All posts by The Trauma Pro

Flying Or Diving After Traumatic Pneumothorax: Part 1

Today, I’m dusting off an old post on flying and diving after pneumothorax. This shows the thinking up until a few years ago. In my next post, I’ll write about a more recent paper that suggests that we can shorten the “no-fly” time considerably.

Hint: no changes to the diving recommendations. One pneumothorax is likely to ground you forever. (pardon the pun)

Patients who have sustained a traumatic pneumothorax occasionally ask how soon they can fly in an airplane or scuba dive after they are discharged. What’s the right answer?

The basic problem concerns Boyle’s Law (remember that from high school?). The volume of a gas varies inversely with the barometric pressure. So the lower the pressure, the larger the volume of gas becomes. Most of us hang out close to sea level, so this is not an issue. But for flyers or divers, it may be.

Flying

Helicopters typically fly only one to two thousand feet above the ground, so the air pressure is about the same as standing on the earth. However, flying in a commercial airliner is different. Even though the aircraft may cruise at 30,000+ feet, the inside of the cabin remains considerably lower though not at sea level. Typically, the cabin altitude goes up to about 8,000 to 9,000 feet. Using Boyle’s law, any volume of gas (say, a pneumothorax in your chest) will increase by about a third on a commercial flight.

The physiologic effect of this increase depends upon the patient. They may never know anything is happening if they are young and fit. But if they are elderly and/or have a limited pulmonary reserve, it may compromise enough lung function to make them symptomatic. And having a medical problem in an aluminum tube at 30,000 feet is never good.

Commercial guidelines for travel after pneumothorax range from 2-6 weeks. The Aerospace Medical Association published guidelines that state that 2-3 weeks is acceptable. The Orlando Regional Medical Center reviewed the literature and devised a practice guideline with a single Level 2 recommendation that commercial air travel is safe 2 weeks after resolution of the pneumothorax, an that a chest x-ray should be obtained immediately before travel to confirm resolution.

Diving

Diving would seem to be pretty safe, right? Any pneumothorax would just shrink while the diver was at depth, then re-expand to the original size when he or she surfaces, right?

Not so fast. You are forgetting why the pneumothorax was there in the first place. The lung was injured, most likely via tearing it, penetration by something sharp, or popping a bleb. If the injured area has not completely healed, then air may begin to escape through it again. And since the air used in scuba diving is delivered under pressure, this could result in a tension pneumothorax.  This is disastrous underwater!

Most injuries leading to pneumothorax heal completely. However, if there are bone spicules stuck in the lung or more complicated parenchymal injuries from penetrating injury, they may never completely heal. This makes the diver susceptible to a tension pneumothorax anytime they use their regulator.

Bottom line: Most patients can safely travel on commercial aircraft 2 weeks after resolution of pneumothorax. Ideally, a chest xray should be obtained shortly before travel to confirm that it is gone. Helicopter travel is okay at any time, since they typically fly at 1,500 feet or less.

Divers should see a physician trained in dive medicine to evaluate their injury and imaging prior to making another dive.

Tomorrow: new info on flying after pneumothorax

References:

  • Divers Alert Network – Pneumothorax – click to download
  • Practice Guideline, Orlando Regional Medical Center. Air travel following traumatic pneumothorax. October 2009.
  • Medical Guidelines for Airline Travel, 2nd edition. Aerospace Medical Association. Aviation, Space, and Environmental Medicine 74(5) Section II Supplement, May 2003.

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.

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.

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.

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.