Category Archives: Head

Everything You Wanted To Know About: Cranial Bone Flaps

Patients with severe TBI frequently undergo surgical procedures to remove clot or decompress the brain. Most of the time, they undergo a craniotomy, in which a bone flap is raised temporarily and then replaced at the end of the procedure.

But in decompressive surgery, the bone flap cannot be replaced because doing so may increase intracranial pressure. What to do with it?

There are four options:

  1. The piece of bone can buried in the subcutaneous tissue of the abdominal wall. The advantage is that it can’t get lost. Cosmetically, it looks odd, but so does having a bone flap missing from the side of your head. And this technique can’t be used as easily if the patient has had prior abdominal surgery.

2. Some centers have buried the flap in the subgaleal tissues of the scalp on the opposite side of the skull. The few papers on this technique demonstrated a low infection rate. The advantage is that only one surgical field is necessary at the time the flap is replaced. However, the cosmetic disadvantage before the flap is replaced is much more pronounced.

3. Most commonly, the flap is frozen and “banked” for later replacement. There are reports of some mineral loss from the flap after replacement, and occasional infection. And occasionally the entire piece is misplaced. Another disadvantage is that if the patient moves away or presents to another hospital for flap replacement, the logistics of transferring a frozen piece of bone are very challenging.

4. Some centers just throw the bone flap away. This necessitates replacing it with some other material like metal or plastic. This tends to be more complicated and expensive, since the replacement needs to be sculpted to fit the existing gap.

So which flap management technique is best? Unfortunately, we don’t know yet, and probably never will. Your neurosurgeons will have their favorite technique, and that will ultimately be the option of choice.

Reference: Bone flap management in neurosurgery. Rev Neuroscience 17(2):133-137, 2009.

What Is: A Hinge Fracture Of The Skull?

Although very few things in medicine are new, I love it when I learn about something I’ve never heard of before. Recently, while reading an autopsy report, I ran across the term “hinge fracture of the skull.” What? Maybe if I were a neurosurgeon, I would have recognized the term. This was the perfect excuse to hit the books (or, more accurately, the internet).

A hinge fracture crosses the skull base transversely and involves the temporal and sphenoid bones. Here are diagrams of two common transsphenoidal fracture patterns, courtesy of radiopaedia.org. The red and green lines can be considered transverse (hinge) fractures.

Why the hinge analogy? Since the fracture extends entirely across the skull base, it splits the skull in two. In theory, the bones could hinge around this line, but the reality is that it usually doesn’t. It’s just a memorable name.

It takes a significant amount of force to fracture the skull like this. Although any major blunt force could do this, there is a higher association with motorcycle crashes. I found an interesting paper (cited below) that showed that if a rider’s face smashes into the back of the cycle driver, the force delivered to the rider’s mandible can cause this fracture pattern. It can also occur in falls from heights and direct trauma to the head (e.g., baseball bat).

Many patients with this injury do not survive very long due to severe CNS injury or other significant blunt-force injuries. Those who do may demonstrate these findings on exam:

  • Bruising typical of a skull base fracture. This includes Battle’s sign (bruising behind the ears over the mastoid process) and raccoon eyes (bruising around the eyes).
  • Evidence of severe TBI. Low GCS is expected due to significant force to the head.
  • Cranial nerve deficits. The path of the fracture can vary considerably and may involve one or more cranial nerves. Patients may manifest hearing loss, double vision (if awake), or facial paralysis.
  • CSF leak. Many basilar skull fractures result in otorrhea or rhinorrhea, and this one is no exception.

If your patient survives the trauma bay, diagnosis is made by CT scan. Given the location of this fracture, CT angiography should be added if a hinge fracture is identified. There is a higher probability of blunt carotid and vertebral arterial injury with this diagnosis.

Treatment of this fracture complex is beyond the scope of this post. Consult your friendly neighborhood neurosurgeon. Only they can appreciate the nuances and reconstructive needs of this injury.

Reference: Mechanism of transverse fracture of the skull base caused by blunt force to the mandible. Legal Medicine,
Volume 54, 101996, 2022.

 

What Is The Zumkeller Index in TBI?

Here’s something you may not have heard of before: the Zumkeller index. Most trauma professionals who take care of serious head trauma have already recognized the importance of quantifying extra-axial hematoma thickness (HT) and midline shift (MLS) of the brain. Here’s a picture to illustrate the concept:

Source: Trauma Surgery Acute Care Open

Zumkeller and colleagues first described the use of the mathematical difference between these two values in prognosticating outcomes in severe TBI in 1996.

Zumkeller Index (ZI) = Midline shift (MDI) – Hematoma thickness (HT)

Intuitively, we’ve been using this all along. At some point, we recognized that if the degree of midline shift exceeds the hematoma thickness, it’s a bad sign. The easiest way to explain this is that there is injury to the brain that is causing swelling so the shift is greater than the size of the hematoma. 

The authors of a recent paper from Brazil decided to quantify the prognostic value of the ZI by doing a post-hoc analysis of a previously completed prospective study.  They limited their study to adult patients with an acute traumatic subdural hematoma confirmed by CT scan. It used data from the 4-year period from 2012-2015.

They compared demographics and outcomes in three cohorts of ZI:

  • Zero or negative ZI, meaning that the midline shift was less than the size of the hematoma
  • ZI from 0.1 mm to 3.0 mm
  • ZI > 3.0 mm

And here are the factoids:’

  • A total of 114 patients were studied, and the mechanism of injury was about 50:50 from motor vehicle crashes vs falls
  • About two thirds were classified as severe and the others were mild to moderate, based on GCS
  • Median initial GCS decreased from 6 in the low ZI group to 3 in the highest ZI group, implying that injuries were worse in the highest ZI group
  • Mortality (14-day) was 91% in the highest ZI group and only in the low 30% range in the others
  • Regression analysis showed that patients with ZI > 3 had an 8x chance of dying within 14 days compared to the others

Source: Trauma Surgery Acute Care Open

Bottom line: This study confirms and quantifies something that many of us have been unconsciously using all along. Of course there are some possible confounding factors that were not quantified in this study. Patients with the more severe injuries tended to also have subarachnoid hemorrhage and/or intra-ventricular blood. Both are predictors of worse prognosis. But this is a nice study that quantifies our subjective impressions.

The Zumkeller Index is an easily applied tool using the measuring tool of your PACS application. It can be used to determine how aggressively to treat your patient, and may help the neurosurgeons decide who should receive a decompressive craniectomy and how soon.

So now go out and amaze your friends! You’ll be the life of the party!

Reference: Mismatch between midline shift and hematoma thickness as a prognostic factor of mortality in patients sustaining acute subdural hematomaTrauma Surgery & Acute Care Open 2021;6:e000707. doi: 10.1136/tsaco-2021-000707

Diagnosing BCVI In Children

Several days ago, in my post on “How Common Is BCVI?” I mentioned a paper recognizing the increasing incidence of BCVI in pediatric patients and the very high stroke rate (37%) and death rate (13%). These numbers are very concerning!

Previous work shows that the Memphis and Denver criteria are not very sensitive in adults. This has led many trauma centers to add CT angiography of the neck automatically in patients with a high-energy mechanism. But what about kids? Are these screening criteria any better?

A consortium of children’s hospital trauma centers has a paper currently in press that evaluated both the Memphis and Denver criteria in children under age 15. It was a four-year prospective, observational study of children with head, face, or neck injuries. Although the Memphis criteria were specifically used in the study, data for applying the original and expanded Denver criteria, EAST practice management guideline criteria, Utah score, and McGovern score were also collected. The last two are pediatric-specific criteria.

Any child who met at least one of the Memphis criteria received a CTA or MRA of the head and neck. In addition, all children with head, face, or neck injuries received a follow-up evaluation two weeks after discharge. This was designed to capture any evidence of BCVI in those who did not meet Memphis criteria and hence had no CTA/MRA. Patients who missed this evaluation or had other missing data were excluded from the analysis.

Here are the factoids:

  • A total of 2,284 children met the criteria for enrollment; nearly one-third were excluded due to no imaging/follow-up or missing data (!)
  • There were 24 BCVI diagnosed (1.6%)
  • Diagnostic accuracy of the various screening criteria were:
Criteria Sens Spec PPV NPV # CTA to detect one BCVI
Memphis 92 71 5 100 20
Denver 73 88 9 100 11
Expanded Denver 88 64 4 100 25
EAST 79 83 7 100 14
Utah 49 96 16 99 7
McGovern 75 90 11 100 9

The Memphis criteria had the highest sensitivity and would have missed the fewest BCVI. The pediatric-specific Utah score had the highest specificity but would have missed more than half of the injuries. The authors recommend refining the Memphis criteria to improve its specificity while maintaining its high sensitivity.

Bottom line: As with adults, we struggle with systematically identifying BCVI. All screening systems leave something to be desired. It’s not practical or prudent to treat children the same as adults and just liberalize the use of CTA. Substituting MRA is not practical because this requires sedation and/or intubation in the younger age groups.

Of interest in this study, the overall incidence was higher (1.6% here vs. less than 0.5% in my previous post). This is probably due to the fact that there was a significant effort to identify criteria for angiography, and follow-up was provided to detect occult injuries.

This paper adds to the previous work I cited describing how important it is to detect this injury. The current research demonstrates that the Memphis criteria are the best we have for pediatric patients at this time. But it clearly shows the need for a better tool. 

But until one is developed, a best practice would be to use the Memphis criteria to screen any pediatric patient with head, neck, or facial trauma due to a high-energy blunt mechanism. Then select CTA or MRA after conferring with your pediatrics and radiology teams.

Reference: Diagnostic accuracy of screening tools for pediatric blunt cerebrovascular injury: An ATOMAC multicenter study. Journal of Trauma, publish ahead of print, DOI: 10.1097/TA.0000000000003888.

 

Treatment Of BCVI

In my last post, I reviewed the grading system for blunt carotid and vertebral artery injury (BCVI). Today, we’ll discuss treatment, and in the next post, we will wrap up with pediatric-specific information.

There are basically three modalities at our disposal for managing BCVIantithrombotic medication (heparin and/or antiplatelet agents), surgery, and endovascular procedures. The choice of therapy is usually based on surgical accessibility and patient safety for anticoagulation. We know that several studies have shown decreased stroke events in heparinized patients. Unfortunately, this is not always possible due to associated injuries. Antiplatelet agents are usually tolerated after acute trauma, especially low-dose aspirin. However, several studies have shown little difference in outcomes in patients receiving heparin vs. aspirin/clopidogrel for BCVI.

So what to do? Here are some broad guidelines:

  • Grade I (intimal flap). Heparin or antiplatelet agents should be given. If heparin can be safely administered, it may be preferable in patients needing other surgical procedures since it can be rapidly reversed by stopping the infusion. These lesions generally heal entirely on their own, so a follow-up CT angiogram should be scheduled in 1-2 weeks. Medication can be stopped when the lesion heals.
  • Grade II (flap/dissection/hematoma). These injuries are more likely to progress, so heparin is preferred if it can be safely given. Stenting should be considered, especially if the lesion progresses. Long-term anti-platelet medication may be required.
  • Grade III (pseudoaneurysm). Initial heparin therapy is preferred unless contraindicated. Stable pseudoaneurysms should be followed with CTA every six months. If the lesion enlarges, surgical repair should be performed in accessible injuries or stenting in inaccessible ones.
  • Grade IV (occlusion). Heparin therapy should be initiated unless contraindicated. Patients who do not suffer a catastrophic stroke may do well with follow-up antithrombotic therapy. Endovascular treatment does not appear to be helpful.
  • Grade V (transection with extravasation). This lesion is frequently fatal, and the bleeding must be addressed using the best available technique. For lesions that are surgically accessible, the patient should undergo the appropriate vascular procedure. Inaccessible injuries should undergo angiographic treatment and may require embolization to control bleeding without regard for the possibility of stroke.

References:

  1. Scott WW, Sharp S, Figueroa SA, et al. Clinical and radiographic outcomes following traumatic Grade 1 and 2 carotid artery injuries: a 10-year retrospective analysis from a Level I trauma center. J Neurosurg 122:1196, 2015.
  2. Scott WW, Sharp S, Figueroa SA, et al. Clinical and radiographic outcomes following traumatic Grade 3 and 4 carotid artery injuries: a 10-year retrospective analysis from a Level 1 trauma center. J Neurosurg 122:610, 2015.
  3. Scott WW, Sharp S, Figueroa SA, et al. Clinical and radiological outcomes following traumatic Grade 1 and 2 vertebral artery injuries: a 10-year retrospective analysis from a Level 1 trauma center. J Neurosurg 121:450, 2015.
  4. Scott WW, Sharp S, Figueroa SA, et al. Clinical and radiological outcomes following traumatic Grade 3 and 4 vertebral artery injuries: a 10-year retrospective analysis from a Level I trauma center. The Parkland Carotid and Vertebral Artery Injury Survey. J Neurosurg 122:1202, 2015.