53 Lameness Ischaemia INTRODUCTION Arterial thromboembolism produces limb ischaemia and either paresis or paralysis, depending on the degree of occlusion and amount of collateral circulation. This is most common in the cat and may be the first sign of cardiac disease. More than 70% of cats with this condition have an underlying cardiomyopathy. It is rare in the dog and risk factors include cardiac disease, hyperadrenocorticism, disseminated intravascular coagulation (DIC), protein-losing nephropathy or enteropathy, heartworm, AIHA, neoplasia and sepsis. A saddle thromboembolism (TE) forms at the aortic trifurcation in 90% of affected cats. Clinical signs result from ischaemia of the cauda equina and hindlimb muscles. The proximal limb may retain voluntary movement while the distal limb is paralysed, or vice versa. Tail function and anal tone may be intact. Trauma or neoplasia to the cauda equina tends not to be so selective. Muscles particularly the gastrocnemius and cranial tibial muscles are firm, painful and swollen. Acute thrombosis also occurs in single limbs causing transient or permanent paresis/paralysis. Owners may report transient signs as lameness. Acute and chronic onset of signs have been reported in dogs aged 5–10 years of age. Chronic onset (>24 hr) produces exercise intolerance and pain (restlessness, refusal to move, vocalization from palpation along the spine) for weeks to months prior to diagnosing the causative aortic thromboembolism. The femoral pulse was abnormal in all dogs. Minimal neurological deficits were present. Abdominal ultrasound was 100% successful in demonstrating the thromboembolism. Muscle enzymes were generally within normal limits (cf. acute onset <24 hr). Survival times ranged from 1 month to 2 years. Cavalier King Charles spaniels comprised the majority of dogs affected, although larger breeds were not spared. The dog featured in Figure 53.1 presented with a 24-hour history of shifting hindlimb lameness followed by an arched back and then sudden paraplegia on the day of referral. Femoral pulses were absent bilaterally but the hind paws were warm until they became cold 2 hours later. The right quadriceps femoris muscle was firm and were painful when touched as were the lumbar epaxial muscles. Pain perception and spinal reflexes were absent in both hind limbs. The cause was thought to be a hypercoagulable state from a protein-losing glomerulonephropathy. The dog was euthanized as the prognosis for long-term normality was guarded and the pain was extreme. Figure 53.1 Non-selective angiography of a 9-year-old male collie cross with aortic thromboembolism. (photo courtesy of Dr Jacques Sottiaux). SIGNALMENT A 6-year-old neutered male domestic longhaired cat. CASE PRESENTING SIGNS Intermittent shifting lameness. CASE HISTORY Lethargy, inappetance and weight loss had been present for 2 months. At 6 weeks prior to referral, a 3-day duration of right hindlimb dragging occurred. Three weeks after this improvement, the left fore pad was swollen, had lost fur and was painful, and 48 hours later still, the hindlimbs were dragged on waking up from sleep. One week later, the hindlimbs were momentarily seen to be dragged and the right forelimb was lame and non-weight-bearing. This improvement was followed by the hindlimbs being dragged again which subsequently improved in the 4 days prior to referral. There had been bowls of rat bait in the kitchen but it was not known if the cat had had access to any of it. CLINICAL EXAMINATION The neurological examination found a very quiet but mentally alert and responsive cat with voluntary movement in both hindlimbs but more so in the right hind. The tail had voluntary movement and anal tone was present. The patellar reflex was normal bilaterally. The hindlimbs flexed by hip movement. The forelimb withdrawal reflex was normal. Cranial nerve and fundus examinations were normal. The gastrocnemius muscles were firm and felt enlarged but were not painful. The femoral pulses were poor/very difficult to feel but all paws felt warm and as warm as each other. The respiratory rate was 56 bpm at rest and there was a visible respiratory effort, HR = 140. Only gold members can continue reading. Log In or Register to continue You may also needLMN paresis and paralysis: Flaccid tailThe haematochezic or dyschezic cancer patientLeaks, dribbles urineOtogenic intracranial infectionMiddle ear diseaseEndocrine emergenciesDefecation: Faecal incontinenceChronic feline keratitis Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window)Click to share on Google+ (Opens in new window) Related Tags: Saunders Solutions in Veterinary Practice Small Animal Neurology Sep 3, 2016 | Posted by admin in SMALL ANIMAL | Comments Off on Lameness: Ischaemia Full access? Get Clinical Tree
53 Lameness Ischaemia INTRODUCTION Arterial thromboembolism produces limb ischaemia and either paresis or paralysis, depending on the degree of occlusion and amount of collateral circulation. This is most common in the cat and may be the first sign of cardiac disease. More than 70% of cats with this condition have an underlying cardiomyopathy. It is rare in the dog and risk factors include cardiac disease, hyperadrenocorticism, disseminated intravascular coagulation (DIC), protein-losing nephropathy or enteropathy, heartworm, AIHA, neoplasia and sepsis. A saddle thromboembolism (TE) forms at the aortic trifurcation in 90% of affected cats. Clinical signs result from ischaemia of the cauda equina and hindlimb muscles. The proximal limb may retain voluntary movement while the distal limb is paralysed, or vice versa. Tail function and anal tone may be intact. Trauma or neoplasia to the cauda equina tends not to be so selective. Muscles particularly the gastrocnemius and cranial tibial muscles are firm, painful and swollen. Acute thrombosis also occurs in single limbs causing transient or permanent paresis/paralysis. Owners may report transient signs as lameness. Acute and chronic onset of signs have been reported in dogs aged 5–10 years of age. Chronic onset (>24 hr) produces exercise intolerance and pain (restlessness, refusal to move, vocalization from palpation along the spine) for weeks to months prior to diagnosing the causative aortic thromboembolism. The femoral pulse was abnormal in all dogs. Minimal neurological deficits were present. Abdominal ultrasound was 100% successful in demonstrating the thromboembolism. Muscle enzymes were generally within normal limits (cf. acute onset <24 hr). Survival times ranged from 1 month to 2 years. Cavalier King Charles spaniels comprised the majority of dogs affected, although larger breeds were not spared. The dog featured in Figure 53.1 presented with a 24-hour history of shifting hindlimb lameness followed by an arched back and then sudden paraplegia on the day of referral. Femoral pulses were absent bilaterally but the hind paws were warm until they became cold 2 hours later. The right quadriceps femoris muscle was firm and were painful when touched as were the lumbar epaxial muscles. Pain perception and spinal reflexes were absent in both hind limbs. The cause was thought to be a hypercoagulable state from a protein-losing glomerulonephropathy. The dog was euthanized as the prognosis for long-term normality was guarded and the pain was extreme. Figure 53.1 Non-selective angiography of a 9-year-old male collie cross with aortic thromboembolism. (photo courtesy of Dr Jacques Sottiaux). SIGNALMENT A 6-year-old neutered male domestic longhaired cat. CASE PRESENTING SIGNS Intermittent shifting lameness. CASE HISTORY Lethargy, inappetance and weight loss had been present for 2 months. At 6 weeks prior to referral, a 3-day duration of right hindlimb dragging occurred. Three weeks after this improvement, the left fore pad was swollen, had lost fur and was painful, and 48 hours later still, the hindlimbs were dragged on waking up from sleep. One week later, the hindlimbs were momentarily seen to be dragged and the right forelimb was lame and non-weight-bearing. This improvement was followed by the hindlimbs being dragged again which subsequently improved in the 4 days prior to referral. There had been bowls of rat bait in the kitchen but it was not known if the cat had had access to any of it. CLINICAL EXAMINATION The neurological examination found a very quiet but mentally alert and responsive cat with voluntary movement in both hindlimbs but more so in the right hind. The tail had voluntary movement and anal tone was present. The patellar reflex was normal bilaterally. The hindlimbs flexed by hip movement. The forelimb withdrawal reflex was normal. Cranial nerve and fundus examinations were normal. The gastrocnemius muscles were firm and felt enlarged but were not painful. The femoral pulses were poor/very difficult to feel but all paws felt warm and as warm as each other. The respiratory rate was 56 bpm at rest and there was a visible respiratory effort, HR = 140. Only gold members can continue reading. Log In or Register to continue You may also needLMN paresis and paralysis: Flaccid tailThe haematochezic or dyschezic cancer patientLeaks, dribbles urineOtogenic intracranial infectionMiddle ear diseaseEndocrine emergenciesDefecation: Faecal incontinenceChronic feline keratitis Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window)Click to share on Google+ (Opens in new window) Related