Case 1

A 12 year-old intact male Poodle with history of CCVHD since several years ago. Was treated with Vetmedin, Fortekor, Sildenafil, Furosemide. Noted more coughing and increased respiratory effort in these few nights. Patient was presented last night due to acute collapse, weakness and incontinence. Physical examination found muffled heart sound, crackle lung sound and tachypnea. Chest radiograph revealed severe cardiomegaly, globoid cardiac silhouette, with clear lung fields.

Echocardiographic findings:

1.1

Fig. 1. Right parasternal long axis four chamber view. Massive pericardial effusion and secondary cardiac tamponade.

2.1

Fig. 2. Homogeneous echogenic object in pericardial sac, surrounding the ventricles.

3.1

Fig. 3 Right parasternal short axis view at papillary muscle level. Large homogeneous echogenic object in pericardial sac.

4.1

Fig. 4. Right parasternal heartbase short axis view. Severe left atrial enlargement documented, LA/Ao ratio = 2.32.

5.1

Fig. 5 Left parasternal apical four chamber view. Large homogeneous echogenic object in pericardial sac.

6.1

Fig. 6. Left parasternal apical four chamber view. Severe mitral valve regurgitation documented. Note there is some echogenic objects in pericardial sac.

Echocardiographic diagnosis:

  • Severe pericardial effusion, cardiac tamponade, clot formation in pericardial sac
  • Left atrial tear/rupture, most likely secondary to severe LA enlargement and CCVHD
  • LA enlargement(can be underestimated due to rupture)
  • Stage C CCVHD
  • Mild TR, no pulmonary hypertension
  • Ventricular arrhythmia

Discussion:

Left atrial rupture is a rare consequence of CCVHD in dogs, accounting 2% of all causes of pericardial effusion. It is more common in male dogs, and uncommon in cats. It is mostly acute onset due to rapid accumulation of blood in the pericardium, causing cardiogenic shock and death from a smaller amount of fluid than other causes of pericardial effusion. Diagnosis of left atrial rupture requires echocardiography, however, absence of a thrombus within the pericardial space may not rule out left atrial rupture, as if the accumulation of the blood was slow or if the rupture did not occur acutely, large visible clots may not be seen due to fibrinolysis.

Acute treatment of left atrial rupture is pericardiocentesis if cardiac tamponade is presented. The wound on left atrium maybe obstructed by the clot, and after pericardiocentesis, diuretics are recommended to decrease LA pressure and size. However, if the wound is not obstructed, bleeding may recur and the prognosis would be very poor.

Although rare, left atrial rupture resulting in pericardial effusion should be considered in older small- to medium-sized dogs presenting with collapse, and dyspnea.

Case 1 is written by Dr Eason, December 2017

Reference:

  1. Erica L. Reineke et al. Left atrial rupture in dogs: 14 cases (1990-2005). Journal of Veterinary Emergency and Critical Care 18(2) 2008
  2. Reid K. Nakamura et al. Left Atrial Rupture Secondary to Myxomatous Mitral Valve Disease in 11 Dogs. J Am Anim Hosp Assoc 2014

Ventricular Septal Defect

Chai is a 7 months old Male Mongrel diagnosed with a grade III/VI systolic heart murmur during routine consultation. He was presented for a check prior to considering desexing surgery.

ULTRASONOGRAPHIC FINDINGS:

There is presence of a high membranous ventricular septal defect, just cranial to the aortic valves. VSD flow velocity from left to right is 5.5 M/S.

VSD is a relatively common defect in the cat, but uncommon in the dog.  VSD is a malformation of the interventricular septum, which allows blood to flow from the left side to the right side (high to low pressure). This causes volume overload of the pulmonary circulation, left atrial and left ventricular dilation and can result in left sided heart failure. Clinical signs vary on the size of the defect. With small (“ resisitive”) defects, patients are asymptomatic except for a loud harsh (typically right sided) systolic murmur and may have a normal quality and length of life.

With large (“ non- resistive”) defects, the heart murmur may be softer, but clinical signs related to pulmonary over circulation may develop, such as left sided heart failure or pulmonary hypertension. If pulmonary hypertension is severe enough to result in reversal of blood flow from the right to the left ventricle, cyanosis will occur. This is referred as “ Eisenmenger: s syndrome”. Treatment of this is similar to right- to left shunting PDA.

Echocardiography is used to visualize the defect (if large) and Doppler is used to assess blood flow through the VSD. Dilation of the left atrium and left ventricle can also be assessed, although this can also been observed on thoracic radiography, along with the absence of pulmonary over circulation and pulmonary edema.

Therapy depends upon the size of the VSD. If the defect is small, no therapy is required as a normal full life can be expected. Otherwise, the treatment is usually restricted to managing signs of heart failure or cyanosis if present. Closure with obstructive device might be possible and referral to a board certified cardiologist for management is always a reasonable option for congenital heart defects.