All posts by The Trauma Pro

And Yet Another Update On How Fast Can You Warm Up A Hypothermic Patient

The cold snap has finally broken in Minnesota, but Texans had a severe problem with it last week. Unfortunately, it resulted in several dozen deaths. Most were due to carbon monoxide poisoning, but there were a number of people who died from hypothermia as well.

I published a revised compilation of my rewarming rate table a month ago. Since then, I’ve been informed that we are using a new device here at Regions Hospital, the Zoll Thermoguard XL. I had to do a little legwork to get the rewarming rate estimate for it. I am republishing the whole table, including the new device, for your reference.

Warming Technique Rate of Rewarming
Bladder lavage no data
probably
< 0.5° C / hr
Passive external (blankets, lights) 0.5 – 1° C / hr
Active external (lights, hot water bottle) 1 – 3° C / hr
Bair Hugger (a 3M product, made in Minnesota of course!) 2.4° C / hr
Hot inspired air in ET tube 1° C / hr
Fluid warmer 2 – 3° C / hr
GI tract irrigation (stomach or colon, 40° C fluid, instill for 10 minutes, then evacuate) 1.5 – 3° C / hr
Peritoneal lavage (instill for 20-30 minutes) 1 – 3° C / hr
Cool Guard system 1° C / hr
Cool Guard system with thoracic lavage 2° C / hr
Cool Guard system with peritoneal lavage 2.7° C / hr
Thoracic lavage (2 chest tubes, continuous flow) 3° C / hr
Continuous veno-venous rewarming 3° C / hr
Zoll Thermoguard XP with 4-balloon rewarming catheter 3 – 4° C / hr
Continuous arterio-venous rewarming 4.5° C / hr
Mediastinal lavage (thoracotomy) 8° C / hr
Cardiopulmonary bypass 9° C / hr
Warm water immersion (Hubbard or therapy tank) 20° C / hr

One of the most important things to consider is the length of time for rewarming. Do the math using the numbers above! For most patients with severe hypothermia, it’s going to take several hours to rewarm. So make sure you are in a suitable location, such as an OR or ICU!

Routine Duplex Screening For Venous Thromboembolism

Venous thromboembolism (VTE) is a potential problem for all hospitalized patients, and traumatic injury is yet an additional risk factor for its occurrence. Most trauma centers have some kind of risk assessment tool to help the tailor their chemoprophylaxis regimen to patients most at risk. But far fewer have adopted the use of screening ultrasounds to monitor for new onset VTE that would dictate conversion to therapeutic treatment.

Unfortunately, in the US, the Centers for Medicare and Medicaid Services (CMS) has deemed VTE as a “never” event and penalizes hospitals when they report it. One of the unintentional consequences of this (or is it?) is that hospitals may then pressure trauma programs to avoid surveillance in order to “make the numbers look better.” Remember Law X from Samuel Shem’s House of God?

X. If you don’t take a temperature, you can’t find a fever.

Similarly, if you don’t do a duplex screen, you probably won’t detect VTE. Now granted. some patients develop classic symptoms like edema, pain, and tenderness. But not that many.

But is this wise? My contention has been that if the patient doesn’t develop symptoms that catch your attention, yet they develop VTE that you don’t know about, they are at risk for more serious complications like pulmonary embolism (PE). And you are blithely unaware.

The trauma group at Intermountain Medical Center in Salt Lake City performed an elegant study to determine the impact of screening for VTE in their trauma patients. They performed a prospective, randomized trial on trauma patients admitted over a 30-month period. Patients were included if they were judged to be at moderate to high risk based on their risk assessment profile (RAP) score. Patients were excluded if they were children, had VTE or PE within 6 months prior to hospitalization, or had some type of hypercoagulable state.

Patients were sequentially randomized to no duplex screening vs screening on days 1, 3, 7, and then weekly thereafter. The primary outcome measure was PE during the hospital stay. Secondary outcomes consisted of a number of factors relating to development of DVT.

Here are the factoids:

  • Nearly two thousand patients were enrolled, with about 995 patients in each group and no differences in demographics
  • The ultrasound group had significantly more below-knee (124 vs 8) and above knee (19 vs 8) DVT identified (no surprise there)
  • The ultrasound group had significantly fewer pulmonary emboli than the no ultrasound group (1 vs 9) (lots of surprise here!)
  • Mortality was similar during the hospital stay and for 90 days after

Bottom line: If you look for it, you will find it! This is the definition of surveillance bias. But in in this study, looking for clots in the legs may also decrease the number of patients who develop symptomatic pulmonary embolism. How could this be?

There are a few possibilities. The majority of DVT found in the surveillance group were located distally. Although there is some uncertainty as to how likely these are to embolize, it is probably very low. So let’s ignore them for now and assume that only the proximal clots might embolize.

This leaves an extra 11 DVT found in the surveillance group over and above the no-ultrasound group. Despite that, the surveillance group had only one PE vs 9 in the no-ultrasound group!

Another explanation was that the ultrasound guided changes in management, shifting to management to therapeutic drug dosing. The authors did not find a significant difference between the use of therapeutic vs prophylactic dosing between the groups. But there was a difference. Although the overall study was well-powered, there really weren’t enough numbers to show whether there was a true difference in therapeutic dosing. Fourteen patients in the ultrasound group got therapeutic anticoagulation compared to only 4 in the no-surveillance group. I think this is the actual reason.

Overall, this is a well-designed and well-executed study that shows why taking the Ron Popeil approach to DVT prophylaxis (“set it and forget it”) doesn’t work. Patients do occasionally develop proximal DVT on standard chemoprophylaxis (and frequently develop distal DVT), but it doesn’t always result in obvious signs and symptoms. This study shows that if you don’t look for it, you may not know until they suddenly develop chest pain, air hunger, and worse! So consider carefully if your practice guideline doesn’t yet include surveillance.

Reference: Trauma Patients at Risk for Venous Thromboembolism who Undergo Routine Duplex Ultrasound Screening Experience Fewer Pulmonary Emboli: A Prospective Randomized Trial. J Trauma, publish ahead of print, Publish Ahead of Print. DOI: 10.1097/TA.0000000000003104, February 4, 2021.

Pop Quiz: What’s The Diagnosis? The Answer

Okay, time for the answer. This 12 year old crashed his moped, taking handlebar to the mid-epigastrium. Over the next 3 days, he felt progressively worse and finally couldn’t keep food down.

Mom brought him to the ED. The child appeared ill, and had a WBC count of 18,000. The abdomen was firm, with involuntary guarding throughout and a hint of peritonitis. The diagnosis was made on the single abdominal xray shown yesterday. Here is a close-up of the good stuff?

Emergency docs, your differential diagnosis list with this history is a pancreatic vs a duodenal injury based on the mechanism.

Classic findings for duodenal injury:

  • Scoliosis with the concavity to the right. This is caused by psoas muscle irritation and spasm from retroperitoneal soiling by the duodenal leak.
  • Loss of the psoas shadow on the right. Hard to see on this xray, but the left psoas shadow is visible, the right is not. This is due to fluid and inflammation along this plane.
  • Air in the retroperitoneum. In this closeup, you can actually see tiny bubbles of leaked air outlining the right kidney. There are also bubbles along the duodenum and a few along the right psoas.

We fluid resuscitated first (important! dehydration is common and can lead to hemodynamic issues upon induction of anesthesia) and performed a laparotomy. There was a  blowout in the classic position, at the junction of 1st and 2nd portions of the duodenum. The hole was repaired in layers and a pyloric exclusion was performed, with 2 closed drains placed in the area of the leak.

The child did well, and went home after 5 days with the drains out. Feel free to common or leave questions!

Blunt Duodenal Injury In Children

Blunt injury to hollow organs is rare in adults, but a little more common in children. This is due to their smaller muscle mass and the lack of protection by their more flexible skeleton. Duodenal injury is very rare, and most trauma professionals don’t see any during their career. As with many pediatric injuries, there has been a move toward nonoperative management in selected cases, and duodenal injury is no exception.

What we really need to know is, which child needs prompt operative treatment, and which ones can be treated without it? Children’s Hospital of Boston did a multicenter study of pediatric patients who underwent operation for their injury to try to tease out some answers about who needs surgery and what the consequences were.

A total of 16 children’s hospitals participated in this 4 ½ year study. Only 54 children had a duodenal injury, proven either by operation or autopsy. Some key points identified were:

  • The injury was very uncommon, with one child per hospital per year at best
  • 90% had tenderness or marks of some sort on their abdomen (seatbelt sign, handlebar mark, other contusions).
  • Free air was not universal. Plain abdominal xray showed free air in 36% of cases, while CT showed it only 50% of the time. Free fluid was seen on CT in 100% of cases.
  • Contrast extravasation was uncommon, seen in 18% of patients.
  • Solid organ injuries were relatively common
  • Amylase was frequently elevated

Although laparoscopic exploration was attempted in about 12% of patients, it was universally converted to an open procedure when the injury was confirmed. TPN was used commonly in the postop period. Postop ileus was very common, but serious complications were rare (wound infection <10%, abscess 3%, fistula 4%). There were 2 deaths: one child presented in extremis, the other deteriorated one day after delayed recognition of the injury.

Bottom line: Be alert for this rare injury in children. Marks on the abdomen, particularly the epigastrium, should raise suspicion of a duodenal injury. The best imaging technique is the abdominal CT scan. Contrast is generally not helpful and not tolerated well by children. Duodenal hematoma can be managed nonoperatively. But any evidence of perforation (free fluid, air bubbles in the retroperitoneum, duodenal wall thickening, elevated serum amylase) should send the child to the OR. And laparotomy, not laparoscopy, is the way to go.

Reference: Operative blunt duodenal injury in children: a multi-institutional review. J Ped Surg 47(10):1833-1836, 2012.