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A. L. Goldman , DVM , MS , and S. L. Beckman , DVM

©Veterinary Medical Association, 1989. All Rights Reserved

A 9-year-old 6.1-kg castrated male domestic shorthair cat was referred after being hit by a car approximately 9 hours earlier. The cat had been clinically normal until the time of trauma.  The referring veterinarian had taken pelvic radiographs, which were evaluated further and revealed an oblique fracture of the right ilium, right-sided iliosacral luxation, and tight-sided pubic fracture.

The urinary bladder was not clearly visible radiographically, and the referring veterinarian reported being unable to palpate the bladder.  He further reported that the cat had not urinated while under his care, a period of approximately 6 hours.

The cat was depressed but responsive, with rectal temperature of 37.4 C (100 F).  The mucous membranes were pale pink, and the capillary refill time was 1 second.  Thoracic auscultation revealed heart rate of 180 beats/min, normal sinus rhythm, and no murmurs.  There were no pulse deficits, and the lungs had mildly increased bronchovesicular sounds bilaterally.

Abdominal palpation elicited moderate pain response in the caudal portion of the abdomen, and the urinary bladder was approximately 5 cm in diameter.  There was a 5-cm laceration over the medial aspect of the left hock and abrasions to the right flank and lateral portion of the abdomen.  The penis protruded from the prepuce, was dry, discolored, and flattened at its most distal 0.5 cm, and there was a blood clot in the distal 3 mm of the penile portion of the urethra.

A catheter was placed in a cephalic vein; blood samples were withdrawn, and lactated Ringer solution was infused at a rate of 25 ml/h.  Blood samples were submitted for a CBC and serum biochemical analysis.  The PCV (30%). and total protein (6.9 g/dl) and BUNa (>60 mg/dl) concentrations were determined immediately Abdominocentesis was performed in an effort to detect uroperitoneum; however, fluid was not aspirated.

Abdominal radiography confirmed the aforementioned pelvic fractures and sacroiliac luxation.  The urinary bladder was in the caudal portion of the abdomen, well below the pelvic brim. Thoracic radiography was unremarkable.  The hock laceration was cleansed and partially sutured, and amoxicillin was given (20 mg/kg of body weight) and repeated every 12 hours.  The penis was cleansed, lubricated with sterile lubricant,b and replaced within the prepuce.  Orthopedic repair of the pelvic fractures was planned pending evaluation of urinary tract function.

The cat had not urinated for 4 hours after referral, and abdominal palpation revealed the urinary bladder to be approximately the same size as before, despite IV administration of fluids.  A urethral catheter was placed with some difficulty; repeated retrograde flushing with sterile saline solution and gentle prodding with the catheter allowed its passage into the penis.  From that point, the catheter passed easily; however, urine did not flow from it.  Attempt at aspiration of urine by use of a 5-cc syringe also was nonproductive.

In an effort to assess catheter position, 0.5 ml of 20% diatrizoate sodiumc was flushed retrograde into the catheter, and pelvic radiography (lateral view) was performed (Fig 1).  This revealed the catheter passing through the penis and then curving ventrocaudally in a gentle arc, with its tip apparently lodged in the tissues of the thigh.  The bladder was still visible in the caudal portion of the abdomen and was approximately the same size as in the radiographs taken earlier that day.  The catheter was palpable subcutaneously on the medial aspect of the right thigh. Thus, ruptured urethra was suspected.

Intraveneous pyelography was performed to evaluate the status of the upper urinary tract (Fig 2). Results revealed the ureters and bladders to be intact and functional.

Permission to perform surgery to repair the suspected urethral tear was obtained.  The cat was anesthetized by use of thiamylal sodium and halothane and was prepared in routine manner for celiotomy.  During anesthesia, continuous ECG monitoring was maintained.  A caudal midline celiotomy incision was made, and the urinary bladder was exteriorized.  The bladder was partially distended, but intact, and appeared untraumatized.  Cystotomy was performed, and normal appearing urine flowed from the incision.

A soft rubber catheter (No. 5 F) was introduced into the bladder through the cystotomy incision and was advanced into the urethra to assist in localizing and assessing its patency.  The urethra was traced caudally and found to be completely ruptured at the caudal end of the pelvic portion of the urethra (the preputial fornix).  The urethra was lying in the deep tissues of the inguinal region.  These tissues, as well as the subcutaneous adipose tissue in this region, were swollen and edematous.

After placement of Penrose drains in the subcutaneous tissues of the caudoventral portion of the abdomen, we decided to close the cystotomy and celiotomy incisions and proceed with perineal urethrostomy.

The cat was prepared in routine manner for perineal surgery.  After the skin incisions were made, the urethra was located in the deep tissues of the perineum by use of minimal dissection (Fig 3).  Urethrostomy was completed satisfactorally and the cat recovered from anesthesia without complications.  The decision to repair the pelvic injuries depended on successful recovery from the urethral injury, the type of surgical repair procedure, and the attending metabolic derangements associated with azotemia.

After surgery fluid administration was changed to 5% dextrose in lactated Ringer solution, with added 20 ml of sodium bicarbonate/L and was infused at a rate of 45 ml/h.  The hypertonicity of this solution and the high rate of infusion were selected to initiate diuresis in an effort to improve renal function and resolve the azotemia.  Sodium bicarbonate was added to help counter suspected metabolic acidosis, because blood gas analysis was not available.  The excised penis and prepuce were dissected after surgery and the site of urethral avulsion was found.

Urinary tract injuries are common in animals with pelvic trauma. One study1 reported that 62% (175/281) of animals with urinary tract trauma had ruptured urinary bladder, whereas 11% (31/281) had ruptured urethra.  Another prospective study2 of urinary tract trauma in 100 dogs with pelvic fractures revealed ruptured urinary bladder in 7, compared with 5 that had ruptured urethra.

Although by no means common, urethral injury does occur and should be suspected in animals with a history of pelvic trauma, and intact urinary bladder without urine flow after catheterization.  Nonproductive attempts at abdominocentesis can be misleading, because leaking urine from a ruptured urethra may remain retroperitoneal or within tissue planes.

In retrospect, azotemia, lack of urination during the 13 hours after trauma, and the unchanged size of the palpable urinary bladder in spite of IV administration of fluids provided enough evidence of urinary tract disruption to indicate performing uroradiography even without catheterization of the cat.

From South Shore Veterinary Associates, 595 Columbian St, South Weymouth , MA 02190 .

aAzostix, Miles Laboratories Inc, Elkhart , Ind.

bSurgilube, E. Fougera and Co, Melville , NY .

cHypaque sodium 20%, Winthrop Laboratories, New York , NY .

1.         Kleine U , Thorron GW. Radiographic diagnosis of urinary tract trauma. J Am Anim Hosp Assoc 1971;7:318—327.

2.         Selcer BA . Urinary tract trauma associated with pelvic trauma J Am Anim Hosp Assoc 1982;18:785—793

A. L. Goldman , DVM , M S

Reprinted from the JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION, Vol. 200, No. 12 Pages 1970-1972.
©American Veterinary Medical Association. 1992. All Rights Reserved.

A 10-year-old 7-kg castrated domestic shorthair car was examined because of lethargy, decreased appetite, and weight loss of several months’ duration.  The owner also believed the cat to be drinking more water than in the past.  Weigh loss of 2kg over the preceding 12 months was evident from the medical record.

The cat appeared depressed and had a matted, unkempt coat. The cervical region was extended, and the head was held low and directly in front of the body.  The cat was afebrile (37.8 C), obese, and hydrated.  Palpation revealed the cervical region to be rigidly extended with tense musculature.  A hard mass was palpable in the midcervical region.  Neurologic examination did not reveal abnormalities, except the rigidly extended neck.

The cat had been evaluated 5 months earlier because of lethargy, change-of-voice, a lump in the neck, and abnormal “staring.”  At that time, the diet was reported to be dry-pelleted cat food and fresh beef liver.  Results of physical examination, CBC, serum biochemical analysis, and thyroxine evaluations done at that time were within normal limits.  Also, cervical and thoracic radiographs at that time were considered normal.

At this evaluation, cervical radiography revealed a bone-dense, cervical mass ventral to the C1-C2 intervertebral space (Fig 1).  The substance of this mass was intimately associated with these vertebrae.  Much of the normal vertebral architecture appeared to be obliterated, and the trachea and cervical soft tissue were deviated ventrally and laterally.  The dorsal spinous processes of cervical vertebrae C3 and C4 were abnormally large.

Thoracic radiography revealed ventral, vertebral bony proliferation extending from thoracic vertebrae T2 through T7, with the most severe lesions associated with T2 through T5 (Fig 2). In addition, the sternebrae were similarly involved, with marked bony proliferation evident throughout the length of the sternum and along several of the costal cartilages. The most caudal costal cartilages were most severely affected.

Retrospective evaluation of the cervical and thoracic radiographs taken at the original examination 5 months earlier revealed the cervical vertebral and thoracic vertebral and sternal lesions, respectively.  The thoracic vertebral lesion was less severe at that time, although the other lesions were well developed.

This cat was still on a diet of dry-pelleted cat food and fresh beef liver daily.  The history physical examination findings and radiographic signs are consistent with a clinical diagnosis of hypervitaminosis A.

Blood samples were withdrawn and submitted for a CBC, serum biochemical analysis, feline leukemia virus antigen test (ELISA),a and a serum vitamin A assay.  The CBC revealed leukocytosis (WBC = 20, 800 cells/dl) and mature neutrophilia (16,432 segmented neutrophils/dl).  Serum hiochemical analysis revealed mild hyperglycemia (glucose = 217mg/dl) and hypercholesterolemia (cholesterol = 270 mg/dl).  The feline leukemia virus antigen test result was negative.  Serum vitamin A concentration was markedly high (315.4 µg/dl; normal, 20 to 80 µg/dl).

Hypervitaminosis A in the cat was first described as deforming cervical spondylosis.1 The pathophysiologic characteristics of the disease were later described by Seawright et al,2 in Australia .  Numerous investigators later recognized the disease in other parts of the world.3,4  The disease is usually caused by the excessive intake of vitamin A through diets high in raw liver, usually beef or sheep liver.  Excessive intake of vitamin A supplements can also produce the disease.

The disease develops most commonly in cats from 2 to 9 years old, and no breed or gender predilection has been recognized. Months or years of a diet high in liver precede signs of toxicosis.5 Early in the disease, cats are lethargic and resent handling.  After several months, cervical stiffness or forelimb lameness may develop.  Signs of cutaneous pain over the cervical and forelimb regions increase as osseous proliferation impinges on spinal nerves6.  Ankylosis follows in the cervical diarthrodial joints.  The elbows and occasionally the shoulders maybe affected, as well as the rest of the spine.

Additionally, an unkempt coat, weight loss, constipation, and a kangaroo-like sitting posture may be seen.  An unkempt coat is likely a result of the affected cat’s inability to groom.  Weight loss and constipation can he attributed to inactivity and muscle atrophy.  The kangaroo-like sitting posture is likely a sign of spinal ankylosis.2

In this case, the history was suggestive of the disease.  The cat was examined because of lethargy, signs of depression, and anorexia.  A diet high in raw beef liver was mentioned.  Although the owner described increased thirst, evidence of polydipsia or polyuna was not found.  However, a urinalysis was not done.  The physical examination findings of rigidly extended head and neck cervical mass, and unkempt coat are also characteristic of hypervitaminosis A.

The history and physical examination findings obtained at first examination, 5 months earlier, were also suggestive of hypervitaminosis A. A diet high in raw liver, a voice change, weight loss, and a staring posture are characteristic of this syndrome.  The voice change perceived by the client was probably attributable to direct pressure by the ventral cervical vertebral mass of proliferative bone on the larynx, laryngeal muscles, and nerves.

The radiographic lesions of bony proliferation of the cervical vertebrae, the sternum, and the costal cartilages are characteristics of the disease.  The cervical vertebral and sternal lesions were apparent in the earlier radiographs; however, the thoracic vertebral lesion was less pronounced, compared with the later radiographs.

In cases of hypervitaminosis A, laboratory findings are nonspecific.  Neutrophilic leukocytosis is consistent with a stress leukogram: however lymphopenia and eosinopenia were not found.  Hyperglycemia is common in cats stressed by disease or hospitalization.  Hypercholesterolemia, often found in cats with hyperthyroidism was not explained in this case.  Thyroxine concentration at the first examination was normal; however, it was not evaluated at the second examination.  The finding of high serum vitamin A concentration (4 times normal) was suggestive of hypervitaminosis A.  The serum alkaline phosphatase activity was normal in this cat, although Riser et al3 reported it to he high in one case.

The cat of this report was given a single intramuscular injection of 1 mg of dexamethasone sodium phosphate and was discharged from our hospital.  We prescribed 13 mg of phenylbutazone to be given PO every 12 hours for analgesia.  The owner was advised to cease the feeding of liver and to feed only a balanced feline diet.  The owner was further advised to encourage the cat to eat with treats and handfeeding.  A follow-up appointment was not kept, and evaluation of the case was lost to follow up.

Six months later, the cat was euthanatized for reasons unrelated to the condition of hypervitaminosis A.  It was reported that the cat had been eating fairly well, although the stiff-necked posture remained.

A necropsy was performed.  The cat was slightly thin, and the cervical region and skull were rigidly extended and immobile.  A firm mass was palpable in the ventral, midcervical region. The skull, cervical portion of the spine, and thoracic cage were dissected free and cleaned of their respective soft tissues.

Severe cervical vertebral spondylopathy was found from the atlanto-occipital articulation caudal to the third thoracic vertebral body.  The entire cervical spine was solidly fused, and bony proliferation was evident on all sides of the vertebrae.  Many of the intervertebral foramina were virtually obliterated by new bone formation.  A large bony mass was ventral to the C1-C2 intervertebral interspace.  The sternum and costal cartilages were obscured by a 0.5-cm-thick collar of bone, which was brittle.

On the basis of findings in the cat of this report, I recommend that in the case of any sick cat on a diet consisting wholly or partly of raw liver, hypervitaminosis A should be suspected.  The feeding of raw liver should he stopped and a balanced feline diet instituted.  Analgesics should be used as required.  Those cats that are anorectic should be evaluated for concurrent disease and treated appropriately.  With the cessation of feeding of raw liver, progression of lesions will stop and pain will lessen; however, ankylotic lesions will remain.

From Warwick Animal Hospital , 1950 Elmwood Ave , Warwick , RI 02888 . Dr. Goldman ’s present address is The Animal Medical Center, 510 E 62nd St. New York City , NY 10021 .

aLeukassay FII, Pitman-Moore Inc, Washington Crossing, NJ.

1. Seawright AA , English PB. Deforming cervical spondylosis in the cat. J Pathol Bacteriol 1964;88:503—509.2. Seawright AA , English PB, Gartner RJW. Hypervitaminosis A of the cat. Adv Vet Sci Comp Med 1970;14:1—27.

3. Riser WH, Brodey RS, Shirer JF . Osteodystrophy in mature cats: a nutritional disease. J Am I Vet Radiol Soc 1968; 9:37 —46.

4. Lucke VM, Baskerville A, Bardgett PL, et al. Deforming cervical spondylosis in the cat associated with hypervitaminosis A. Vet Rec 1968:82:141—142.

5. English PB, Seawright AA. Deforming cervical spondylosis of the cat. Aust Vet J 1964;40:376—381.

6. Herron MA . Hypervitaminosis A. In: Bojrab MJ,ed. Pathophysiology in small animal surgery. Philadelphia : Lea & Febiger, 1981:685—686.

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