Category Archives: Complications

Top 10 Worst Complications: #1 Nasocerebral Tube

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 The tube must not be withdrawn, because it will cause significant injury to the base of the brain. A stat neurosurgical consultation must be obtained, and if the patient is salvageable, the tube must be withdrawn through a craniectomy.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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Nausea In The Trauma Bay: Gastric Tube vs Anti-Emetic Drugs?

Nausea and vomiting are common problems in trauma patients, particularly those in a trauma activation. Inciting factors include pain, full stomach from food eaten before the event or blood swallowed after, or reaction to pain medications. For years, trauma professionals reached for the lowly gastric tube to evacuate stomach contents to “solve” the problem.

But how many of you have seen a patient forcefully empty their stomach as soon as the tube touches the oropharynx? And of course, your patient is lying supine, so the vomitus goes straight up, then back down into their airway. And if their mental status is not quite right, they may aspirate, causing even bigger problems.

We’ve had anti-emetic medications for a long time, some more effective than others. Only recently have we begun to rely on these as a first line defense in the trauma resuscitation room. But do they work? Are they safer?

The University Medical Center Utrecht in the Netherlands looked at this problem. They changed their policy from inserting a gastric tube to administering anti-emetics at the beginning of 2014. They studied their experience for the 6 months before and 6 months after the policy change. They inserted an orogastric (OG) tube preferentially before the switch, and used ondansetron and/or metoclopramide after.

Here are the factoids:

  • A total of 1446 trauma patients were admitted during this period. After excluding patients who were intubated or did not complain of nausea, 453 were analyzed (30%)
  • 20% of patients who had an OG tube placed vomited vs only 3% receiving medication (significant)
  • After therapy, 14% of patients receiving an OG were still nauseated vs only 2% getting meds (also significant)
  • 3 patients vomited and aspirated after OG placement, and 1 developed a pneumonia. 2 patients became bradycardic and med administration, and one developed QT-prolongation

Bottom line: This is a relatively small, retrospective study. Furthermore, the choice of gastric tube route (oral) is a setup for gagging and vomiting. Nasogastric tubes are a bit less noxious, but can’t be inserted in all patients (see next week’s post). Even so, the use of anti-emetics in trauma patients complaining of nausea seems like the kinder, gentler way to go. 

Which drug to use? Previous studies have shown that ondansetron 4mg is as effective as 8mg, and that this drug is about equally as effective as metoclopramide. There is also some evidence that giving both is more effective than just giving one.

Gastric tubes are still important, particularly in the comatose patient. But since these patients are at risk for cribriform plate injury, only the oral route should be used.

Reference: Analysis of two treatment modalities for the prevention of vomiting after trauma: orogastric tube or anti-emetics. Injury (accepted manuscript, in press) online 8 July 2017.

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Colonic Pseudo-Obstruction In Trauma Patients – Part 2

In my last post, I discussed a paper describing the incidence of colonic pseudo-obstruction (CPO), or Ogilvie syndrome, in trauma patients. The paper confirmed my bias that this condition could be a problem in a specific subset of trauma patients. They are generally older men with pelvic or spine fractures, with or without surgical fixation. In addition, some comorbidities like diabetes, obesity, and concomitant head injury increase the incidence.

The usual dogma is that a cecal diameter > 12cm places the patient at risk of perforation. Therefore, as the size of the colon increases, steps should be taken to decompress it definitively. This typically involves neostigmine infusion, which usually requires transfer to the ICU, or colonoscopic decompression.

Until about eight years ago, we managed this issue at Regions Hospital using the IV neostigmine option in the ICU. But then, one of our colorectal surgeons described his experience managing CPO with subcutaneous neostigmine. A light bulb turned on! Intravenous neostigmine requires admission to an ICU at our hospital for continuous monitoring to quickly identify the development of bradycardia.

But subcutaneous neostigmine was not on the naughty list! We developed a practice guideline to identify and exclude patients for whom this drug was contraindicated. And it required monitoring that could be accomplished in a floor bed with brief episodes of continuous EKG monitoring. Our inpatient trauma unit could easily do this. However, it might require a step-down bed in yours.

Here is the guideline. Click the image of the link at the end of this post to download a copy.

Here are the major features of the guideline:

  • Identification. Any patient, especially those with the previously described risk factors, begins daily monitoring with a flat plate abdominal x-ray. Patients with abdominal distension with subjective discomfort or nursing concerns with the distension fall into this category.
  • Trigger. Once distension of any part of the colon, particularly the cecum, exceeds 10 cm, it is time to act. Otherwise, daily monitoring and a bowel regimen continue.
  • Contraindications to neostigmine. If the patient has a recent history of MI, bronchospasm, is on beta-blocker therapy, or has SBP < 90 torr, heart rate < 60, or weight < 50kg, colonoscopic decompression should be carried out.
  • Continuous monitoring must be available for one hour after injection. This requires an appropriate nurse and an EKG monitor. Atropine must be present at the bedside in case bradycardia develops.
  • Up to three doses of SQ neostigmine (1mg) can be given 12 hours apart. If the patient responds with a large bowel movement or passage of gas, it should be confirmed with an abdominal x-ray.
  • Patients with insufficient response must transfer to ICU for IV neostigmine or should be scheduled for an urgent colonoscopy.

Our experience has shown that this guideline is usually very effective. However, a few patients have had a recurrence after 24-48 hours, which is uncommon. The guideline can be repeated if necessary.

Bottom line: A low index of suspicion for CPO in trauma patients is critical. Once the colon perforates, these patients do poorly, and serious complications are common. This guideline allows the trauma service to keep these patients out of the ICU while treating it. But before you implement this, please work closely with your pharmacists to ensure that hospital policy allows using neostigmine outside of an ICU setting.

Colonic Pseudo-Obstruction in Trauma – Practice guideline. Click to download.

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Colonic Pseudo-Obstruction In Trauma Patients – Part I

A funny thing happened eight years ago. During one of our morbidity and mortality conferences at Regions Hospital, we got the first hint of an emerging pattern. We noted occasional trauma patients who developed colonic pseudo-obstruction (CPO), also known as Ogilvie’s syndrome.

In reviewing our experience, it seemed to occur mostly in men who had sustained pelvic or thoracolumbar spine injuries. Surgical instrumentation for these injuries also appeared to be a common factor, as was middle-aged or older, obesity, and metabolic diseases like type II diabetes.

We continued to see the pattern and treated it in a highly variable way depending on the attending surgeon. Abdominal x-rays were obtained semi-randomly, and if the cecum was considered as the ill-defined term “large,” the patient was sent to the ICU for an injection of neostigmine or endoscopic evacuation. If a perforation occurred, patients often got very sick.

As always, variable practice patterns are fodder for developing a practice guideline. This is the first part of a two-part series on CPO in trauma patients. First, I’ll review a new article describing this condition’s incidence in orthopedic patients. Then, in my next post, I will share a practice guideline we developed for use at Regions Hospital.

The paper was a retrospective cohort study performed by the surgical group at Copenhagen University Hospital in Denmark. They focused on patients who underwent pelvic or acetabular procedures for traumatic injury over twelve years. One cohort consisted of patients who developed CPO; the other did not.

The definition of CPO was based on standard procedures that this surgical group already used, although the specifics were not fully explained. It was based on a physical examination of the abdomen, laboratory tests, and radiographic images. Patients with a colonic diameter >10 cm were treated with neostigmine infusion. Colonoscopic decompression was used if neostigmine did not work or was contraindicated.

Here are the factoids:

  • Of 1060 patients who underwent pelvic or acetabular procedures for trauma, 25 developed CPO (2.4%)
  • The incidence was only 1.6% for pelvic fractures and about 2.6% for acetabular fractures or combined fracture patterns
  • Risk factors identified included motorcycle crash, preperitoneal packing, concomitant skull fracture or intracranial hemorrhage, paraplegia or tetraplegia, internal fixation, congestive heart failure, diabetes, and sepsis or nosocomial infection
  • CPO development increased ICU length of stay by 9 days and added a month to the hospital stay
  • Mortality was higher in the CPO group (8% vs. 6%), but this was not statistically significant

Bottom line: This is the first paper I’m aware of that quantifies what I have already seen regarding Ogilvie’s syndrome in trauma. It should be an eye-opener for everyone who sees seriously injured orthopedic patients. The increased lengths of stay are enormous, which adds to the cost and the potential for even more complications.

Obviously, this is a problem that needs to be taken very seriously. Use of the ICU for neostigmine infusion or procedural decompression should be common. But recognition and initial management should be standardized, so all appropriate patients are treated for the condition.

In my next post, I’ll share the practice guideline we developed at Regions hospital. It is designed to identify the condition early and provide decompressive therapy without moving the patient to the ICU.

Reference: Ogilvie Syndrome in Patients With Traumatic Pelvic and/or
Acetabular Fractures: A Retrospective Cohort Study. J Orthop Trauma 37(3):122-129, 2023.

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Best Of EAST 2023 #12: VTE Prophylaxis In Severe TBI

Time for another abstract on venous thromboembolic disease (VTE) prophylaxis, but this time in patients with severe head injury. VTE is a significant problem for trauma patients. Those with a potential source of bleeding from their injuries cause us to hesitate and consider the timing of chemical prophylaxis closely. Do we really want to cause more bleeding?

This is particularly problematic with intracranial hemorrhage, as the treatment is major brain surgery. Over recent years, the literature has been leaning toward earlier prophylaxis as soon as the intracranial blood has stopped evolving.

The EAST Multicenter Trials Group performed a seven-year retrospective review at 24 Level I and II trauma centers to assess the safety and efficacy of VTE chemoprophylaxis.  They divided patients into three groups: no prophylaxis, early prophylaxis (within 24 hours), and late prophylaxis (after 24 hours).

The authors assessed two endpoints: VTE occurrence and expansion of intracranial hemorrhage (ICH). They used several regression models to check their hypotheses.

Here are the factoids:

  • A total of 2,659 patients met the inclusion criteria. This averages out to 15 eligible patients per month per center. This is probably reasonable when combining a few high-volume centers with more lower volume centers.
  • Compared to early prophylaxis, patients who received late prophylaxis were twice as likely to develop VTE, although this was not statistically significant (p = 0.059)
  • Compared to early prophylaxis, patients who received no prophylaxis were a third less likely to develop VTE, although this, too, was not statistically significant (p = 0.39
  • About 25% of patients who received either early or late prophylaxis suffered an extension of their ICH, but only 17% of the no-prophylaxis group did
  • The regression model showed that the no prophylaxis group was 36% less likely to develop ICH extension compared to either early or late prophylaxis groups.

The workgroup concluded that the development of VTE was not dependent on the timing of the start of prophylaxis. Furthermore, patients who did not receive any prophylaxis had significantly decreased odds of ICH extension. The group recommended larger randomized studies to extend this work.

Bottom line: Shocker! This multicenter study suggests that the no prophylaxis and early prophylaxis groups had fewer VTE events than the late group, although these results were not statistically significant. This means that there wasn’t an advantage to giving the shot.

And the other major conclusion was that both early and late prophylaxis was associated with a significantly higher incidence of ICH extension. 

Roll these together, and you will find that neither early nor late prophylaxis help prevent VTE, yet they are both associated with additional bleeding in and around the brain! 

Heresy! I am trying to figure out what to make of these results. Perhaps the retrospective nature of the study and the wildcards this introduces influenced the results. It could be a study power problem, except the numbers were approaching significance that was unfavorable for prophylaxis.

I will be very interested to hear how the authors explain these findings. And yes, a well-powered randomized study would be great, but I don’t think many institutional review boards will be keen on a no-treatment group given our current fear of VTE. So don’t count on any real answers soon.

Reference: EARLY VTE PROPHYLAXIS IN SEVERE TRAUMATIC BRAIN INJURY: A PROPENSITY SCORE WEIGHTED EAST MULTICENTER TRIAL. EAST 2023 Podium paper #38.

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