Postmortem diagnosis of venous air embolism in a Wielkopolski horse

In a standing horse, venous air embolism associated with an open blood vessel may occur if a pressure gradient develops between the catheter entry point into the jugular vein and the right atrium. A catheter directed toward the heart promotes air aspiration, whereas a catheter directed toward the head promotes bleeding. ¹¹ The entry of a small amount of air into a vein is generally harmless, as small air bubbles can diffuse through the alveolar-capillary membrane into the pulmonary circulation. ¹¹ A small amount of air can reduce cardiac output and perfusion of the lungs, heart, brain, and other organs. ⁴ However, the entry of a large volume of air into the circulation poses a serious threat. A large volume of air can obstruct the right ventricular outflow tract, leading to obstructive shock and acute cardiovascular failure. ¹³ Reports indicate that 0.25 mL of air per kg of body weight or a single injection of 100 mL into the jugular vein may not cause clinical signs in horses, but a 500-mL injection can result in sudden death.^9,10

In human pathology, postmortem computed tomography (CT) prior to autopsy is the method of choice for suspected air embolism.^2,7 Radiography and MRI are also mentioned in the literature as useful methods.^5,6 In veterinary medicine, ultrasound was reported as a diagnostic tool for venous air embolism in 2 horses. ³ A brain infarct was also detected by MRI in a horse 17 mo after the event. ¹¹ However, these have been isolated cases.

In contrast to imaging, the Richter method, developed in human medicine, provides a definitive diagnostic approach to venous air embolism at autopsy when imaging is unavailable or inconclusive. This method can only be applied to fresh cadavers and relies on specific modifications of the autopsy technique.^8,12 The skull must not be opened before the thoracic cavity to prevent postmortem air suction caused by negative venous pressure. The sternum is removed only below the second rib to prevent damage to the subclavian veins. The pericardium is opened and filled with water. The right ventricle is punctured underwater to check for rising gas bubbles. Similarly, the left ventricle is also punctured. If gas is present only in the right ventricle, it indicates pulmonary embolism. If only a few gas bubbles are observed, they are usually considered incidental findings. A large or moderate volume of gas suggests fatal pulmonary air embolism. Air in the left atrium and ventricle may indicate an open foramen ovale, air passage through pulmonary capillaries, or improper preparation technique. However, it is most often a result of putrefaction, rendering the air embolism test invalid. The technique is assumed to be applicable to cooled corpses up to 2-d postmortem.^8,12 The validity of the Richter method and its advantage over standard autopsy techniques for diagnosing venous air embolism were supported in one study. ¹⁴

A 9-y-old female Wielkopolski horse was presented to the clinic with an acute injury to the hoof capsule of the left hindlimb. The horse underwent surgical treatment under general anesthesia. Both the surgical procedure and the recovery period were uneventful. To facilitate regular administration of anti-inflammatory and antibiotic medications, a permanent intravenous catheter (IV catheter 14 G × 13 cm, extended use; Mila International) was placed under aseptic conditions in the left jugular vein. The catheter was connected to a 10-cm extension line (Microextension with clip; Walter) and sealed with a pierceable plug. On postoperative d 9, the horse was found in left lateral recumbency in its stall. The animal was unresponsive, had bilateral horizontal nystagmus, and pale mucous membranes. The pulse was weak, and ~2 L of blood were observed near the horse’s neck. The plug of the intravenous catheter was missing, and the locking clip of the extension line was open. The exact time the catheter remained open could not be determined, but it is estimated to have been up to 1.5 h since the last examination, when the infusion tube was still properly connected to the catheter. Resuscitation efforts were initiated immediately, including compression of the left jugular vein, intravenous administration of adrenaline, infusion of Ringer solution via a right-sided intravenous catheter, and cardiac massage. Unfortunately, these measures were unsuccessful, and the horse could not be resuscitated.

Given the severity of the acute clinical problem, ultrasound was not possible in our case. We attempted a postmortem radiograph of the heart in dorsal recumbency. Unfortunately, the heart was severely displaced due to a postmortem diaphragmatic hernia. It was not possible to perform an assessment; only intestinal contents could be detected in the chest cavity (Fig. 1). CT and MRI were impossible due to the limited size of the gantry.

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Figure 1.

Postmortem sinistrodextral radiographic image of the thoracic cavity of our case in dorsal recumbency. The thoracic cavity of the horse is almost completely overlaid with nonhomogeneous intestinal contents within the cecal apex (arrows) due to postmortem diaphragmatic herniation. The heart is displaced far to the cranial side and cannot be assessed. Collapsed lung tissue is suspected. The free air in the thorax is suggested to be a postmortem artifact. Figure 2. Thoracic cavity of the horse, opened from the right side. The head is on the right of the figure. Postmortem diaphragmatic rupture with displacement of the cecal apex (arrow) into the thoracic cavity.

The autopsy was performed ~38 h postmortem, with special emphasis on the venous circulatory system of the neck and thorax. A 2.1-mm diameter catheter was present in the left jugular vein directed towards the heart, with a 10-cm open, unplugged extension. Both the catheter and the extension were secured to the skin with 2 individual sutures each. A 2.1-mm plugged catheter was observed in the right jugular vein, secured to the skin with a single suture.

The horse was positioned in left lateral recumbency to optimize access to the right side of the heart for examining the atria and venous sinuses in situ. The skin of the neck and thoracic inlet was dissected and reflected. All major blood vessels, including the cranial and caudal vena cava, as well as the right subclavian vein, were clamped near the heart using arterial clamps. Subsequently, the musculature between the right forelimb and thorax was incised ventrally to dorsally, and the limb was retroflexed and secured in a laterodorsal position. The right ribs were partially removed by making 2 cuts starting from the second rib: one lateral to the sternum and another approximately at the upper third of the chest. Within the thoracic cavity, we observed a postmortem rupture of the diaphragm and prolapse of the cecal apex into the thoracic cavity (Fig. 2), consistent with the radiographic findings.

The pericardium was opened on its right lateral side and filled with water (Fig. 3A). Before opening the myocardium, an assistant submerged the heart beneath the water surface (Fig. 3B). The right atrium and ventricle were incised separately with a scalpel. This revealed gas bubbles rising from the right atrium and ventricle (Fig. 3C; Suppl. Video). The same procedure was applied to the left atrium and ventricle, revealing no gas bubbles.

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Figure 3.

Adaptation of the Richter method to diagnose venous air embolism in a horse. A. The pericardium is opened on the right lateral side and filled with water. B. An assistant submerges the heart beneath the water surface. C. Upon incision of the right atrium, gas bubbles (arrow) escape.

Following the venous air embolism test, we conducted the autopsy according to our standard protocol. Minor adherent thrombi were observed at the puncture sites in both jugular veins (Fig. 4); their low grade rendered them clinically insignificant. Pulmonary congestion, alveolar emphysema, and edema were diagnosed and suspected to be agonal changes.

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Figure 4.

Left jugular vein of the horse. A small thrombus (arrow) is attached to the catheter and the adjacent venous endothelium.

The autopsy confirmed venous air embolism, with significant gas bubbles escaping from both the right atrium and ventricle. Hence, venous air embolism was determined to be the cause of death, and obstructive shock the direct mechanism of death. In the cascade of events leading to death, air bubbles obstruct the right ventricular outflow tract and the pulmonary circulation, maximizing resistance in the pulmonary vessels and causing acute overload on the right heart, while at the same time preventing blood return to the left atrium. No gas was detected in the left atrium and ventricle, and no foramen ovale was present. If doubts arise about whether the detected gas is of putrefactive origin, a chemical-toxicologic examination can be performed.^1,2,8 Although gas was detected, we did not measure its volume and quality. For such analysis, a spirometer and headspace tubes would be needed to aspirate and store the gas for subsequent analysis. ¹ In some human cases of air embolism, histopathology has revealed organized fibrin precipitates in the lumens of small pulmonary arterial branches, with visible rounded lacunae assumed to be air bubbles. ² In our case, histologic examination revealed only agonal changes in the lungs. Research indicates that specific histologic findings for either venous or arterial air embolism are lacking. ⁸ Thus, the diagnosis of fatal venous air embolism is primarily a macroscopic diagnosis.

Veterinary pathologists should be familiar with the adapted Richter method for diagnosing air embolism in large animals. This method is particularly valuable for determining the cause of death in peracutely deceased animals when imaging methods are unavailable or inconclusive.