Delayed Splenic Rupture: Part 1

This post was prompted by a paper that somehow got into the Journal of Trauma this month on nonoperative management of delayed splenic rupture after trauma. It’s a bad retrospective review of 15 patients which I’ll say more about tomorrow. There’s very little good literature on this topic, so I wanted to share some personal observations.

Back in the days before CT scan (and unfortunately, I remember them), the diagnosis of abdominal injury was much more difficult. It was primarily qualitative, meaning that we somehow figured out that they either had it or they didn’t. We could not very easily figure out what specific injuries a given patient had. However, management was simple: we went to the operating room, found out and fixed it.

Sometimes, though, we would encounter a patient who had been involved in some type of blunt trauma a week or two earlier who presented to the ED with left-sided abdominal pain, shock and anemia. The diagnosis was “delayed splenic rupture” and they were taken to OR for a splenectomy.

When CT scan came along, we found out that these were actually “delayed recognition of splenic injury.” We still took them to the OR for splenectomy, but with experience this slowly gave way to splenic repair, and then to nonoperative management. 

There is still one subset of these injuries that is problematic: spleen injury with a contrast blush. It turns out that there are really two types of blush: contrast seen within a pseudoaneurysm within the splenic pulp, and extravasation. And furthermore, the pseudoaneurysm is the culprit in most “delayed splenic ruptures.”

Tomorrow, I’ll write about how to recognize this potential problem, what to do about it acutely, and what to do if it was missed and the patient presents to your ED ten days later in shock.

Related post:

Reference: Nonsurgical management of delayed splenic rupture after blunt trauma. J Trauma 72(4):1019-1023, 2012.

New Technology: Help Brain Injured Patients To Talk

It is can be extremely difficult to communicate with some brain injured patients. Many have global damage that precludes the processing necessary to formulate thoughts. However, some may be able to think but can’t effectively make themselves understood. Patients with the “locked in” syndrome are a perfect example.

A company called NeuroVigil has developed technology and data analysis techniques for extracting a wealth of information from a single-channel EEG. The iBrain system uses two sensors that do not require being stuck to the head with adhesive. A simple elastic band can hold them in place. 

Last year, the company fitted the device on Stephen Hawking to begin testing and training the system to assist with his communication efforts. Currently, Hawking uses an IR sensor that detects twitches in his cheek. These are painstakingly translated into letters and then words that are spoken by a computer. The iBrain system is being trained to recognize words via his EEG patterns and should speed up his communication with the outside world.

If this technology pans out, it may be used to communicate with moderate to severely injured TBI patients who have expressive language problems. It could also be used to test for and communicate with patients who are “locked in.”

The video was recorded at TEDMED 2009. Much of the key information is presented beginning at 10:10 into the video.

I have no financial interest in NeuroVigil

New Technology: The End Of Handwashing?

All healthcare professionals are notoriously bad about washing their hands, especially doctors. A variety of things have been developed to help us keep our hands clean, including simple soap and water, barriers like gloves, and various gels and foams (which I swear I can taste in my mouth 10 minutes later, even though I’m pretty sure I’m not putting my fingers there).

A recently published paper from China is shining new light on this topic (get it?). Researchers developed a hand-held, battery-powered plasma flashlight that gets rid of bacteria on skin in a flash. It costs less than $100 to produce and runs on a 12V battery. 

This device was found to inactivate all bacteria in a 17-layer biofilm containing a very hardy organism, enterococcus faecalis. It does not produce UV radiation, and the exact mechanism for the bacterocidal effect is unclear. There was no adverse effect on skin.

The main drawbacks to this device are that it only produces a small area of plasma, and it takes 5 minutes to kill all the bacteria. But take this to the next logical step. Many of you are familiar with the Dyson Airblade hand dryers found at many airports. Suppose you could produce a more intense plasma field using a more robust power supply (power line or ambulance power system) in a device that you could just pass your hands through to disinfect them? 

And if you really want to improve compliance, hook the unit to the door control so the doctor can’t even walk into a patient room without passing his hands through it!

Reference: Inactivation of a 25.5µm Enterococcus faecalis biofilm by a room-temperature, battery-operated, handheld air plasma jet. Journal of Physics D: Applied Physics 45(2012):165205 (5p), 2012.

Best Of: Flying After Pneumothorax

Patients who have sustained a traumatic pneumothorax occasionally ask how soon they can fly in an airplane after they are discharged. What’s the right answer?

The basic problem has to do with Boyle’s Law (remember that from high school?). The volume of a gas varies inversely with the barometric pressure. So the lower the pressure, the larger a volume of gas becomes. Most of us hang out pretty close to sea level, so this is not an issue.

However, flying in a commercial airliner is different. Even though the aircraft may cruise at 30,000+ feet, the inside of the cabin remains considerably lower though not at sea level. Typically, the cabin altitude goes up to about 8,000 to 9,000 feet. Using Boyle’s law, any volume of gas (say, a pneumothorax in your chest), will increase by about a third on a commercial flight. 

The physiologic effect of this increase depends upon the patient. If they are young and fit, they may never know anything is happening. But if they are elderly and/or have a limited pulmonary reserve, it may compromise enough lung function to make them symptomatic.

Commercial guidelines for travel after pneumothorax range from 2-6 weeks. The Aerospace Medical Association published guidelines that state that 2-3 weeks is acceptable. The Orlando Regional Medical Center reviewed the literature and devised a practice guideline that has a single Level 2 recommendation that commercial air travel is safe 2 weeks after resolution of the pneumothorax, and that a chest xray should be obtained immediately prior to travel to confirm resolution.

Bottom line: Patients can safely travel on commercial aircraft 2 weeks after resolution of pneumothorax. Ideally, a chest xray should be obtained shortly before travel to confirm that it is gone. Helicopter travel is okay at any time, since they typically fly at 1,500 feet or less.

References:

  • Practice Guideline, Orlando Regional Medical Center. Air travel following traumatic pneumothorax. October 2009.
  • Medical Guidelines for Airline Travel, 2nd edition. Aerospace Medical Association. Aviation, Space, and Environmental Medicine 74(5) Section II Supplement, May 2003.

Best Of: The Downside Of Not Taking Your Anticoagulant

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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