Category Archives: Complications

Abdomen, Complications

Leukocytosis After Splenic Injury

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Any trauma professional who has dealt with spleen injuries knows that the white blood cell (WBC) count rises afterwards. And unfortunately, this elevation can be confusing if the patient is at risk for developing inflammatory or infectious processes that might be monitored using the WBC count.

Is there any rhyme or reason to how high WBCs will rise after injury? What about after splenectomy or IR embolization? An abstract is being presented at the Clinical Congress of the American College of Surgeons next month that examines this phenomenon.

This retrospective study looked at a convenience sample of 75 patients, distributed between patients who had splenic injury that was either not treated, removed (splenectomy), or embolized. Data points were accumulated over 45 days.

Here are the factoids:

  • 20 patients underwent splenectomy, 22 were embolized, and 33 were observed and not otherwise treated
  • Injury severity score was essentially identical in all groups (19)
  • Splenectomy caused the highest WBC counts at the 30 day mark (17.4K)
  • Embolized patients had mildly elevated WBC levels (13.1K) that were just above the normal range at 30 days
  • Observed patients had high normal WBC values (11.0K) after 30 days
  • Values in observed and embolized patients normalized to about 7K after 30 days; splenectomy patient WBC count remained mildly elevated at 14.1K.
  • The authors concluded that embolization does not result in permanent loss of splenic function (bad conclusion, rookie mistake!)

Bottom line: This study is interesting because it gives us a glimpse of the time course of leukocytosis in patients with injured spleens. If you need to follow the WBC for other reasons, if gives a little insight into what might be attributable to the spleen. Splenectomy generally results in a chronically elevated WBC count, which tends to vary in the mid-teens range. Embolization (in this study) transiently elevates the WBC count, but it then drops back to normal.

The big problem with this study (besides it being small) is that it fails to recognize that there are many different shades of embolization. Splenic artery? Superselective? Selective? I suspect that the WBC count in main splenic artery embolization may behave much like splenectomy in terms of leukocytosis. And the conclusion about splenic function being related to WBC count was pulled out of a hat. Don’t believe it.

Reference: Leukocytosis after Splenic Injury: A Comparison of Splenectomy, Embolization, and Observation. American College of Surgeons Scientific Forum Abstracts pg S164, 2015.

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Complications

How Fast Do Trauma Patients Die?

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For years, I’ve taught my residents participating in trauma activations, “Your patient is bleeding to death until proven otherwise.” This concept served as the basis of the [poorly documented] “Golden Hour” and for decades has directed our efforts at getting patients to a center with an immediately available OR as quickly as possible.

Donald Trunkey published the first paper illustrating the trimodal distribution of death in 1983 in Scientific American. A crude graph showed the large spike in early deaths that occurred within this first hour. But the paper was mainly observational and was not based on quantitative data.

Wouldn’t it be nice to know how quickly these injured patients were dying, and of what? The trauma group at the University of Pennsylvania massaged data in the state trauma database, focusing on patients who died of their injuries during the first four hours. They created two variables to more objectively compare times, the TD5 and the TD50. These are the time at which 5% and the time at which 50% (median) had died, respectively.

The Pennsylvania Trauma Outcomes Study database contains a huge amount of data. During the 11 years of the study, a total of 6,547 met the mortality criteria for analysis.

Here are the factoids:

  • The mechanism of injury was about 60% blunt / 40% penetrating, with an average ISS of 33
  • The majority of these patients (85%) were hypotensive before their death, meaning that they were likely bleeding to death on arrival
  • The  overall TD5 was 23 minutes, and the TD50 was 59 minutes
  • These numbers were shorter for penetrating injuries, TD5=19 minutes and TD50=43 minutes
  • Patients who were not hypotensive lived a little longer: TD5=44 minutes and TD50 = 2 hours 18 minutes
  • 77% of patients died in the ED and 19% in the OR. The remainder died in the ICU.

This chart shows the TD5 by mechanism and type of surgery. This represents when after arrival, patients start dying due to their injuries. Penetrating injury plus hypotension kills the fastest at 19 minutes and head injuries the slowest at 1:20.

Bottom line: The authors clearly show how soon seriously injured patients start to die. It’s less than 20 minutes in victims of penetrating injury with early hypotension. And the time between the “just start do die” point (TD5) and the “half are dead” point (TD50) is frighteningly short, just an additional twenty minutes!

There appears to be a bit of a grace period in patients who arrive with a normal blood pressure. Their TD50 is extended out to about two hours. All this means is that they are bleeding more slowly, but it is still killing them.

A good rule of thumb is that ANY hypotensive patient should make you justify why you are NOT ALREADY IN THE OPERATING ROOM! Dawdling in the trauma bay or performing unnecessary scans will push your patient much closer to the point of no return. Look at the huger percentage of patients in this study who died in the ED.

Remember, your patient is bleeding to death in front of your eyes, and the only place you can stop it is the OR!

Reference: Defining the optimal time to the operating room may
salvage early trauma deaths, J Trauma 76(5):1251-1258, 2014.

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Complications

Predicting VTE Risk In Children

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There’s a lot of debate about if and at what age injured children develop significant risk for venous thromboembolism (VTE). In the adult world, it’s a little more clear cut, and nearly every patient gets some type of prophylactic device or drug. Kids, we’re not so certain about at all.

The Children’s Hospital of Wisconsin tried to tease out these factors to develop and implement a practice guideline for pediatric VTE prophylaxis. They prospectively reviewed over 4000 pediatric patients admitted over a 6 year period.

It looks like the guideline was developed using some or all of this data, then tested using regression models to determine which factors were significant. The guideline was then tweaked and a final model was implemented.

Here are the factoids:

  • 588 of the patients (14%) were admitted to the ICU, and 199 of these were identified as high-risk by the guidelines
  • Median age was 10 (this is always important in these studies)
  • VTE occurred in 4% of the ICU patients, and 10% of the high-risk ones
  • Significant risk factors included presence of central venous catheter, use of inotropes, immobilization, and GCS < 9

Bottom line: This abstract confuses me. How were the guidelines developed? What were they, exactly? And the results seem to pertain to the ICU patients only. What about the non-ICU kids? The abstract just can’t convey enough information to do the study justice. Hopefully, the oral presentation will explain all.

I prefer a very nice analysis done at the Oregon Health Science University in Portland. I wrote about this study earlier this year. The authors developed a very useful calculator that includes most of the risk factors in this model, and a few more. Input the specific risks, and out comes a nice score. The only issue is, what is the score threshold to begin prophylaxis and monitoring? Much more practical (and understandable) than this abstract. Check it out at the link below.

References:

  1. Evaluation of guidelines for injured children at high risk for venous thromboembolism: A prospective observational study. J Trauma Acute Care Surg. 2017 May;82(5):836-844.
  2. A Clinical Tool for the Prediction of Venous Thromboembolism in Pediatric Trauma Patients. JAMA Surg 151(1):50-57, 2016.
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Complications

NSAIDs And Fracture Healing Revisited – Yet Again!

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I’ve written so many posts about the use of non-steroidal anti-inflammatory drugs (NSAIDs) it’s practically getting old. To summarize, some old animal studies suggested that using NSAIDs during fracture healing could impair the process. However, human studies were not so convincing.

Over the years, there has been quite a bit of conflicting evidence. This generally means the association between healing and NSAID use is weak. However, after this period of time, we should have become aware of a significant cause/effect relationship.

The Eastern Association for the Surgery of Trauma recently released a practice management guideline regarding the use of NSAIDs for the treatment of acute pain after orthopedic trauma. They used a standard methodology to identify and analyze published research. They focused on human studies specifically relating to this drug class’s use in fractures. The group ultimately identified 19 pertinent research papers for analysis, 10 of which were prospective, randomized studies.

Here are the three questions they asked, with their answers:

  • Should NSAIDs be used in analgesic regimens for adult patients
    (≥18 years old) with traumatic fracture versus routine analgesic
    regimens that do not include NSAIDs to improve analgesia and
    reduce opioid use without increases in non-union and acute kidney
    injury rates? Although the quality of the studies for this question was low, EAST conditionally recommended using NSAIDs in pain control regimens. In the higher-quality studies in this group, there was no increased risk of non-union.
  • Should ketorolac be used in analgesic regimens for adult patients with traumatic fracture versus routine analgesic regimens that do not include ketorolac to improve analgesia and reduce opioid use without increasing non-union
    rates? This is the same question asked above, but with a specific drug rather than the class in general. The answer was basically the same.
  • Should selective NSAIDs (COX-2 inhibitors) be used in analgesic
    regimens for adult patients (≥18 years old) with traumatic fracture versus routine analgesic regimens that include non-selective NSAIDs to improve analgesia and reduce opioid use without increasing non-union rates?     COX-2 inhibitors are a subset of NSAIDs that are more selective in their action, blocking only the COX-2 receptor. Several years ago, there was a scandal regarding the COX-2 inhibitor rofecoxib (Vioxx). These selective drugs tended to have a higher incidence of cardiac complications. The manufacturer covered up this fact for several years, resulting in many unneeded deaths before it was removed from the market. The only COX-2 inhibitor available in the US is celecoxib. Only a few studies were performed using this drug during bone healing. There were not enough to make a recommendation.

Bottom line: EAST made conditional recommendations for using NSAIDs in general and ketorolac specifically in adults with fractures. “Conditional” only means that the authors did not have a consensus. Some voted to strongly recommend, and the remainder to conditionally recommend. There were no votes to recommend against their use.

The use of NSAIDs should complement a well-thought-out opioid regimen, which should also be combined with other non-narcotic medications and appropriate mobilization and therapy.

Reference: Efficacy and safety of non-steroidal anti-inflammatory
drugs (NSAIDs) for the treatment of acute pain after orthopedic trauma: a practice management guideline from the Eastern Association for the Surgery of Trauma and the Orthopedic Trauma Association. Trauma Surg Acute Care Open. 2023 Feb 21;8(1):e001056. doi: 10.1136/tsaco-2022-001056. PMID: 36844371; PMCID: PMC9945020.

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Complications

Top 10 Worst Complications: #1 Nasocerebral Tube

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Minor complications from nasogastric tube insertion occur relatively frequently. Emesis is fairly common when the gag reflex is stimulated by the tube in the back of the oropharynx. An infrequent but possibly fatal one is insertion through the cribriform plate. 

The cribriform plate is located directly posterior to the nares and is part of the ethmoid bone. It is very porous in nature and weaker than the surrounding portions of the ethmoid. It is easily fractured, and can be seen is association with basilar skull fractures. This is one source for rhinorrhea in patients with these fractures.

Cribriform fracture is a contraindication to unprotected insertion of a nasogastric tube. If you look at the sagittal section below, the plate lies directly behind the nares. When inserting the NG tube, we are usually taught to aim the tube straight back. Unfortunately, this aims it directly at the cribriform. If a fracture is present, it is possible that you may be inserting a nasocerebral tube!

Cribriform plate - sagittal section

The usual symptoms when this occurs consist of immediate neurologic deterioration to coma, and a unilateral or bilateral blown pupil. The tube must not be withdrawn, because it will cause significant injury to the base of the brain. A stat neurosurgical consultation must be obtained, and if the patient is salvageable, the tube must be withdrawn through a craniectomy.

To avoid this dreaded complication, identify patients at risk for cribriform injury. They are:

  • patients with signs of trauma from eyebrows to zygoma
  • comatose patients
  • patients with signs of basilar skull fracture (Battle’s sign, raccoon eyes, oto- or rhinorrhea)

If your patient is at risk, follow these guidelines:

  • first, does the patient really need a gastric tube?
  • if comatose, insert an orogastric tube
  • if awake, don’t put the tube in their mouth, as they will gag continuously. Instead, place a lubricated, curved nasal airway. Then lube up a slightly smaller Salem sump tube and pass it through the airway.
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