Here’s an interesting case to consider. A young male is assaulted and stabbed to the back. Paramedics bring him to your ED as a trauma team activation, and the full team is assembled prior to his arrival.
He is brought into the room on the stretcher in the prone position. Here is a representative picture. This is not the actual patient, just a picture I found on another blog site that looks pretty close to the real case.
Let’s walk through the thought processes of managing this over the next few days.
First, what do you need to know right now to navigate your critical decision points? And what are you going to do regarding positioning, evaluation, and imaging?
Tweet or comment with your replies! More on Monday.
We’ve all been faced with injured patients who are taking some kind of anticoagulant, and it complicates their care. Many trauma professionals just say, “they just shouldn’t take this stuff any more." Why can’t we just stop them in patients at risk for injury (e.g. an elderly patient who falls frequently)?
Two major risk groups come to mind: those taking the meds who have DVT (or a propensity to get it), and patients with atrial fibrillation who take them to decrease stroke risk. I was not able to find much info (yet) on the former category. But there is a series of nicely done studies based on work from the Framingham Heart Study.
The Framingham study started in 1948, and has been following over 5,000 people for the development of cardiovascular disease. In this particular analysis, 5070 patients who were initially free of disease were analyzed for development of atrial fib and occurrence of stroke. Anticoagulants were seldom used in this group.
The authors found that the prevalence of stroke increased with age in patients with atrial fib. The percentage that could be attributed to a-fib also increased. The following summarizes their numbers:
- Age 50-59: 0.5 strokes per 100 patients, attributable risk 1.5%
- Age 60-69: 1.8 strokes per 100 patients, attributable risk 2.8%
- Age 70-79: 4.8 strokes per 100 patients, attributable risk 9.9%
- Age 80-89: 8.8 strokes per 100 patients, attributable risk 23.5%
Bottom line: The risk of having a stroke just because a patient has atrial fibrillation goes up significantly with age. So setting an age cutoff for taking an anticoagulant doesn’t make sense. Unfortunately, increasing age also means increasing risk of injury from falls. Warfarin definitely cuts that risk, and it happens to be relatively easily reversbile. However, the newer non-reversible drugs change the equation, shifting the risk/benefit ratio too far toward the dark side. We need some good analyses to see if it really makes sense to move everybody to these new (expensive) drugs just to make it easier to dose and monitor. The existing studies on them only look at stroke, but don’t take injury morbidity and mortality into account.
Reference: Atrial fibrillation as an independent risk factor for stroke: the Framingham study. Stroke 22:983-988, 1991.
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This is a perfect example of why you cannot just simply read an abstract. And in this case, you can’t just read the paper, either. You’ve got to critically think about it and see if the conclusions are reasonable. And if they are not, then you need to go back and try to figure out why it isn’t.
A study was recently published regarding bleeding after nonoperative management of splenic injury. The authors have been performing an early followup CT within 48 hours of admission for more than 12 years(!). They wrote this paper comparing their recent experience with a time interval before they implemented the practice.
Here are the factoids. Pay attention closely:
- 773 adult patients were retrospectively studied from 1995 to 2012
- Of 157 studied from 1995 to 1999, 83 (53%) were stable and treated nonoperatively. Ten failed, and all the rest underwent repeat CT after 7 days.
- After a “sentinel delayed splenic rupture event”, the protocol was revised, and a repeat CT was performed in all patients at 48 hours. Pseudoaneurysm or extravasation initially or after repeat scan prompted a trip to interventional radiology.
- Of 616 studied from 2000-2012, after the protocol change, 475 (77%) were stable and treated nonoperatively. Three failed, and it is unclear whether this happened before or after the repeat CT at 48 hours.
- 22 high risk lesions were found after the first scan, and 29 were found after the repeat. 20% of these were seen in Grade 1 and 2 injuries. All were sent for angiography.
- There were 4 complications of angiography (8%), with one requiring splenectomy.
- Length of stay decreased from 8 days to 6.
So it sounds like we should be doing repeat CT in all of our nonoperatively managed spleens, right? The failure rate decreased from 12% to less than 1%. Time in the hospital decreased significantly as well.
Wrong! Here are the problems/questions:
- Why were so many of their patients considered “unstable” and taken straight to OR (47% and 23%)?
- CT sensitivity for detecting high risk lesions in the 1990s was nothing like it is today.
- The accepted success rate for nonop management is about 95%, give or take. The 99.4% in this study suggests that some patients ended up going to OR who didn’t really need to, making this number look artificially high.
- The authors did not separate pseudoaneurysm from extravasation on CT. And they found them in Grade 1 and 2 injuries, which essentially never fail
- 472 people got an extra CT scan
- 4 people (8%) had complications from angiography, which is higher than the oft-cited 2-3%. And one lost his spleen because of it.
- Is a 6 day hospital stay reasonable or necessary?
Bottom line: This paper illustrates two things:
- If you look at your data without the context of what others have done, you can’t tell if it’s an outlier or not; and
- It’s interesting what reflexively reacting to a single adverse event can make us do.
The entire protocol is based on one bad experience at this hospital in 1999. Since then, a substantial number of people have been subjected to additional radiation and the possibility of harm in the interventional suite. How can so many other trauma centers use only a single CT scan and have excellent results?
At Regions Hospital, we see in excess of 100 spleen injuries per year. A small percentage are truly unstable and go immediately to OR. About 97% of the remaining stable patients are successfully managed nonoperatively, and only one or two return annually with delayed bleeding. It is seldom immediately life-threatening, especially if the patient has been informed about clinical signs and symptoms they should be looking for. And our average length of stay is 2-3 days depending on grade.
Never read just the abstract. Take the rest of the manuscript with a grain of salt. And think!
Reference: Delayed hemorrhagic complications in the nonoperative management of blunt splenic trauma: early screening leads to a decrease in failure rate. J Trauma 76(6):1349-1353, 2014.
The serial hemoglobin (Hgb) determination. We’ve all done them. Not only trauma professionals, but other in-hospital clinical services as well. But my considered opinion is that they are not of much use. They inflict pain. They wake patients up at inconvenient hours. And they are difficult to interpret. So why do them?
First, what’s the purpose? Are you looking for trends, or for absolute values? In trauma, the most common reason to order is “to monitor for bleeding from that spleen laceration” or some other organ or fracture complex. But is there some absolute number that should trigger an alarm? If so, what is it? The short answer is, there is no such number. Patients start out at a wide range of baseline values, so it’s impossible to know how much blood they’ve lost using an absolute value. And we don’t use a hemoglobin or hematocrit as a failure criterion for solid organ injury anymore, anyway.
What about trends, then? First, you have to understand the usual equilibration curve of Hgb/Hct after acute blood loss. It’s a hyperbolic curve that reaches equilibrium after about 3 days. So even if your patient bled significantly and stopped immediately, their Hgb will drop for the next 72 hours anyway. If you really want to confuse yourself, give a few liters of crystalloid on top of it all. The equilibration curve will become completely uninterpretable!
And how often should these labs be drawn? Every 6 hours (common)? Every 4 hours (still common)? Every 2 hours (extreme)? Draw them frequently enough, and you can guarantee eventual anemia.
Bottom line: Serial hemoglobin/hematocrit determinations are nearly worthless. They cost a lot of money, they disrupt needed rest, and no one really knows what they mean. For that reason, my center does not even make them a part of our solid organ injury protocol. If bleeding is ongoing and significant, we will finding it by looking at vital signs and good old physical exam first. But if you must, be sure to explicitly state what you will do differently at a certain value or trend line. If you can’t do this and stick to it, then you shouldn’t be ordering these tests in the first place!
Reference: Serial hemoglobin levels play no significant role in the decision-making process of nonoperative management of blunt splenic trauma. Am Surg 74(9):876-878, 2008.
Again, I’m not a fan of animal studies. But this one, presented at EAST 2012 and now published, involves both pigs and humans and is so intriguing I just have to share it. The authors have a track record of studying coagulation issues with thromboelastography (TEG) in both animals and people. They previously showed that hypercoagulability detectable by TEG occurs after insertion of pulmonary artery catheters in swine and critically ill humans.
In this follow-on study, they looked at TEG profiles in 16 healthy swine and 8 critically ill humans after insertion of a central venous catheter (CVC). They found that CVC insertion induced the same type of hypercoagulable state. TEG clotting time and initial clot formation time decreased, and fibrin cross-linking accelerated. The changes were somewhat less in humans, but were still significant in both groups. All coag tests (PT, PTT, INR) and measured coag factors (von Willebrand, AT III) were unchanged.
Interestingly, in the animal group the hypercoagulable state persisted for at least 3 hours after CVC removal. And the hypercoagulability could be prevented with enoxaparin, but not heparin.
Bottom line: The idea that hypercoagulability could be induced by central arterial or venous catheter placement is intriguing, although this work has not been replicated by others yet. What if hypercoagulability occurs with any invasion of the vascular system? We may eventually discover that the increased incidence of DVT we have been fighting in the hospital setting is in part due to our ubiquitous use of IVs and routine blood draws.
Reference: Insertion of central venous catheters induces a hypercoagulable state. J Trauma 73(2):385-390, 2012.