Imaging

The Times They Are A Changin': the "No Zone" Approach to Management of Penetrating Neck Trauma

Clinical Case: You're working a busy evening shift when a middle aged woman is brought in by EMS from the scene of a car accident.  She has a deep laceration to her anterior neck near the level of the cricoid cartilage from a glass shard.  She is neurologically intact, talking with a normal voice and is in no respiratory distress.  However, there is a continuous and brisk oozing of blood from the wound.

Clinical Question: What imaging is indicated in hemodynamically stable, neurologically intact patients with penetrating neck injuries?  What should the typical disposition be?

Literature Review:
Any neck wound that extends deep to the platysma is considered a penetrating neck wound, and it is estimated that they represent 5-10% of all trauma patients who arrive to the emergency department. Two common ways of anatomically dividing the neck include using the sternocleidomastoid to divide the neck into anterior and posterior triangles, or dividing the neck into three zones [1]:


    In the event of penetrating injury to the neck, airway compromise should be immediately assessed, with early intubation for airway protection if there is any concern for expanding neck hematoma or concerns for airway injury.  An attempt can be made to orotracheally intubate (bougies have been suggested as excellent initial adjuncts [2]), but plans should be made to move to early cricothyroidotomy if the airway is unable to be secured from above. After securing the airway and establishing hemodynamic stability, the neck wound should be carefully inspected.  Injuries that breach the platysma may have caused significant underlying injury, and it is best to avoid probing these wounds at the bedside, as this could disrupt hemostasis.  Aside from risk of vascular disruption, patients with penetrating neck injuries warrant consideration of tracheal and esophageal compromise.  Signs of tracheal injury include air bubbling at the wound, hemoptysis, subcutaneous emphysema, and stridor.  Esophageal injuries can be initially be asymptomatic, and a missed injury can lead to neck space infection and mediastinitis [3].   Emergent surgical consultation is warranted, as patients with hemodynamic instability and/or "hard signs" of vascular or aerodigestive tract injury should go for emergent neck exploration [3].

    Classically, management of hemodynamically stable patients with penetrating neck injuries was based on an anatomic "zone-based" approach mentioned above, with zone II injuries often going directly to surgical exploration and zone I and III injuries undergoing angiography, bronchoscopy, and esophagoscopy.  This approach was developed in the 1970’s, but it had several problems [4].  First, there may be poor correlation between the location of the neck wound and internal organ involvement, as there may be traversing of zones internally. Secondarily, the adoption of a mandatory-exploration policy lead to a high negative exploration rate (53% - 56%)[4,5].

    With the rapid improvement and dissemination of the use of  CT over the past few decades, a “No Zone” management approach based on careful physical exam with CT angiography has been shown in surgical literature to decrease resource utilization and unnecessary surgical exploration, making the rigid zone approach less relevant [3].   Several studies have examined the sensitivity and specificity of CT angiography in stable patients with penetrating neck injury.  A study by Inaba et. al. prospectively evaluated an algorithm in which patients with "soft signs" of injury (venous oozing, non-expanding hematoma, minor hemoptysis, dysphonia, dysphagia, or small amount of subcutaneous emphysema) underwent an initial evaluation with CT-angiography and asymptomatic patients were observed [6].  Over a 31-month period, 453 patients with penetrating neck trauma were prospectively evaluated in their study.  186 of these patients had "soft signs" of clinical injury, and underwent CT angiography as their initial method of evaluation.  38.2% of these patients had an injury to zone II of the neck.  Using an aggregate gold standard of the final diagnosis at discharge which included operative exploration, catheter-based angiography, bronchoscopy, esophagogram and esophagoscopy results and clinical follow-up (duration not specified),  the sensitivity and specificity of CT Angiography for vascular or aerodigestive injury was 100% and 97.5 % respectively.  There were two patients who had false-positive findings of vascular injury (irregularities in the ICA) that were not present on follow-up with surgical exploration and/or angiography, and three patients had air tracking suspicious for aerodigestive tract injury that was not confirmed on follow-up imaging and endoscopic studies. 

    As mentioned above, the "No Zone" approach combining clinical exam with imaging evaluation has the potential to decrease unnecessary neck exploration. A study by Osborn et. al. examined the rate of negative neck explorations in patients who were taken to the OR who did not have hard signs of injury.  They compared the rate of negative neck explorations amongst those patients who had a CT-A as part of their initial evaluation and those who did not, and found that CT angiography significantly reduced the negative neck exploration rate [7]:

    Source: Osborn et al. (2008)
     In their review of penetrating neck trauma management, Shiroff at al. shared the algorithm below, comparing the traditional vs. "no zone" approach:

    Image Source:  Reference 3



    Take Home Points: Patients with penetrating neck trauma who are hemodynamically unstable or  display hard signs of vascular or aerodigestive should receive immediate surgical consultation with consideration for operative or invasive management.  As the traditional, anatomic approach to management of penetrating neck trauma is associated with a high rate of negative neck exploration, patients with soft signs of injury should be initially evaluated with CT angiography which has a high sensitivity for clinically-significant injury.

    Submitted by Philip Chan, PGY-3
    Edited by Maia Dorsett (@maiadorsett), PGY-4
    Faculty reviewed by jason wagner (@TheTechDoc)

    References
    [1] Tintinalli’s Emergency Medicine, 7e.  Ch 257. 
    [2] Daniel, Y., de Regloix, S., & Kaiser, E. (2014). Use of a Gum Elastic Bougie in a Penetrating Neck Trauma. Prehospital and disaster medicine, 29(02), 212-213.
    [3] Shiroff, A. M., Gale, S. C., Martin, N. D., Marchalik, D., Petrov, D., Ahmed, H. M., ... & Gracias, V. H. (2013). Penetrating neck trauma: a review of management strategies and discussion of the ‘No Zone’approach. The American Surgeon, 79(1), 23-29.
    [4] Prichayudh, S., Choadrachata-anun, J., Sriussadaporn, S., Pak-art, R., Sriussadaporn, S., Kritayakirana, K., & Samorn, P. (2015). Selective management of penetrating neck injuries using “no zone” approach. Injury.
    [5] Varghese, A. (2013). Penetrating neck injury: a case report and review of management. Indian Journal of Surgery, 75(1), 43-46.
    [6] Inaba, K., Branco, B. C., Menaker, J., Scalea, T. M., Crane, S., DuBose, J. J., ... & Demetriades, D. (2012). Evaluation of multidetector computed tomography for penetrating neck injury: a prospective multicenter study. Journal of Trauma and Acute Care Surgery, 72(3), 576-584.
    [7] Osborn, T. M., Bell, R. B., Qaisi, W., & Long, W. B. (2008). Computed tomographic angiography as an aid to clinical decision making in the selective management of penetrating injuries to the neck: a reduction in the need for operative exploration. Journal of Trauma and Acute Care Surgery, 64(6), 1466-1471.

    An Imperfect Science: Diagnosis of CSF Shunt Malfunction

    Clinical scenario: Your patient is a 20 yo male with a history of VP shunt placement as a child for obstructive hydrocephalus. He was brought to the emergency department by his family because of decreased responsiveness over the past day. On arrival to the emergency department, he has aniscoria (L greater than R), no verbal response, and withdraws his extremities symmetrically. An emergent non-contrast head CT shows no change in ventricular size from prior CT scan one year prior and a VP shunt series demonstrates no evidence of fracture of the shunt line. Clearly, something is critically wrong with the patient, but is it his VP shunt to blame?

    Clinical question: What is the spectrum of shunt complications? What is the sensitivity of clinical exam and various imaging modalities in detecting shunt malfunction?

    Literature Review: There are multiple forms of CSF shunts, the most common of which is the Ventriculo-Peritoneal shunt (as opposed to ventriculo-atrial & ventriculo-pleural) which shunts CSF into the peritoneal cavity. A CSF shunt is composed of a proximal catheter, reservoir, valve and distal catheter [1]. The proximal catheter starts in the frontal horn of the lateral ventricle and exits through a burr hole to connect to the reservoir which is located in the subcutaneous tissue (this is what is accessed when neurosurgery taps a shunt). Flow from the reservoir to the distal catheter is regulated by a one way valve. Programmable shunts allow for the setting of a specific pressure above which fluid drains through a valve. This is sometimes adjusted in one direction or another for VP shunt patients who experience headaches, lightheadedness or other symptoms related to the pressure when their evaluation is negative for obstruction, infection etc. For VP shunts, the distal catheter is then tunneled into the peritoneum


    Image Source: Cancer Research UK / Wikimedia Commons


    As an emergency physician, one must be familiar with the presentation and diagnosis of shunt complications because they are relatively common; incidence of VP shunt failure is close to 40% at one year and 50% at two years from initial shunt placement, at least in the pediatric population where it has been most actively studied[2]. There are multiple types of shunt malfunctions leading to increased intracranial pressure, including but not limited to:

    1. Mechanical Obstruction - Most proximally, the catheter can be obstructed by blood, debris or in-growth of the choroid plexus. The catheter position within the lateral ventricle can also migrate. Kinking or fracture along the catheter track at any point will also lead to shunt failure, as will distal obstruction which can occur when the catheter adheres to the omentum or erodes into intra-abdominal organs.

    2. Infection - This often presents with shunt failure, and occurs most commonly within 6 months of placement due to intraoperative contamination with skin flora. The overall incidence of shunt infection is common (8-10%).

    3. Ventricular Loculations - Loculations within the ventricle can create non-communicating pockets of CSF that are not drained by the VP shunt. If these grow, they can cause symptoms of hydrocephalus.

    At least in very young children, depressed level of consciousness, nausea/vomiting, headache, irritability, and fluid tracking along the shunt site are highly predictive of shunt malfunction (see positive LR below). However, none of these clinical signs and symptoms are adequately sensitive to rule out shunt malfunction in their absence [2,3]. Some signs like abdominal pain/peritonitis are less commonly seen, but more highly predictive of shunt infection.

    LR, Sensitivity, & Specificity for clinical signs and symptoms associated with shunt failure in two large pediatric studies


    In addition to overall clinical exam and picture, radiographic imaging plays a central role in the emergency department evaluation of VP shunt malfunction.

    CT scans are the most commonly used imaging modality to evaluate for shunt malfunction. While enlarged ventricles (when compared with prior imaging studies) are the canonical feature of shunt obstruction, other CT findings correlated with increased intracranial pressure include effacement of the cortical sulci, loss of the basal cisterns and periventricular edema due to transependymal CSF absorption [4]. Based on multiple retrospective pediatric studies using surgical shunt revision as a "gold standard", CT has a sensitivity for shunt malfunction of anywhere between 53% to 92% [4,5; see Table below]. In one small retrospective study of 174 adults evaluated for shunt malfunction with both shunt series and head CT, head CT had a sensitivity of only 52%, a specificity of 78% and negative predictive value of 88% for shunt malfunction [6]. This study only included patients who had had shunt series performed, so it may have underestimated the sensitivity of CT by excluding patients who were evaluated with CT alone. While this is a wide range of estimations for sensitivity, the important point is that a negative head CT does not completely rule out a shunt malfunction.

    Shunt series radiographs are used to identify mechanical shunt defects such as shunt discontinuity or kinking. Studies in both children [4,7] and adults [6] support the conclusion that although the yield and sensitivity of radiographic shunt series is very low (see Table below), it is not zero. Shunt series rarely (~ 1-2%) detect abnormalities not identified on initial CT that prompt surgical revision. Therefore, shunt series are still indicated in the evaluation of potential shunt malfunction.


    Table 2 from Boyle and Nigrovic, 2015. Reference 4.


    In some cases, more commonly in pediatric institutions, MRI protocols have been instituted to reduce cranial radiation in children [4,8,9]. This has been made possible in part due to advances in MRI technology that have allowed for development of "ultra-fast" or Rapid MRI protocols that can acquire images in a span of ~ 1-4 minutes. Rapid Cranial MRI has been studied in comparison to CT for detection of ventricular shunt malfunction in the pediatric population, and appears to be comparable at least with respect to specificity and accuracy [8]. When considering using MRI in place of CT, the provider should be aware that some VP shunts have a programmable shunt valves that can be affected by the magnetic force of the MRI machine and may need to be readjusted after the exam. For this reason, it is common practice to obtain coned-down radiographs of a small indicator usually located near the proximal portion of the distal catheter to identify the setting prior to MR and then again after MR. If the programmed setting has changed, the neurosurgeon can use a magnet to reprogram the setting. The radiologist uses an indicator that looks like a clockface to determine the settings. 


    Image source: http://www.ajnr.org
    Take home Points: Malfunction and infection are common complications of CSF shunts. No single clinical exam finding or image study is sufficient to rule out shunt malfunction, and clinical management should take into account patient history, overall clinical picture, diagnostic data and neurological assessment.
     

    Submitted by Maia Dorsett @maiadorsett
    Faculty Reviewed by Peter Panagos and Richard Griffey
     

    References
    1. Wallace, A. N., McConathy, J., Menias, C. O., Bhalla, S., & Wippold, F. J. (2014). Imaging Evaluation of CSF Shunts. American Journal of Roentgenology, 202(1), 38-53.2.Garton, H. J., Kestle, J. R., & Drake, J. M. (2001). Predicting shunt failure on the basis of clinical symptoms and signs in children. Journal of neurosurgery, 94(2), 202-210.3. Piatt Jr, J. H., & Garton, H. J. (2008). Clinical diagnosis of ventriculoperitoneal shunt failure among children with hydrocephalus. Pediatric emergency care, 24(4), 201-210.4. Boyle, T. P., & Nigrovic, L. E. (2015). Radiographic Evaluation of Pediatric Cerebrospinal Fluid Shunt Malfunction in the Emergency Setting. Pediatric emergency care, 31(6), 435-440.
    5.Lehnert, B. E., Rahbar, H., Relyea-Chew, A., Lewis, D. H., Richardson, M. L., & Fink, J. R. (2011). Detection of ventricular shunt malfunction in the ED: relative utility of radiography, CT, and nuclear imaging. Emergency radiology, 18(4), 299-305.
    6. Griffey, R. T., Ledbetter, S., & Khorasani, R. (2007). Yield and utility of radiographic “shunt series” in the evaluation of ventriculo-peritoneal shunt malfunction in adult emergency patients. Emergency radiology, 13(6), 307-311.
    7. Desai, K. R., Babb, J. S., & Amodio, J. B. (2007). The utility of the plain radiograph “shunt series” in the evaluation of suspected ventriculoperitoneal shunt failure in pediatric patients. Pediatric radiology, 37(5), 452-456.
    8.Boyle, T. P., Paldino, M. J., Kimia, A. A., Fitz, B. M., Madsen, J. R., Monuteaux, M. C., & Nigrovic, L. E. (2014). Comparison of rapid cranial MRI to CT for ventricular shunt malfunction. Pediatrics, 134(1), e47-e54.
    9. Koral, K., Blackburn, T., Bailey, A. A., Koral, K. M., & Anderson, J. (2012). Strengthening the argument for rapid brain MR imaging: estimation of reduction in lifetime attributable risk of developing fatal cancer in children with shunted hydrocephalus by instituting a rapid brain MR imaging protocol in lieu of head CT. American Journal of Neuroradiology, 33(10), 1851-1854.10.

    Does cardiac standstill on bedside echo equal 100% mortality?

    You’re in the midst of catching up on notes during a hectic overnight shift when out of the corner of your eye you see a stretcher zoom into the trauma bay – with an EMT leaning over the side performing chest compressions. As the team gathers, the paramedics give report. The patient is a middle-aged male, no known past medical history, who was acting normally about half an hour ago when he suddenly collapsed in front of his family. They started CPR within a couple minutes of the patient collapsing, and called EMS. The paramedics continued CPR, placed a supraglottic airway, and placed the patient on the monitor. He has had a slow, organized rhythm without pulse throughout the arrest. He has received several doses of epinephrine without response. The patient has been pulseless for a little over half an hour by the time he arrives. The ED crew takes over CPR, IV access is obtained, and the patient switched over to the ER monitors, which show a slow, wide-complex, relatively disorganized rhythm. The patient shows no signs of life. Your attending physician calls for the ultrasound, and calls out to the team that if the bedside echo shows cardiac standstill, you will consider terminating further resuscitative efforts.

    Clinical Question:

    Does cardiac standstill on bedside echo universally predict mortality in OHCA?

    Literature Review:

    A systematic review of studies investigating the diagnostic accuracy of bedside echo in OHCA was published by a Canadian group in Annals in 2012 [1]. This was a well-done study, with a broad search strategy, rigid but logical inclusion & exclusion criteria, and quality assessment with a modified version of the QUADAS instrument.
    Eight studies were included in the final analysis, with a total of 568 patients. Of the 378 patients with cardiac standstill on bedside echo, only 9 (2.4%, 95% CI 1.3% – 4.5%) achieved ROSC. The authors pooled results of the included studies to devise a 2x2 table and determine test characteristics of bedside echo. This revealed a sensitivity of 91.6% (95% CI 84.6% - 96.1%) and specificity of 80.0% (95% CI 76.1% - 83.6%). The positive likelihood ratio is 4.26 (95% CI 2.63 - 6.92) and the negative likelihood ratio is 0.18 (95% CI 0.10 - 0.31). Heterogeneity was minimal (0.0%) for the negative likelihood ratio, but was significant (82.1%) for the positive likelihood ratio. The authors conclude, “While there is insufficient evidence to support using echo in isolation to decide whether or not to continue with cardiopulmonary resuscitations, the presence or absence of VWM in the context of the pretest survival likelihood can provide emergency personnel with further information to assist making that difficult decision whether to stop cardiopulmonary resuscitation with more confidence.”

    It is important to note that the outcome of interest in this systematic review was survival to admission, which is not necessarily a good predictor of neurologically-intact long-term survival past discharge, which is the ultimate patient-centered outcome of OHCA. Further limitations included variable inclusion/exclusion of traumatic arrest patients in the included studies, and variability in application of bedside ultrasound. Namely, there were significant differences in training level of examiners, degree of external review of OCHA studies, and definition of “cardiac standstill” between the included studies.
    This paper was the focus of a “Systematic Review Snapshot,” authored by our very own Dr. Brian Cohn and published in Annals in 2013 [2].

    I attempted a PubMed search using the same search strategy as the authors in the original systematic review (available in the online supplementary material), but I did not discover any further studies on this topic that have been published since that paper in 2012.

    Take-home Points:

    - Cardiac standstill does not universally lead to failure of resuscitation of OHCA.
    - The best-available current evidence does not support the use of bedside echo alone to predict outcomes in OHCA patients.
    - Other factors influencing likelihood of neurologically-intact survival (down time, underlying rhythm, patient age/comorbidities, etiology of arrest, etc.) should be taken into account when interpreting bedside echo results.
    - More research is needed to determine true prognostic factors associated with survival from OHCA.

    Submitted by C. Sam Smith, MD. @CSamSmithMD
    Faculty review by Brian Cohn +EMJClub 

    References:
    [1] Acad Emerg Med. 2012 Oct;19(10):1119-26.
    [2] Ann Emerg Med. 2013 Aug;62(2):180-1.

    Needle that belly!

    An infant female with no significant history presents to your trauma bay after reported accidental blunt trauma to the abdomen, the patient arrives from a referral hospital where plain films demonstrated free air. On arrival the patient show signs of hemodynamic instability and an elevated lactate. The patient was decompressed with "needle peritoneumostomy" prior to going to the OR for exploration. 

    Clinical Question:

    Can “tension pneumoperitoneum” cause hemodynamic instability?

    Literature Review:

    The presence of "free air" in the peritoneum is often diagnostically significant; however, the gas itself is rarely of clinical importance. An exception to this rule is in the case of a tension pneumoperitoneum. Tension pneumoperitoneum (TPP), also known as hyperacute abdominal
    Example of pneumoperitoneum & football sign
    compartment syndrome [1], or abdominal tamponade [2], is a rare, but potentially deadly event. Similar to tension pneumothorax, the underlying mechanism is a tissue flap that acts as a one-way valve for air release, resulting in a progressive increase in intra-abdominal pressure. The increasing peritoneal pressures may rapidly lead to respiratory compromise due to diaphragmatic elevation and a drop in cardiac output resulting from decreased venous return or aortic outflow due to occlusion. [3] This can progress to cardiovascular collapse and respiratory failure and eventually death. [2]

    In one of the earliest reported cases in 1913, tension pneumoperitoneum was theorized to be a consequence of gas forming bacteria in the abdominal cavity. [4] Now it is known that tension pneumoperitoneum is usually a consequence of hollow viscus perforation, post-operative complications, positive pressure ventilation or other insulflation-dependent procedures (eg, colonoscopy, endoscopy, cystoscopy or air enema). There has even been reported cases from CPR. [9,10] However, there are few published case reports of TPP as a result of blunt force trauma. [3,6]


    Signs and symptoms of TPP include abdominal distension and fullness. The additional presence of a tympanitic, rigid abdomen, hypotension, dyspnea, and jugular vein congestion can be considered as signs of TPP, requiring immediate management.

    The diagnosis of tension pneumoperitneum should be based physical exam and supported by imaging of the abdomen. Plain films of the abdomen show large amounts of intraperitoneal air. Lateral supine and left lateral decubitus films show the air best. Elevation of the diaphragm or medial displacement of the liver, called the “saddlebag sign” is suggestive of tension physiology.[1] The viscera may appear more distinct as they are outlined by the air tissue interface as in the double-wall sign (the visualization of the outer wall of bowel loops caused by the presence of extraluminal and intraluminal gas). Another radiographic sign of a large pneumoperitoneum is football sign - the intraperitoneal air outlines the abdominal cavity and the falciform ligament appears like the laces of a football.

    With this said, plain films of the abdomen are rarely obtained in the setting of trauma. If hemodynamically stable, the patient is imaged using computed tomography (CT scan) which will show posterior liver compression by superiorly located free air. However, because CT scanning is contraindicated in the hemodynamically unstable patient, the diagnosis may have to rest on the clinical presentation and/or portable plain films. It can be confirmed by needle decompression or paracentesis with a rush of air and improvement of hemodynamic stability. [7]
    Treatment of tension pneumoperitoneum depends on the stability of the patient. If the patient is acutely unstable with labile blood pressures and signs of shock, treatment is emergent needle decompression using a 14g angiocatheter. There are no large trials that recommend a specific location based on success and/or safety rates. However, several small case series suggest using the same sites for decompression: two centimeters below the umbilicus in the midline (through the linea alba) or five centimetres superior and medial to the anterior superior iliac spines on either side. [8]. If the patient is stable, a paracentesis catheter/drain can be placed. The definitive treatment is to determine what initially caused the air accumulation, which may necessitate an exploratory laparotomy. It should be noted that a nasogastric tube turned to suction is unlikely to evacuate the pneumoperitoneum due to the ball and valve mechanism that created it initially. [3]


    Take-home Points: 
    -Pathophysiology and treatment is similarly to pneumothorax, it can lead to cardiovascular collapse, respiratory failure, and eventually death if untreated. Unstable patients should be recognized on exam, however x-ray and CT have utility based on stability. Decompression is the treatment and can be performed with an angiocath placed two centimeters below the umbilicus in the midline. 


    References:
    [1] Lin B, Tension Pneumoperitoneum. The Journal of Emergency Medicine, Vol. 38, No. 1, pp. 57–59, 2010.
    [2] Khan ZA. Conservative management of tension pneumoperitoneum. Ann R Coll Surg Engl. 2002 May;84(3):164-5.
    [3] Ogle JW Tension Pneumoperitoneum after Blunt Trauma. The Journal of Trauma: Injury, Infection, and Critical Care. 1996 Nove; 41(5): 909-911.
    [4] Falkenburg C. Ein Fall von Gasansammlung in der freien Bauch-Hohle. Dtsch Z Chir 1913;124: 130-6.
    [5] Olinde A, Carpenter D, Maher J. Tension pneumo-peritoneum. Arch Surg 1983;118:1347-50.

    [6] Ferrera PCChan L. Tension pneumoperitoneum caused by blunt trauma. Am J Emerg Med. 1999 Jul;17(4):351-3.
    [7] Yakobi-Shvili RCheng D. Tension pneumoperitoneum--a complication of colonoscopy: recognition and treatment in the emergency department. J Emerg Med. 2002 May;22(4):419-20.
    [8] Fu KIshikawa TYamamoto TKaji Y. Paracentesis for successful treatment of tension pneumoperitoneum related to endoscopic submucosal dissection. Endoscopy. 2009;41 Suppl 2:E245.
    [9] Williams DTManoochehri PKim HT. Tension pneumoperitoneum. Emerg Med J. 2014 Nov;31(11):943.
    [10] Mills SAPaulson DScott SMSethi G. Tension pneumoperitoneum and gastric rupture following cardiopulmonary resuscitation. Ann Emerg Med. 1983 Feb;12(2):94-5.
    Submitted by Decompression Danny Kolinsky, PGY-2
    Edited by Louis Jamtgaard, PGY-3. @Lgaard
    Faculty review by Rebecca Bavolek

    As Low As Reasonably Achievable

    Your patient is a 40-something female who has never been to your facility before but reports a history of chronic abdominal pain of undetermined etiology. She has had an appendectomy and a cholecystectomy. She is now presenting with two days of right-sided cramping abdominal pain associated with nausea without vomiting and lightheadedness. Screening labs protocoled by the triage nurse are unremarkable, and a bedside RUQ ultrasound is negative for significant pathology. After two doses of morphine she is still visibly uncomfortable in the stretcher. The team is reticent to pursue further diagnostics, but given the fact that she currently carries no diagnosis for her symptoms and is still in considerable distress, and the lack of any prior imaging in your EMR, the decision is made to order a CT abdomen/pelvis with contrast.

    Clinical Question:

    Given the fact that the pre-test probability for finding significant pathology in this patient is low, how worried should you be about exposing your patient to further ionizing radiation?



    Literature Review:

    Several groups of experts, including the American Association of Physicists in Medicine, the National Council on Radiation Protection & Measurements, and the US FDA, all report the median effective dose of ionizing radiation (IR) from an abdomen/pelvis CT (the most common CT ordered in the US) as 8 - 10 millisieverts (mSv) [1]. This is compared to 0.065 mSv for a two-view chest X-ray, and 0.42 mSv for a screening mammography series [12].

    At the risk of turning this into a physics lecture, the Sievert is the SI unit of measurement for “dose equivalent” and for "effective dose" of radiation. “Dose equivalent” includes a weighing factor that accounts for the relative biological impact of different types of radiation. “Effective dose” takes this a step further, by utilizing weighing factors to account for the relative effect of radiation on different types of tissues. It represents the probability of cancer induction, and is commonly used in medical research. Conventionally, “effective dose” is used to measure low doses of IR which carry the stochastic (i.e., somewhat random and not entirely predictable) risk of inducing malignancy. This is in contrast to high doses of IR that cause deterministic effects -- what we would consider radiation poisoning -- that are certain to occur with exposure to high levels of IR. These exposures are typically measured in Grays, the SI unit of absorbed dose (simply the mean energy imparted to each unit of mass). For more detailed information on radiation quantities and exposures, click here.

    So when should we be concerned? There is no "safe" dose of radiation. We are all exposed to a certain level of "background" radiation which probably leads to a certain rate of malignancy all on its own; any exposure to IR beyond this can only increase this risk. Thus the radiation safety doctrine of "As Low As Reasonably Achievable" governing IR exposure.

    The National Academy of Sciences' National Research Council published phase 2 of its Biological Effects of Ionizing Radiation (BEIR) VII report in 2006. In this report, the group gathered available biological and epidemiological data related to human IR exposures. This included survivors of the atomic bomb blasts in Japan during WWII, people who lived close to nuclear power accident sites, workers with occupational exposures, and patients who underwent medical radiologic studies [2]. The breadth of available data suggest that increased cancer risk is associated with acute exposures of 10-50 mSv, and protracted exposures of 50-100 mSv [3]. Data also suggest a "linear, no threshold" dose-response relationship -- again, no "safe" level of IR exposure exists and any exposure, no matter how small, carries a nonzero risk of developing malignancy [2].

    It doesn't take a particle physicist to see that the high end of the commonly reported dose of a CT scan overlaps with the low end of the dose range leading to increased malignancy. While the absolute risk of developing malignancy from a single CT scan may be quite low, the sheer number of scans performed would suggest that, from a population standpoint, many new malignancies are being induced by medical imaging.

    Indeed, a group of authors used radiation risk models from the BEIR report to estimate incidence of future cancers resulting from the 72 million CT scans performed in the US in 2007 (excluding those scans performed on patients already diagnosed with cancer or those performed in the last five years of a patient's life) [4]. They concluded that approximately 29,000 new cancers (95% CI 15,000 - 45,000) could result from these scans, with the largest contributor being CT scans of the abdomen & pelvis with 14,000 new cancers (95% CI 6,900 - 25,000). About a third of these projected cancers resulted from scans performed on patients aged 35 - 54, and 15% from scans performed on pediatric patients less than 18 years old. Lung cancers were projected to be most common, followed by colon cancer and leukemia. Two thirds of cancers were projected to occur in females.

     
    Projected number of future cancers (mean and 95% uncertainty limits) that could be related to computed tomographic scan use in the United States in 2007, according to age at exposure.
    From Reference [4]
    From Reference [4]
    These were not the only authors to reach such concerning conclusions. Again using BEIR VII data & models, one group estimated that annual chest CT screening for lung cancer in adults starting at age 40 would result in a 1/10,000 estimated excess lifetime risk of radiation-induced lung cancer mortality for men and 3/10,000 for women, which would likely negate any mortality benefit gained by early identification of lung malignancy from such screening [5]. Another group examined risk from CT coronary angiogram, using simulated exposure doses and BEIR VII models, and found a 1/284 lifetime attributable risk for a 40-year-old woman, with risk inversely proportional to age [6]. Several other groups have used calculated doses of common scans and BEIR VII models to conclude that exposure to CT scans likely significantly increases lifetime risk of cancer [7,8,9].

    Two chief limitations affect all of these studies. First, they all rely on BEIR VII models of lifetime attributable risk. Unfortunately, accurately quantifying risks directly would require long-term follow-up of very large patient populations. The BEIR VII models are based on direct evidence of the carcinogenic behavior of IR in other populations, such as nuclear accident & atomic bomb survivors. As such, they likely represent the best models we have for estimating long-term risk of IR in medical imaging. In fact, in vitro studies suggest that the form of IR utilized in medical imaging (x-rays) may have even greater potential to damage cellular DNA than gamma rays (the primary form of IR released in atomic bomb blasts) [4].

    The second limitation to the prior studies is that they almost universally relied on estimated doses of IR from the various scans, with the majority falling in the previously-suggested 8 - 10 mSv range. Practically speaking, it is nearly impossible to truly quantify the IR absorbed by a human body in a CT scanner. Some degree of estimation & calculation will always be necessary, but most of the aforementioned studies relied on previously-published estimates of dose or dose estimates from "phantom studies," not exams performed on actual patients.

    In 2009, a group of authors in San Francisco attempted to more directly quantify the radiation dose of common CT study types, compare intra- and inter-site variability, and determine what impact this variability has on attributable cancer risk [10]. They estimated this effective dose using the Dose-Length Product, which is recorded as part of the CT scan metadata. The DLP is an approximation of the total energy a patient absorbs from the scan, determined by multiplying the energy absorbed from a single slice (the CT Dose Index or CTDI) by the total length of the body scanned. The authors combined the DLP with details of the area imaged and used conversion factors to translate this into an effective dose. This approach is used elsewhere in the literature, and is described in a report by the American Association of Physicists in Medicine's report on The Measurement, Reporting, and Management of Radiation Dose in CT [11]. They also utilized methods & risk estimates published in the BIER report to calculate the lifetime attributable risks of cancer above baseline based on the magnitude of a single exposure.

    Based on the study group's data, doses of many scans were significantly higher than the commonly-reported 8 - 10 mSV. Abdomen/pelvic CTs had the highest radiation doses, ranging on average from 15 - 31 mSv. The corresponding median adjusted lifetime attributable risk of cancer was 4 cancers per 1000 patients. For a routine abdomen/pelvis CT with contrast, one attributable cancer would be expected for every 470 scans of 20-year-old females, or for every 870 scans of 40-year-old females. These numbers are even more concerning for multiphase scans (e.g., angiography studies), which impart effective doses up to 90 mSv based on the authors' calculations. At this end of the scale, a 20-year-old female undergoing multiphase abdomen/pelvis CT could face as high as a 1/250 risk of cancer attributable to the scan. One of the takeaways from this study was that the same CT scan type could yield effective dosages with over 13-fold variability between sites, or even between different scans on the same equipment.

    From Reference [10]

    From Reference [10]

     The American College of Radiology addressed these concerns in their White Paper on Radiation Dose in Medicine in 2007 [13]. In this document, the ACR acknowledges that effective dose of commonly-used CT scans may exceed 10 - 25 mSv. They further state that, while there are no hard data as of yet showing an increased incidence of cancer with CT scans, the boom of CT ordering has just occurred in the past 5 - 10 years, and cancer due to IR usually does not occur until 1 - 2 decades or longer after exposure.

    Overall, data suggest that anywhere between 1 - 3% of cancer cases in the US may be due to exposure to IR from medical imaging [4,13]. The ACR White Paper states that the massive increased use of CT scanning in the past decade "may likely result in an increase in the incidence of imaging-related cancer in the US population in the not-too-distant future."


    Faculty commentary:
    Dr. Richard Griffey, Director of Quality and Safety for Washington University Emergency Medicine and evidence-based diagnostics advocate, had this to add:

    “One of the things people often ask/wonder about…is what strategy makes sense on an individual patient level?
    • What is the incremental harm of an additional study?
    • Does the benefit of the study far outweigh the risks?
    • What are the other options – ultrasound, watchful waiting, serial exams, MRI, etc.?
    • If someone has already undergone multiple scans, how much additional risk does one more scan actually incur?
    • Who should we be focusing on in avoiding ionizing radiation?"

    Take-home:
    - While it is highly impractical to conduct a longitudinal study of cancer incidence based on exposure to medical imaging, based on the best data we have it is highly likely that such exposure will lead to tens of thousands of new malignancies in the future.
    - The risk of malignancy is most pronounced in females, and is inversely proportional to age.
    - Patients undergoing repeat CT scans are almost certainly exposed to a level of ionizing radiation that increases their risk of cancer above baseline.
    - It is our responsibility as patient caregivers to be responsible in our ordering of CT scans and other studies that expose patients to ionizing radiation. They carry a nonzero risk of harm which must be weighed against possible diagnostic yield.

    Submitted by C. Sam Smith (@CSamSmithMD), PGY-3
    Faculty Reviewed by Richard Griffey 

    References:
    [1] National Council on Radiation Protection and Measurements, Ionizing Radiation Exposure of the Population of the United States. 2009;NCRP report 160 http://www.ncrponline.org/.
    [2] BEIR VII Phase 2.  Washington, DC National Academies Press 2006.
    [3] Proc Natl Acad Sci U S A 2003;100(24);13761-13766.
    [4] Arch Intern Med. 2009;169(22):2071-2077.
    [5] J Med Screen 2008;15(31):153- 158.
    [6] JAMA 2007;298(3):317-323.
    [7] Radiology 2004;232(3):735- 738.
    [8] Radiology 2009;251(1):175- 184.
    [9] AJR Am J Roentgenol 2009;192(4):887- 892.
    [10] Arch Intern Med. 2009;169(22):2078-2086.
    [11] American Association of Physicists in Medicine, The Measurement, Reporting and Management of Radiation Dose in CT: Report of AAPM Task Group 23 of the Diagnostic Imaging Council CT Committee.  College Park, MD American Association of Physicists in Medicine2008;AAPM report 96.
    [12] National Cancer Institute, Radiation risks and pediatric computed tomography (CT): a guide for health care providers. 2009.
    [13] J Am Coll Radiol 2007;4(5):272- 284.

    Imaging in Renal Colic

    You are working in the Emergency Department when a 30ish year-old female is wheeled by, clasping on to her right flank and clearly in pain.  You head into the room and find out that she had the acute onset of right flank pain that has been coming and going for the last hour.   She is otherwise healthy and denies any prior history of renal stones.  Thinking that this is probably a kidney stone, you order some pain medication, a UA, and a urine pregnancy test.  She is (thankfully) not pregnant and has 2+ blood in her UA.

    You log back in to order your next diagnostic test of choice.  You start to click on “renal stone protocol CT” but pause…  and think to yourself: “Do I need to irradiate this woman to make the diagnosis?  Will the results of the CT scan change my management in some way?  What are the alternatives?”

    Clinical Question #1:

    Does a CT scan change management in cases of suspected uncomplicated renal colic?
                    
    The Literature:

    There are several smaller studies that addressed whether a CT scan changes the clinical management in a patient where there is a high suspicion for renal stone.
                    
    Zwank et. al. [1] published a prospective observational study addressing this question.  The study enrolled providers caring for 93 “clinically stable” patients  > 18 yo with abdominal or flank pain, > 18 years of age and the  “most likely diagnosis” of renal colic.   Patients at higher risk of complication, i.e. those with a history of chronic kidney disease, nephrectomy, renal transplant, UTI, prior renal stones, were excluded from the study.  Prior to the CT, providers were surveyed as to what their top 3 differential diagnoses were and whether they thought that the CT scan might change management.    In the end, 62/93 patients who were scanned were diagnosed with renal colic (as a side note only 84% of these had hematuria on UA).   Five (5.3%) patients received an alternative diagnosis after CT scan – two ovarian cysts, one ovarian tumor, diverticulitis, and mesenteric edema.  Of the 16 patients where CT scan was obtained even though the provider thought it was very unlikely to change management, 10 had symptomatic renal stones and reportedly none had a change in management (unclear why the disparity if a diagnosis was not reach in 6/16 cases).    On this small pool of data, the authors conclude that “This result indicates that providers who are confident with the diagnosis of renal colic and who do not anticipate benefit from a CT scan can trust their low pre-test probability or ‘gestalt’ of low likelihood of benefit and should strongly consider not ordering a CT scan.” 
                    
    Another way of framing the question about whether CT scans change management in patients thought to have renal colic is to examine the incidence of alternative diagnoses that are found on CT in these patients.   In their prospective study, Pernet et. al. [2] examined this question by following the CT diagnosis of 155 patients with suspected uncomplicated renal colic (i.e. exclusion of patients with compromised renal function, UTI, fever, suspected bilateral renal stones).  118/155 (77%) were found to have uncomplicated stones, while 10 (6%) of these patients were found to have alternative diagnoses after CT.  These diagnoses included large calculi needing urology intervention, pyelonephritis, biliary colic, appendicitis, ileitis, small bowel obstruction and intra-renal hemorrhage.  Though a similar proportion of alternative diagnoses were found in this study when compared with Zwank et. al. above, these authors argue that CT(low-dose radiation) should be performed in cases of predicted uncomplicated renal colic because of the proportion of alternative diagnoses that mandated other intervention or hospitalization.  They further argue, that the population of patients which people would least want to irradiate (young women) are also the most likely to have some alternative diagnoses.   

    Clinical Question #2:

    Given that stones requiring urologic intervention and alternative diagnoses are found on CT imaging, how does ultrasound measure up as an imaging modality?

    The Literature:

    An older article in the British Journal of Radiology published in 2001  [3] [around the advent of use of CT and Ultrasound for diagnosis of renal calculi as opposed to intravenous urography (IVU)] prospectively evaluated the sensitivity and specificity of non-contrast CT and ultrasound for renal calculi.  They prospectively enrolled 62 patients with suspected uncomplicated renal colic.  These patients underwent both renal ultrasound and CT scan.  The gold standard was stone recovery or urological intervention.  43 (69%) of patients with suspected renal colic were confirmed by the “gold standard”.  Ultrasound showed 93% sensitivity and 95% specificity in the diagnosis of ureterolithiasis, while CT showed 91% and 95%.    Alternative pathology was found in six patients (~ 10%).  These alternative pathologies were cholelithiasis, cholecystitis, ovarian torsion, adnexal masses and appendicitis.  Both CT and ultrasound detected these, with the exception of the case of appendicitis, which was detected by CT scan alone.  Given advances in imaging technology, it is likely the sensitivity of CT has increased with time, but this is an impressive comparison.

    Another study compared KUB + ultrasound versus CT scan for detection of clinically significant renal stones [4].   This was a retrospective study of 300 patients evaluated with KUB, US, non-contrast CT or some combination of the above for renal colic.  The study is overall very confusing because of the number of combinations of imaging modalities that patients had.  Despite this, one interesting observation was that among 147 patients who underwent KUB and/or US and CT scan, 22 had a normal KUB or US (unclear what proportion had what) and a CT scan positive for stone.  Of these, mean stone size was < 5 mm suggesting that this was a population of patients who was unlikely to need any type of urologic intervention.

    Along the same lines of sensitivity of ultrasound for renal stones requiring urologic intervention, two separate studies examined the incidence of urologic intervention needed in patients with “normal” renal ultrasounds [5, 6].  In one of these studies (Yan et. al.) ,  they prospectively followed 341 patients with renal colic who were evaluated with ultrasound.   Of the 105 (30.8%) patients were classified as “normal”, none had urologic intervention in the following 90 days.  Alternative pelvic pathologies were identified on ultrasound (such as ovarian cysts and pregnancy) but there was no avenue for direct comparison with CT in this study.  A similar study from Edmonds et. al. retrospectively reviewed the records of all patients undergoing renal ultrasound for suspected nephrolithiasis over the course of a year.  Of a 352/817 (43%) that were classified as “normal”, only 2 patients (0.6%) required urologic intervention in the following 90 days.  They did not comment on alternative diagnoses.

    Take home:

    Renal ultrasound is a reasonable initially imaging modality for patients with suspected uncomplicated renal colic.  While we are overall pretty good an predicting who has renal colic based on history and exam (~ 60- 70% of all patients with this as a suspected diagnosis had imaging confirming it in the above studies), we should keep in mind that anywhere between 5 – 10% of these patients will have an alternative diagnosis requiring alternative management.   Ultrasound is good at picking up these alternative diagnoses as well.

    References:

    1. Zwank et. al. “Does computed tomographic scan affect diagnosis and management of patients with suspected renal colic?” American Journal of Emergency Medicine 32 (2014) 367–370
    2. Pernet et. al. “Prevalence of alternative diagnoses in patients with suspected uncomplicated renal colic undergoing computed tomography: a prospective study.” CJEM. 2014 Feb 1;16(0):8-14.
    3. Patlas et. al. “Ultrasound vs CT for the detection of ureteric stones in
    patients with renal colic”. The British Journal of Radiology, 74 (2001), 901–904
    4. Ekici and Sinanoglu. “Comparison of conventional radiography combined
    with ultrasonography versus nonenhanced helical computed
    tomography in evaluation of patients.” Urol Res (2012) 40:543–547
    5. Yan et. al. “Normal renal sonogram identifies renal colic patients at low risk for urologic intervention: a prospective cohort study” CJEM 2014:1-8.


    6. Edmonds et. al.  “The utility of renal ultrasonography in the diagnosis of renal colic in emergency department patients” CJEM 2010;12(3):201-6.

    Kindly submitted by Maia Dorsett, PGY-3.

    Does a cervical seatbelt sign mandate advanced imaging?

    You are working in the emergency department when EMS brings in a middle aged female who was the restrained driver in a low speed head-on MVC. In the emergency department, she is slightly hypertensive and complaining of generalized stiffness. Her physical exam (including C-spine exam and neurologic exam) is unremarkable with the exception of an abrasion to the left side of her neck without surrounding hematoma concerning for a cervical seat belt sign.

    Clinical Question:


    In this otherwise well appearing patient you wonder – what is the best course of action? Does the physical finding of a cervical seat belt sign warrant additional imaging for vascular injury, such as a CT-A?

    Literature:


    One study that addressed this question was a retrospective review of patients who received neck CT angiograms based on the presence of a seatbelt sign alone at a Level I trauma center from 2008-2010. Over this time period, 418 patients underwent a CT-A. Eleven patients had positive vascular findings, two with blunt carotid injury (BCA) – giving an overall frequency vascular injury of 2.6%. Importantly, all of the patients who were found to have vascular injuries had a cervical spine fracture, rib fracture, thoracic spine fracture, facial fracture, skull fracture, large hematoma on the neck or a combination of the above injuries. The correlation between seatbelt sign and positive CT-A finding was overall very weak (r = .007). The above findings lead the authors to reasonably conclude that CT-A of the neck vascular injury can be “safely reserved for patients with a seatbelt sign and obvious injuries on physical examination and/or positive findings on standard trauma imaging.”

    A second study prospectively evaluated trauma patients with cervical or thoracic seatbelt signs at a level I trauma center over a 17 month period. Out of 131 trauma pts with cervical or thoracic seatbelt signs, four (3%) were found to have carotid artery injuries. The presence of a carotid injury was strongly associated with a GCS < 14 (p< 0.0003), ISS > 16 (p < .0001), and the presence of a clavicle or first rib fracture (p < .0037). No vascular injuries were identified in patients with thoracic-only seatbelt signs. Each of the four patients had at least one identifiable significant injury ranging from scalp laceration + extremity fracture to clavicle + bilateral superior rib fractures. The authors of this study concluded that the cervical-thoracic seatbelt sign combined with an abnormal physical examination is an “effective screening combination for cervico-thoracic vascular injury.”

    Take Home:


    CT-angiogram is not necessarily indicated based on the finding of a cervical seatbelt sign alone in the absence of significant hematoma, neurologic symptoms, or other traumatic injuries.

    References:

    1) Dhillon, Ramandeep Singh, et al. "Seatbelt sign as an indication for four-vessel computed tomography angiogram of the neck to diagnose blunt carotid artery and other cervical vascular injuries." The American Surgeon 79.10 (2013): 1001-1004.
    2) Rozycki, Grace S., et al. "A prospective study for the detection of vascular injury in adult and pediatric patients with cervicothoracic seat belt signs." The Journal of Trauma and Acute Care Surgery 52.4 (2002): 618-624.