All posts by The Trauma Pro

Another Worthless Test? Serum / Urine Myoglobin

We often rely on diagnostic testing to augment our physical examination skills. These tests may be in the form of imaging that allows us to see things that we normally cannot, or measurements of body composition using laboratory testing.

If you look at the “menu” of tests that your hospital laboratory offers, it is very extensive. You can order just about any assay imaginable on any body fluid or tissue. Diagnosis of many of the clinical diseases or disorders that we treat has come to rely on some of these assays.

Let’s take rhabdomyolysis, for example. I’ve been writing about compartment syndrome in the last few posts. One of the byproducts of a full-blown compartment syndrome is muscle breakdown. Two of the well-known substances released from injured muscle are creatine kinase (CK) and myoglobin.

Many textbooks advise the clinician to monitor levels of these substances, since myoglobin is toxic to nephrons and may lead to kidney injury. So most trauma professionals routinely write orders for serial CK, myoglobin, as well as creatinine to monitor renal function.

But most clinicians do not know their laboratory as well as they think. Your lab has the capability to perform commonly requested tests rapidly and on site. But what about assays that are rarely ordered? Does it make sense to have the reagents necessary for these uncommon tests on hand at all times? They degrade over time, and may very well expire before they are ever used, costing money to replace.

So most hospital labs send uncommon assays out to larger labs that perform the test for a large geographic area. But how does the “send out” specimen get to that lab? By courier (if local) or more commonly, by delivery service (if remote). And obviously, this takes time. And some assays are complex and may take hours or days to perform.

At my hospital lab, a serum or urine myoglobin assay is a “send out” test. And if you ask, the lab will tell you that it takes 3-4 business days to get the result. So if you send it out Wednesday, you will have the result the following Monday! Does it make any sense to get serial myoglobins? Or even a single myoglobin test? By the time you get the result, your patient will be treated and gone!

Bottom line: Think about the tests that you order very carefully. If you are ordering something out of the ordinary, check with your lab. Is it a “send out” test? How long does it take to get a result? And more importantly, how expensive is it? These tend to be pricey due to the low frequency of processing.

Then do the math. Is it worth the wait and expense? Or can you get the same information using routine, in house testing? In the case of rhabdomyolysis, serum CK levels are good markers, as is visual inspection of the urine. If it’s any darker than a light yellow, there may be myoglobin present. A quick and dirty way to confirm is some inexpensive testing: a urine specimen that is dipstick positive for blood, and with microscopic analysis shows few if any RBCs usually means myoglobin. Voila! Diagnosis now, not in 4 days.

What The Heck? Final Answer: Progressive Back Pain After Heavy Lifting

In my last two posts, I described an athlete who developed significant pain in his lower back after rapidly escalating his weight lifting regimen. The pain was very localized to the paraspinal areas bilaterally, and serum CPK was elevated.

Congrats to Jay Slutsky for being the first to figure this one out. The suspected diagnosis was lumbar paraspinous muscle compartment syndrome. Compartment pressures were measured, and were found to be 78 and 26 mm Hg. A contrast MRI was obtained that showed swelling of both sets of paraspinal muscles.

The patient was taken to the OR for fasciotomy.Source: Published paper

Note the bulging musculature above. Some areas appeared to be necrotic and did not bleed or contract. There were sharply debrided. The patient recovered quickly, with significant pain relief. The skin incisions were closed after several days, once swelling had subsided. He was well-healed and pain-free at his one month postop visit.

As you can see, any muscle surrounded by a rigid fascial compartment can develop a compartment syndrome. Typically, this requires direct trauma, but exertional compartment syndromes as in this case have been described in the legs of athletes as well. A history of a blow to the muscle group, or of very intense exercise should raise suspicion.

Physical findings of extreme pain that is very focal, coupled with discrete tenderness and firm muscle compartments, should confirm the potential diagnosis. Serum CPK is helpful for trending. Normal pressures in this muscle group tend to be in the single digits to low teens. They rise transiently during exercise, but usually return to normal shortly afterwards. “Normal” compartment pressures are not really known, so findings need to be coupled with CPK levels. Once the compartment pressure reaches the 30s, and especially if accompanied by high and rising CPKs, the syndrome is present. MRI is interesting, but not terribly helpful.

Treatment is typical for any compartment syndrome: release the muscle! A vertical incision centered over the bulging and tight muscle compartment is used. The wound is left open until swelling subsides enough to close the skin. Recovery is usually rapid, although some complain of a persistent low level of pain for a period of time. It is not known how soon these patients may resume sports or training.

Bottom line: Any patient with direct trauma or extreme exertion involving a muscle group is at risk for compartment syndrome. Physical exam, coupled with compartment pressure measurement if in doubt, are the mainstays of diagnosis. CPK levels may help in cases of uncertainty. As with any compartment syndrome, rapid diagnosis and fasciotomy is the key to preserving function and decreasing the likelihood of disability and chronic pain.

Related posts:

References:

  • Acute Exertional Lumbar Paraspinal Compartment Syndrome. Spine 35(25):E1529-E1533, 2010.
  • Lumbar paraspinal compartment syndrome. International Orthopaedics 36:1221-1227, 2011.
  • Paravertebral compartment syndrome after training causing severe back pain in an amateur rugby player: report of a rare case and review of the literature. BMC Musculoskelet Disord 14:259, 2013.

 

 

What The Heck? Part 2: Progressive Back Pain After Heavy Lifting

Yesterday, I described a case of a young athlete who developed progressive back pain after rapidly increased his deadlift weights. He presented to the hospital with back pain and inability to get up from a supine position. He had firm and tender paraspinal muscles in his lower back, but no other findings.

What to do next? Obviously, we need a bit more information on the bony structures. Other than run of the mill muscle strain, a compression fracture would be the next most common diagnosis. In this young, healthy athlete, a simple set of AP and lateral spine images should be sufficient. But if you opted for a CT scan, I won’t argue. In either case, the images were normal.

Since there is significant muscle pain and tenderness, a lab panel with a few extras is in order, as well. The usual electrolytes, etc were normal. Creatinine was 0.9, but CPK was 60,000!

Now what are you thinking? What’s the diagnosis, and what is the decision tree for treatment?

Add your comments below, or tweet them out. I’ll finish this topic up in the next post.

 

What The Heck? Progressive Back Pain After Heavy Lifting

What the heck?! Here’s an interesting case of back pain! Can you figure it out?

A 20 year old male athlete has been performing 125 pound deadlift exercises recently. During his last session, he rapidly escalated to 6 reps at 235 pounds. He developed crampy lower back pain two hours later. The pain became rapidly worse, and he was evaluated at a hospital two days later.

He complained of unrelenting back pain, and could not get up or turn from a supine position. He denies taking any medications or supplements. There is no history of trauma.

On exam, he had firm and painful paraspinal muscles. Buttocks, thighs, and legs were nontender. All pulses were present. Straight leg raise and reverse straight leg raise tests were normal bilaterally. The abdomen was soft and nontender.

What are you thinking? What additional workup is needed at this point?

Post your comments below, or tweet them out. Tomorrow, we’ll walk through the diagnostic stuff, and Monday will be the big reveal.

Do We Really Need To Consult Neurosurgery For Mild TBI?

We consult our neurosurgeons too often. Think back on all the head injured patients you have admitted and placed a neurosurgical consult. How many times did they recommend something new or different, or take them to surgery? Not very often, I would guess.

This is becoming a hot topic. Check out the references below to read about a few other studies that have taken a similar approach.

The trauma group at Scripps Mercy in San Diego retrospectively reviewed their admissions to determine how often patients with mild TBI (GCS > 13) and some degree  intracranial hemorrhage required neurosurgical intervention, even if they were intoxicated or taking anti-platelet or anticoagulant drugs. A total of 500 patients were studied over a 28 month period.

Here are the factoids:

  • 49 (10%) of patients required some sort of neurosurgical intervention (41 craniotomy/craniectomy, 8 ICP monitors)
  • 93% of patients had neurosurgical consultation, and made additional recommendations in only 10 (2%),none of which changed management
  • There was no clinical difference in GCS between those who received an intervention and those who did not
  • Epidural and subdural hematomas were significant predictors of neurosurgical intervention
  • Intoxication or use of anti-platelet or anticoagulant drugs was not associated with intervention. These were present in 30% of all patients!
  • Unsurprisingly, ICU and hospital length of stay were longer in patient who underwent an intervention

Bottom line: As I said, this seems to be a hot research topic. And in this study, the numbers are getting larger and the criteria more inclusive (alcohol and anticoagulants allowed).

Neurosurgeons play a very important role in patients with more moderate to injury to their brain, and with spine injuries. But their input may not be needed in many patients with milder injuries. These data suggest that, in patients with GCS > 13, only subdural and epidural hematomas require consultation because they are much more likely to require intervention. 

This parallels a practice guideline we have in place where patients with subarachnoid or small intraparenchymal hemorrhage, or a linear skull fracture are managed by the trauma service without neurosurgical consultation. We do involve them if there is any intracranial hemorrhage with a history of anticoagulant use, however.

We all need to use our neurosurgeons wisely, and this paper helps to clarify situations where they may and may not be needed. 

Related posts:

Reference: Routine neurosurgical consultation is not necessary in mild blunt traumatic brain injury. J Trauma 82(4):776-780, 2017