All posts by TheTraumaPro

Treating Numbers: Pulse Oximetry

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. 

DVT Prophylaxis After Solid Organ Injury

Nonoperative management of solid organ injury is the norm, and has reduced the operative rate significantly. At the same time, the recognition that development of deep venous thrombosis (DVT) in trauma patients is commonplace creates uncertainty? Is it safe to give chemical prophylaxis with low molecular weight heparin (LMWH)? How soon after injury?

The trauma group at USC+LAC published the findings of a retrospective review of 312 patients undergoing nonoperative management for their liver, spleen or kidney injuries. They looked at chemical prophylaxis administration and its relationship to failure of nonop management of solid organ injury.

As expected, as the grade of the solid organ injury increased, so did the failure rate of nonoperative management. Administration of low molecular weight heparin, such as enoxaparin, did not increase failure rate in this study. All but one failure occurred in patients who had not yet received the injections. Likewise, two DVT and two pulmonary embolisms occurred, but only in patients who had not yet received prophylaxis. 

Bottom line: This small study offers some assurance that early prophylaxis is okay, and a few prospective studies do exist. UCSF / San Francisco General is comfortable beginning chemical prophylaxis 36 hours postop, regardless of solid organ injury. Look for more guidance on this issue in the near future. Until then, consider starting LMWH prophylaxis early to avoid complications from DVT or PE.

Reference: Thromboembolic prophylaxis with low-molecular-weight heparin in patients with blunt solid abdominal organ injuries undergoing nonoperative management: current practice and outcomes. J Trauma 70(1): 141-147, 2011.

The Value Of Repeated Head CT

Repeating the head CT in patients with head injury has almost become routine. This practice varies greatly and depends on the neurosurgeon’s preference in many centers. It occurs most commonly when there is blood inside the skull, any type of blood. But does this practice make sense? Sure, if you’ve got a small epidural it seems reasonable. But what about that wisp of subarachnoid blood?

Another paper being presented at the Congress of Neurologic Surgeons this fall describes a review of 445 cases at their hospital and a meta-analysis of 15 studies in the literature. The authors looked at the practice of repeat CT scanning with respect to the good old clinical exam. They stratified all patients who underwent an intervention after repeat CT into two groups, based on changing clinical exam or CT findings.

They found that a significant number of patients required some management change based on deteriorating neurologic exam, whereas very few required it based on the repeat CT. The authors concluded that it is not necessary to rescan a head trauma patient if their neurologic status is stable or improving. 

Bottom line: This is preliminary data, and it is only available in abstract form, so don’t change your practice yet. We need more information on how many patients were reviewed and how good the meta-analysis was. However, you should begin to question whether rescanning everyone is necessary or prudent. Not all head injuries are alike, and some of the trivial ones, like subarachnoid blood in a young adult probably don’t need a repeat scan. More to come when this is presented and/or published.

Reference: The Value of Scheduled Repeat Cranial Computed Tomography Following Mild Head Injury: Single Center Experience and Meta-Analysis. Paper 152, presented at the Congress of Neurologic Surgeons, October 2012.

Subdural Hematomas and Hygromas Simplified

There’s a lot of confusion about subdural pathology after head trauma. All subdural collections are located under the dura, on the surface of the brain. In some way they involve or can involve the bridging veins, which are somewhat fragile and get more so with age.

Head trauma causes a subdural hematoma by tearing some of these bridging veins. Notice how thick the dura is and how delicate the bridging veins are in the image below.

When these veins tear, bleeding ensues which layers out over the surface of the brain in that area. If the bleeding does not stop, pressure builds and begins compressing and shifting the brain. A subdural hematoma is considered acute from time of injury until about 3 days later. During this time, it appears more dense than brain tissue.

After about 3-7 days, the clot begins to liquefy and becomes less dense on CT. Many hematomas are reabsorbed, but occasionally there is repeated bleeding from the bridging veins, or the hematoma draws fluid into itself due to the concentration gradient. It can enlarge and begin to cause new symptoms. During this period it is considered subacute.

It moves on to a more chronic stage over the ensuing weeks. The blood cells in it break down completely, and the fluid that is left is generally less dense than the brain underneath it. The image below shows a chronic subdural (arrows).

Hygromas are different, in that they are a collection of CSF and not blood. They are caused by a tear in the meninges and allow CSF to accumulate in the subdural space. This can be caused by head trauma as well, and is generally very slow to form. They can lead to slow neurologic deterioration, and are often found on head CT in patients with a history of falls, sometimes in the distant past. CT appearance is similar to a chronic subdural, but the density is the same as CSF, so it should have the same appearance as the fluid in the ventricle on CT.

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