Signalment:

Neptune, 8 year old, cm Doberman pinscher

Patient History:

Neptune was admitted to Tufts University Foster Hospital for Small Animals for evaluation of severe dyspnea of ~24 hours duration. Neptune had a previous history of hypothyroidism, chronic limping on left hind leg due to past injury and a 1 1/2 year history of dilated cardiomyopathy (DCM). Medications upon presentation were: Enalapril 10 mg SID; Rimadyl 75 mg PRN; Soloxine 0.8 mg BID; Chondroflex TID. Neptune had been in a boarding kennel for 8 days while the owners were away, and was dyspneic upon returning home. There were no reports of breathing difficulty while at the kennel, but Neptune lost 5# while being boarded. Owners noted heavy breathing, a "gurgling" sound and cough. Owners took Neptune to RDVM, who did not auscult any abnormalities; Neptune was scheduled for a chest radiograph and echocardiogram the following week. The dog seemed calmer at home and was able to sleep, though did not eat; he continued to have pronounced abdominal respiratory effort with cough that evening, which prompted presentation to Tufts.

Patient's Status Upon Presentation:

Upon presentation, Neptune was alert but distressed. He was hypothermic at 99.7 (Fahrenheit), slightly tachycardic at 134 bpm, with increased respiratory rate (RR) of 112 breaths per minute, increased respiratory effort (RE), and respiratory noise / "gurgling". Weight was 97# (44 kg) with a BCS of 5/9. Neptune had a productive cough, bringing up blood-tinged fluid. Lateral thoracic radiographs showed an interstitial and patchy alveolar pattern most severe in the caudal lung fields and perihilar area, most consistent with cardiogenic pulmonary edema; cardiomegaly was noted with a vertebral heart score (VHS) of 13. Further physical exam was not possible due to respiratory distress.

The problem list included: respiratory distress with elevated RR, productive cough, weight loss, cardiomegaly and pulmonary edema. Differential diagnosis included: DCM, left-sided congestive heart failure (LCHF) and historical hypothyroidism.

A poor prognosis was given to the owner on initial presentation.

Initial Diagnostics and Results:

Initially Neptune was placed in an oxygen cage. An intravenous (IV) bolus of Lasix (70 mg - 1.5 mg/kg) was given to begin clearance of fluid from the lungs. Nitroglycerin ointment was applied to the inner surface of the pinna, for its vasodilatory effects in reducing preload (left end-diastolic pressure), as well as afterload (resistance to ejection of blood by the ventricles). An IV catheter was placed. A Dobutamine infusion was started at 5 mcg/kg/min; this was given in 0.9% NaCl @ 10 ml/hr (316 mg of Dobutamine was added to 240 mls of NaCl); the rate was increased to 15 ml/hr after 4 hours. Dobutamine is a direct beta 1 adrenergic agonist with mild beta 2 and alpha 1 adrenergic effects; it is used as a rapid acting positive inotropic agent for short term treatment of CHF.

A CBC / chemistry profile were submitted and were normal with the exception of mildly elevated ALP.

A continuous ECG was initiated, as well as hourly RR / RE checks. Though sinus tachycardia was seen on admission, after a few hours, atrial fibrillation with a rate of 300 bpm was detected. After 20 minutes, a bolus of Diltiazem (0.44 ml - 0.05 mg/kg) was given IV. Diltiazem is a calcium channel blocker that inhibits the transmembrane influx of extracellular calcium ions in myocardial cells and vascular smooth muscle, but does not alter serum calcium concentration; this inhibits cardiac smooth muscle contractility, dilating systemic and coronary arteries, lowering peripheral resistance and blood pressure, and reducing cardiac afterload. Diltiazem also slows AV nodal conduction, prolonging refractory times, and for this reason is used to treat atrial fibrillation.

Daily SOAP Notes - Day 1:

Subjective: mentation was dull, but dog was responsive to sound; mildly dyspneic in oxygen.

Objective: weight: 44 kg; T: 100.1; P: 100; HR: 250-280 bpm with an irregularly irregular rhythm; pulses were weak with pulse deficits and an occasional strong pulse; RR 48 with mild effort; respiratory crackles were heard bilaterally; MM: pink, CRT < 2 sec. PU/PD. No vomiting or diarrhea; appetite was decreased (Neptune did eat a small amount of canned food. Medications included:

1. Lasix 70 mg (1.5 mg/kg) bolus IV X 1; oral Lasix 100 mg (2.3 mg/kg) TID was begun

2. oxygen cage

3. Diltiazem 5 mg (0.11 mg/kg) bolus IV slowly over 30 mins X 2; oral extended release Diltiazem (Dilacor) was started at 60 mg BID

4. Digoxin 0.25 mg (0.01 mg/kg) PO BID was initiated; Digoxin is a positive inotropic agent which causes increased cardiac output, increased diuresis with reduction in edema secondary to a reduction in sympathetic tone, reduction in heart size, heart rate, blood volume and pulmonary and venous pressures; it also causes decreased conduction velocity through the AV node; it is used in veterinary medicine to treat CHF, atrial fibrillation and supraventricular tachycardia.

5. Enalapril 20 mg PO SID (increased from historical dose of 10 mg SID)

6. Soloxine 0.8 mg PO BID

7. Nitroprusside CRI @ 3 mcg/kg/min IV was begun (1.26 ml was added to 60 ml D5W to make a solution 50 mcg/ml and infused @ 15 ml/hr). Nitroprusside is a potent, immediate-acting intravenous hypotensive agent that directly causes peripheral vasodilation (arterial and venous); it causes lowering of blood pressure, increase in heart rate, mild decrease in cardiac output and significant reduction in total peripheral resistance. It is used for the management of refractory CHF, often in combination with Dobutamine. Continuous blood pressure monitoring is critical. The solution needs to be protected from light.

8. Dobutamine was discontinued, due to its potential to worsen tachycardia in atrial fibrillation.

Treatments included continuous ECG monitoring, which initially showed atrial fibrillation with a rate of 240 bpm; this converted to sinus rhythm with a rate of 115 bpm late on the first night after the above medication regimen was given. Blood pressure monitoring showed blood pressure of 110-115 mmHg systolic. An intracath was placed in the left saphenous vein for nitroprusside administration. Catheters were flushed every 4 hours, except for the Nitroprusside catheter.

Lab results were within normal limits.

Nursing notes: Neptune remained somewhat refractory to treatment for LCHF with increased RR and RE and inability to tolerate more than a few minutes out of the oxygen cage; conversion from atrial fibrillation to sinus rhythm, as well as normotension were good prognostic indicators.

Assessment: Cardiogenic pulmonary edema (LCHF) likely secondary to DCM

Plan: Continue current treatments / medications for LCHF

Daily SOAP notes - Days 2 - 5:

Subjective: Neptune was mostly quiet, alert and responsive; on day 5, he was brighter.

Objective: Weight loss of 6 kgs occurred over the 4 days; appetite was poor with no vomiting or diarrhea; he was PU/PD from the diuretics; by day 5, he was eating small amounts of cooked chicken and rice; HR varied from 97 to 170 bpm, with a II/VI systolic murmur PMI left apex, an S3 gallop and occasional arrhythmia (VPCs); RR was 48-80 on the second day with moderate to marked RE in oxygen, gradually slowing to 28-40 with mild RE out of oxygen by day 5. Medications on day 5 (upon discharge) included:

1. Lasix 75 mg (2 mg/kg) PO BID; owner was instructed to give up to 100 mg BID if RE was increased, or to decrease to 50 mg SID to BID if breathing comfortably but seemed weak, lethargic or reluctant to eat

2. Enalapril 20 mg PO AM, 10 mg PM

3. Digoxin 0.25 mg PO AM, 0.125 mg PM

4. Soloxine 0.4 mg PO SID

5. Pimobendan 10 mg PO BID

6. Amiodarone 400 mg PO BID; with instructions to give for 5 days, then decrease to 200 mg BID

Medications were adjusted daily during Neptune's 5 days in the ICU. Lasix was given IM, by IV boluses, as an IV CRI, and orally, usually at a dose of 2-2.3 mg/kg. Enalapril was increased on the last 2 days, to help with forward blood flow, since blood pressure readings remained WNL. Digoxin dose remained the same from days 2-5. Soloxine dose was reduced by half on day 2 due to its pro-arrhythmic, increased afterload and LV oxygen demand properties. Pimobendan was added on day 4; Pimobendan is a phosphodiesterase inhibitor and a calcium channel sensitizer, having positive inotropic properties without increasing myocardial oxygen demand, as well as decreasing sympathetic stimulation; it has been shown to have a significant benefit in veterinary use for the treatment of CHF secondary to DCM and CVD. Amiodarone was added on day 5 for control of ventricular arrhythmias which were refractory to other therapies; Amiodarone is a class III anti-arrhythmic agent with properties including prolongation of myocardial cell-action potential duration and refractory period, and non-competitive alpha and beta adrenergic inhibition. Diltiazem and Nitroprusside were discontinued on day 4 due to general improvement.

Treatments included continuous ECG monitoring, lab work and blood pressure measurements, as well as TPR's; Neptune was able to be moved from the oxygen cage to a regular cage on day 3. Laboratory values showed mild elevation in BUN and decreased sodium, chloride and potassium, all consistent with diuretic administration. On day 3, an echocardiogram was performed which showed a dilated left ventricular chamber with thin walls and markedly depressed systolic function, especially in one region of the free wall, suggestive of possible myocardial infarct. Marked left atrial enlargement was noted, as well as moderate mitral and trivial tricuspid and aortic insufficiencies.

Neptune's condition was somewhat refractory to treatment, and, though more stable on the day of discharge from the hospital, his arrhythmia continued to put him at risk for collapse or sudden death. His complex medication regimen would require careful monitoring of blood values, blood pressure, ECG, respirations, heart rate and appetite. A low sodium diet was recommended, as well as low sodium treats. Exercise restriction was limited to leash walks only, and situations of excessive excitement or anxiety were to be avoided. A recheck in one week was recommended, to include bloodwork and an ECG.

Final Outcome:

Over the next 4 months, Neptune presented for 6 recheck appointments. There was considerable difficulty in adjusting medications to adequately manage heart failure and arrhythmia. Neptune had 2 episodes of decreased appetite and diarrhea due to Digoxin toxicity; Digoxin was discontinued for at least 48 hours each time and restarted at half the previous dose. Renal values showed elevated BUN and decreased sodium, chloride and potassium, all consistent with diuretic administration. On the second recheck, thoracic radiographs showed early LCHF, and the Lasix dose was increased to 75 mg TID for 2 days, with instructions to decrease the dose gradually down to 50 mg BID, with constant RR and RE monitoring by the owner; over the next few months, Lasix was tapered down to 50 mg SID. Liver values became elevated, possibly a result of Amiodarone toxicity; Amiodarone dose was decreased to 150 mg BID; subsequent chemistry profiles showed liver enzymes trending downward, with only mild elevations by the sixth recheck. Hypotension was measured at the fourth recheck, and Enalapril dose was decreased to 10 mg BID. At the sixth recheck, Neptune was doing very well with good appetite, desirable respiratory rate of 24 at home with no extra effort, and a heart rate of ~104 bpm with only occasional arrhythmia. Medications at this time included: Pimobendan 10 mg BID; Enalapril 10 mg BID; Lasix 50 mg SID; Amiodarone 150 mg BID; Digoxin 0.06125 mg BID; Soloxine 0.4 mg SID. DCM and CHF appeared to be well-controlled on the current medical regimen. The plan was to recheck in 2-3 months if continuing to do well.

Discussion of Case:

Dilated cardiomyopathy (DCM) is the term given to diseases in which myocardial failure (or decrease in myocardial contractility) is present. DCM is characterized by a primary increase in left ventricular end-systolic diameter and volume, accompanied by thinning of the LV myocardium and dilation of all cardiac chambers. In most veterinary cases, there is no known etiology for DCM, and it remains an idiopathic disease, except for known causes such as taurine or carnitine deficiency or adriamycin-induced cardiotoxicity. Doberman pinschers account for the vast majority of DCM cases (33% in one study at U.C.- Davis). Because of this breed predilection, DCM is thought to be genetic in origin and most likely heritable. It is most commonly diagnosed in Dobermans between the ages of 7 and 10 years, though can be identified in both younger and older dogs.

Ventricular arrhythmias are a consistent finding in affected Doberman pinschers, and these can be present over a long period during which the dog may have myocardial failure with no clinical signs. Arrhythmias, particularly ventricular tachyarrhythmias and rapid atrial fibrillation, can contribute to the genesis of CHF. In the Doberman pinscher breed, the first diagnosis of the disease is often coincident with the onset of heart failure, as it is common for Doberman to be outwardly asymptomatic until they present in fulminant congestive heart failure.

Common clinical signs of DCM / CHF include dyspnea, tachypnea, cough (which may produce pink-tinged pulmonary edema fluid), weight loss, hypothermia secondary to poor perfusion, episodes of weakness or syncope secondary to arrhythmias. Many Dobermans will die suddenly from their disease, likely as a result of tachyarrhythmias. Once Dobermans have had an episode of heart failure, the short and long term prognosis is poor, and these cases can be difficult to manage, often requiring several adjustments in medical therapy.

Neptune's case demonstrated a typical presentation and management of Doberman pinscher DCM.