A 60-year-old man known to have DM type 2 was brought by the family as a camel hit his knee. He was not able to walk on it at the scene and in ED. It was swollen with no open wound.
Tips Although patients come with isolated injuries, we always have to make sure that they do not have other injury findings. Therefore, approaching systematically to the patient is important. At this moment, please remember primary and secondary surveys of multiple trauma. The animal attacks may create multiple injuries on patients, and they should be evaluated as multiply injured patients. After you ruled our multiple or life, organ, extremity threatening injury, you can deep dive into isolated injuries. In this case, knee injury after a direct hit.
Of course, inspection and palpation are essential in every extremity injury. Evaluating the patient for neurovascular problems and range of motions are applied in almost every extremity trauma. But sometimes, clinical presentations or findings can be subtle and you may need a better tool. In these case, we recommend using Ottawa Knee Rules.
The image shows tibia plateau fracture on AP knee x-ray.
Her father brought a 9-year-old girl due to deformed right extremity. He was playing at home and fell from a hight on his hand. No open wounds. No past medical and surgical. Vaccination: up to date.
Examination: radial pulse is intact. He can move the fingers but with limitation due to pain. Sensation is normal. The X-ray showed both radius and ulna fracture. The patient underwent procedural sedation with IV ketamine, and the reduction was made with ortho oncall.
The EMS brought a 39-year man as his right upper extremity was stuck in a machine in a factory where he works. He came with deformity and severe pain in his right arm. Pain management was given. He received tetanus toxoid as well. X-ray shows oblique humeral shaft fracture with shortening and angulation. He underwent procedural sedation to reduce it.
It is common to hear that “when you work in an Emergency Department (ED), you have to be prepared for everything”. In my experience as a medical student, this could not be more true. I’ve seen tea overdose, collision scooter vs horse, and anything in between. All these experiences will contribute to my formation and made me realize that we are not prepared for many situations. Some of these situations may involve specific populations we’re not so familiarized with and sometimes can change the way we manage an emergency.
Here, I want to discuss some of these “special populations” which may demand a different approach than the usual – and that is what makes emergency medicine so interesting. Let’s talk about one of these subgroups of patients: athletes, and what makes them unique.
Athletes: What do I need to know about them?
Heart and Hemodynamic: The “athlete’s heart syndrome (1)”
Morphological, functional and electrical changes
Lower heart rate;
Hypertrophic left ventricle (LV)
Lifelong cardiac remodelling could lead to arrhythmogenic pathways
Changes in autonomic nervous system – vagal tonus
Unlike what may be the first thought, the respiratory system does not differ greatly in athletes from non-athletes (2).
High energy trauma:
Be aware that professional athletes are constantly at risk of high energy traumas, in special head traumas (concussions) and limb trauma (fractures);
How could this be a problem?
Late signs of hypovolemia
The athlete’s autonomic nervous system has pronounced vagal tonus, which leads to the famous resting bradycardia – this could disguise a tachycardia, one of the early signs of hypovolemia (2).
Delay in seeking help
Elite athletes may delay seeking help or admit they are not feeling well for fear of losing a competition or training sessions.
Besides that, in amateur (and sometimes even in professional) level competitions, staff and coaches often are not trained to identify conditions that need prompt medical assistance
Common situations and how to manage
Exercise and health always have been put together in a “cause and consequence” relation. Besides their undeniable positive effects, exercise on the professional level also has its sidebacks and associated risks. Here I want to discuss some physiological changes we observe in the elite athletes and a very common condition in the ED: the sport-related concussion.
Sport-related concussion (3,4) is a traumatic brain injury induced by biomechanical forces. It may be caused either by a direct impact to the head or by a force transmitted from the impact elsewhere in the body; It typically presents with rapid onset of short-lived signs and symptoms; However, the course is sometimes unpredictable and may evolve in minutes to hours; It may or may not have a decreased level of counsciousnes.
The current literature organize the signs and symptoms of sport-related concussion in 4 domains
Headache, dizziness, gait disturbances, vertigo, nausea and vomiting, near vision impairment
Given the rapid onset and short duration, the patient might present to the ED with minor or no symptoms; However, the emergency physician still plays an important role, providing supportive care to relieve remaining symptoms and rule out more severe conditions.
Due to the mechanism of trauma, always rule out cervical spine lesions or instability.
A Glasgow Coma Scale < 13 should raise awareness for a more severe brain lesion.
Does this patient need a head CT?
Canadian CT head rule (adults)
PECARN CT rule (under 16)
Headache: 86% had significant pain reduction, and 52% had complete headache resolution after receiving an intravenous dose of one or more of the following: ketorolac, prochlorperazine, metoclopramide, chlorpromazine, and ondansetron. Common orally administered analgesics such acetaminophen, non-steroidal anti-inflammatories and triptans have shown efficacy for pain relief, but there are no studies in the ED setting.
Dizziness: Suspicion for peripheral vertigo can be confirmed by the Dix-Hallpike manoeuvre and treated with the Epley manoeuvre. Meclizine (vestibular suppressant) and diazepam can be used with caution because of potential side effects on cognition and alertness.
To date, rest continues to be recommended for the acute (24-48h) injury period. After that period, patients can be encouraged to become gradually more active, always below their cognitive and physical limits.
When to admit
This decision is based on the patient’s clinical status. Persistent symptoms and alterations on head CT are the most common indications for admission.
Discharging to home: Education is key for recovery and prevention of recurrence (4). Current evidence indicates that written educational material is more effective than orally given instructions only; Important information that should be present in the educational material are expected symptoms, their management and a timeframe of resolution.
Carbone A, D’Andrea A, Riegler L, Scarafile R, Pezzullo E, Martone F, America R, Liccardo B, Galderisi M, Bossone E, Calabrò R. Cardiac damage in athlete’s heart: When the “supernormal” heart fails! World J Cardiol 2017; 9(6): 470-480 Available from: URL: http://www.wjgnet.com/1949-8462/full/v9/i6/470.htm DOI: http:// dx.doi.org/10.4330/wjc.v9.i6.470
ACSM’s advanced exercise physiology. — 2nd ed.;Peter A. Farrell, Michael Joyner, Vincent Caiozzo ISBN 978-0-7817-9780-1
McCrory P, Meeuwisse W, Dvorak J, et al. Br J Sports Med 2018;51:838–847
Bazarian JJ, Raukar N, Devera G, et al. Recommendations for the Emergency Department Prevention of Sport-Related Concussion. Ann Emerg Med. 2020;75(4):471-482. doi:10.1016/j.annemergmed.2019.05.032
A 39-year-old woman presented to ED with mouth pain. She was cleaning the bathroom and suddenly slipped and fell. She hit her mandible with the floor. She was able to speak minimally—no avulsed teeth. She had teeth 23 and 24 subluxations.
This is a high energy impact trauma. Ensure that you evaluate the patient systematically for trauma and not forget to pay attention to a neck injury. Violence, assault, partner abuse should be in your mind. Specific mandibular and panoramic imaging may give excellent views for diagnosis. In some cases, CT may be necessary to evaluate the maxillofacial injury. Besides, know the teeth universal numbering. If you see this kind of damage in the examination, always rule out an alveolar fracture.
Cite this article as: iEM Education Project Team, "iEM Image Feed: Camel Bite," in International Emergency Medicine Education Project, February 10, 2021, https://iem-student.org/2021/02/10/camel-bite/, date accessed: April 18, 2021
In this post, we will share the traumatic (Epidural, subdural, cerebral contusion, subarachnoid hemorrhage, cerebral edema) and atraumatic (intracranial parenchymal hemorrhage, subarachnoid hemorrhage) brain computerized tomography (CT) findings. We will also provide GIF images and one final image, which includes all pathologies in one image.
Traumatic brain injury (TBI) has been noted as a leading cause of death and disability in infants, children, and adolescence (Araki, Yokota and Morita, 2017). In the UK alone, it’s approximated 1.4 million individuals attend the emergency department (ED) with head injury, and of those, 33%-50% are children under the age of 15; on top of this, a fifth of those patients admitted have features suggesting skull fracture or brain damage – that’s no small figure (NICE, 2014)! The particular importance of TBI in the paediatric population is that the treatment and management approach differs to adults; this is largely due to the anatomical and physiological differences in children. Furthermore, neurological evaluation in children proves more complex. All in all, children are complicated, and it is of great importance that we are aware of these differences when a paediatric patient arrives at the ED with TBI presentations.
Why is the paediatric population at risk for TBIs?
To delve slightly deeper into physiology and anatomy, there are several reasons children are at high risk of acquiring serious injury from TBIs. The paediatric brain has higher plasticity and deformity. As such, their less rigid skulls and open sutures allow for greater shock absorbance and response to mechanical stresses (Ghajar and Hariri, 1992). This ‘shaking’ of the brain inside the skull can stretch and tear at blood vessels in the brain parenchyma, resulting in cerebral haemorrhage.
Children also have a larger head-to-body size ratio, making the probability of head involvement in injury consequently higher (in comparison to adults); the head is also relatively heavier in a child, making it more vulnerable (especially in injury caused by sudden acceleration).
Young children have weaker neck muscles on top of having relatively heavier heads. Ligaments in the neck are relied on for craniocervical stability more so than the vertebrae. Hence, not only are TBIs more likely, but craniocervical junction lesions can also result from traumatic injury.
How does TBI in children come about?
The common causes of TBI in the paediatric population varies with age (Araki, Yokota and Morita, 2017). Some of these causes can be seen in the table below, which has been adopted from Araki, Yokota, and Morita (2017).
How can TBI in children present?
History: dangerous mechanism of injury (e.g. road traffic accidents or fall from a height greater than 1 meter)
Glasgow Coma Scale (GCS) less than 15 (at 2 hours after injury)
Visible bleeding, bruise, swelling, laceration
Signs of base-of-skull fracture:
‘Panda’ eyes – haemotympanum
Battle’s sign – cerebrospinal fluid leakage from ear or nose
Seizure (ask about history of epilepsy)
Focal neurological deficit
Loss of consciousness
Amnesia lasting more than 5 minutes
Note some children won’t have any of these signs, but if there is any suspicion of possible TBI, it should be investigated further.
There are various causes to paediatric TBI – also subdivided into primary and secondary TBI. Primary TBI includes skull fractures and intracranial injury. Secondary TBI can be caused by diffuse cerebral swelling. Primary and secondary TBI will be managed similarly in initial treatment (i.e. in the ED). The goal of baseline treatment is to:
maintain blood flow to the brain
prevent ischaemia (and possible secondary injury)
Analgesia, Sedation, Seizure Prophylaxis
A level of anaesthesia needs to be achieved to allow for invasive procedures, such as airway management and intracranial pressure (ICP) control. Normally opioids and benzodiazepines are using in combination for analgesia and sedation in children. Instances where a child presents with a severe TBI (defined as a ‘brain injury resulting in a loss of consciousness of greater than 6 hours and a Glasgow Coma Scale of 3 to 8’), a neuromuscular block is used to improve mechanical ventilation, stop shivering, and reduce metabolic demand.
Anticonvulsants have been used in children, in particular infants, as they have a lower seizure threshold. Risk factors for early onset of seizures in infants under the age of 2 include hypotension, child abuse, and a GCS of ≤ 8; note, all of which may occur as a result of, or preceding, a TBI! For severe paediatric TBI cases, immediate prophylactic administration of anticonvulsants has been recommended.
Maintaining Cerebral Perfusion
The gold standard to measure ICP is an external ventricular drain (EVD); which can be used not only to measure ICP but can also be opened to drain additional CSF to reduce ICP. An intraparenchymal intracranial pressure sensor is an immediate invasive method used to detect early increased ICP in children with TBI. Monitoring of both ICP and cerebral perfusion pressure (CPP) is considered standard practice in TBI management in both paediatric and adult populations, as it is associated with better outcomes.
CPP is the pressure gradient which allows for cerebral blood flow. If this pressure is not maintained, the brain will lose adequate blood flow (Ness-Cochinwala and Dwarakanathan, 2019). Elevated CPP can accelerate oedema and increase chances of secondary intracranial hypertension.
A CPP of around 40-60 mmHg (40-50mmHg in 0-5 year-olds and 50-60mmHg in 6-17 year-olds) is considered ideal. Achieving an adequate CPP can be done by increasing MAP or reducing ICP (using the above equation). Hence it is necessary to have a good understanding of what good target values for MAP and ICP are.
A good target value for MAP is the upper end of ‘normal’ for the child’s age. Reaching this can be done by using fluids (if fluid deficient) or by use of inotropes. The recommended ICP target is < 20mmHg (normal is between 5-15 mmHg and raised ICP is regarded as values over 20mmHg).
When thinking about ICP, it’s useful to remember a mass in the brain; a mass being possible haemorrhage or any other space-occupying lesion. In TBI, oedema is most prominent at around 24-72 hours post-injury. As a result of increased mass, the initial consequence is a displacement of cerebrospinal fluid (CSF) into the spinal cord. Following this, venous blood in the cranium will also be displaced.
If ICP is further elevated, herniation can result – which is serious and often fatal! Signs of uncal herniation can present as unilateral fixed and dilated pupil. Signs of raised ICP can include pupillary dilatation and series of responses known as the ‘Cushing’s Triad’: irregular, decreased respiration (due to impaired brainstem function), bradycardia, and systolic hypertension (widened pulse pressure). Cushing’s triad results from the response of the body to overcome increased ICP by increasing arterial pressure.
Using the Monroe-Kellie Doctrine as a guide, we can predict how to reduce ICP. One management is head positioning. Head-of-bed should be elevated to 30˚, with the head in mid-line position, to encourage cerebral venous drainage. The EVD can also be used to drain CSF.
Commonly, intravenous mannitol and hypertonic saline are used to manage intracranial hypertension in TBI. Mannitol is traditionally used at a dosage of 20% at 0.25-1.0 g/kg – this is repeatedly administered. The plasma osmolality of the patient needs to be kept a close eye on; it should be ≤ 310 mOsm/L. 3% NaCl can be used to raise sodium levels to 140-150 mEg/L – this is slightly higher than normal sodium levels as a higher blood osmolarity will pull water out of neurons and brain cells osmotically and reduce cerebral oedema (Kochanek et al., 2019). Mannitol works in the same manner, however, use with caution as mannitol, being an osmotic diuretic, can cause blood pressure drops and compromise CPP! In last-resort emergency cases, where ICP need to be immediately reduced, a decompressive craniotomy can be performed.
Intravascular Volume Status
Measuring the patient’s central venous pressure (CVP) is a good indicator of the child’s volume status; 4-10 mmHg have been used as target thresholds. Alternatively, you can also monitor urine output (>1mL/kg/hr), blood urea nitrogen, and serum creatinine. Low volume status should be corrected with a fluid bolus. If the patient’s volume status is normal or high, but they remain hypotensive, vasopressors may improve blood pressure. At all costs, hypotension must be avoided, as if can lead to reduced cerebral perfusion and lead to brain ischaemia; on the other end, hypertension can cause severe cerebral oedema and should also be kept an eye on.
Other considerations - There have been reports of pituitary dysfunction in 25% of paediatric TBIs (during the acute phase). Do consider this if the patient had refractory hypotension – keep ACTH deficiency in mind!
Prevent hypoxia at all costs! Hypoxia goes hand-in-hand with cerebral vasodilation – and as we already know, this increases the pressure in the cranium. Additionally, with hypoxia, there will be ischaemia. A minimum haemoglobin target of 7.0 g/dl is advised in a severe paediatric TBI case.
Other considerations - Whilst we are on the blood topic, also take care to correct and control any coagulopathies.
At a Paediatric Glasgow Coma Scale (PGCS) of less than 8, airways must be secured with a tracheal tube and mechanical ventilation commenced. SpO2 should be maintained at greater than 92%.
Of course, hypercapnia (CO2 > 6 kPa) and hypocapnia (CO2 < 4 kPa) are both not ideal, and we should maintain paCO2 at 4.5 – 5.3 kPa. However, some sources have suggested a quick fix to reduce ICP is to acutely hyperventilate the patient (as low CO2 results in cerebral vasoconstriction) – it’s suggested that paCO2 can safely go as low as 2.67 kPa before ischaemia kicks in! Mild hyperventilation is recommended (3.9 – 4.6 kPa)(Araki, Yokota and Morita, 2017).
Decreasing Metabolic Demand of the Brain
What we want is to prevent hyperthermia, as it increases cerebral metabolic demands. Normothermia (36.5˚C – 37.5˚C) can be maintained by use of cooling blankets or antipyretics. There has been debate on whether therapeutic hypothermia has shown any benefit. Some studies have shown that moderate hypothermia for up to 48 hours, followed by slow rewarming, has prevented rebound intracranial hypertension as well as decreased ICP, however, there have not been any confirmed functional outcomes or decreased mortality rates benefits of this method (Adelson et al., 2013; Hutchinson et al., 2008).
Persistent hyperglycaemia (glucose > 10 mmol/L) should be treated. Hypoglycaemia (< 4 mmol/L) is much more dangerous. Persistent hyperglycaemia can be managed by reducing the dextrose concentration in IVF (which is usually administered in the first 48 hours of ICU care), or by starting an insulin drip.
A comment on imaging methods
In the UK, the initial investigation choice for detecting acute brain injuries is a CT head scan. A CT scan should be done within an hour of suspected head injury. If there are no indications for a CT head scan (i.e. the signs/symptoms listed previously), a CT head scan should be performed within 8 hours of injury (NICE, 2014).
MRI scans are not usually done as the initial investigation, however, they have shown to provide information on the patient’s prognosis.
A final and most important note:
Don’t ever forget Safeguarding in children. Unfortunately, child maltreatment is common and can present anywhere. Have a look at the NICE guidelines below for more on how to identify child maltreatment.
Adelson PD, Wisniewski SR, Beca J, Brown SD, Bell M, Muizelaar JP, Okada P, Beers SR, Balasubramani GK, Hirtz D; Paediatric Traumatic Brain Injury Consortium. Comparison of hypothermia and normothermia after severe traumatic brain injury in children (Cool Kids): a phase 3, randomised controlled trial. Lancet Neurol. 2013 Jun;12(6):546-53. doi: 10.1016/S1474-4422(13)70077-2.
Araki T, Yokota H, Morita A. Pediatric Traumatic Brain Injury: Characteristic Features, Diagnosis, and Management. Neurol Med Chir (Tokyo). 2017;57(2):82-93. doi:10.2176/nmc.ra.2016-0191
Finnegan R, Kehoe J, McMahon O, Donoghue V, Crimmins D, Caird J, Murphy J. Primary External Ventricular Drains in the Management of Open Myelomeningocele Repairs in the Neonatal Setting in Ireland. Ir Med J. 2019 May 9;112(5):930.
Ghajar J, Hariri RJ. Management of pediatric head injury. Pediatr Clin North Am. 1992;39(5):1093-1125. doi:10.1016/s0031-3955(16)38409-7
Hutchison JS, Ward RE, Lacroix J, Hébert PC, Barnes MA, Bohn DJ, Dirks PB, Doucette S, Fergusson D, Gottesman R, Joffe AR, Kirpalani HM, Meyer PG, Morris KP, Moher D, Singh RN, Skippen PW; Hypothermia Pediatric Head Injury Trial Investigators and the Canadian Critical Care Trials Group. Hypothermia therapy after traumatic brain injury in children. N Engl J Med. 2008 Jun 5;358(23):2447-56. doi: 10.1056/NEJMoa0706930.
Kochanek PM, Tasker RC, Bell MJ, Adelson PD, Carney N, Vavilala MS, Selden NR, Bratton SL, Grant GA, Kissoon N, Reuter-Rice KE, Wainwright MS. Management of Pediatric Severe Traumatic Brain Injury: 2019 Consensus and Guidelines-Based Algorithm for First and Second Tier Therapies. Pediatr Crit Care Med. 2019 Mar;20(3):269-279. doi: 10.1097/PCC.0000000000001737.
Elevated cardiac troponin levels, or troponinemia, are one sign that the myocardium may be infarcting or under some type of stressful condition. Cardiac troponin levels are assessed in conjunction with the clinical history, physical exam, EKG, and another laboratory testing in deciding if troponinemia is due to cardiac ischemia or another condition. Conditions associated with elevated cardiac troponin levels include cardiac ischemia (i.e. STEMI, NSTEMI), cardiac contusion, cardiac procedures, congestive heart failure, renal failure, aortic dissection, tachy- or bradyarrhythmias, rhabdomyolysis with cardiac injury, Takotsubo syndrome, pulmonary embolism, acute stroke, myocarditis, sepsis, severe burns, extreme exertion, and other conditions. It is unlikely that this patient had elevated troponin levels from Acute coronary syndrome (Choice D) as her cardiac catheterization results showed no significant occlusive lesions in the coronary arteries. D-Dimer levels do increase with patient age, but cardiac troponin levels do not increase with patient age (Choice B). Sepsis (Choice C) is a cause for elevated troponin levels, but this patient has no clinical signs or sepsis symptoms. Atrial fibrillation with a rapid rate (Choice A) is the most likely cause of this patient’s elevated troponin level. Correct Answer: A
This patient sustained a penetrating traumatic injury to the left chest and presented to the emergency department with hemodynamic instability (tachycardic and hypotensive). Some differential diagnoses to consider on arrival include tension pneumothorax, cardiac tamponade, aortic injury, or aero-digestive tract injury. Prior to taking a detailed history on any trauma patient, a primary survey should be performed. The goal of the primary survey in a trauma patient is to identify and treat any life-threatening injuries as soon as possible. The primary survey is also known as the “ABCs.” Sometimes it is referred to as the “ABCDEFs.” This acronym stands for Airway, Breathing, Circulation, Disability, Exposure, and FAST exam (How to learn eFAST exam for free). Each letter is addressed and assessed in the order they exist in the alphabet. This creates a methodical, algorithmic approach to assist the practitioner in assessing the trauma patient for life-threatening injuries. The sonographic view shown in this question is the subxiphoid (cardiac) view and demonstrates the presence of free fluid. Free fluid on ultrasound appears black, or “anechoic” and is assumed to be blood in the setting of trauma. The free fluid is highlighted by red stars in the image below. The collapse of the right ventricle is shown by the yellow arrow in the below image.
In conjunction with hemodynamic instability and a history of penetrating chest trauma, this sonographic view strongly supports the diagnosis of cardiac tamponade. Consulting the general surgery team for exploratory laparotomy (Choice A) would be the correct course of action for a patient with hemodynamic instability and free fluid on the other abdominal views of the FAST exam. Needle decompression of the chest (Choice B) would be the correct initial treatment for a tension pneumothorax. The patient described in the case has clear bilateral lung sounds, no tracheal deviation mentioned, normal O2 saturation on room air, and sonographic demonstration of cardiac tamponade. A CT scan of the chest, abdomen, and pelvis (Choice D) would be indicated in this patient if he had normal vital signs and no free fluid on the FAST exam. A pericardiocentesis (Choice C) is the most appropriate next step in the management of this patient with cardiac tamponade to relieve signs of obstructive shock. It should be noted that this procedure has limitations and is not always effective. Pericardiocentesis is a temporizing treatment with pericardiotomy being the definitive therapy. Blood in an acute hemopericardium may clot and be unable to be aspirated with a large-bore needle. The procedure may injure surrounding organs, such as the liver, intestines, or heart itself. Ultrasound-guidance should be used whenever possible to avoid injury to surrounding organs. Emergent thoracotomy to relieve the cardiac tamponade should be performed on any patient with confirmed cardiac tamponade and cardiac arrest in the Emergency Department. Correct Answer: C
This patient has sustained blunt abdominal trauma from his seat belt. This is indicated by the linear area of ecchymoses, known as a “seat belt sign”. This is a worrisome physical exam finding that should raise a concern about a severe intra-abdominal injury. All trauma patients presenting to the emergency department should be assessed using an organized approach, including a primary survey (“ABCs”) followed by a secondary survey (more detailed physical examination). The FAST (Focused Assessment with Sonography in Trauma) examination is part of the primary survey in a trauma patient. Some sources abbreviate the primary survey in trauma as “ABCDEF”, which stands for Airway, Breathing, Circulation, Disability, Exposure, FAST exam. The primary survey attempts to identify any life-threatening diagnoses that need to be addressed in a time-sensitive manner. Examples include cardiac tamponade, tension pneumothorax, and intra-abdominal bleeding. The FAST exam includes 4 basic views: the right upper quadrant view (liver and right kidney), pelvis view (bladder), left upper quadrant view (spleen and left kidney), and cardiac/subxiphoid view (heart). An E-FAST, or extended FAST, includes the four standard FAST views plus bilateral views of the lungs to evaluate for pneumothorax. An abnormal FAST exam demonstrates the presence of free fluid on ultrasound. In the setting of trauma, free fluid is assumed to be blood. Free fluid on ultrasound appears black, or anechoic (indicated by yellow arrows in below image).
The space between the liver and right kidney (“Morrison’s Pouch”) is often the first location or blood to accumulate in a patient with intra-abdominal bleeding. Trauma patients who are hemodynamically unstable with a positive FAST exam (this patient) should go to the operating room for emergent exploratory laparotomy (Choice C) to determine the source of their bleeding. Performing a CT scan of the abdomen and pelvis (Choice A) would be the correct answer if the patient was hemodynamically stable and had a positive FAST exam. Allowing this patient to leave the emergency department for a CT scan would be dangerous as this patient could rapidly decompensate. Performing a Diagnostic Peritoneal Lavage (Choice B) would be the correct answer if the patient was hemodynamically stable but had a normal FAST exam. An emergent thoracotomy (Choice D) is more typically performed in patients with penetrating trauma who have cardiac arrest shortly before presenting to the emergency department. This intervention attempts to identify and treat any reversible causes of cardiac arrest. Correct Answer: C
Hoffman JR, Wolfson AB, Todd K, Mower WR. Selective cervical spine radiography in blunt trauma: methodology of the National Emergency X-Radiography Utilization Study (NEXUS). Ann Emerg Med. 1998;32(4):461-469. doi:10.1016/s0196-0644(98)70176-3