History
A 2-day-old 44-kg (97-lb) purebred female Holstein calf was evaluated for weakness, signs of depression, and inability to stand unsupported. Immediately after birth, the calf could stand and was tube fed with approximately 4 L of colostrum. Twenty-four hours after birth, the calf was standing and suckled its daily requirement of milk replacer, but 48 hours after birth, the calf was recumbent and only drank half of its 2-L morning milk replacer feeding. The owner had treated the calf with 100 mg of tulathromycin that morning. On initial examination, rectal temperature (39°C [101.5°F]) and heart rate (120 beats/min) were within reference ranges, but the respiratory rate was high (100 breaths/min; reference range, 30 to 60 breaths/min). Auscultation of the lungs revealed bronchovesicular sounds with no crackles or wheezes. Given the high respiratory rate in the absence of fever or auscultable pulmonary changes, a venous blood gas analysis was performed to rule out metabolic acidosis as a cause of the high respiratory rate. Findings included a pH of 7.28 (reference range, 7.35 to 7.50) with a high PCO2 (79.7 mm Hg; reference range, 34 to 45 mm Hg), bicarbonate concentration (36.3 mEq/L; reference range, 20 to 30 mEq/L),1 and total CO2 concentration (38.6 mEq/L; reference range, 20 to 20 mEq/L)1 consistent with respiratory acidosis with metabolic compensation. Respiratory acidosis in the face of the high respiratory rate suggested either shunting of blood away from the respiratory tract or diffusion impairment in the lungs. A suitable arterial sample could not be obtained for an arterial blood gas analysis. To further evaluate the lungs and heart, radiographs of the thorax were obtained (Figure 1).
Right lateral (A) and dorsoventral (B) radiographic views of the thorax of 2-day-old 44-kg (97-lb) female Holstein calf that was evaluated for weakness, depression, and inability to stand.
Citation: Journal of the American Veterinary Medical Association 234, 6; 10.2460/javma.234.6.739
Determine whether additional imaging studies are required, or make your diagnosis from Figure 1—then turn the page →
Diagnostic Imaging Findings and Interpretation
A severe unstructured interstitial pattern mixed with a patchy alveolar pattern is evident; it is most severe in the perihilar region but extends to include the entire caudodorsal lung fields (Figure 2). The ventral aspect of the caudal segment of the left cranial lung lobe has an alveolar pattern with faint air bronchograms. Pulmonary vessels are partially obscured by the severity of pulmonary parenchymal changes on the lateral view, but on the dorsoventral view, the right pulmonary artery and vein are enlarged. The radiographic diagnosis is cardiogenic pulmonary edema secondary to a congenital heart defect. The most likely anomaly is a ventricular septal defect or patent ductus arteriosus. The alveolar pattern in the ventral left cranial lung lobe is the result of bronchopneumonia caused by aspiration, sepsis, or an atypical distribution of pulmonary edema.
Same radiographic views as in Figure 1. On the lateral view (A), notice the area of severe mixed interstitial and alveolar pulmonary pattern (black arrows) in the perihilar region that obscures the caudal vena cava. A faint air bronchogram is observed in the dependent caudal segment of the left cranial lung lobe (white arrow). The dorsoventral view (B) has considerable obliquity, but a peripheral pulmonary mixed interstitial and alveolar pattern is evident. Notice the enlarged right caudal pulmonary artery (black arrows) and the enlarged pulmonary vein (white arrows).
Citation: Journal of the American Veterinary Medical Association 234, 6; 10.2460/javma.234.6.739
Comments
Echocardiography was performed and revealed a 2-cm-diameter opening in the middle portion of the interatrial septum (Figure 3). A large, loose membranous flap was observed extending from the margins of the defect into the left atrium. The defect was most consistent with a patent foramen ovale. The right ventricle had moderate hypertrophy. The blood flow velocity out of the pulmonary artery was normal on continuous-wave Doppler, ruling out pulmonic stenosis. However, pulmonic valve regurgitation was moderate to severe. The velocity of pulmonic regurgitation measured 3.4 m/s, equivalent to a pressure gradient of 46 mm Hg (reference range, 8 to 10 mm Hg), which indicated pulmonary diastolic hypertension. A 3-mL bolus of agitated saline (0.9% NaCl) solution was injected into a jugular catheter, revealing right-to-left shunting across the foramen ovale during systole that was indicative of severe pulmonary hypertension. In early diastole when right ventricular pressure was low, mild left-to-right shunting through the defect was observed. The echocardiographic diagnosis was patent foramen ovale with bidirectional shunting.
Right parasternal 4-chamber long-axis echocardiograms of the same 2-day-old female Holstein calf as in Figure 1 before (A) and after (B and C) administration of a bolus of agitated saline (0.9% NaCl) solution. Notice the large defect in the middle portion of the interatrial septum and loose membranous flap (dashed arrow) extending from the margins of the defect into the left atrium (LA). Right-to-left shunting of the hyperechoic bubbles is evident (B) as they fill the right atrium (RA) and right ventricle (RV) and can be seen streaming across the patent foramen ovale. A small number of bubbles can be seen in the left ventricle (LV) as well. Hyperechoic bubbles are observed in the LA and LV during the late phase filling (C).
Citation: Journal of the American Veterinary Medical Association 234, 6; 10.2460/javma.234.6.739
A CBC revealed leukopenia characterized by neutropenia with a left shift, neutrophils with toxic changes, and lymphopenia and a low Hct; findings were consistent with sepsis caused by gram-negative bacteria.
Treatment included intranasal oxygen, antimicrobials, flunixin meglumine, and furosemide. The calf's condition worsened, and the calf was euthanatized 5 days later.
A large patent foramen ovale and a 2-mm-diameter patent ductus arteriosus were found on necropsy. Approximately 40% of the right lung and 25% of the left lung were dark red and firm, and some sections did not float in formalin. Histologically, the pulmonary parenchyma was hyperemic with many bronchi and bronchioles containing foreign material (food) and inflammatory cells consistent with aspiration and acute bronchopneumonia.
Cattle have a highly reactive pulmonary vasculature,1 and insults such as endotoxemia, hypoxemia, and cold weather can induce pulmonary hypertension. If pulmonary arterial pressure equals or exceeds systemic pressure, right-to-left shunting can occur through a patent foramen ovale or ductus arteriosus. In this calf, the severe pulmonary hypertension was most likely secondary to aspiration pneumonia and septicemia. Although this calf had a pulmonary pattern in the left cranial lung lobe suggestive of aspiration pneumonia, radiographic changes in the caudodorsal portion of the lungs were most consistent with cardiogenic edema.
Anderson FL, Sutton RB, Tsagaris TJ, et al. Spontaneous pulmonary hypertension in the bovine. Am J Physiol 1972;222:561–564.
