Heartbroken: traumatic myocarditis/myocardial contusions

Traumatic cardiac injury is probably not something that many people give much consideration to. When we see dogs and cats that have suffered blunt thoracic trauma we think a lot about the thoracic injuries that can compromise respiration such as pneumothorax or pulmonary contusions. But how often do we wonder how the heart is? Some of the potential consequences of traumatic cardiac injury include: reduced contractility, even resulting in cardiogenic shock; dysrhythmias; haemorrhage including into the pericardial space; and potential rupture.

Some traumatic cardiac injuries are more spectacular and significant than others. I imagine that animals with the most severe cardiac injuries make up a reasonable proportion of the ones that die before we ever see them. Some of the more spectacular and unusual injuries that have been reported in the literature include for example Gerbode defect (Hezzell et al, 2011), bradydysrhythmia with 3rd degree AV block (Nicholls et al, 1995) and right atrial rupture (Witt et al, 2000).

But undoubtedly what is more common is so-called traumatic myocarditis or myocardial contusion, trauma-induced bruising of the myocardium. Histopathological findings in such cases might include subendocardial, subepicardial, and intramyocardial haemorrhage, as well as acute degeneration or necrosis of muscle fibres. As with other types of contusions these will clearly vary in their severity and their clinical significance. In some cases, traumatic myocarditis may declare itself by giving rise to sometimes quite spectacular dysrhythmias, typically ventricular in nature; for example see Macintire, Snider, 1984. These are often animals that have sustained severe impact and typically have other injuries too. Suspecting cardiac injury in these cases is less of a challenge. It should also be noted that the myocardial injury in such cases is likely multifactorial in origin; aside from the contusion, other relevant sources of myocardial injury might include hypoxic insult if shock has occurred or oxygenation is poor or the effects of reactive oxygen species/inflammatory mediators.

One test that can be run to confirm the presence of myocardial cell injury is to measure plasma cardiac troponin (cTn) concentration. I am not going to elaborate much on this here suffice to say that there are different forms of cTn; both cTnI and cTnT are meant to increase quickly and reliably when myocardial cell injury occurs and cTn is specific to the myocardium (a test with good specificity and sensitivity). Another marker that has been used to detect myocardial cell injury is CK-MB but it is probably less useful as levels can rise with not just myocardial but also skeletal muscle injury; the latter is also likely to be present in these blunt thoracic trauma patients.

A small number of reports can be found in the veterinary literature describing cTn measurement in patients with blunt thoracic trauma, e.g. Burgener et al (2006), DeFrancesco et al (2002), Dinizl et al (2007), Schober et al (1999). One question that we must ask is what is the point of measuring cTn in such cases? Say I have a patient with thoracic trauma and dysrhythmias, it is extremely likely that this patient has some degree of traumatic myocarditis/myocardial contusion. There is no specific therapy for this other than supportive care, treating dysrhythmias if they are clinically significant, and a good old tincture of time. Measuring cTn in such a case will give me an indication of how severe the injury is but it does not in itself afford other treatment options or prompt other decisions to be made. The half-life of cTn is relatively short such that it should decrease relatively quickly; serial cTn measurements (e.g. after 48-72 hours) could be used to provide evidence that myocardial cell injury is not on-going. Personally I have only ever measured plasma cTn concentration in those cases that also had significant dysrhythmias; unsurprisingly it has come back as high and consistent with myocardial injury…I have really wanted to know how high the cTn concentration was in these patients for my own interest and have obtained consent from the pet’s carer all the while explaining the background usefulness or otherwise. Was it money well spent?

I should say that my own personal experience of patients with thoracic trauma and significant dysrhythmias is limited to dogs. Despite having seen many more cats than I care to remember that have suffered thoracic trauma, typically due to vehicular injury, I do not recall dysrhythmias as something that has stood out. I wonder whether that is because those that sustain severe enough injury to cause dysrhythmias die before presentation. Maybe?

What about echocardiography? If we did echocardiography soon after presentation in all patients with blunt thoracic trauma, would we note any decreases in cardiac contractility either focally or globally? Ultrasound is being used more and more by emergency veterinary surgeons for a variety of uses. This started with looking for free fluid in various sites but now we are also doing emergency scans of the heart for contractility, left atrial size and pericardial effusion. I wonder if as we scan more and more of these trauma cases we will detect anything interesting about their contractility.

I imagine that at least for dogs that present following blunt thoracic trauma the incidence of traumatic myocarditis or myocardial contusion may be higher than we know. However in many cases it is occurring in a sub-clinical way without causing any clinically significant consequences…or at least no consequences that we are sophisticated enough to detect. In that regard I suppose we could ask well who cares then? Traumatic myocarditis/myocardial contusion: often overlooked – with good reason?

Is this something you have ever given much thought to?

 

Papers mentioned:

Burgener IA, Kovacevic A, Mauldin GN, Lombard CW. Cardiac Troponins as Indicators of Acute Myocardial Damage in Dogs. J Vet Int Med 2006. 20:277–283.

DeFrancesco TC, Atkins CE, Keene BW, et al. Prospective Clinical Evaluation of Serum Cardiac Troponin T in Dogs Admitted to a Veterinary Teaching Hospital. J Vet Int Med 2002. 16(5): 553-557.

Dinizl PPVP, Schwartzll DS, Collicchio-Zuanazel RC. Cardiac trauma confirmed by cardiac markers in dogs: two case reports. Arq Bras Med Vet Zootec 2007. 59(1).

Hezzell M, Dennis S, Lewis DH, Luis Fuentes V. Gerbode defect associated with blunt trauma in a dog. J Vet Cardiol 2011. 13:141-146.

Macintire DK, Snider TG. Cardiac arrhythmias associated with multiple trauma in dogs. J Am Vet Med Assoc 1984. 184(5):541-5.

Nicholls PK, Watson PJ. Cardiac trauma and third degree AV block in a dog following a road accident. J Sm Anim Pract 1995. 36(9):411-415. [Had an atrial septal tear]

Schober KE, Kirbach B, Oechtering G. Noninvasive assessment of myocardial cell injury in dogs with suspected cardiac contusion. J Vet Cardiol 1999. 1(2):17-25.

Witt AL, Mathews KA, Holmberg DL. Successful Management of Traumatic Right Atrial Rupture. J Vet Emerg Crit Care 2000. 10(2):85-89.