All posts by TheTraumaPro

Serial Hemoglobin / Hematocrit – Huh?

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!

Related post:

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.

Central Line Insertion Causes Hypercoagulability?

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.

Best Of: What You Need To Know About Falls From a Height

 Falls from a height can be either accidental or intentional (suicide attempt). There are several prognostic factors for survival that have been identified:

  • Height
  • Age
  • Type of surface
  • Body part that touches the ground first

Two other factors are important, but do not have a significant effect on mortality:

  • Circumstances of the fall (suicide, accident, escape)
  • Initial impact with an object before impacting the ground

Height. Overall, about half of victims die at the scene, and a total of 70% die before they reach the hospital. The median height leading to death is about 49 feet, or about 4 to 5 storeys. 100% of victims die after falling 85 feet, or about 8 storeys.

Age. Mortality increases with age due to pre-existing medical conditions and decreased physiologic reserve.

Type of surface. The type of surface struck (i.e. grass, water, construction debris) can also have an effect on secondary injuries and survival. Mortality after striking a hard surface is nearly double that of hitting a soft one (39% vs 22%)

Body part touching the ground first. The highest mortality is seen when the victim lands in a prone position (57%). Striking head first has the next highest mortality at 44%. The best striking position is feet first, with a mortality of 6%.

Circumstances of the fall. Suicide attempts have the highest death rate at 46%. This may be attributable to pre-planning, and the increased likelihood that the fall may lead to additional trauma mechanisms (struck by car after jumping from land bridge, drowning after jumping from bridge over water). Accidental falls have a lower 17% mortality.

Initial impact before final impact. Striking wires or scaffolding before the final impact is protective, decreasing the death rate from 37% to 15%.

It is important for the trauma professional to obtain as much information from bystanders or EMS as possible about the fall details. This will ultimately enable to trauma physician to pursue appropriate diagnostic techniques to pinpoint specific injuries associated with various types of falls.

Reference:

Crit Care Med 33(6): 1239-1242, 2005.

Spinal Cord Concussion In Student Athletes

Spinal cord injuries are typically devastating injuries with profound consequences for function and life expectancy. However, a small percentage result in rapidly reversible symptoms. Because these temporary injuries are rare, they tend to cause confusion among clinicians.

Technically, a spinal cord concussion (a “zinger” or “stinger” is an example) is a mild cord injury that results in transient neurologic disturbances. The deficits can be sensory, motor or both, and typically resolve in less than 48 hours. The injuries tend to involve the mid-portion of the cervical cord or the cervico-thoracic junction, since these are the areas of maximum mobility. In a few cases, the athlete has congenital narrowing of the spinal canal which predisposes them to injury. In most cases, the injury probably occurs due to the flexibility of the young spine.

The usual management consists of an MRI of the spine followed by admission and frequent neurologic checks to ensure ongoing resolution. MRI is typically negative in a true concussion. If a signal change is seen, then technically a cord contusion is present. Management is the same for both. There is no indication to give steroids. Evaluation of the ligaments is critical to determine if a collar will be necessary.

Recovery is rapid and complete. But what is the answer to the inevitable question, “when can he/she return to play?” In adult players, the literature suggests that it may be safe to return once they have fully recovered. There is little guidance for kids.

Here’s what I tell the parents: This event has shown that, given the right force applied to your child’s neck, the bones can move enough to injure their spinal cord. This time, the cord was just tickled a little bit. But if the bones had moved just another millimeter or two, this injury could have been permanent and they would never have walked again. I recommend that they do not play this sport again.

Some of you may disagree. I’d be very interested in hearing your comments. 

Reference:

  • First mention: About concussion of the spinal cord. Wein Med Jahrb 34:531, 1879.

But The Radiologist Made Me Do It!

The radiologist made me order that (unnecessary) test! I’ve heard this excuse many, many times. Do these phrases look familiar?

  1. … recommend clinical correlation
  2. … correlation with CT may be of value
  3. … recommend delayed CT imaging through the area
  4. … may represent thymus vs thoracic aortic injury (in a 2 year old who fell down stairs)
Some trauma professionals will read the radiology report and then immediately order more xrays. Others will critically look at the report, the patient’s clinical status and mechanism of injury, and then decide they are not necessary. I am firmly in the latter camp.
But why do some just follow the rad’s suggestions? I believe there are two major camps:
  • Those that are afraid of being sued if they don’t do everything suggested, because they’ve done everything and shouldn’t miss the diagnosis
  • Those that don’t completely understand what is known about trauma mechanisms and injury and think the radiologist does
Bottom line: The radiologist is your consultant. While they are good at reading images, they do not know the nuances of trauma. Plus, they didn’t get to see the patient so they don’t have the full context for their read. First, talk to the rad so they know what happened to the patient and what you are looking for. Then critically look at their read. If the mechanism doesn’t support the diagnosis, or they are requesting unusual or unneeded studies, don’t get them! Just document your rationale clearly in the record. This provides best patient care, and minimizes the potential complications (and radiation exposure) from unnecessary tests.
Related post: 

Reference: Pitfalls of the vague radiology report. AJR 174(6):1511-1518, 2000.