How many times has this happened to you? You walk into a young, healthy trauma patient’s room and discover that they have nasal prongs and oxygen in place. Or better yet, these items appear overnight on a patient who never needed them previously. And the reason? The pulse oximeter reading had been low at some point.
This phenomenon of treating numbers without forethought has become one of my pet peeves. Somehow, it is assumed that an oximetry value less than the standard “normal” requires therapy. This is not the case.
In young, healthy people the peripheral oxygen saturation values (O2 sat) are typically 96-100% on room air. As we age, the normal values slowly decline. If we abuse ourselves (smoking, working in toxic environments, etc), lung damage occurs and the values can be significantly lower. Patients with obstructive sleep apnea will have much lower numbers intermittently through the night.
So when does a trauma inpatient actually need supplemental oxygen? Unfortunately, the literature provides little guidance on what “normal” really is in older or less healthy patients. Probably because there is no norm. The key is that the patient must need oxygen therapy. How can you tell? Examine them! Talk to them! If the only abnormal finding is patient annoyance due to the persistent beeping of the machine, they don’t need oxygen. If they feel anxious, short of breath, or have new onset tachycardia, they probably do. Saturations in the low 90s or even upper 80s can be normal for the elderly and smokers.
Bottom line: Don’t get into the habit of treating numbers without thinking about them. There are lots of reasons for the oximeter to read artificially low. There are also many reasons for patients to have a low O2 sat reading which is not physiologically significant. So listen, talk, touch and observe. If your patient is comfortable and has no idea that their O2 sat is low, turn off the oxygen and toss the oximeter out the window.
You’re running a trauma activation, and everything is going great! Primary survey – passed. Resuscitation – lines in, fluid going. You are well into the exam in the secondary survey.
Then it happens. The automated blood pressure cuff shows a pressure of 72/44. But the patient looks so good!
You recycle the cuff. A minute passes and another low pressure is noted, 80/52. You move the cuff to the other arm. Xray comes in to take some pictures. You roll the patient. 76/50. Well, you say, they were lying on the cuff. Recycle it again.
A minute later, the pressure is 56/40, and the patient looks gray and is very confused and diaphoretic. It’s real! But how long as it been real? An easy 5 minutes have passed since the first bad reading.
Bottom line: Sometimes it’s just hard to believe that your patient is hypotensive. They look so good! But don’t be fooled. If you get a single hypotensive reading, STOP! You have 90 seconds to figure out if it’s real, so don’t do anything else but. Check the pulse rate and character with your fingers. Do a MANUAL blood pressure check. It’s fast and accurate. If you have the slightest doubt, ASSUME IT’S REAL. Remember, your patient is bleeding to death until proven otherwise. And it’s your job to prove it. Fast!
Enjoy this parody of the Dos Equis “Most Important Man In The World” commercials. This video was part of the Trauma Education: The Next Generation conference produced last week. Enjoy, and please comment or give it a thumbs up on YouTube!
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.