Most trauma professionals have heard of OPSI, but few have ever seen it. The condition was first described in splenectomized children in 1952. Soon after, it was recognized that this infection occurred in asplenic adults as well.
OPSI is principally due to infection by encapsulated organisms, those with a special polysaccharide layer outside of the bacterial wall. This layer is only weakly immunogenic, and confers protection from the normal immune mechanisms, particularly phagocytosis. However, these bacteria are more easily identified and removed in the spleen.
OPSI may be caused by a number of organisms, the most common being Strep. pneumonia, Haemophilus influenza, and meningococcus. For this reason, the standard of care has been to administer vaccines targeting the usual organisms to patients who have lost their spleen.
How common is OPSI? A recent paper from Gernany reviewed comprehensive data from 173 intensive care units over a 2-year period. Here are some of the more interesting factoids:
- 2,859 ICU beds were screened, but the number of unique patients was not given. This is very disappointing because incidence cannot be calculated!
- 52 cases of OPSI occurred
- Only half of the patients had received vaccines
- Pneumococcus was the most common bacterium (42%). There were no H. Flu or meningococcal infections.
Bottom line: Yes, OPSI exists and can occur in your asplenic patients. It is uncommon enough that you and your colleagues will probably never see a case. But proper vaccination remains important. Papers consistently show that we are collectively not very good at ensuring that our splenectomized patients receive all their vaccines, ranging from only 11-50%. We collectively need to make better efforts to provide them to our at-risk patients.
Reference: Overwhelming Postsplenectomy Infection: A Prospective Multicenter Cohort Study. Clin Infec Diseases 62:871-878, 2016.
Here’s the most recent newsletter that was released at the end of October; the topic is Potpourri.
In this issue, I cover:
- Femoral Traction And Open Fractures
- Nursing: My Doc Won’t Listen!
- Zones Of The Retroperitoneum
- CT After Laparotomy For Penetrating Trauma
To download the current issue, just click here! Or copy this link into your browser: http://bit.ly/TME201910
The next newsletter will be released to subscribers at the end of November. I’ll release it to everyone else via this blog in December, so subscribe now if you want it sooner! Click this link right away to sign up now and/or download back issues.
Got a suggested theme for later issues? Just let me know what you’d like to read about by emailing or leaving a comment here.
On occasion (but not routinely) trauma patients need to have their stomach decompressed. The reflex maneuver is to insert a nasogastric (NG) tube. However, this may be a dangerous procedure in some patients.
Some patients may be at risk for a cribriform plate fracture, and blindly passing a tube into their nose may result in a nasocerebral (NC) tube (see picture). Immediate and profound neurologic decompensation usually occurs. This is a neurosurgical catastrophe, and the outcome is uniformly dismal. It generally requires craniectomy to remove the tube.
The following patients are at risk:
- Evidence of midface trauma (eyebrows to zygoma)
- Evidence of basilar skull fracture (raccoon eyes, Battle’s sign, fluids leaking from ears or nose)
- Coma (GCS<8)
If you really need the tube, what can you do? If the patient is comatose, it’s easy: just insert an orogastric (OG) tube. However, that is not an option in awake patients; they will continuously gag on the tube. In that case, lubricate a curved nasal trumpet and gently insert it into the nose. The curve will safely move it past the cribriform plate area. Then lubricate a smaller gastric tube and pass it through the trumpet.
You are seeing a young man in the emergency department who gives a history of falling two days ago. He experienced chest pain at the time which has persisted, but he did not immediately seek medical care. He has noticed that he now gets winded when walking quickly or climbing stairs, and describes pleuritic chest pain.
He presents to your emergency room and on exam has a bruise over his left lateral chest wall. Subcutaneous emphysema is present, and breath sounds are absent. Chest x-ray shows a complete pneumothorax on the left.
You carefully prepare and insert a chest tube in the usual position. A significant rush of air occurs, which tapers off over 15 seconds. Here is the followup image:
About 10 minutes later you are called to his room because he is complaining of dyspnea and his oxygen saturation has decreased to 86%. Breath sounds are somewhat decreased and the tube appears to be functioning properly. You immediately obtain another chest x-ray:
What just happened? This is a classic case of unilateral “flash” pulmonary edema after draining the chest cavity. This phenomenon was first described in 1853 in a patient who had just undergone thoracentesis. It is very uncommon, but seems to occur after rapid drainage of air or fluid from the chest cavity.
Here are some interesting factoids from case reports:
- It occurs more often in young men
- It is most common when draining large hemo- or pneumothoraces
- Rapid drainage seems to increase the incidence
- It is likely due to increased pulmonary capillary permeability from inflammatory mediators or changes in surfactant
- Symptoms typically develop within an hour after drainage
What should you do? First, if you are draining a large collection of air or blood, do it slowly. Clamp the back end of the chest tube prior to insertion (you should always do this if you value your shoes) and use it to meter the amount of fluid or air released. I typically let out about 300cc of fluid, then wait a minute and repeat until all the blood has been drained. For air, vent it for 10 seconds, then wait a minute and repeat.
In patients at high risk for this condition, apply pulse oximetry and follow for about an hour. If they still look and feel great, nothing more need be done.
- Fulminant Unilateral Pulmonary Edema After Insertion of a Chest Tube. Dtsch Arztebl Int 105(50):878-881, 2008.
- Reexpansion pulmonary edema after chest drainage for pneumothorax: A case report and literature overview. Respir Med Case Rep 14:10-12, 2015.
- Re-expansion pulmonary edema following thoracentesis, Can Med Assn J 182(18):2000-2002, 2010.
Radiologists sure know their anatomy! The vast majority of the time, I actually know what they are describing. But every once in a while they’ll toss in some term that I know I probably learned about in medical school (last century). For whatever reason though, I’m just not able to retrieve it.
Which brings me to the pars fracture. Hmm. I figure that if I have to hit the books again to look something up, there are probably a few other trauma professionals out there who are dying to know what it is, too. Here’s a diagram of a typical vertebra:
The arch extending away from the vertebral body consists of the pedicles, which are connected by the lamina. A number of things jut off from this arch, including the transverse and spinous processes and the articular processes.
The area between the lamina and pedicle and adjacent to the articular process is called the pars interarticularis. This area is a bit thinner and flatter than the rest of the arch and can fracture if sufficient acute stress is applied. It can also fracture if enough chronic stress in the area occurs. This pattern is typically seen in the lumbar spine, but may also occur at the cervical level. Thus, a pars fracture or pars defect is simply a fracture through this area.
Another term you may see with regard to the pars is spondylolysis. This is defined as a defect in the pars interarticularis, typically from a fracture. So if you see either of these terms in a radiology report, recognize that they are basically one and the same.
Here is a nice image showing the location of the pars, and the axial CT appearance of “bilateral pars defects.”
Mystery solved! Amaze your friends!