2 Ways To Perform A Pericardial Window For Trauma: Part 1 with Video!

In this two-part post, I’ll describe two ways to perform a pericardial window for trauma. The pericardial window should be considered in any trauma patient who has one of the following:

  • A suspected diagnosis of pericardial tamponade. These patients do not yet have classic signs and symptoms. If they did, a thoracotomy or sternotomy is in order, not a window.  But they do have a mechanism that could produce bleeding into the pericardial sac, and a positive imaging study. Typically, this study is a FAST exam of the heart. Occasionally, pericardial fluid may be seen on chest CT. This is uncommon but significant when detected.
  • An injury in proximity to the heart that is of concern for cardiac injury with a negative or indeterminant FAST. These are typically penetrating injuries so close to the heart that it’s hard to believe it wasn’t injured. If the FAST is not helpful, a window will make the definitive diagnosis.

Pericardial window is a very invasive procedure. For trauma, it is usually performed in the operating room and requires general anesthesia. It could be performed in the ED if the patient is already intubated and sedated.

There are two ways to perform this procedure. Today, I’ll discuss the old-timey subxiphoid approach.  The equipment required is minimal:

  • Scalpel
  • Tissue (Metzenbaum) scissors
  • Once or two toothed forceps
  • Your finger
  • Good lighting

A 4-8 cm incision is made extending from the top of the xiphoid, extending about 4 cm down onto the abdominal midline. Enter the retrosternal space with your finger, and head to the heart. Usually, some fatty tissue must be bluntly dissected out of the way. Note: the heart is frequently further away than you think!

Sweep the fat out of the way, exposing the pericardium. Grasp the pericardium with the toothed forceps and tent it away from the heart. Use the Metzenbaum scissors to incise the pericardium immediately adjacent to the forceps. If this is difficult, then have an assistant grasp the pericardium with another pair so a short line of pericardium is elevated. (Note: sometimes having a second set of forceps in the incision makes it too difficult to see, which is why I prefer the single forceps technique).

Make sure that the wound is bloodless when you incise the pericardium! There is always at least a small amount of pericardial fluid that will squirt out, and you are looking at its color. If it is anything but amber, you have a positive result. If you have a bloody field that contaminates the fluid, a false positive diagnosis could occur leading to an unnecessary thoracotomy.

If the window is positive, cover the wound and head immediately to the OR if your’re not already there. Your patient has a cardiac injury until proven otherwise. If negative, then close the skin wound with your sutures / staples of choice. Do not attempt to close the tiny pericardial hole!

Here’s a video that shows the basic technique. The procedure depicted is being performed for non-trauma, so the operator takes his time. He has the luxury of dissecting and exposing the field well. But in trauma, we don’t usually have time to resect the xiphoid or take 10 minutes to dissect out the field.

In my next post, I’ll discuss the technique that is used if you already find yourself in the abdomen when a cardiac injury is suspected.

Best Of EAST #10: MTP With Whole Blood

Here’s one last abstract to consider before the EAST meeting kicks off this afternoon. Every trauma center must have a massive transfusion protocol (MTP). But not every one has access to whole blood. And whole blood is all the rage now for transfusion in the trauma world.

Believe it or not, we must still ask the question “is using whole blood safe?” More than 50 years ago, all we had was whole blood. But we didn’t use it in trauma the way we do today. And we didn’t have the tools then to determine whether there were any adverse effects from its use. Now we do, and we are slowly rediscovering the nuances of using it. Some work has shown that small volumes of whole blood appear to be safe. But there is little information on the safety of using large volumes in MTP.

The group at Oregon Health Sciences University in Portland attempted to do this with a quick shot paper to be presented tomorrow morning. They reviewed their experience over a two year period. For the first 18 months, they used standard component therapy (PRBC + plasma + platelets) in their MTP. For the final six months, they used cold-stored uncrossmatched, low-titer group O blood. Any patient who had MTP activated and received even a single unit of blood was included in the study. 

Here are the factoids:

  • 83 patients received component therapy and 42 received whole blood; demographics were the same
  • The component therapy patients received an average of 6 PRBC, 5 plasma, and 0 platelets; the whole blood group received 6.5 units (4 PRBC, 4 plasma, and 1 platelets based on the usual composition of a unit)
  • Plasma:RBC ratio was 0.8:1 for the component group and 0.94:1 in the whole blood group (statistically significant, but not clinically significant, see below)
  • The authors described a component-equivalent unit of product which is not defined. It was 12 for component therapy and 27 for whole blood.
  • There were no differences in 24-hour or 30-day mortality, and no transfusion reactions

The authors concluded that MTP using whole blood is feasible, and that it appeared to be safe and effective. They also commented that it may lead to more balanced resuscitation.

My comment: Alright, this is the last time I’ll mention study power (for a while). If a study does not have the statistical power to show a difference between groups, then seeing no difference means nothing. The absence of a difference does not mean that the two groups are equivalent. And this study of 125 patients is small potatoes for showing any difference in a crude outcome like mortality.

Besides having a small number of subjects, the average number of units given was low for an MTP. For most trauma centers, this was just over one cooler of products. Although ISS was 29, the patients don’t sound like they had huge blood replacement requirements, so it’s no wonder that mortality was the same between the two groups.

And finally, the statement about more balanced resuscitation is open to debate. The difference between 0.8 units of plasma and 0.94 units is 35cc per unit of red cells given, a little over 1 tablespoon. It’s hard to believe that this would ever make a difference clinically.

To those who read only the title or the conclusion of an abstract (or paper for that matter), beware. The devil is in the details. This study is a good start toward addressing the question posed, but needs several hundred more subjects (and a lot more blood products given) to close in on an answer.

Reference: Massive transfusion with whole blood is safe compared to component therapy. EAST Annual Assembly Quick Shot #8, 2020.

Best Of EAST #9: Is TXA Associated With VTE?

Most trauma programs can be divided into two types: those that believe in tranexamic acid (TXA) and those that don’t. I won’t get into the details of the CRASH-2 study here. But those centers that don’t believe usually give one of two reasons: they don’t think it works or they think the risk of venous thromboembolism (VTE) is too high.

EAST put together a multi-institutional trial to see if there was an association between TXA administration and subsequent VTE. The results are being reported as one of the paper presentations at the meeting this week. A retrospective study of the experience of 15 trauma centers was organized. A power analysis was preformed in advance, which showed that at least 830 patients were needed to detect a positive result.

Adult patients who received more than 5 units of blood during the first 24 hours were included. There were a lot of exclusionary criteria. They included death within 24 hours, pregnancy, pre-injury use of anticoagulants, interhospital transfer, TXA administration after 3 hours, and asymptomatic patients that had duplex VTE surveillance (huh?). The primary outcome studied was incidence of VTE, and secondary outcomes were MI, stroke, length of stay, and death.

Here are the factoids:

  • There were 1,333 eligible patients identified, and 887 (67%) received TXA
  • Females were significantly (over 2x) more likely to receive TXA (46% vs 19%)
  • 80% of patients given TXA received VTE prophylaxis, whereas only 60% of those who did not receive TXA got prophylaxis (also significant)
  • TXA patients had a statistically significantly higher ISS (27) compared to non-TXA patients (25) but this is not clinically significant
  • Mortality in the TXA group was significantly lower (17% vs 34%)
  • The number of units of blood, plasma, and platelets transfused were significantly lower in the TXA group
  • VTE rate appeared lower in the TXA group, but once multivariate analysis was applied, there was no difference

The group concluded that there was no association between TXA and VTE, but that it was linked to decreased mortality and transfusion need.

My comment: This was a study done the way they are supposed to be! Know your objectives and study outcomes up front. Figure out how many patients are needed to tease out any differences. And use understandable statistics to do so.

But, of course, it’s not perfect. No retrospective study is. Nor is any multi-institutional trial. There are lots of little variations and biases that can creep in. But the larger than required sample size helps with reducing the noise from these issues.

Basically, we have a decent study that shows that the clinical end points that we usually strive for are significantly improved in patients who have TXA administered. We don’t know why, we just know that it’s a pretty good association.

This study shows that the usual reasons given for not using TXA don’t appear to hold true. So hopefully it will convert a few of the TXA non-believers out there. I’m excited to hear more details during the presentation at the meeting.

Reference: Association of TXA with venous thromboembolism in bleeding trauma patients: an EAST multicenter study. EAST Annual Assembly, Paper #13, 2020.

Best Of EAST #8: Early vs Late Full Anticoagulation In TBI

Trauma professionals are always reluctant to anticoagulate TBI patients with demonstrated blood in their head. In recent years, we’ve become more comfortable providing prophylactic doses of low molecular weight heparin after a suitable period. This is typically 24-48 hours after a stable head CT in patients with select types of intracranial hemorrhage (ICH) who are at increased risk for venous thromboembolism.

But what about therapeutic dose anticoagulation in these patients? Let’s say that you have a patient with ICH who has developed a significant pulmonary embolism (PE)? Is is safe to give full dose anticoagulation? And if so, when?

The group at Shock Trauma in Baltimore attempted to answer this in one of the EAST Quick Shot presentations scheduled for this week. The did a retrospective review of 4.5 years of their own data on these patients. They specifically selected patients who had both ICH and PE and compared those who received full anticoagulation within 7 days of injury vs those who were dosed after 7 days. Outcomes studied included death, interventions for worsening ICH, and pulmonary complications.

Here are the factoids:

  • A total of 50 patients had both ICH and PE, but only the 46 who received therapeutic anticoagulation were analyzed
  • 19 patients (41%) received early anticoagulation, and 27 received it late (59%)
  • There were 4 deaths in the early group (2 from the PE, 1 from multi-system organ failure, 1 from the TBI) vs none in the late group, and this was statistically significant
  • 3 patients in the early group (18%) vs 2 in the late group (7%) had an increase in their ICH (p=0.3), and none required intervention

The authors concluded that their study failed to show any instances of clinically significant progression of ICH after anticoagulation, and that it is not associated with worse outcomes, even if started early. Thus they recommend that ICH should not preclude full anticoagulation, even early after injury.

My comment: I always say that you shouldn’t let one paper change your practice. Even a really good one. In order to ensure that you are providing the best care, more work must always be done to confirm (or refute) the findings of any provocative research. And this little Quick Shot, with little opportunity for questions from the audience, should definitely not change it!

The major issues to consider here are common ones: 

  • This was a retrospective study and it does not appear that any guideline was followed to determine who got early vs late anticoagulation. So who knows what kind of selection bias was occurring and how the surgeon decided to prescribe anticoagulation? It’s very possible that patients with a “bad CT” were put into the late group, and the not so bad ones in the early group. This would bias the results toward better outcomes in the early anticoagulation group.
  • It’s also a very small study that is extremely underpowered. The authors comment on the fact that the outcomes of the early group were not worse than the late group. However, looking at their sample size (46) shows that they would only be able to show differences if they were about 5x worse in the early group. They would realistically need about 350 total patients to truly show that the groups behaved the same. Their small numbers also preclude saying that there were no ICH progressions. There very well could have been if 300 more patients were added to the series.
  • And isn’t death a significant outcome? The authors indicated that 2 of the 4 deaths were a result of the PE. Yet there was a significant association (p=0.02) of increased death in the early anticoagulation patients that can’t be discounted.

Bottom line: It’s way too early to consider giving early anticoagulation to patients with ICH and pulmonary embolism. It may very well be shown to be acceptable, eventually. But not yet. And a much bigger prospective study will be required to confirm it.

Reference: Therapeutic anticoagulation in patients with traumatic brain injuries and pulmonary emboli. EAST Annual Assembly Quick Shot #7, 2020.

Best Of EAST #7: Is There A Relationship Between Number Of Transfusions And Infection?

It has long been known that blood transfusion decreases immunocompetency for a period of time. This has been taken advantage of in transplant surgery for decades. And blood transfusions are used liberally in major trauma. So could blood transfusion make it more likely for a trauma patient to suffer complications such as pneumonia, sepsis, and surgical site infections?

The group at the Massachusetts General Hospital explored this possibility. The analyzed four years of TQIP data, examining patients who received blood transfusions within four hours of arrival. They excluded transfers in, patients with incomplete transfusion counts, and those who died within 48 hours.

They focused on pneumonia, sepsis, and surgical site infections and statistically controlled for demographics, comorbidities, injury severity, and surgical/procedural interventions.

Here are the factoids:

  • A million patients (!) were reviewed and about 41,000 met study criteria
  • The odds ratio of infectious complications increased from 1.23 after 2 units to 4.89 after 40 units
  • Each additional unit after 40 increased the odds of an infection by another 4.9%

The authors concluded that blood transfusion is associated with a dose dependent risk of infectious complications and that patients should be resuscitated to achieve prompt hemorrhage control (really?).

My comment: Well, this certainly looks fairly straightforward. Of course, it suffers from the usual drawbacks of massaging large databases. And remember, it shows an association, not cause and effect. How can we tease out whether the higher infection risk is due to badly hurt patients who need major surgery and prolonged ICU stays with pneumonia? The authors have tried to reduce this as much as possible using logistic regression. Unfortunately, many of the variables are very interdependent and I don’t believe the methods can fully overcome this. And there may be other factors not available for analysis in the TQIP data.

Here is my only question for the authors and presenter:

    • How can you be sure that you have fully controlled for the key variables that might influence your final analysis? Yes, you considered demographics, three listed comorbidities (cirrhosis, diabetes, and steroid use), injury severity, and some interventions. But might there be other factors not listed and maybe not even in the TQIP data? Ideas?

This is one of those papers that makes you say “hmm”. But don’t we always try to stop the bleeding promptly. I’m not sure what alternative we have to giving blood.

Reference: Overtransfusion comes at a significant cost: the dose-dependent relationship between blood transfusions and infections after major trauma. EAST Annual Assembly abstract #26, 2020.