Case Studies In Small Animal

Cardiovascular Medicine

Home Up 1    Pleural Fluid 2              Cough 3   Heart Murmur 4           Syncope 5       Tachypnea 6           Cyanosis 7   Heart Murmur 8   Heart Murmur 9              Cough 10    Heart Failure 11              Ascites 12    Pleural Fluid 13           Syncope 14     Bradycardia 15     Tachycardia 16                Blind 17   Heart Murmur 18   Resp. Distress 19        Collapsing 20    Heart Failure 21          Paralysis 22    New Murmur 23              Cough 24          Vomiting 25       Tachypnea 26   Heart Murmur 27      Hemoptysis 28  Limb Swelling 29  Heart Murmur 30 Acute Collapse 31 Enlarged Heart 32               Blind 33             Cough 34         Collapse 35         Collapse 36 Thromboembolus 37  Heart Murmur 38  Heart Murmur

Diagnosis

Case 16

Signalment

bullet14-year-old FS miniature schnauzer cross weighing 8 kg ("Mitzie")

Presenting Complaints

bulletBumping into objects, weakness

Pertinent History

bulletMitzie was brought to her veterinarian 3 weeks ago for a routine examination. Blood work was submitted as a pre-screen for a proposed dental procedure. The blood work: BUN 106, creatinine 4.1, PO4 10.8, Ca 11.9, K 6.1, cholesterol 330, amylase 3,470, lipase 757, RBC 5.3, and PCV 41%. The referring DVM was concerned about renal disease and a possible pancreatitis and/or neoplasia. Mitzie was admitted, treated with 700 - 900ml 0.9% NaCl per day for three days, and with 6cc Amphojel and 250mg Cefazolin BID. During her hospital stay, Mitzie was not eating well and vomited repeatedly. Blood work 6 days later: BUN 75, creatinine 4.0, PO4 12.1, RBC 4.3, and PCV 33%. The Ca, K, cholesterol, amylase, and lipase were within normal limits. Mitzie was sent home on the Amphojel and 400mg amoxicillin BID. The owners report that when Mitzie returned home she continued to vomit and refuse food. She bumped into objects in the house, was very ataxic, collapsed frequently, got stuck in corners, and appeared to circle to the left. Repeat blood work 1 week ago: BUN 75 and creatinine 3.1. Mitzie was given 350ml 0.9% NaCl IV and her medications were discontinued. She continued to show signs of disorientation, weakness and inappetence.

Physical Examination

bulletAlert and responsive to touch or loud noises. Stands with left elbow rotated axially. Very ataxic and weak in all four limbs but worse in the front. Collapses with thoracic limbs abducted. Wanders restlessly in the exam room, runs into objects, and gets into corners and pauses before moving on. Eyes: cloudy lenses OU. Severe tartar and moderate gingivitis. HR=150, irregular rhythm. Panting. No menace response, normal PLRs, anisocoria - OD>OS, positional horizontal nystagmus with the fast phase to the right. All tendons were hyporeflexic. Conscious proprioception absent in the front limbs and depressed in the hind limbs.

Problems

bulletHistorical renal insufficiency
bulletAtaxia
bulletVisual impairment
bulletNystagmus
bulletArrhythmia

Plans and Progress Notes

First Day

bulletProblem 1 - Historical renal insufficiency. S/O: Most recent blood work on Mitzie from the referring veterinarian shows an elevated BUN and creatinine.  A: Mitzie's history of renal insufficiency is very concerning. Although she was brought to the VMTH for a work-up of her ataxia and acute visual impairment, we feel that her renal parameters are more critical at this time. P: CBC, Chem Panel Lipase, Urinalysis w/ P:C ratio, blood pressure measurement, and abdominal ultrasound. Offer her water q 4hrs, feed k/d disguised with something tastier. Carry outside to urinate.
bulletProblem 2 - Ataxia. S/O: Stands with left elbow rotated axially. Very ataxic and weak in all four limbs but worse in the front. Collapses with thoracic limbs abducted. Hyporeflexic tendon responses and absent CPs in the thoracic limbs, diminished in the hind. A: When watching Mitzie walk around, it appears that her ataxia and collapsing are due to weakness. She has not been eating well and she could be suffering from uremia. The lack of CPs could also be due to weakness. On the other hand, there could be a neurologic basis to her unsteadiness. She does exhibit some other neurologic abnormalities (see problems 3 and 5). If this is the case, we feel that her metabolic problems are more of a threat to her well-being at this time. Neurologic disease will not be pursued at this time. P: See problem 1.
bulletProblem 3 - Visual Impairment. S/O: Wanders restlessly in the exam room, runs into objects, and gets into corners and pauses before moving on. Eyes: cloudy lenses OU. No menace response, normal PLRs, and intact blink response to tactile stimulation. A: Mitzie is able to blink so we can assume that CN III is intact. We need to assess whether or not the lack of menace is due to damage to CN II or its associated tracts, or there is a problem in the eye with the retina or optic disc. Acute onset of the visual impairment associated with the renal insult makes us suspicious that Mitzie has suffered retinal hemorrhage as a result of hypertension from her renal disease. P: Ophthalmology consult to R/O a problem of the eye.
bulletProblem 4 - Nystagmus. S/O: Positional horizontal nystagmus, fast phase to the right. Anisocoria OD>OS. A: The presence of nystagmus in Mitzie adds to our suspicion of neurologic disease. It could be from a primary neurological abnormality or related to a metabolic encephalopathy. We will first rule out metabolic disease. P: See problem 1.
bulletProblem 5 - Arrhythmia. S/O: Questionable arrhythmia on cardiac auscultation. A: We felt that the heart rhythm was abnormal but we were unable to assess the nature of the arrhythmia. P: Cardiology consultation. Thoracic radiographs (also performed because of her advanced age).

Second Day

bulletProblem 1: Historical renal insufficiency. S/O: CBC: RBC 5.92, PCV 45%, WBC 18,300 - mild neutrophilia and monocytosis. Chem panel: BUN 124, creatinine 6.5, PO4 14.5, Ca 13.2, K 6.1 and cholesterol 385. Ultrasound: bilateral abnormal renal architecture, left renal cortical cysts, mineralized left adrenal gland and mild hepatomegaly. A: The elevated values on the blood chemistry panel in conjunction with the abnormal renal architecture are consistent with chronic renal failure. The mineralized adrenal gland is the result of the PO4 and Ca imbalances. The damaged kidney fails to excrete PO4 leading to secondary hyperparathyroidism. Increased PTH, activation of the renin-aldosterone-angiotensin system, and sodium retention lead to volume expansion and hypertension. Hypertension could be the cause of many of the Mitzie's signs, so we need to measure her blood pressure. P: Urinalysis with P:C ratio and blood pressure measurement. Start Mitzie on 0.9% NaCl at 30ml/hr IV (maintenance rate), start her on a diet of cottage cheese and rice. Repeat blood work after overnight fluid therapy. Rename Problem 1 to Problem 6 - Chronic renal failure.
bulletProblem 3 & 4: S/O: Optho consult: anisocoria - OD; bilateral retinal hemorrhages - severe.
bulletProblem 5: S/O: Thoracic radiographs: prominent aorta. Cardio consult: Thickened left ventricle, intermittent tachycardia and second degree AV block. A: The cardiac arrhythmia may be consistent with metabolic disease - chronic renal failure in this instance. The left ventricular thickening and prominent aorta could be explained by hypertension. P: Correct electrolyte abnormalities with fluid therapy and look for hypertension. See plan for problem 1.

Third Day

bulletProblem 6: S/O: Lethargic, weak, alert. No menace bilaterally. T=101.4,Wt=10.8 kg. BUN 125, creatinine 4.9, PO4 12.7, Ca 10.7, K5.5, cholesterol 330. Urinalysis: S.G. 1.011 with 1+ protein on dipstick, urine protein 85, creatinine 39.2, P/C 2.17. Blood pressure measurement performed (Dinamap): systolic=185 mm of Hg, diastolic=133 mm of Hg, mean=153 mm of Hg. Pulse=168 beats/minute with an erratic rhythm. A Doppler was done to confirm elevated pressures, which showed a systolic of 190 mm of Hg. Mitzie is urinating large amounts  of very dilute urine. A: Mitzie's chronic renal failure has caused hypertension, which most likely explains the retinal hemorrhages bilaterally that caused her blindness. Her BUN is still very high on 1 1/2 times maintenance 0.9% NaCl plus 1 mg/kg/min mannitol. We will increase her fluid rate to 2x maintenance and continue the mannitol at the same rate, and recheck her kidney panel. She also has a marked hyperphosphatemia, which is also caused by chronic renal failure. We will start her on a phosphate binder with her meals to try to decrease that value.
bulletNew problem 7: HYPERTENSION A: Mitzie has severe hypertension which can explain her ataxia and central neurologic signs and retinal hemorrhages. We need to treat this aggressively due to severity. P: We will begin with diltiazem at 1.5 mg/kg PO TID and recheck blood pressure tomorrow. If no improvement, we will increase the dose to 2 mg/kg.
bulletProblem 2:A: Mitzie continues to be ataxic. We think this is a combination of weakness and possibly bleeding in her brain due to hypertension. We will try and control her hypertension, however this may be permanent damage. P: Control hypertension, see problem 7 plan.
bulletProblem 3: A: Mitzie has bilateral retinal hemorrhages as the cause of her acute blindness. A problem in clotting and hypertension are the two main rule outs for bilateral retinal hemorrhages. Since she has severe hypertension, this is the most likely cause. Treatment of the hypertension may resolve the blindness, however there is a chance it could be permanent. P: Treat the hypertension (see problem 7) and monitor daily. Rename to problem 8 Retinal Hemorrhages (bilateral).

Fourth Day

bulletProblem 6: Chronic Renal Disease S/O: Mitzie is eating better. She seems to be less weak, and possibly less ataxic. Still no menace. We can't see the horizontal nystagmus. BUN=61, CR=3.1, Phos:8.2. BP still at 190 mm of Hg systolic and 130 mm of Hg diastolic. A: Mitzie's renal values have decreased with diuresis, which probably increased her appetite and decreased her weakness. However if this is chronic, her values most likely will increase once we taper the fluids. As she is a small dog, she is a candidate for SQ fluids. We will continue to keep her at 2x maintenance until tonight, when we will decrease back to 1 1/2x maintenance. We will also discontinue the mannitol at that time. P: Begin tapering her off her fluids this evening and discontinue mannitol.
bulletProblem 7: Hypertension. A: We have still not controlled the blood pressure, which is our biggest concern. We will increase the dosage of diltiazem to 2 mg/kg TID and recheck blood pressures tomorrow morning. P: Increase diltiazem to 3/4 tablet (22.5 mg) PO TID and recheck blood pressures. If no change, switch medications to prazosin.
bulletProblem 2: Ataxia: A: Mitzie's ataxia seems to be resolving, however she is also becoming stronger, so it is hard to differentiate. If it is resolving, it may indicate the hypertension did not cause permanent damage. P: Request a neurology consult to fully evaluate if she is improving.

Fifth Day

bulletProblem 7: Hypertension. S/O BARH, P=144, RR=18. Repeat BP indicates systolic of 185 (done with Doppler in ICU). Appetite is good. Much stronger than yesterday. Still urinating large amounts. Still no menace. Neurology feels she is not as weak, however they feel her ataxia is the same. A: Hypertension has not improved so we will switch to prazosin .5 mg PO TID. Again, we will recheck pressures in the morning. We will send her home tomorrow, as we feel she is stable to go home and will recover better there. She will continue on the prazosin. We will recheck her on Tuesday, and evaluate her blood pressures again. If normal, we will repeat the echocardiogram and ECG to reevaluate her arrhythmia. P: Start prazosin .5 mg TID PO. Recheck blood pressures in the morning. Send Mitzie home tomorrow and recheck her on Tuesday.
bulletProblem 6: Chronic Renal Failure: A: Although Mitzie is improved, we are afraid that this episode has increased damage to the kidneys. Therefore, we are going to taper her off fluids to maintenance this morning and 1/2 maintenance tonight, and then send her home on SQ fluids. We will also continue the Basalgel at home, and start Pepcid AC 1/2 tab SID to protect her stomach against ulcers that are common in chronic renal failure. P: Taper fluids to 33mls/hr this morning, and then again to 16 mls/hr this evening, discontinue tomorrow. Send Mitzie home on 150-200 mls SQ LRS BID, Pepcid AC 1/2 tab (5 mg) PO SID, Basalgel 1/2 capsule (250mg) in food BID. Recheck her kidney values on Tuesday when she comes in to check her hypertension.

Sixth Day

bulletProblem 7: Hypertension: S/O Mitzie is again stronger today, and is eating and drinking well. She is still urinating normally and defecated a large amount of normal stool today. Systolic pressure 195 mm of Hg, diastolic = 133 mm of Hg, mean = 155 mm of Hg. Still no menace, still very ataxic but not weak. A: We have not improved her hypertension at all. We will increase prazosin to 1 mg TID PO, and send her home on that dose to recheck her pressures on Tuesday. If normal, we will recheck her echocardiogram and ECG.
bulletProblem 6: Chronic Renal Failure: P: We taught owners how to administer SQ fluids, which they did well, although they were worried they wouldn't have any success. They will bring in Mitzie on Tuesday for a recheck of her kidney values.

Discharge Summary

bulletMitzie was admitted due to acute onset of marked ataxia and apparent blindness. She was referred to Medicine due to marked azotemia, retinal hemorrhages and suspected hypertension. Systemic arterial blood pressure was 195 mm of Hg systolic and 133 mm of Hg diastolic, which was uncontrolled during entire visit, despite switching medications and increasing dosages. Diuresis decreased azotemia, but due to chronic nature of disease we sent her home on Basalgel, SQ LRS, and Pepcid AC to help control the symptoms. We will be seeing her for a recheck on Tuesday.

Two days later

bulletPatient is hypertensive. Pressure was measured at 8:30 am. It was 177 mm of Hg systolic and 133 mm of Hg diastolic with a mean (average) of 156 mm of Hg.

 

Mark D. Kittleson, D.V.M., Ph.D. All rights reserved.