CLINICAL REASONING – EMERGENCY MEDICINE
Clinical Reasoning: Traumatic brain injury
When an external force damages the head - the result is head trauma, and if there's temporary or permanent
brain dysfunction, we call it a traumatic brain injury, or TBI.
This external force could be a blunt impact, like a baseball bat, a penetrating injury, like a gunshot wound, a blast
wave, like an explosion, or an accelerating-decelerating force, like in a motor vehicle accident.
The most common causes of TBIs are falls and motor vehicle accidents, and high-risk groups include the elderly
and individuals using alcohol and illicit drugs.
When TBIs occur in children, non-accidental trauma, or child abuse, should always be a primary concern.
TBIs can cause primary injuries which are a direct result of the external force.
These include skull injuries like fractures; blood vessel injuries like an epidural or subdural hematoma, or a
subarachnoid or intracerebral hemorrhage; and brain parenchymal injuries like brain contusions and diffuse
axonal injury.
Sometimes, primary injuries can lead to secondary injuries - like cerebral herniation, seizures, and increased
intracranial pressure.
When an individual has a suspected head trauma, the initial evaluation starts with the primary survey, during
which the “ABCDEs” are assessed.
“A” is for airway, and individuals with a traumatic brain injury may not be able to protect their airway, leading to
aspiration and hypoxia, which can worsens the brain injury. These individuals may require endotracheal
intubation and mechanical ventilation.
“B” is for breathing, and if there’s increased intracranial pressure, it can lead to an irregular breathing pattern -
which is part of the Cushing triad.
“C” is for circulation, and hypertension and bradycardia are the two remaining features in the Cushing’s triad.
There may also be hypotension, which can reduce brain perfusion.
“D” is for disability, which can be assessed using a 15-point Glasgow Coma Scale, or GCS, where the minimum
possible score is 3.
The GCS score has 3 parts: eye movement, verbal response, and motor response.
For eye movement, if the individual spontaneously opens their eyes, that’s 4 points. If they open their eyes only
when asked, that’s 3 points. If they open their eyes only with a mild amount of pain like rubbing the orbit of the
eye, that’s 2 points. If they don’t open their eyes, that’s 1 point.
For verbal response, if the individual can say what year it is, that’s 5 points. If they get the year wrong, that’s 4
points. If they respond with inappropriate words, like “yesterday or dog”, that’s 3 points. If they respond with a
sound like a moan, that’s 2 points. If they don’t respond, that’s 1 point.
For motor response, if the individual can obey a motor command, like: “show me three fingers”, that’s 6 points.
If not, you can rub the orbit of the eye, and if they smack your hand out of the way, then they’re localizing well,
and that’s 5 points. If not, you can prick the tip of their finger, and if they withdraw, that’s 4 points. If not, if the
upper limbs are flexed and lower limbs are extended, then that’s 3 points. If the upper and lower limbs are
extended, that’s 2 points. Finally, if there is absolutely no tone, that’s 1 point. To remember the point system,
think “4 eyes” for eye movement, the “Jackson 5” for verbal response, and a “6 cylinder motor” for the motor
response.
Finally, there’s “E” is for exposure, during which the individual is log-rolled to expose the back, which may help
identify other injuries like spinal fractures.
Next is the secondary survey, which includes a history and head-to-toe physical examination. Key elements in
the history are captured in the mnemonic “AMPLE”.
“A” for allergies, “M” for medications, like anticoagulants and antiplatelet medications that increase the risk of
intracranial bleeding. “P” for pregnancy and past medical history, “L” for last meal, and “E” for the events that
caused the trauma, such as the mechanism of injury and whether there was loss of consciousness.
It’s helpful to get information from eyewitnesses, because sometimes there can be post-traumatic memory loss
or amnesia.
Important physical examination findings to look for include an asymmetric or fixed, dilated pupils which can
indicate an impending cerebral herniation.
Also, contralateral hemiparesis due to compression of the ipsilateral cerebral peduncle which occurs in uncal
cerebral herniation.
That can also cause ipsilateral paralysis of the third cranial nerve, causing ptosis, a dilated pupil and a “down and
out” eyeball.
Sometimes, the contralateral cerebral peduncle is compressed, producing an ipsilateral hemiparesis - that’s
called Kernohan’s notch syndrome.
Also, it’s important to look for signs of a basilar skull fracture and an underlying hematoma. Signs include
periorbital ecchymosis or “raccoon eyes”, a battle sign - which is a hematoma behind the ear, hemotympanum -
which is bleeding in the tympanic cavity, and otorrhea or rhinorrhea, which is often bloody discharge mixed with
clear cerebrospinal fluid.
If cerebrospinal fluid is mixed in with blood, then on gauze, the cerebrospinal fluid travels further along than the
blood, producing a “halo sign”; which is a halo or a ring of fluid around a center of blood.
After the primary and secondary survey, you can now classify the TBI.
A mild TBI, also known as a concussion, typically has a GCS of 13 to 15, and a complete loss of consciousness is
for less than 30 minutes. Also, the duration of post-traumatic memory loss or amnesia, as well as a change in the
level of consciousness - like feeling lethargic or confused - lasts for less than 1 day.
Moderate TBI has an GCS of 9 to 12, loss of consciousness for 30 minutes to 24 hours, post-traumatic amnesia
for 1 to 7 days, and a change in the level of consciousness for more than 24 hours.
Finally, severe TBI has a GCS less or equal to than 8. Think - “if the GCS is less than 8, it’s time to intubate”,
because individuals often can’t maintain their airway. Also, severe TBI has a loss of consciousness for more than
24 hours, post traumatic amnesia for more than 7 days, and similar to moderate TBI, a change in the level of
consciousness for more than 24 hours.
1|Page
CLINICAL REASONING – EMERGENCY MEDICINE
In terms of labs and imaging, a CBC should be obtained, to make sure that the platelet count is at least 100,000
cells per microliter, which is the minimum threshold for neurosurgery.
Additionally, PT, PTT, and INR should be checked to make sure that they are normal - since that can worsen a
bleed.
A urine toxicology, blood alcohol level, and glucose levels should be checked to identify any other potential
causes of an altered mental status.
Initially, a non-contrast brain CT should be done to see if there’s any shift in the midline of the brain due to a
mass effect.
A mass effect can compress other structures of the brain, and can cause a cerebral herniation, which is life-
threatening. The reason that the scan is done without contrast, is that both blood and contrast are white,
making it difficult to detect a bleed.
The CT is normal in mild TBI, but may be abnormal in moderate and severe TBI.
In terms of TBI treatment, there are general measures which applies to all cases of TBI, and specific measures
which apply to specific types of brain injuries.
One general measure that starts immediately is lowering the intracranial pressure. That’s because the cerebral
perfusion pressure, or CPP equals the mean arterial pressure, or MAP minus the intracranial pressure, or ICP.
Since we can’t measure cerebral blood flow, we use the CPP to represent it, and in the setting of TBI, the CPP
needs to be above 60 mmHg to ensure that the brain gets enough blood. To do that, we can keep the systolic
blood pressure above 100 mmHg using intravenous fluids and transfusions, if necessary.
Now to measure ICP, an intracranial ICP monitor can be placed in the epidural or subdural space, the brain
parenchyma, the lateral ventricle, or the 3rd ventricle of the brain. Usually an ICP monitor is placed in individuals
with a GCS less than or equal to 8 and an abnormal CT scan.
The ICP is normally around 10 millimeters of mercury, and should be kept below 20 mmHg.
One way is by simply elevating the head of the bed to 30 degrees. This level helps increase venous outflow from
the brain. Before doing this, it’s important to make sure that the individual doesn’t have a cervical spine injury.
Another method is by using sedatives like propofol which lowers the ICP by decreasing the cerebral activity and
metabolic demand, therefore lowering the cerebral blood flow, which is reflected as a low CPP. However, the
blood pressure must be monitored as propofol can cause hypotension.
Now, a major determinant of cerebral blood flow is the partial pressure of carbon dioxide or PaCo2.
When the PaCO2 is high, cerebral vasodilation occurs, the cerebral blood flow increases, and therefore the ICP
increases.
When the PaCO2 is low, cerebral vasoconstriction occurs, and the cerebral blood flow decreases, and therefore
the ICP decreases.
Historically, hyperventilation was used to lower the PaCO2, but that caused so much cerebral vasoconstriction
that it resulted in cerebral ischemia!
So, now the goal is to have a normal PaCO2 level between 35 and 45 mmHg, which lowers the ICP, but maintains
adequate cerebral blood flow.
Now, if the ICP monitor is placed in the ventricles of the brain, then we also have surgical access to place an
external ventricular drain, or EVD, which can remove cerebrospinal fluid, lowering the ICP.
Another way to lower the ICP is using osmotic diuretics like mannitol or hypertonic saline, which work by
extracting free water from the neurons.
Now, although previously steroids were thought to be helpful in reducing cerebral edema, they currently have
no role in TBI treatment, and may in fact worsen outcomes.
Finally, if the elevated ICP is refractory to medical therapy, then neurosurgical intervention is necessary.
A decompressive craniectomy essentially removes a portion of the skull, allowing the squished brain to
“breathe” and the ICP to go down.
Two more extreme methods of lowering the ICP are a barbiturate coma and therapeutic hypothermia.
A barbiturate coma puts the brain to sleep - lowering the metabolic rate - using barbiturate medications like
pentobarbital.
Therapeutic hypothermia involves cooling the body, which not only lowers ICP, but also protects the brain
against secondary injury.
Alright, now let’s move on to some specific injuries and their management. Let’s start with skull fractures, which
are classified into linear fractures, depressed fractures, or basilar skull fractures - all of which can be seen on a
CT scan.
A linear fracture is a single fracture that runs through the entire thickness of the skull. They’re usually clinically
insignificant, and require no treatment, unless it disrupts an underlying blood vessel like the middle meningeal
artery - causing an epidural hematoma.
A depressed skull fractures is when the fractured segment folds inwards into the brain parenchyma. These are
clinically important because they directly damage the underlying brain, and often require surgery.
If a basilar skull fracture is present, it suggests that there was a significant amount of force. That means that
there’s a high risk of a hematoma as well as a cervical spine injury. So in that situation, a cervical spine CT should
be obtained. Also, basilar skull fractures cause cerebrospinal fluid to leak out through the ear and nose,
increasing the risk of meningitis.
After skull fractures, comes specific brain injuries, which can be classified as extra-axial and intra-axial injuries.
Extra-axial injuries are within the skull, but don’t involve the brain parenchyma. These include epidural and
subdural hematomas, as well as a subarachnoid hemorrhage.
Intra-axial injuries involve the brain parenchyma, and include intracerebral hemorrhage, cerebral contusion, and
diffuse axonal injury.
Epidural hematomas are when blood collects in the space between the dura mater and inner aspect of the skull
periosteum. This happens when a linear fracture at the temporo-parietal region of the skull tears open the
middle meningeal artery, causing profuse bleeding.
2|Page
CLINICAL REASONING – EMERGENCY MEDICINE
Because of the high amount of force required to produce an epidural hematoma, they’re more common among
young individuals at risk of such an injury, such as those playing sports or getting into fights.
Individuals classically have a period of loss of consciousness, and then can have a lucid-interval; during which the
individual regains consciousness and feels fine - but a lucid interval isn’t always seen.
If there’s a rapidly growing epidural hematoma it can cause symptoms to progress rapidly, potentially leading to
a cerebral herniation.
A brain CT is diagnostic, and classically shows a convex, “lens-shaped” hyperdense collection of blood.
Additionally, epidural hematomas do not cross the suture lines of the skull.
In addition to the bleeding, there can be surrounding cerebral edema, and if the edema is significant, it can
cause a shift of the midline to the contralateral side, which signifies an impending cerebral herniation.
Epidural hematomas are often an emergency, and neurosurgical intervention is often necessary to evacuate the
epidural hematoma and suture up the epidural space, preventing re-accumulation of the hematoma.
Optimally, a craniotomy; which is removing a portion of the skull is done, and this magnificently cures most
individuals.
In some settings, a life-saving alternative is to drill a hole in the skull, which is called Burr hole trephination.
Finally, non-operative management with serial neurological exams and CT scans may be considered if all of the
following criteria are met: the epidural hematoma is less than 30 milliliters in size, the midline shift is less than 5
millimeters, the GCS is greater than 8, and individual has no focal neurological deficits.
All right, now a subdural hematoma occurs when blood collects between the dura and arachnoid mater.
Unlike epidural hematomas, the bleeding source is usually the bridging veins that connect the cerebral venous
sinuses to the superficial veins of the skull.
Now, because the source is venous, the bleeding is slower than an arterial bleed, and the onset of symptoms
depends on how quickly the hematoma accumulates.
A subdural hematoma is considered acute if it develops within 2 days of a head trauma, subacute if it develops
between 2 days and 2 weeks of a head trauma, and chronic if it develops 2 weeks or more after a head trauma.
Now, unlike epidural hematomas, even minor head trauma, like walking into a door, can lead to a subacute or
chronic subdural hematoma, especially in individuals with brain atrophy, like the elderly and individuals who
abuse alcohol. That’s because when the brain shrinks, the bridging veins get stretched, making them more
susceptible to tearing.
Often times, individuals don’t even remember the traumatic event, so it’s important to considers a subdural
hematoma in individuals with an altered mental status.
Also, if a subdural hematoma is detected in an infant or young child, it could be due to non-accidental trauma.
Infants and children have large heads with relatively small brains, so vigorously shaking a young child can cause a
subdural hematoma, as well as other signs of non-accidental trauma like retinal hemorrhages on fundoscopy. In
these situations, the history often doesn’t fit the developmental age of the child, like a 2 month old infant who
“rolled off the bed”.
A brain CT is usually diagnostic, and classically shows a concave, “crescent-shaped” density that crosses the
suture lines. And the density on the brain CT helps determine the age of the hematoma.
Acute subdural hematomas are hyperdense, while chronic subdural hematomas are hypodense.
Subacute subdural hematomas appear isodense, meaning they blend in with the adjacent brain parenchyma,
making them easy to miss.
Also, a midline shift may also be seen on CT.
Similar to epidural hematomas, the mainstay of treatment is a craniotomy or Burr hole trephination.
However, relative to epidural hematomas, the morbidity and mortality of subdural hematomas are high because
they can develop more insidiously and are therefore harder to detect in the early stages.
Next, there’s a subarachnoid hemorrhage which is bleeding between the arachnoid and pia mater.
Head trauma is the most common cause of subarachnoid hemorrhage, but a non-traumatic subarachnoid
hemorrhage can occur if there’s a spontaneous rupture of an intracranial berry aneurysm.
In both traumatic and non-traumatic subarachnoid hemorrhage, a brain CT shows blood in the ventricular
cisterns, interhemispheric fissures and within the sulci. The more blood that’s seen, the worse the outcome.
Now, in cases of a non-traumatic subarachnoid hemorrhage, if the brain CT is negative, then the diagnosis can
be made with a lumbar puncture and cerebrospinal fluid analysis, which shows red blood cells or
xanthochromia; which is a result of red blood cell breakdown.
However, in cases of a traumatic subarachnoid hemorrhage, a lumbar puncture is contraindicated due to the
high intracranial pressure and the risk of cerebral herniation.
A complication that can occur about 2 days to 2 weeks after a subarachnoid hemorrhage is post-traumatic
vasospasm of the subarachnoid vessels, which can cause cerebral ischemia. Therefore, individuals are given a
specific calcium channel blocker called nimodipine, which relaxes the cerebral vascular smooth muscle,
preventing vasospasm.
A 3 week course of nimodipine should be started within 96 hours of the subarachnoid hemorrhage.
All right, onto the intra-axial injuries. Intracerebral hematomas form when the arterioles underneath the pia
mater rupture due to the shearing forces of trauma, causing a small hematoma to form. These rarely happen in
isolation, and instead happen alongside extra-axial injuries.
On brain CT, intracerebral hematomas are well-demarcated, homogenous, regularly shaped border hematomas
located deep in the brain.
The mortality rate for intracerebral hematomas is high, and individuals often require surgical decompression
with a craniotomy.
Next, is a cerebral contusion which literally translates to a “brain bruise”. This is similar to an intracerebral
hematoma, but the key difference is that on a brain CT, contusions are often poorly demarcated,
heterogeneous, irregularly shaped border and are found near the surface the brain.
When a cerebral contusion occurs on the same side as the impact, it’s called a “coup” injury, but if it happens on
the opposite side of the impact, it’s called a “contrecoup” injury.
3|Page
CLINICAL REASONING – EMERGENCY MEDICINE
Just like skin bruises, cerebral contusions and the surrounding edema often get bigger over time so early surgical
intervention with a craniotomy is often necessary.
Now, of all of the intra-axial injuries, the most common ones are diffuse axonal injuries. They result from the
shearing forces on the white matter axons in the brain, causing them to stretch or tear apart. This leads to a
prolonged post-traumatic coma, defined as more than 6 hours, which is not adequately explained by a mass
lesion like a big hematoma or contusion.
If individuals recover from the coma, they often have a lasting cognitive deficit, such as memory loss or
problems with language.
The brain CT typically shows multiple, small, hyperdense, punctate lesions along the gray-white matter junction.
But the diagnosis is best made with a brain MRI, which offers better resolution and can more accurately detect
diffuse axonal injury.
Now, even though a TBI is an intense acute event, it can lead to chronic complications.
For example, post-traumatic seizures can occur up to a week after a moderate or severe TBI, so those individuals
are given prophylactic antiepileptic medications like phenytoin for 1 week.
There’s also an increased risk of developing post-traumatic epilepsy months to years after the event, however,
prophylactic antiepileptic medications do prevent this.
Also, a prolonged increased intracranial pressure can cause a type of stress gastric ulcer called a Cushing ulcer,
so these individuals should get prophylactic IV proton pump inhibitors.
Finally, mild TBI or concussion is treated with a combination of rest, analgesia, and observation.
Now, due to the radiation, in mild TBI or concussion, a brain CT is only recommended when the individual
develops a worsening headache, has persistent confusion, has a focal neurological deficit, or is on
anticoagulation therapy like warfarin.
Usually, individuals with a mild TBI can be discharged after 4 to 6 hours of observation or a negative brain CT.
A complete recovery can take a couple of weeks, and if there are symptoms like headaches, dizziness, confusion,
depression, or a decline in cognitive function, that persist beyond those two weeks, then it’s called post-
concussive syndrome.
Treatment of post-concussive syndrome is mainly focused on symptoms, such as analgesics for headache or
selective serotonin-reuptake inhibitors for depression.
Now, when it comes to athletes, any athlete who has had a concussion should be immediately removed from
play.
The concussion can be graded depending on symptoms.
A grade 1 concussion is when there’s no loss of consciousness and no amnesia, and the athlete should sit out the
game.
A grade 2 concussion is when there’s a loss of consciousness, but no amnesia, and the athlete should sit out for
at least a week.
Finally, a grade 3 concussion is when there’s a loss of consciousness and amnesia, and the athlete should sit out
the rest of the season.
It’s really important for an athlete to stay out of play because although the athlete may feel fine after a while, a
second blow to the head after a concussion can be fatal, and this is called second-impact syndrome. That’s
because a concussion can make the cerebral blood vessels weak and leaky, and a second blow can cause massive
and irreversible cerebral edema.
Another complication of concussion injuries is called chronic traumatic encephalopathy, or CTE.
CTE usually occurs after repetitive head trauma, such as in contact sports like american football, boxing, and
football or soccer.
The exact amount of head trauma needed to cause CTE is unknown but it turns out that CTE develops 8 to 10
years after the initial head trauma.
In the early stages, CTE causes mood and behavior changes, but later it can affect cognitive domains like
memory.
Summary
All right, as a quick recap. A mild TBI, or concussion, has a GCS of 13 to 15, a moderate TBI has a GCS of 9 to 12,
and a severe TBI has a GCS of 8 or less.
The major investigation that helps identify most primary brain injuries is a non-contrast brain CT.
The brain CT is done for moderate and severe TBI, as well as in mild TBI where the individual has a worsening
headache, persistent confusion, a focal neurological deficit, or is on anticoagulation therapy like warfarin.
General measures for treating TBI include lowering the ICP by elevating the head of the bed to 30 degrees,
sedation, intubation and hyperventilation in order to achieve a partial pressure of carbon dioxide or PaCO2
between 35 and 45 millimeters of mercury, osmotic diuresis with mannitol or hypertonic saline, and finally if all
else fails, a decompressive craniectomy.
Specific lesions identified on CT scan such as epidural and subdural hematomas should be identified and
evacuated.
Epidural hematomas appear as a convex, “lens-shaped” hyperdense collection of blood that does not cross the
suture lines.
Subdural hematomas appear as a concave, “crescent-shaped” density that crosses the suture lines.
Subarachnoid hemorrhage is seen as blood in the ventricular cisterns, interhemispheric fissures and within the
sulci.
Diffuse axonal injury results from the shearing forces on the white matter, and presents as a coma lasting more
than 6 hours with no obvious cause on CT scan.
Mild TBI, or concussion, can also result in some complications like second-impact syndrome and chronic
traumatic encephalopathy, and is treated with rest, analgesia, and observation.
4|Page
CLINICAL REASONING – EMERGENCY MEDICINE
Clinical Reasoning: Chest trauma
The chest wall houses a number of vital structures in the body - the heart and the pericardium, the lungs and the
pleura, the aorta, and the esophagus - all protected within the rib cage and sternum.
And trauma to the chest wall is responsible for over one-fourth of trauma deaths.
Chest trauma can be blunt, such as from motor vehicle accidents, or penetrating, such as from a stab or gunshot
wound.
Chest trauma evaluation starts with the primary survey, which includes the ABCDEs: airway, breathing,
circulation, disability, and exposure, and the goal is to quickly assess and treat life-threatening injuries.
It starts with checking the patency of the airway and whether the individual requires endotracheal intubation.
As for breathing, you can look, listen, and feel.
So look at the respiratory rate, oxygen saturation, and breathing pattern.
If the person is hypoxemic, a 100% oxygen non-rebreather mask should be given.
Also if there's asymmetric breathing it could indicate a weak chest segment due to rib fractures.
Next, listen for breath sounds for signs like decreased air entry in tension pneumothorax or hemothorax, or
muffled heart sounds in cardiac tamponade.
After that feel for tenderness along the chest wall, which can occur with rib fractures.
In circulation, check the blood pressure and heart rate.
If there are signs of shock it could be due to a number of causes like bleeding into the pleura or pericardium,
obstruction of cardiac output in the setting of a tension pneumothorax, or inadequate cardiac output in the
setting of myocardial injury.
Also, as part of circulation, it’s important to look for other sources of bleeding, to insert two large-bore
intravenous lines, and to prepare for the need for blood products.
It’s specifically important to assess for signs of inadequate end-organ perfusion, such as altered mental status,
decrease urine output, cool or pale skin, and a delayed capillary refill.
Bedsides ultrasound can also be used in the primary survey - and it’s called focused assessment with sonography
for trauma, or the FAST exam.
When views are added to look for a pneumothorax, hemothorax, or cardiac tamponade, it’s called an extended
FAST or E-FAST.
“Disability” means neurological disability, and is assessed by checking the pupils and using the Glasgow Coma
Scale, or GCS.
Finally, exposure is assessed by turning the individual on their side, and assessing their back for any occult
injuries.
Alright, now the secondary survey focuses on taking a history, and performing an elaborate head-to-toe
examination with the goal of detecting more subtle injuries.
Now, if a life-threatening injury is recognized, then life-saving interventions are immediately performed, like a
needle decompression for a tension pneumothorax, covering an open pneumothorax wound, inserting chest
tubes for pneumothorax or hemothorax, or performing a pericardiocentesis for a cardiac tamponade.
Initially, a chest x-ray should also be done to help identify rib fractures, pulmonary contusions, a pneumothorax,
a hemothorax, or an aortic injury.
An electrocardiogram or ECG and cardiac enzymes, should be done to help identify myocardial injury.
A CBC can help identify a baseline for bleeding since there may be a dilutional anemia that will begin hours to
days after the trauma, a blood type and crossmatch for blood transfusions, and a PT, PTT, and INR.
Alright, let’s get into specific chest wall injuries, starting with rib fractures, which are the most common chest
wall injuries.
Usually a rib fracture causes point tenderness over the rib along with bruising.
In fact, the pain can be really severe and it can lead to very shallow breathing.
So to help maintain good ventilation, encouraging deep breathing and good pain control is the key.
Analgesics like acetaminophen and NSAIDs are a good start.
Sometimes, opioid medications are used even though they can cause respiratory depression.
Intercostal nerve blocks are a great option for pain control.
Under the guidance of ultrasound, a local anesthetic medication like bupivacaine is injected just below the edge
of the fractured rib, because that’s where the intercostal nerves run.
Complications of rib fractures include a pneumothorax, hemothorax, or a splenic or liver laceration, which are all
the result of the sharp edge of a displaced rib injuring a nearby structures.
Now, if there’s inadequate pain control and ventilation the lung can collapse, and that’s called atelectasis.
Atelectasis predisposes a person to developing a post-traumatic pneumonia.
Generally speaking, individuals younger than 65 years with no comorbidities and 1 or 2 rib fractures are
discharged home.
On the other hand, individuals over age 65, or those with comorbidities like COPD, or those with 3 or more rib
fractures should be admitted for observation.
Alright, now if three or more adjacent ribs are each fractured in at least two locations, this creates a free-floating
segment called a flail chest.
A flail chest can have paradoxical movement during respiration. In other words, the flail segment will move
inwards during inspiration, and outwards during expiration, which is the opposite of the remaining normal chest.
5|Page
CLINICAL REASONING – EMERGENCY MEDICINE
The respiratory failure in a flail chest is not due to the mechanical issue, instead it’s directly related to injury to
the underlying lung, which is called a pulmonary contusion - or a “lung bruise”.
Pulmonary contusions happen in the context of blunt chest trauma, and can be diagnosed on a chest x-ray.
But the thing is, the chest x-ray may not show any changes until 6 hours after the injury. This makes sense,
because you’d expect the same delay in the appearance of a skin bruise.
So the classic presentation of a pulmonary contusion is someone who was initially oxygenating well, but then
began to deteriorate over time.
In a pulmonary contusion, a chest x-ray typically shows patchy opacities representing pulmonary edema and
hemorrhage.
Now a chest CT is more sensitive and can pick up signs of a pulmonary contusion earlier, so it’s usually preferred
for that reason.
Management of a flail chest and pulmonary contusion includes pain control, as well as oxygenation and
ventilation with non-invasive positive pressure ventilation, or if necessary, endotracheal intubation.
Also, it’s important to avoid giving IV fluids, because that can exacerbate the pulmonary edema. If IV fluids are
needed, sometimes they’re given along with a diuretic like furosemide.
Finally, it’s unclear if surgical fixation of the fractured ribs provides any additional benefit.
A pneumothorax is a collection of air in the pleural space.
A tension pneumothorax occurs when the injured pleura forms a one-way valve, allowing air to go in, but not go
out. This means that with every breath, the pneumothorax gets bigger and bigger.
Individuals present with chest pain, shortness of breath, and hypoxia, and examination reveals decreased air
entry on auscultation and hyperresonance on percussion.
Now, in cases of a tension pneumothorax, it can compress the right atrium of the heart and the vena cavae,
decreasing venous return. This results in decreased cardiac output manifesting as hypotension, altered mental
status and an elevation of the jugular venous pressure, and this is typical of obstructive shock.
Additionally, in a tension pneumothorax, the mediastinum and trachea may be shifted to the contralateral side.
A tension pneumothorax is a clinical diagnosis, meaning that if it’s suspected, it’s a medical emergency that must
be immediately treated by inserting a needle in the 2nd or 3rd intercostal space at the midclavicular line,
decompressing the pneumothorax.
Following decompression, a chest tube is inserted in the 4th or 5th intercostal space along the anterior axillary
line.
An open pneumothorax, also called a “sucking chest wound” is a pneumothorax that communicates with
atmospheric air due to an open chest wound.
An open pneumothorax occurs if the chest wound is greater than two-thirds the diameter of the trachea,
because atmospheric air likes to take the path of least resistance, preferring the open wound over the trachea.
One key difference between an open pneumothorax and a tension pneumothorax is the absence of obstructive
shock. This is because air is not being trapped in the pleural space, instead it’s free to go in and out of the chest.
So, pressure does not build up, and the surrounding structures aren’t compressed.
Initial management of an open pneumothorax is applying dressing over the wound, and then taping it from 3
sides, leaving one side open. This creates a unique valve mechanism that allows air to go out, but does not allow
air in.
Eventually, a chest tube needs to be inserted, and the wound needs to be repaired.
Next up is a hemothorax which is a collection of blood in the pleural space. Individuals have shortness of breath,
hypoxia, decreased air entry on auscultation and dullness on percussion.
Because the pleural cavity can accommodate large amounts of blood, the major concern in hemothorax is
hemorrhagic shock.
The diagnosis is made with an upright chest x-ray, because a supine chest x-ray may miss a smaller hemothorax.
The chest x-ray shows a concave opacity blunting the costophrenic angle, which is the angle between the pleura
covering the ribs and the pleura covering the diaphragm.
The FAST exam may also help with the diagnosis of a hemothorax.
Although a hemothorax usually originates from injury to the lung parenchyma or the intercostal vessels, it’s
important to consider an intra-abdominal source of bleeding that may have leaked through an injured
diaphragm.
The FAST exam or a CT scan of the abdomen can usually detect an intra-abdominal source, and if there is one,
then the individual is taken to the operating room to control the bleeding.
Treatment of a hemothorax consists of inserting a chest tube, and restoring the circulating blood volume.
If the amount of blood drained from the chest tube is more than 1500 milliliters in a day, or if the rate of
bleeding is more than 200 milliliters per hour for 2 to 4 hours, or the individual decompensates after initial
stabilization, then a surgical thoracotomy should be done. This involves surgically opening the chest to identify
and stop the bleeding.
A unique intervention to restore blood volume is autotransfusion. This means taking the hemothorax blood from
the chest tube, and giving it back to the individual intravenously. This eliminates the risk of transfusion reactions,
because it’s their blood.
Okay, cardiac injury can be blunt or penetrating.
Blunt cardiac injuries include myocardial concussion, contusion, or rupture, and coronary vessel injury.
A myocardial concussion, also called commotio cordis, is a rare form of cardiac injury that manifests as sudden
collapse of the individual due to a life-threatening arrhythmia like asystole, ventricular fibrillation, or cardiac
arrest. This is thought to occur when the blow to the chest happens just before the T-wave; a period of electrical
vulnerability. In other words, bad timing.
Treatment should follow the advanced cardiac life support, or ACLS protocols, including cardiopulmonary
resuscitation, or CPR, and if necessary, defibrillation.
6|Page
CLINICAL REASONING – EMERGENCY MEDICINE
A myocardial contusion is a “heart bruise”. Because of its anterior and retrosternal location, the right ventricle is
most commonly injured.
The signs and symptoms of a myocardial contusion depend on the extent of injury, but commonly include chest
pain, arrhythmias, hypotension, and even cardiogenic shock.
Now, in the context of chest trauma, hypotension and arrhythmias should be initially presumed to be from
hemorrhage, rather than a cardiogenic cause, because bleeding is so much more common.
Now, an ECG should be done on all individuals with chest trauma to help identify any resulting arrhythmias; with
sinus tachycardia being the most common, conduction blockade, or ischemia.
Additionally, troponin levels are obtained as a marker of cardiac myocyte injury.
A normal ECG and negative troponin levels effectively rule out myocardial contusion.
In a hemodynamically stable individual, if there are ECG changes or if there are elevated troponin levels, then
the individual should be admitted for continuous ECG monitoring.
In a hemodynamically unstable individual, any ECG changes or elevated troponin levels should prompt an
emergent echocardiogram to look for signs of decreased cardiac contractility, valvular damage, or rupture of the
myocardial wall.
Any serious arrhythmias should be medically treated and inotropic agents like dobutamine should be given if
cardiac output is decreased.
Fortunately, most individuals with myocardial contusion recover with no residual cardiac damage.
Myocardial rupture is perforation of the ventricular or atrial walls, and usually leads to a rapid death.
Rarely, the bleeding is limited by the pericardium, leading to a pericardial tamponade.
An echocardiogram aids with the diagnosis, and a thoracotomy should be performed to evacuate the pericardial
tamponade, control the bleeding, and repair the defect.
Coronary vessel dissection secondary to trauma can obstruct coronary blood flow, leading to myocardial
infarction.
ECG changes are identical to a myocardial infarction caused by atherosclerosis, and so is the management.
This means individuals should be sent to the catheterization lab for percutaneous coronary intervention or PCI.
Finally, cardiac arrest in the setting of any blunt cardiac injury is an indication for a thoracotomy.
As for penetrating cardiac injury, the main concern is acute pericardial tamponade, which is accumulation of
blood in the pericardial sac that encroaches on the ventricles and atria, limiting their filling capacity, and as a
result, decreasing the cardiac output.
As little as 50 milliliters of blood is sufficient to produce a tamponade physiology, because it’s not about the
amount of blood accumulating, it’s about the rate of accumulation.
In a trauma, blood accumulates rapidly, giving little time for the heart to adapt.
The classical Beck’s triad includes hypotension, jugular venous distension, and muffled heart sounds.
However, in trauma, individuals may be hypovolemic, so the jugular veins could be flat.
The FAST exam during the primary survey is the best diagnostic tool for a pericardial tamponade.
On ultrasound, a pericardial tamponade is defined as presence of a pericardial effusion and diastolic collapse of
the right ventricle or atrium.
Electrical alternans, which is alternating amplitudes of the QRS complexes on ECG is highly specific for a
tamponade, but it’s usually found in chronic pericardial effusions and less commonly in the acute setting.
Treatment includes giving IV fluids to maintain the blood pressure, and performing an ultrasound-guided
pericardiocentesis just below the xiphoid process to aspirate the effusion.
Unfortunately, if the blood has clotted, a needle aspiration isn’t possible, and a thoracotomy becomes necessary
to evacuate the blood.
Aortic injury is usually blunt, resulting from rapid deceleration like in motor vehicle accidents.
Based on severity, aortic injuries are classified into 4 grades.
Grade I is a tear in the tunica intima, the innermost layer of the aorta.
Grade II is a collection of blood within the aortic wall, also called an intramural hematoma.
Grade III is a pseudoaneurysm; which is a breach in aortic wall causing leakage of blood, but is contained by the
tunica adventitia, the outermost layer. This gives the appearance of an aneurysm, but because it does not
involve all 3 layers, it is not a true aneurysm.
Grade IV is a full-blown rupture of the aorta.
Now, the most common site of injury is the aortic isthmus; which the portion of the descending aorta between
the origin of the left subclavian artery and the ligamentum arteriosum.
This is because the aorta is strongly tethered by the ligamentum arteriosum at this site, which limits free
movement of that part during rapid deceleration.
The injury typically causes chest pain, interscapular pain, or shortness of breath.
Rupture of the aorta causes rapid hemorrhagic shock that usually results in a rapid death.
Bleeding from the aorta may also cause a mediastinal hematoma to develop which may lead to hoarseness from
compression of the recurrent laryngeal nerve, dysphagia from esophageal compression, or a left-sided
hemothorax by getting through the pleura.
Arterial flow may be limited, causing ischemia to the distal extremities, which causes extremity pain.
Similar to aortic dissection, aortic injury may result in hypertension in the upper extremities, and hypotension in
the lower extremities.
Now, because of the non-specific presentation and high mortality, aortic injuries should always be suspected in
any individual with a potential mechanism.
7|Page
CLINICAL REASONING – EMERGENCY MEDICINE

The chest x-ray is the best initial investigation, and classically shows a wide mediastinal diameter, which is
defined as greater than 8 centimeters on a supine chest x-ray, or greater than 6 centimeters on an upright chest
x-ray.
A wide mediastinum is a sensitive but non-specific sign of aortic injury.
Lastly, diaphragmatic injury may lead to herniation of abdominal contents through the defect and into the chest
cavity.
Loops of bowel can become strangulated passing through the defect, and therefore individuals may have
symptoms of bowel obstruction like vomiting.

Other signs on chest x-ray include an abnormal aortic contour, a left hemothorax, or a downward displacement
of the right mainstem bronchus.
Now, if there is a wide mediastinum on chest x-ray, the next step is a CT angiography, which is the gold-standard
test for detecting aortic injury.
This involves injecting contrast material into the femoral artery, then taking pictures of the chest using a CT scan.
Abdominal contents can compress the adjacent lung, causing respiratory distress.
On auscultation, bowel sounds may be heard in the thorax.
Chest x-ray findings include dilated loops of bowel in the chest, mediastinal shift to the opposite side, an
abnormal contour of the affected hemidiaphragm, and the tip of a nasogastric tube would abnormally above the
diaphragm.

Sometimes the CT angiogram does not accurately identify the injury, in which case the next step is an A CT scan is better than the chest x-ray at identifying diaphragmatic injuries, and treatment is surgical repair.
intravascular ultrasound, which assesses aortic injuries in real-time, but unlike the CT, doesn’t require exposure
to radiation or contrast material. Summary

Okay, if the individual’s systolic blood pressure is greater than 100 mm Hg, the blood pressure should be Alright a quick recap, chest trauma can be blunt, such as from motor vehicle accidents, or penetrating, such as
lowered with beta-blockers, specifically esmolol. That’s to reduce the shearing effect of a high blood pressure from stab and gunshot wounds.
which can worsen the aortic injury.
Evaluation starts with the primary survey or the ABCs, which is aimed at identifying and promptly treating life-
Grade I injuries can be managed without surgery, while surgical repair is the definitive management for the threatening injuries.
remaining aortic injuries, and should be performed as soon as possible.
In airway, evaluate if the individual can maintain their own airway, or require endotracheal intubation.
An alternative to open surgery is thoracic endovascular aortic repair, or TEVAR, which involves inserting a stent
In breathing, look, listen and feel for signs of tension pneumothorax, hemothorax, and pericardial tamponade.
graft through the femoral artery and up to the aorta.
In circulation, hypotension usually indicates hemorrhagic shock, but can also be from obstructive shock in
TEVAR can be performed with local anesthesia right after the CT angiogram, and unlike open surgery, TEVAR
tension pneumothorax, or cardiogenic shock in myocardial injury.
does not require placing the individual on cardiopulmonary bypass.
As part of the primary survey, the focused assessment with sonography for trauma, or the e-FAST exam is done
Injury to the tracheobronchial tree can result from both penetrating or blunt trauma.
to diagnose conditions like pericardial tamponade.
Clinical features include hemoptysis and subcutaneous emphysema, which is air under the skin.
The secondary survey includes a head-to-toe examination to look for injuries that may have been missed.
Auscultation of the chest may reveal a crunching sound that is synchronous with the pulse. This is called
A chest x-ray is done on all individuals with chest trauma. Rib fractures are managed with pain control, and when
Hamman’s crunch, and is thought to be due to the heart beating against the air-filled mediastinum.
three or more adjacent ribs are each fractured in at least two locations, it’s called a flail chest.
If the wound opens into the pleural space, a pneumothorax may develop.
A flail chest may lead to respiratory failure by causing pulmonary contusions.
However, a chest tube would fail to evacuate the pneumothorax and re-expand the lung, because the original
Both are managed with pain control, oxygenation, and positive pressure ventilation, or even endotracheal
injury is in the tracheo-bronchial tree.
intubation.
A chest x-ray will reveal pneumomediastinum, or air in the mediastinum, subcutaneous emphysema, and
A tension pneumothorax is managed with needle decompression, followed by chest tube insertion.
possibly a pneumothorax.
Open pneumothorax is managed by applying dressing and taping it from 3 sides, followed by chest tube
When tracheobronchial injury is suspected, a bronchoscopy is performed to determine the site and extent of
insertion and surgical repair of the wound.
injury.
Hemothorax is treated by inserting a chest tube, or if the amount or rate of bleeding is too much, a resuscitative
During the bronchoscopy, endotracheal intubation may be performed to protect the airway, but it should never
thoracotomy may be indicated.
be performed blindly because that risks worsening the injury.

Definitive treatment includes surgical repair and placement of a tracheostomy tube.

8|Page
CLINICAL REASONING – EMERGENCY MEDICINE

All individuals with suspected myocardial injury get an ECG and troponin levels, and if they’re normal, that rules
out myocardial injury.

Pericardial tamponade is diagnosed during the FAST exam, and is treated by performing a pericardiocentesis, or
if necessary, a resuscitative thoracotomy.

Blunt aortic injury shows a wide mediastinum on chest x-ray, and is confirmed by a CT angiogram.

Additionally, the blood pressure should be lowered using the beta-blocker esmolol, to decrease the shearing
effect on the aortic wall.

Endovascular repair is preferred over open surgical repair.

9|Page
CLINICAL REASONING – EMERGENCY MEDICINE
Clinical Reasoning: Burns
The skin is the largest organ of the body, and is made of the epidermis, the dermis, and the hypodermis.
Burns result from exposure of skin cells to an overwhelming amount of energy in the form of heat, causing
cellular necrosis.
The degree of injury depends on the temperature, the duration of exposure, and the baseline structural integrity
of the skin; which means younger children and elderly individuals are at higher risk of injury, because their skin is
relatively weaker.
Okay, burns can be classified based on the cause, or by the depth of injury which corresponds to the severity of
the burn.
Burns are most commonly thermal, which can result from scalds, such as hot water, or flames, such as from
house-fires.
Less commonly, burns can be electrical, like from exposure to lightning strike or high-voltage electrical current,
or from exposure to chemical substances, which can be acidic or alkaline.
Based on depth, burns can be first, second, or third degree.
First degree burns are also called superficial burns, and involve the epidermis only.
A prime example would be a simple sunburn from a day on the beach, which appears red, with no blisters.
Second degree burns are further subclassified into superficial partial thickness burns, which involve the
epidermis and the superficial dermis, and deep partial-thickness burns, which involve the epidermis and the
deep dermis.
Superficial partial thickness burns appear red and are often blistered, whereas deep partial thickness burns
appear red or white, with no blisters.
Third degree burns are full-thickness burns, extending through and destroying the entire dermis.
These appear leather-like with a charred appearance and tense feel.
Usually, third degree burns are surrounded by a rim of second degree burns.
Fourth degree burns extend beyond the dermis, destroying fascia, muscle or bone.
Because third and fourth degree burns destroy the entire skin, they destroy the skin nerve endings, and
therefore can feel relatively painless.
Due to their strength and velocity, electrical burns have an entrance and an exit wound, similar to a gunshot. But
aside from that, the skin actually looks fine.
However internally, the muscles are injured and even heart can be severely damaged, so don't let normal skin
fool you.
Sadly, in children, specific burn patterns raise suspicion for physical abuse. These include burns with a sharply
demarcated edge, small circular burns matching a cigarette tip, or burns in the perineal region matching a
pattern that could only be explained if the child was dipped into scalding water.
Management of burns begins at the scene.
First, remove the individual from the source, making sure you don’t expose yourself to electrical current or
chemicals.
Additionally, remove all clothing, accessories or jewelry from the individual, as they may be contributing to
injury.
On the way to the hospital, cool the injured areas with room-temperature water.
It may be intuitive to use ice or iced-water, but this should be avoided because it can worsen the injury.
At the emergency department, management starts with the ABCs; that is airway, breathing and circulation.
Using a fiberoptic or direct laryngoscope, look for edema and obstruction of the airway.
The decision to intubate is based on the presence of oropharyngeal swelling, stridor and respiratory distress
causing hypoxemia. But sometimes, it’s more subtle.
Clinical signs like hoarseness of the voice, facial burns, drooling, soot in the airway, or even singed nasal or facial
hairs should encourage you to secure the airway prophylactically, even if the airway isn’t swollen yet or they are
not in obvious respiratory distress.
Sometimes it’s too late and the airway has closed, and in that case a surgical cricothyroidotomy is performed. In
other words, if the main airway door is closed, you better break in through the window.
Also, If exposure to carbon monoxide is a concern, like in the setting of a closed house-fire, 100 percent oxygen
is provided using a non-rebreather mask, and carboxyhemoglobin levels are measured.
Alright, so burns cause a tremendous amount of fluid loss, but it’s not as obvious as the fluid loss seen in
diarrhea, vomiting or bleeding.
Burns increase capillary permeability, causing a tremendous amount of fluid to shift from the plasma to the
interstitial space, which is called “third-spacing”.
To replace the loss, place two large-bore intravenous lines on an unburnt area of the skin. The amount of fluid to
give depends on the total body surface area affected. Importantly, first degree burns are not included in the
calculation.
To measure this, the “rule of 9s” is used in adults. This method divides the body into eleven areas, each equal to
9 percent.
The head is 9, each arm is 9, each leg is 18; that is 9 for the anterior aspect and 9 for the posterior aspect.
The chest, abdomen, upper back, and lower back each represent 9 percent. Nine times 11 is 99, so that last 1
percent is the perineum.
Sometimes, the burn areas are patchy, and it can be difficult to ascertain a percentage.
To tackle this issue, the palm can be used to estimate, as the palm approximates 1 percent of a person’s total
body surface area.
10 | P a g e
CLINICAL REASONING – EMERGENCY MEDICINE
Because children have larger heads and smaller extremities, the “rule of 9s” cannot be applied to them. Instead,
the more complex Lund and Browder chart is used, which takes into account the child’s age. This chart may also
be applied to adults.
Alright, once you got the percentage, it’s inserted into the Parkland formula, which calculates how much
intravenous Ringer’s lactate the individual should receive.
Ringer’s lactate is used because its composition is closest to the extracellular fluid.
In the first 24 hours, the amount of Ringer’s lactate to give in milliliters is equal to: 4 multiplied by the weight in
kilograms, multiplied by the percentage of the total body surface area involved. Half of the number you get is
given in the first 8 hours, and the other half is given over the next 16 hours.
Alright, so the adequacy of fluid resuscitation is determined by inserting a Foley catheter and measuring the
urine output hourly. In adults, 0.5 milliliters per kilogram per hour is considered adequate, whereas in children 1
milliliter per kilogram per hour is adequate.
The idea behind this strict fluid regimen is Jackson’s burn model, which states that a burn injury is divided into
three zones, a central zone of coagulation, which is dead and unsalvageable, a middle zone of stasis, and an
outer zone of hyperemia.
Adequate fluid resuscitation may potentially save the zones of stasis and hyperemia from irreversible injury.
Under- or over-resuscitation may result in more tissue injury.
Also, under-resuscitation may cause acute kidney injury, while over-resuscitation may worsen compartment
syndrome or cause pulmonary edema.
Also, tetanus toxoid should be given if the individual had not received it in the past 5 years.
Tetanus immunoglobulin is added if they haven’t received the primary series during childhood.
In addition to fluid resuscitation, individuals with electrical burns should be placed on a continuous cardiac
monitor, because they might have cardiac arrhythmias.
Electrical burns and burns that damage muscle tissue may cause rhabdomyolysis, which releases myoglobin into
the circulation.
Myoglobin is toxic to the renal tubular epithelial cells, causing acute tubular necrosis.
In addition to fluids, alkalization of the urine with the osmotic diuretic mannitol is recommended.
In addition, extensive tissue necrosis releases potassium, causing hyperkalemia.
Okay, now full-thickness burns appear as a leathery, necrotic eschar. If that eschar circumferentially covers and
pressures the neck, chest or an extremity, it can impair perfusion, and this is called compartment syndrome.
Also, an eschar around the neck can compress the trachea, and an eschar around the chest can impair breathing
mechanics.
To prevent tissue necrosis and hypoventilation, an escharotomy is performed. This involves making an incision
through the eschar, relieving the pressure. Anesthesia is usually not needed because eschars are usually
painless, since all the nerve endings in the dermis have been destroyed.
Okay, a crucial aspect of burn management is analgesia.
In minor burns, acetaminophen or non-steroidal anti-inflammatory drugs can be given.
However, in more severe burns, IV opioids like morphine can help especially if they’re given early on.
However, a challenging balance should be maintained, because opioids also cause hypotension and respiratory
depressions; side effects that we don’t want in burns.
Additionally, sedation with benzodiazepines or ketamine may be initiated, to ease taking care of the wounds.
Because burns increase the risk of stress peptic ulcers, or Curling ulcers, intravenous proton pump inhibitors are
given.
The risk of venous thromboembolism such as deep venous thrombosis or pulmonary embolism is also increased
in the setting of burns, and therefore prophylaxis is instituted using unfractionated or low-molecular weight
heparin.
Burns cause a hypermetabolic state, and individuals often cannot feed themselves. Therefore nutritional support
is important.
Enteral feeding using a nasogastric tube is preferred, but if they can’t tolerate it, total parenteral nutrition or
TPN may be required.
Next, is local wound management. The skin is the most important barrier to infection, so if that barrier is
damaged, the skin needs help preventing infection and augmenting healing.
The wound should be cleaned with soap and water or sterile saline.
Povidone-iodine solutions on the other hand have been shown to delay wound healing and should be avoided.
Acidic chemical burns should be irrigated continuously with water only for 20 to 30 minutes, and alkaline burns
should be irrigated for hours, since they are far worse.
And it’s actually not a good idea to neutralize an acid with a base and vice versa - in fact it’s contraindicated,
because this results in the release of thermic energy, which further damages the tissue.
Okay, so any eschar or necrotic tissue should be debrided, because dead tissue serves as a habitable
environment for bacteria.
Debridement is done in a tangential method, meaning that thin layers of the necrotic tissue should be removed
until there’s uniform capillary bleeding throughout the wound. This indicates that you’ve reached viable tissue.
An important aspect of preventing infection is giving antibiotics, but because blood flow is often compromised at
the necrotic burn area, systemic antibiotics may not adequately reach it.
Therefore, topical antibiotics are usually preferred, with a large number of options to choose from.
Silver sulfadiazine covers most gram positive and gram negative bacterial organisms as well as fungi, and it’s
application is not painful.
It’s downsides however are that it doesn’t cover Pseudomonas aeruginosa, which is the most common cause of
sepsis from burns, and it’s not conducive to wound healing.
11 | P a g e
CLINICAL REASONING – EMERGENCY MEDICINE

Mafenide acetate covers Pseudomonas, but it is painful to apply.

Silver nitrate is a good option for individuals with sulfa allergies, who cannot be given silver sulfadiazine.

However, it leaves a blackish stain, making it difficult to assess the wound.

If a wound infection is suspected, a tissue biopsy is obtained, and topical as well as systemic antibiotics are
tailored to the offending organism.

Sterile dressings should be applied daily, as they aid in wound healing.

Summary

Alright, a quick recap. Burns can be categorized by cause, and include thermal, chemical and electrical burns, or
by depth, and include first, second, third and fourth degree burns.

Evaluation begins at the scene. Management begins at the scene, and includes removing the individual from the
source, and applying room-temperature water to the affected areas.

Analgesia should be initiated as soon as possible.

In the emergency department, evaluation begins with the ABCs: airway, breathing and circulation.

Early endotracheal intubation is indicated if the individual has any of: oropharyngeal swelling, stridor,
respiratory distress causing hypoxemia, hoarseness of the voice, facial burns, drooling, soot in the airway, or
singed nasal or facial hairs.

When carbon monoxide poisoning is a concern, 100 percent oxygen is provided, and carboxyhemoglobin levels
are measured.

Two-large bore intravenous lines are inserted to initiated intravenous Ringer’s lactate.

Using the “rule of 9s” or the Lund-Browder chart, estimate the total body surface area affected, and insert it into
Parkland’s formula to determine the amount of fluid in milliters to give in the first 24 hours.

This is equal to 4 multiplied by the weight in kilograms multiplied by the total body surface area.

Half is given in the first 8 hours, and the other half is given in the next 16 hours.

Urine output should be monitored to make sure you’re not over-or-under-resuscitating the individual.

Additional therapeutic measures include providing analgesia, the tetanus toxoid vaccine, initiating stress ulcer
and venous thromboembolism prophylaxis, and inserting a nasogastric tube for enteral feeding.

If the necrotic eschar is causing compartment syndrome, an escharotomy is performed.

Burn wounds are cleaned, irrigated and thoroughly debrided.

Topical antibiotics are often indicated to prevent infection, and options include silver sulfadiazine, mafenide
acetate, silver nitrate, and many more.

12 | P a g e