3rd Summative Outline

ًَّ‫س ْهال‬
َ ‫ْت‬
ََّ ‫شئ‬
ِ ‫ن إِذا‬ ََّ ‫ َوأَ ْن‬،ًَّ ‫سهال‬
ََّ ‫ت تَجْ عَ َُّل ا ْلح ََز‬ َ ‫اللّهُمَّ ال‬
َ ُ‫س ْه ََّل إِ َّالّ ما َجعَلتَ َّه‬
MEDICAL EMERGENCIES 2. Compression rate should be 100 to 120

per minute.
OXYGEN IS VITAL FOR LIFE 3. Compression depth should be 2 to 2.5 in.
• Primary concern (5 to 6 cm).
o Initiating and maintaining 4. Do not lean hands on the chest between
circulation through compressions compressions to allow complete recoil
o Delivering oxygen to vital organs between compressions.
• Airway obstructions impede (or hinder) 5. Continue compression-only CPR until
oxygen delivery arrival of automated external defibrillator
• Time is important when an unconscious
or rescuers with additional training.
person is not breathing. Permanent brain
6. If trained in rescue breathing, add rescue
damage begins after only 4 minutes
breaths after 30 compressions, using two
without oxygen and death can occur as
soon as 4 – 6 minutes. breaths then and every 30 compressions
• Immediate action is crucial to survival until skilled help arrives.
7. Naloxone may be given for suspected life-
Oxygen is essential for life and required for threatening opioid associated
cellular function emergencies.
• Hypoxia is oxygen deficiency 8. Assessment of breathing and pulse checks
• Anoxia is the absence of oxygen may be done first by basic life support
Respiratory system provides the interface healthcare providers, but must be done in
between the atmosphere and the bloodstream <10 seconds.
for gas exchange
• Intake of oxygen STEPS OF BASIC CPR
• Removal of CO2
STEP 1 AND STEP 2 IN BASIC CPR: RECOGNITION
AND CALL FOR HELP
BASIC LIFE SUPPORT/ CARDIOPULMONARY
▪ Before approaching a collapsed individual,
RESISCITATION assess the scene for risks to healthcare
▪ The time sensitivity of CPR in sudden providers. Potential risks include the
cardiac death is emphasized in the
presence of hazardous materials, an
American Heart Association Chain of
unstable physical environment, or
Survival
personal violence.
▪ Once the patient is reached, determine
CRITICAL GOAL OF CPR: provide critical blood flow
to vital organs the patient’s level of responsiveness to
noxious stimuli.
• Probably will not restart the heart a. VERBAL STIMULI - “Sir/Ma’am! Are
• Delays damage to vital organs you okay? Are you alright?”
b. PAINFUL STIMULI – tap firmly but
SEQUENCE OF STEPS FOR BASIC CPR gently the shoulders of the patient
▪ State your name and desire to help:
1. C-A-B (chest compressions, airway, and
1. If the injured responds, leave in
breathing) is the recommended sequence position found
for a single rescuer. Provide chest 2. If the injured does not respond,
compressions before giving rescue scan quickly to determine if he is
breaths.
What is meant for you, will reach you even if its beneath two mountains MUKHALALATI | 2025
What isn’t meant for you, won’t reach you even if it’s between your two lips.
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breathing normally, and Pulse Check: Adult/Child

simultaneously check for a pulse • Use carotid artery in the neck to
▪ If the patient is without normal breathing,
check for pulse
get help first before starting chest
• Place two fingers on “Adam’s Apple”
compressions (asking a bystander to activate
• Slide fingers toward you and slightly
the local EMS system)
upward into groove on side of neck
STEP 3 IN BASIC CPR (HEALTHCARE PROVIDER • Allow 5-10 seconds
ONLY): ASSESS CIRCULATION • Adjust pressure to locate pulse but
avoid excessive pressure
▪ The carotid artery is generally the most
reliable and accessible location to palpate
a pulse. The artery is located by placing STEP 4 IN BASIC CPR: BEGIN CARDIAC
two fingers on the trachea and then COMPRESSIONS
sliding them down to the groove between When the lack of a pulse is confirmed, begin
the trachea and the sternocleidomastoid serial rhythmic closed chest compressions.
muscle.
CLOSED CHEST COMPRESSIONS
Note: Simultaneous palpation of both carotid
arteries should not be performed because, in low- ▪ Place the victim supine on a firm surface,
pressure states, this could obstruct cerebral blood with the rescuer at the victim’s side.
flow and may interfere with the ability to detect a ▪ Place the heel of one hand midline on the
pulse lower half of the sternum, 4 to 5 cm (∼2
in.) cephalad of the xiphoid process.
▪ The femoral artery may be used as an ▪ The heel of the hand should be parallel
alternative site to palpate a pulse. This with the long axis of the patient’s body.
can be found just below the inguinal Then place the second hand on top of the
ligament approximately halfway between first hand, so the hands are parallel with
the anterior superior iliac spine and the each other.
pubic tubercle. ▪ Keep the arms straight and the elbows
If no definite pulse is felt within 10 seconds, locked. The vector of the compression
chest compression should begin. force should start from the rescuer’s
shoulders and be directed downward.
Pulse Check: Infant ▪ Depress the sternum 2 to 2.5 in. (5 to 6
• Use brachial artery on upper arm cm) in an adult at a rate of 100 to 120
• Place two fingers on inner arm just compressions per minute. Rates lower
under armpit than this are inadequate. The
• Find groove formed by muscles compression-release phases should be
• Use gentle pressure roughly equal in length.
• Allow 5-10 seconds ▪ With a single rescuer or with two rescuers
• Adjust pressure to locate pulse but if the patient is not intubated, give two
avoid excessive pressure ventilations after every 30 compressions.
With two rescuers assisting an intubated
patient, ventilate at a rate of 8 to 10 per
minute, without interrupting chest
compressions.
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Note: Although assisting ventilation is important, compressions, and before attempting breaths,
not everyone is willing to perform mouth-to- look for an object and, if seen, remove it.
mouth breathing due to concerns over infectious
disease transmission. Chest compressions alone
can be effective and should be provided even if
rescue breathing is not being performed.
COMPRESSION-VENTILATION RATIO
Patient Rescuers How to

compress and
depth
Infant 1 rescuer – Two or three
STEP 5 IN BASIC CPR: DEFIBRILLATE
30:2 fingers – 1.5
2 rescuer– inches (4 cm) Defibrillation
15:2 – 1/3 chest
depth ▪ is the therapeutic use of electricity in
Child 1 – 30:2 One or two cardiac arrest to depolarize the entire
2 – 15:2 hands – 2 myocardium to eliminate ventricular
inches (5 cm) fibrillation or non-perfusing ventricular
– 1/3 chest tachycardia so that coordinated
depth contractions can resume.
Adult 1 – 30:2 Two hands – 2 ▪ It should be performed in close
2 – 30:2 -2.5 inches (5- coordination with CPR of the cardiac
6 cm) arrest patient.
Note: Allow complete recoil of the chest between ▪ The indications for defibrillation include
compressions, with approximately equal ventricular fibrillation and pulseless
compression and relaxation times. Minimize ventricular tachycardia.
interruptions. ▪ Defibrillation is not “jumpstarting the
Two rescuers, intubated patient: give breaths at a heart” and is thus not indicated for
rate of 8–10 breaths/min without interrupting asystole or pulseless electrical activity.
chest compressions. ▪ It is contraindicated for sinus rhythm,
conscious patients with a pulse, or when
1. Use head-tilt-chin-lift to open airway there is danger to the operator or others
2. Create seal with barrier device (or mouth (e.g., from a wet patient or wet
to mouth directly on victim while pinching
surroundings).
nose closed)
3. Rescue breaths sufficient for gentle chest Ventricular tachycardia
rise-and-fall, no more
1. 1 second breath
2. 1 second exhale
3. 1 second for next breath
Ventricular Fibrillation
Note: If the chest does not rise with the initial
rescue breath, re-tilt the head before delivering
the second breath. If the chest does not rise with
the second breath, the person may be choking.
After each subsequent set of 30 chest
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Electrical cardioversion defibrillators will require an operator to manually

deliver the shock after analysis and charging.
▪ is the application of a synchronized
electrical impulse to convert a still- 1. Ensure that the scene is safe for
perfusing tachydysrhythmia back to a performing defibrillation, including water
normal sinus rhythm. and environmental scene dangers such as
▪ Cardioversion may also be performed traffic. The patient should be in the supine
pharmacologically or position with ongoing CPR
nonpharmacologically for the stable 2. Expose the chest to apply the pads or
patient. paddles. To avoid skin burns, remove all
▪ Electrical cardioversion is indicated for metallic objects, jewelry, or medication
patients with ventricular tachycardia, patches (wipe off any residue). If there is
supraventricular tachycardia, atrial flutter, excessive chest hair over the areas where
or atrial fibrillation, who are the pads or paddles are to be placed,
hemodynamically unstable as a quickly shave the hair off to ensure a good
consequence of the rhythm. contact with the skin.
▪ It may also be considered after 3. If the patient is on a wet or conducting
unsuccessful pharmacologic therapy for surface, move the patient to a safe area
the previously mentioned arrhythmias, and dry the body before delivering any
even if the patient remains shocks. Sweat or moisture on the chest
hemodynamically stable. will conduct the current and may reduce
▪ Electrical cardioversion should be the adhesion of pads.
synchronized, which means the electric 4. Remove all direct sources of oxygen to
impulse will be timed with the patient’s avoid fire
intrinsic QRS complexes, to minimize the
POSITIONING
risk of inducing ventricular fibrillation.
There are several possible positions for the
Note: The energy used for defibrillation or
placement of the pads or paddles:
electrical cardioversion is delivered as a wave and
may be monophasic or biphasic. Monophasic
waveforms are found in older defibrillators and
deliver the energy in a single direction, while
biphasic waveforms deliver the energy forward
and back in two phases within the same amount
of time.
Manual defibrillators require a manual analysis
of the patient’s cardiac rhythm, as well as manual
delivery of the shock through paddles or self-
adhesive pads (see below) by the operator.
Automated external defibrillators (AED) may be
fully or semi-automated. Fully automated
external defibrillators will analyze the rhythm
automatically, and if indicated, charge and deliver • Antero-apical position:
the shock, whereas semi-automated external o Place one paddle/pad to the right
of the upper half of the sternum,
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just below the patient’s right o Chest compression fraction >80%

clavicle, and place the other pad o Compression rate of 100-120/min
just below and to the left of the o Compression depth of at least 2 inches
left nipple. in adults or 1/3 the AP dimension in
o With a female patient, place the infants and children
paddle/pad just below and to the o No excessive ventilation
left side of the breast. Do not place
it over the breast STEP 7 IN BASIC CPR: OPEN THE AIRWAY AND
RESCUE BREATHING
Note: This is the preferred position for a supine
patient, such as in cardiac arrest, and when using The seventh step is to assess the upper airway of
defibrillation paddles. The idea is to maximize the victim. This usually requires positioning the
current flow across the cardiac chambers rather individual supine on a flat, firm surface with the
than along the chest wall. arms along the sides of the body.
▪ Unless trauma can be definitely excluded,
any movement of the victim should
consider the possibility of a spine injury.
▪ As the patient is placed supine, stabilize
the cervical spine by maintaining the
head, neck, and trunk in a straight line. If
the neck is not already straight, then it
▪ Anteroposterior position: should be moved as little as possible to
o Place one pad/paddle at the left establish the airway.
lower sternal border and the ▪ If the patient cannot be placed supine,
posterior pad/paddle below the the jaw thrust maneuver can be applied
left scapula with the rescuer at the victim’s side.
STEP 6 IN BASIC CPR: CONTINUE HIGH-QUALITY ▪ Common causes of airway obstruction in
CARDIAC COMPRESSIONS an unconscious patient are occlusion of
the oropharynx by the tongue and laxity
Continuing high-quality compressions as much as of the epiglottis.
possible while minimizing interruptions is critical ▪ With loss of muscle tone, the tongue or
to increase the chances of achieving return of the epiglottis can be forced back into the
spontaneous circulation and optimizing the oropharynx upon inspiration. This can
chance of survival to hospital discharge. create the effect of a one-way valve at the
Chest compressions fraction refers to the entrance to the trachea, leading to airway
proportion of time spent performing obstruction. After positioning the patient,
compressions. Current guidelines recommend a inspect the mouth and oropharynx for
chest compression fraction of at least 60%. secretions, foreign objects, loose (floppy)
dentures, partial dentures, or broken
According to the American Heart Association teeth.
(AHA), a high quality CPR is the primary ▪ If secretions are present, they can be
component in influencing survival from cardiac removed with the use of oropharyngeal
arrest.
suction if available; a visualized foreign
body may be dislodged by use of a finger
A high quality CPR metrics include:
sweep and then manually removed. In
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contrast to earlier recommendations, a

blind finger sweep should never be
performed as there is a risk of worsening
airway obstruction.
▪ Once the oropharynx has been cleared,
two basic maneuvers for opening the
airway may be tried. These are the head
tilt–chin lift and the jaw thrust. JAW THRUST MANEUVER
▪ These maneuvers help to open the airway
by mechanically displacing the mandible The jaw thrust is the safest method for opening
and the attached tongue out of the the airway if there is the possibility of cervical
oropharynx spine injury. This maneuver helps to maintain the
cervical spine in a neutral position. The rescuer,
who is positioned at the head of the patient,
places the hands at the sides of the victim’s face,
grasps the mandible at its angle, and lifts the
mandible forward. This lifts the jaw and opens
the airway with minimal head movement.
RESCUE BREATHING
After opening the airway, assess respiratory
HEAD TILT–CHIN LIFT MANEUVER effort and air movement. Look for chest
expansion, and listen and feel for airflow. The
To perform the head tilt–chin lift maneuver, simple act of opening the airway may be
gently extend the patient’s neck by placing one adequate for the return of spontaneous
hand under the patient’s neck and the other on respirations. However, if the victim remains
the forehead and extending the head in relation without adequate respiratory effort, then further
to the neck. This maneuver should place the intervention is required. If rescuers are reluctant
patient’s head in the sniffing position, with the to perform mouth-to-mouth ventilation and the
nose pointing up. In conjunction with the head patient is in cardiac arrest, chest compressions
tilt, perform the chin lift. The chin lift is done by alone can be effective.
carefully placing the hand that had been
supporting the neck for the head tilt under the
symphysis of the mandible, taking care not to
--FROM SAFE INSTRUCTORS—
compress the soft tissues of the submental
triangle and the base of the tongue. Then lift the Scene Safety and Assessment
mandible forward and up, until the teeth barely
1. Scene safety – “The scene is safe, I am
touch. This supports the jaw and helps tilt the
safe, move over”
head back.
2. Check for responsiveness
a) Verbal stimuli (shout on both sides of the
head) “Hey are you OK?”, “Hey are you
alright?”
b) Painful stimuli (tap firmly but gently) – tap
patient’s shoulders
3. Call for Help – “Help! Someone help!”
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4. Check for pulse and breathing (atleast 5 o if has pulse and has breathing,
seconds, not more than 10 seconds) recovery position (except for trauma
a) Pulse (carotid pulse closest to you) victims)
b) Breathing (observe for rise and fall
of the chest)
5. “Activate emergency response system”
a) “Get an AED”
b) “Start High-Quality CPR”
Component of High-Quality CPR: (SPAMGA)

S- Start compressions within 10 seconds upon
recognition of cardiac arrest
P – Push hard [2-24 inches (5-6 cm) (adult)], push
fast 9100-120 compressions/minute (Macarena
beat)]
A – Allow complete chest recoil
M – Minimize interruption to chest compression
to < 10 seconds
G – Give effective breaths
A – Avoid excessive ventilations
FOREIGN BODY OBSTRUCTION/RESPIRATORY
4 Universal Steps of AED Operation OBSTRUCTION
1. Turn on AED
2. Attach pads (below right clavicle, below ▪ condition where patency of respiratory
left nipple) passages are compromised
3. Let AED analyze ▪ It is important to recognize and be able to
4. Give shock (200J recommended) assist someone with an airway
Shockable rhythms: obstruction due to a foreign body
• Ventricular fibrillation ▪ An individual in distress from a
• Pulseless ventricular tachycardia (no pulse compromised airway is likely to use the
based on ECG, but has carotid pulse) universal sign for an airway obstruction,
Non-shockable rhythms: which is for the individual to grab his or
• Asystole (as a rule, no electric shock) her neck with both hands.
• Pulseless electrical activity (PEA) (has ▪ Foreign bodies can cause partial or
pulse on ECG, but no carotid pulse) complete obstruction. With a partial
airway obstruction, air exchange may be
Note: adequate or inadequate. If the victim is
o if no pulse and no breathing, CPR able to speak, cough, and exchange air,
o if has pulse but no breathing, do rescue then he or she should be encouraged to
breathing continue spontaneous efforts.
▪ Obtain assistance, such as activation of
the local EMS system
▪ Do not interfere with the patient’s attempts
to cough or expel the foreign body and do not
perform a blind finger sweep.
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▪ If air exchange becomes inadequate as aggressively, with the intention of removing the
indicated by an inability to speak, increased obstruction.
difficulty breathing, weak and ineffective
cough, worsening stridor, or cyanosis, - Can be performed with the victim standing,
immediate medical intervention is needed. sitting, or lying down, or it can be self-
▪ Inadequate air exchange from a severe administered.
partial or a complete airway obstruction
1. To perform the maneuver with the patient
should be managed the same way. In an
standing or sitting, stand behind the
unconscious person, the presence of
patient and place the thumb side of a fist
airway obstruction may be ascertained by
against the victim’s abdomen midline
noting inadequate airflow and poor chest
just above the umbilicus and well below
rise with efforts to ventilate
the xiphoid process.
▪ Maneuvers used to relieve foreign body
2. Grasp the fist with the other hand, and
obstructions include the Heimlich
forcefully push the fist into the victim’s
maneuver (subdiaphragmatic abdominal
abdomen with a quick upward thrust.
thrusts), chest thrusts, back blows and
Repeat until the item is dislodged or the
the finger sweep.
patient becomes unconscious.
In a conscious individual, the obstructed airway 3. For an unconscious patient, place the
(Heimlich) maneuver is the recommended victim supine on a firm surface and sit
maneuver in most adults for relieving airway astride the victim’s thighs
obstruction due to a solid object. It is not useful 4. Place the heel of the dominant hand
for liquids. midline just above the patient’s
umbilicus, and the other hand directly on
In an unconscious individual suspected of having
top of the first. Then deliver quick upward
an aspirated foreign body and in whom the
thrusts.
foreign body is visualized, the recommended
5. To self-administer thrusts, the individual
first step is the finger sweep.
can either use his or her own fist to
Note: A blind finger sweep is no longer deliver the thrusts or lean forcibly against
recommended as it may worsen airway a firm object, such as a porch rail or the
obstruction by pushing an unseen object into an back of a chair.
even less favorable position.
Potential complications of the Heimlich
In an unconscious patient whose foreign body maneuver include injury or rupture of abdominal
cannot be visualized, the recommended or thoracic viscera and regurgitation of stomach
sequence is to perform the obstructed airway contents.
maneuver up to five times, open the mouth and
BACK BLOWS
perform a finger sweep if a foreign body has
become visible, and then attempt to ventilate. 1. Administer 5 back blows with heel of
hand over spine between shoulder
OBSTRUCTED AIRWAY (HEIMLICH) MANEUVER
blades while supporting patient with
- Creates an artificial cough by forcefully elevating other hand on sternum.
the diaphragm and forcing air from the lungs. 2. Apply in rapid succession
3. Have patient’s head lower than his
- It may be repeated multiple times. Each chest.
individual thrust should be performed
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CHEST THRUSTS 2. with infant’s torso positioned

prone and head down along
- Is used primarily if someone is morbidly obese
rescuer’s arm or older child draped
or in the late stages of pregnancy and the rescuer
prone and head down cross
cannot reach around the patient’s abdomen to
across rescuer’s knees, five blows
perform abdominal thrusts
are delivered to interscapular
1. To perform chest thrusts with the patient area
standing or sitting, stand behind the 3. infant is repositioned supinely
patient and place the thumb side of a fist along rescuer’s arm, or larger
against the victim’s sternum, avoiding the infant placed on floor, five chest
costal margins and the xiphoid process. thrusts are delivered
2. Grasp the fist with the other hand, and 4. older children: Heimlich maneuver
press the fist into the victim’s chest with a (Age 1 yr old and older???)
quick backward thrust. ▪ if unconscious
3. Repeat until the item is dislodged or the 1. attempt ventilation
patient becomes unconscious. 2. standard CPR (lone rescuer 30:2;
4. For an unconscious patient, place the two or more rescuers 15:2
victim supine on a firm surface and kneel
close to the victim’s side. Place the hands ADVANCED CARDIAC LIFE SUPPORT (ACLS)
in the same position as for chest
The basic life support assessments and
compression (i.e., the lower sternum),
interventions include the Primary Survey, and the
and deliver quick thrusts.
advanced life support assessments and
FINGER SWEEP interventions include the Secondary Survey.
- The finger sweep maneuver is used only in ▪ The Primary Survey addresses the
unconscious patients. identification of cardiac arrest and
performance of good-quality CPR
1. Using the thumb and fingers of one hand,
(including ventilation) and defibrillation.
grasp both the tongue and the mandible
▪ The 2015 Advanced Cardiac Life Support
and lift them. This may partially relieve
guidelines and 2017 International
the obstruction by lifting the tongue away
Consensus on Cardiopulmonary
from the back of the throat.
Resuscitation and Emergency
2. With the other hand, insert the index
Cardiovascular Care Science with
finger into the back of the throat, and use
Treatment Recommendations Summary
a hooking action in an attempt to dislodge
emphasize chest compressions, starting
the foreign body to move it into the
with circulation-airway-breathing as
mouth for manual removal.
opposed to airway-breathing-circulation.
3. Use care so the foreign object is not
▪ Maximize chest compression fraction to
pushed deeper into the throat.
>60% with minimal pauses in
FOR CHILDREN: compressions.
▪ Defibrillate as soon as possible for VF or
▪ if conscious:
pulseless VT. Start at 200 J biphasic or at
1. five back blows and five chest
maximum energy. Make sure CPR
thrusts
interruptions are as brief as possible when
defibrillating
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▪ Maintain continuous compressions during

rhythm analysis and defibrillator
recharging. Resume one cycle of CPR
immediately after defibrillation even with
ROSC.
▪ The 2015 updates and 2017 International
Consensus on Cardiopulmonary
Resuscitation and Emergency
Cardiovascular Care Science With
Treatment Recommendations Summary
recommend a 30:2 compression-to-
breath ratio, maximizing compression
time, with no pauses longer than 10
seconds.
▪ The target compression rate is 100 to 120
per minute, rather than at least 100 per
minute. The maximum compression rate
is 120 per minute because quality ▪ Defibrillation may be done with either an
decreases with rates greater than this. automated external defibrillator or a
The maximum depth of compressions is 6 manual defibrillator
cm, with a target of 5 to 6 cm, rather ▪ Deliver shocks for VF or pulseless VT with
than at least 5 cm in the 2010 guidelines. minimal interruption of chest
▪ For one- and two-rescuer CPR, the 2015 compressions only during actual shock
Advanced Cardiac Life Support guidelines delivery. Make sure that the position of
recommend 30 compressions followed by the defibrillator pads does not interfere
two breaths (30:2 ratio) in patients with monitoring leads.
without an advanced airway, similar to ▪ After delivery of the first shock, resume
the 2017 International Consensus on CPR immediately for 2 minutes before
Cardiopulmonary Resuscitation and reviewing the ECG monitor for a rhythm
Emergency Cardiovascular Care Science diagnosis.
With Treatment Recommendations ▪ If a viable rhythm has returned, check for
Summary. During breaths, compressions pulse and breathing. If breathing and
may be withheld. If an advanced airway pulse have returned, begin care for post-
is in place, the 2015 updates recommend ROSC management.
a breath rate of 10 per minute, or one ▪ If breathing is absent, continue rescue
breath every 6 seconds, asynchronous breathing with a BVM at the rate of about
from compressions. 10 breaths per minute; if pulse is not
▪ The critical rhythms associated with present, continue CPR and move to the
cardiac arrest are VF (Figure 24-5), Secondary Survey.
pulseless VT (Figure 24-6), asystole (Figure ▪ The Secondary Survey includes
24-7), and pulseless electrical activity endotracheal intubation or the
(PEA) (Figure 24-8). placement of another airway adjunct,
assessment of ventilatory status, gaining
IV access, identifying ECG rhythms,
delivering drugs to enhance circulation,
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and addressing the reasons for the

occurrence or persistence of cardiac
arrest. SHOCK
▪ Shock is a state of circulatory insufficiency
that creates an imbalance between tissue
oxygen supply (delivery) and demand
(consumption), resulting in end-organ
dysfunction
▪ The mechanisms that can result in shock
are frequently divided into four
categories: (1) hypovolemic, (2)
distributive, (3) cardiogenic, and (4)
obstructive.
▪ A state of widespread inadequate tissue
perfusion. Although we often think of
oxygen when we read this statement, do
not forget that the cells are deprived of
electrolytes, hormones, and glucose in
addition to oxygen, and that wastes are
not taken away from the cells.
▪ Tissues deprived of oxygen turn to
anaerobic (without oxygen) sources for
energy.
▪ Although these pathways may allow cells
to continue to function for a time, they
result in high levels of toxic substance
building up in the body.
▪ Toxins in the blood change the pH
towards acidity and acidity can inactivate
medications like epinephrine. Toxins in
the blood can also cause cardiac
dysrhythmias.
Note: Low BP does not equal shock.

It is important to evaluate many factors:
Baseline BP info from patient when possible
Presence of sustained tachycardia
LOC
MOI and suspected injuries from MOI
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CATEGORIES OF NON-TRAUMATIC SHOCK o Compensatory responses to

decreased SVR may include
The four categories of shock can be described in
increased CO (increased
terms of their respective physiologic changes and
contractility and heart rate) and
common causes, recognizing that a single
tachycardia.
etiology may manifest the clinical findings of
o The concurrent decreased SVR
more than one shock type.
results in a decreased preload and
▪ Hypovolemic shock may hinder CO overall.
o occurs when decreased o When your blood vessels lose their
intravascular fluid or decreased tone, they can become so open
blood volume causes decreased and floppy that not enough blood
preload, stroke volume, and pressure supplies your organs.
cardiac output (CO).
There are a number of types of distributive
o Severe blood loss (hemorrhage)
shock, including the following:
can cause decreased myocardial
oxygenation, which decreases Anaphylactic shock is a complication of a severe
contractility and CO. allergic reaction known as anaphylaxis. Allergic
o This action may lead to an reactions occur when your body mistakenly treats
autonomic increase in the systemic a harmless substance as harmful. This triggers a
vascular resistance (SVR). dangerous immune response. Anaphylaxis is
o Hypovolemic shock can also occur usually caused by allergic reactions to food, insect
due to volume loss from other venom, medications, or latex.
etiologies
Septic shock is another form of distributive
Associated with: shock. Sepsis, also known as blood poisoning, is a
condition caused by infections that lead to
1. Trauma
bacteria entering your bloodstream. Septic shock
o Severe hemorrhage – external or
occurs when bacteria and their toxins cause
internal
serious damage to tissues or organs in your body.
o Sever injury – esp fracture of
bones and crushing of tissues Neurogenic shock is caused by damage to the
o Surgical procedure – esp if central nervous system, usually a spinal cord
anesthesia is not adequate injury. This causes blood vessels to dilate, and the
o Burning – esp where extensive skin may feel warm and flushed. The heart rate
surface damage allows loss of a slows, and blood pressure drops very low.
large amount of exudate
▪ Cardiogenic shock
2. Dehydration – in cases of severe diarrhea
o The left ventricle fails to deliver
and vomiting
oxygenated blood to peripheral
tissues due to variances in
▪ Distributive shock
contractility, as well as preload,
o there is relative intravascular
afterload, and right ventricular
volume depletion due to marked
function.
systemic vasodilatation. This is
o Myocardial infarction is the most
most commonly seen in septic
common cause of cardiogenic
shock.
shock.
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o Dysrhythmia are another common

cause because they can lead to a
decreased CO.
o Bradyarrhythmias result in low
CO, and tachyarrhythmias can
result in decreased preload and
stroke volume.
o Patients with cardiogenic shock
may soon develop clinically
evident infection (up to 46%)
and/or demonstrate an
inflammatory response similar to
but less pronounced than with
septic shock.
▪ Obstructive shock CATEGORIES OF TRAUMATIC SHOCK

o is uncommon (1%) and is due to a ▪ Hemorrhagic Shock
decrease in venous return or o creates a state of impaired
cardiac compliance due to an oxidative metabolism and
increased left ventricular outflow homeostasis, due to inadequate
obstruction or marked preload oxygen delivery to meet metabolic
decrease. demand, and hypoperfusion
o Cardiac tamponade, pulmonary leading to inadequate cellular
embolism, and tension waste removal.
pneumothorax are causes of o Hemorrhagic shock triggers a
obstructive shock. complex range of physiologic
responses that may temporarily
compensate for intravascular
volume loss and maintain
perfusion to the most important
vascular beds.
o When uncorrected, coagulopathy,
additional inflammation, and
organ system damage will result.
o The hemodynamic response to
acute severe hemorrhage-induced
hypovolemia traditionally includes
tachycardia, hypotension, and
signs of poor peripheral perfusion
(cool, pale, clammy extremities
with weak peripheral pulses and
prolonged capillary refill).
o Arterial and venous
vasoconstriction leads to a
narrowing of the pulse pressure.
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o Cerebral hypoperfusion causes more severe hypothermia, the patient

alterations in mental status. With may demonstrate paradoxical
increasing blood loss, signs and undressing—removal of clothing in
symptoms become more response to prolonged cold stress. Slurred
pronounced. speech and/or ataxia may mimic a stroke
o Classification of hemorrhage or alcohol intoxication
severity as a percentage of blood ▪ The prehospital treatment of hypothermia
volume loss estimated based on should be focused on maintaining the
systolic blood pressure, heart rate, patient’s core body temperature and
and Glasgow Coma Scale is not preventing any further heat loss.
reliable and should not be used to
guide ED resuscitation. 2. ACIDOSIS
▪ Is the result of excessive acid
TRAUMA TRIAD OF DEATH accumulation in body fluids. Causes
include excessive acid in the blood,
In the ED and OR environments, the critical
decreased clearance of acidic byproducts,
parameter is the time the patient spends there
loss of bicarbonate from the blood,
before certain clinical conditions develop. These
buildup of carbon dioxide in the blood
conditions include hypothermia, acidosis and
resulting from poor lung function, and
coagulopathy. Jointly they comprise the trauma
slow breathing.
triad of death
▪ Prehospital treatment of acidosis should
1. HYPOTHERMIA focus on managing the suspected cause
▪ Occurs when the body’s mechanisms for (e.g., the injury) and contributing
temperature regulation are overwhelmed. underlying diseases. In the setting of
▪ The brain’s hypothalamus produces multisystem trauma, management of
hormones that influence a variety of hypoxia and hypoperfusion is important.
bodily functions, including body Providers should ensure that the patient’s
temperature. airway is patent and oxygen is
▪ Core body temperature normally ranges administered.
between 36.5–37.5°C.
▪ Hypothalamic control of temperature 3. COAGULOPATHY
occurs through several mechanisms, ▪ can result from a number of different
including heat conservation with events, including excessive fluid dilution,
peripheral vasoconstriction and heat metabolic events (e.g., acidosis),
production through shivering, influenced hypothermia and disseminated
by epinephrine. intravascular coagulation (DIC).
▪ Heat production increases with muscle ▪ Prehospital treatment options for
contractions and shivering. Some consider coagulopathies are limited and tend to be
shivering one of the last resorts by which supportive. Providers should focus on
the body attempts to maintain securing the patient’s ABCs, administering
temperature. supplemental oxygen, managing external
▪ There are numerous signs and symptoms hemorrhage with direct pressure, wound
associated with hypothermia, including care, maintaining the patient’s
confusion, dizziness, chills, dyspnea, mood temperature, and providing overall
change and irritability. In situations of support.
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Note: Between hypothermia, coagulopathy Orthopedic injuries to these structures

and acidosis, it is important to correct or include the following:
address first the body temperature of the
patient because as the core temperature Fracture: A disruption of bone tissue.
goes down, the ability to stop the bleeding Fractures may be caused by (1) an application
also goes down. It can also contribute to of force exceeding the strength of the bone,
the development of acidosis due to (2) repetitive stress, or (3) an invasive process
decreased tissue perfusion, shivering and a that undermines the bone’s integrity.
decrease in the removal of lactic acid from
the body. Dislocation: Complete disruption of a joint,
such that the articular surfaces of the bones
that comprise the joint are no longer in
FRACTURES contact with one another.
ANATOMY: Subluxation: Partial disruption of a joint, in

which some degree of contact between the
Musculoskeletal trauma involves injury to one articular surfaces remains.
or more of the following structures:
Fracture-dislocation or fracture-subluxation:
Bone: A unit of the skeleton composed of the Disruption of a joint combined with fracture
hardest variety of connective tissue. Bones of at least one of the bones involved in the
give shape and support to the body. In articulation.
addition to surrounding and protecting vital
organs, they serve as points of attachment for Diastasis: A separation of the interosseous
the muscles of the limbs, making movement membrane connecting two syndesmotic joints
possible. as seen between the radius and ulna and tibia
and fibula.
Joint: The area where two or more bones
articulate with one another. Joints are usually Strain: A tearing injury to muscle fibers
classified in terms of the amount of motion resulting from excessive tension or overuse.
permitted at the articulation. Most joints of Strains can be further subdivided in first,
the extremities are synovial joints, which second, and third based on their level of pain
allow the greatest amount of motion. and functional ability.
Ligament: A bundle of connective tissue Sprain: A tearing injury to one or more

forming part of the fibrous capsule ligaments of a joint, which occurs when the
surrounding a joint and attached to it. Every joint is forced beyond the limits of its normal
joint of the extremities is reinforced by two or planes of motion. These injuries can be
more ligaments, whose purpose is to stabilize further classified into first-, second-, and
the joint by confining its movements to third-degree sprains depending on their
specific planes and preventing movement extent.
beyond physiologic limits. TYPES OF FRACTURES (ADULTS):
Tendon: The fibrous structure connecting a • “Common” Fractures - Most fractures are
voluntary muscle to bone, cartilage, or the result of significant trauma to healthy
ligaments. Tendons enable muscles to effect bone. The bony cortex may be disrupted
motion in the joint or body area to which they by a variety of forces, including a direct
are attached. blow, axial loading, angular (bending)
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forces, torque (twisting stress), or a - Damage to the epiphyseal plate during a

combination of these. child’s growth may destroy part or all of
its ability to produce new bone substance,
• Pathologic Fractures - Fractures that resulting in aborted or deformed growth
result from relatively minor trauma to of the limb.
diseased or otherwise abnormal bone are
ORTHOPEDIC EMERGENCIES
termed pathologic fractures.
- In such cases, a preexisting process has • Open fracture (compound fracture): The
weakened the bone and rendered it bone pokes through the skin and can be
susceptible to fracture by forces that, seen. Or a deep wound exposes the bone
under normal circumstances, would not through the skin. It is a fracture associated
disrupt the cortex. with overlying soft tissue injury, creating
- Common examples of such injuries are communication between the fracture site
fractures through metastatic lesions, and the skin.
fractures through benign bone cysts, and
• A potential major complication of open
vertebral compression fractures in
fracture is osteomyelitis.
patients with advanced osteoporosis.
• Closed fracture (simple fracture). The
• Stress Fractures - Bone may undergo a bone is broken, but the skin is intact.
“fatigue” fracture by being subjected to
low-intensity trauma or repetitive forces
before the bone and its supporting tissues
have had adequate time to accommodate
to such forces.
- often involve the lower extremity, are
common in athletes such as runners or
dancers, and occur in deconditioned
individuals who begin new exercise • Subluxation and dislocation
programs. o Subluxation is a condition in which
the articular surfaces of a joint are
• Salter (Epiphyseal Plate) Fractures - nonconcentric to any degree.
Fractures involving the physis, the Dislocation is the most extreme
cartilaginous epiphyseal plate near the form of subluxation.
ends of the long bones of growing o A joint is dislocated when the
children, were originally classified by articular surfaces of the bones that
Salter and Harris and are commonly called normally meet at the joint are
Salter fractures. completely out of contact with one
- New bony material needed for the another.
elongation of bones during growth is o The urgency of reducing a
provided by specialized cells within the dislocation is based on several
physis. When growth is completed, the factors. One is the potential for
physis transforms from cartilage into neurologic or circulatory
bone, ultimately fusing with the bone compromise. The neurovascular
surrounding it, and disappearing as a bundle passing close to the
distinct entity.
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affected joint may become

“kinked” around the dislocation.
This may result in neurologic or
vascular deficit that might be
temporary if the deformity is
reduced promptly but irreversible
if treatment is delayed.
o Another consideration is that the
longer a joint has been dislocated,
the more difficult it may be to
reduce and the less stable the
reduction is likely to be. This is
probably due, at least in part, to
edema, muscle spasm, and other
tissue changes that increase over
time.
o Dislocation of the hip also carries
the potential for avascular necrosis
of the femoral head.
Definition of Terms: PREHOSPITAL SPLINTING DEVICES
• Greenstick. This is an incomplete break. A Sling and Swath
part of the bone is broken, causing the
▪ For injuries of the wrist or forearm,
other side to bend.
consider using a sling to supplement the
• Transverse. The break is in a straight line
splint, because optimal immobilization
across the bone.
includes the joint above and the joint
• Spiral. The break spirals around the bone.
below the fracture, and a sling helps keep
This is common in a twisting injury.
the elbow at rest.
• Oblique. The break is diagonal across the
▪ For suspected injuries to the shoulder,
bone.
humerus, or elbow, a sling-and-swathe
• Compression. The bone is crushed. This
arrangement works well. This method
causes the broken bone to be wider or
involves applying a sling, then binding the
flatter in appearance.
affected arm to the thorax with a gauze
• Comminuted. The bone has broken into 3
wrap.
or more pieces. Fragments are present at
▪ An exception to this principle is
the fracture site.
immobilization of patients with suspected
• Segmental. The same bone is broken in 2
anterior dislocation of the shoulder.
places. So there is a "floating" piece of
bone.
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Splints HISTORY TAKING

Pelvic Binding • Knowing the precise mechanism of injury
may be the key to diagnosing some
▪ An outdated device is military antishock
fractures or dislocations.
trousers, which historically were applied
• History taking should not necessarily be
during ambulance transport for patients
limited to orthopedic issues. Depending
in shock with already diagnosed pelvic
on the situation, a general medical history
ring fracture, or for patients with a
should be obtained because it may have
clinically apparent femoral fracture when
implications for further workup, the
a traction device is not at hand, as the
potential for complications, or ultimate
device immobilizes the joints above and
prognosis for recovery of function.
below the fracture.
• Relevant issues may include a history of
cancer, heart disease or neurologic
disease, taking anticoagulant medication,
falling due to syncope or transient
hemiparesis, or an unsteady baseline gait
that cannot withstand further
impairment.
PHYSICAL EXAMINATION
Essential components of the examination for
CLINICAL FEATURES musculoskeletal trauma are (1) inspection for
• Orthopedic diagnosis is sometimes wounds, swelling, discoloration, or deformity;
thought of as being as simple as taking a (2) assessment of active and passive range of
radiograph of the painful area. Although motion of the joints proximal and distal to the
imaging is an important adjunct, it is not injury; (3) palpation for tenderness or deformity;
the ultimate diagnostic resource. The pain and (4) assessment of neurovascular status.
of a fracture or a dislocation may be Inspection and Range of Motion
referred to another area.
• Imaging decisions should be based not • Gross deformity along the shaft of a long
only on the chief complaint but also on bone is pathognomonic for fracture.
systematic palpation, observation of • Deformity at a joint, loss of range of
subtle deformity or significant point motion, and severe pain at rest suggest
tenderness, and mechanism of injury. the presence of a dislocation or fracture
• Some injuries might not be near the joint.
radiographically apparent on the first day, • An exception is posterior dislocation of
regardless of what views are taken. the shoulder, which, although intensely
Common examples are fracture of the painful, might not be accompanied by
scaphoid, non-displaced fracture of the obvious deformity, although the humeral
radial head, and stress fracture of a head may be palpable posteriorly
metatarsal.
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Palpation to a minimum or at least halting its

progression.
• When gross deformity is not present,
▪ Jewelry, watches, or rings that may cause
presumptive diagnosis strongly depends
compression or constriction as an
on findings noted on palpation.
extremity swells should be removed
• Palpation may disclose areas of bony step-
immediately and prior to imaging.
off and the precise location of point
▪ Administer analgesics as necessary. If the
tenderness.
patient is relatively comfortable at rest,
• The palpation examination should be medication may not be required.
done systematically and consistently
from one patient to the next. The area WITHHOLD ORAL INTAKE
palpated should extend well beyond the
▪ Any patient who might be a candidate
location of pain described by the patient,
for prompt surgical fixation,
as the pain may be referred.
manipulation, or any other procedure
o when an injured patient complains under general anesthesia or
of shoulder pain, palpation should
procedural sedation should not be
begin at the sternoclavicular joint,
allowed to eat or drink from the
then proceed along the clavicle
moment of arrival until the need for,
onto the acromioclavicular joint, and timing of, such a procedure has
then onto the humeral head and
been ascertained.
along the entire humeral shaft.
REDUCE FRACTURE DEFORMITY
Neurovascular Assessment
▪ The long-term purpose of reducing
• When injury involves an extremity, as significant deformity associated with
opposed to the vertebral column, fractures is restoration of normal
sensorimotor testing should be performed appearance and function of the
on the basis of peripheral nerve function, extremity.
rather than nerve root and dermatomal ▪ Short-term benefits to reducing
distribution. deformity early: (1) alleviating pain,
• Assess vascular status early. The sooner (2) relieving the tension on nerves or
circulatory compromise is identified and vessels that may be stretched as they
addressed, the better the chance of pass along the deformity, (3)
avoiding tissue ischemia or necrosis. eliminating or significantly minimizing
TREATMENT the possibility of inadvertently
converting a closed fracture to an
CONTROL PAIN AND SWELLING open one when the skin is tented by a
▪ Initiate measures to reduce swelling early. sharp bony fragment, and (4) restoring
Severe swelling not only intensifies the circulation to a pulseless distal
pain of injury but also may delay the extremity.
application of a definitive immobilization ▪ After the patient has been
dressing and may make the skin more appropriately sedated, deformity at or
susceptible to skin blisters and pressure near the midshaft of a long bone is
sores. usually reduced with gradual, steady,
▪ The application of cold and elevation are longitudinal traction.
often quite effective in keeping swelling
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▪ Any rotational deformity should be ▪ The purposes of debridement and

corrected only after the angular irrigation are (1) to expose the wound in
component has been addressed and order to allow better identification of the
should be performed while traction is limits of injury and facilitate inspection for
maintained. foreign material; (2) to identify and
▪ The nearer a deformity is to a joint, remove clots, debris, and nonviable
the more difficult it may be to correct tissue; and (3) to reduce bacterial
and the more specialized the contamination and make the wound more
reduction maneuver may have to be. resistant to the effects of any residual
When deformity is associated with contamination.
circulatory deficit, a true emergency
**
exists, and the anticipated delay until
reduction should be considered. ➢ Elevation of the injured part usually helps
minimize pain and swelling. Elevation
REDUCE DISLOCATIONS
must be above the level of the heart to
INITIAL MANAGEMENT OF OPEN FRACTURES be effective. Patients with an injured
lower extremity often sit at home or at
▪ Open fractures warrant prompt and
work with the foot resting on a stool or
meticulous attention. The most important
chair, thinking they are complying with
elements in the treatment of open
instructions.
fractures, aside from tetanus prophylaxis
➢ Recumbent or near-recumbent position,
that applies generally to any wound, are
with the leg supported higher than the
irrigation, debridement, and antibiotics as
rest of the body.
soon as is practical.
➢ If an upper extremity sugar-tong dressing
▪ Early administration of antibiotics can
has been applied, the patient should be
prevent or reduce the clinical
instructed to work the fingers (wiggle or
consequences of bacterial contamination
wave) as much as possible to minimize
in open fractures.
stiffness and swelling.
▪ Initiate antibiotic therapy promptly in the
➢ Patients should be advised to monitor the
ED. There is no standard antibiotic
fingers or toes for excessive swelling,
regimen.
decreased sensation, or cyanosis and to
▪ An accepted approach, but by no means
be alert for a significant increase in pain.
the only regimen in use, is a first-
Any of these signs or symptoms warrants
generation cephalosporin, with the
a return to the ED or prompt evaluation
addition of an aminoglycoside when the
by the follow-up physician.
wound is >10 cm with severe soft tissue
injury and loss of bone coverage.
▪ When there is significant contamination
by plants or soil, consider the addition of
penicillin.
▪ To lower the infection rate, not only
antibiotics but also generous irrigation
and adequate debridement are necessary
to reduce bacterial contamination and
colonization.
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ANATOMY (CHILDREN): TYPES OF FRACTURES (CHILDREN):

The anatomy of the pediatric musculoskeletal FRACTURES INVOLVING THE PHYSIS
system is unique and reflects the active
▪ Salter-Harris Type I Fractures
growth and development that occurs during
o Type I physeal injuries occur when
childhood.
the epiphysis separates from the
• The physis is an area of growth metaphysis.
cartilage and may occur at one (e.g., o The epiphysis may, however,
the phalanges) or both (e.g., the tibia displace from the metaphysis.
and the femur) ends of a long bone. incidence of Type I injuries have a
• The area of bone between a physis very low growth disturbances.
and the adjacent joint is termed the o Suspect a Salter-Harris type I injury
epiphysis. when there is point tenderness
• An apophysis is an outgrowth of bone, over a physis.
usually with its own ossification center
in childhood that often serves as a
point for muscle or ligament
attachment.
• The midshaft of a long bone is
referred to as the diaphysis.
• The metaphysis of a long bone
represents the area between the
diaphysis and the physis.
The long bones of children are less dense and ▪ Salter-Harris Type II Fractures
more porous than the long bones of adults. o In a type II injury, the fracture line
Pediatric long bones respond to mechanical extends a variable distance along
stress by bowing and buckling rather than the hypertrophic cell zone of the
fracturing through and through like fractures in physis and then out through a
adult bones. piece of metaphyseal bone.
o The periosteum overlying the
The weakness of the metaphyseal fragment remains
physis is in part related intact, whereas the periosteum on
to the reduced oxygen the opposite side of the fracture is
tension found in the torn away from the diaphysis while
hypertrophic zone of the remaining adherent to the
physis. This epiphysis.
hypertrophic zone is the
location of frequent
fractures within the
physis. The physis is also
sensitive to alterations
in the blood supply, and
physeal injuries can
result in growth
disturbance.
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▪ Salter-Harris Type III Fractures ▪ Salter-Harris Type V Fractures

o Type III physeal injuries are o Type V injuries typically involve the
intraarticular. The fracture line knee or ankle and are the result of
extends intra-articularly from the a profound compressive force
epiphysis, through the transmitted to the physis, resulting
hypertrophic zone of the physis, in crushing of the chondrocytes in
with the cleavage plane continuing both the reserve and proliferative
along the physis to the periphery. zones. Displacement of the
o The prognosis for subsequent epiphysis is usually only minimal
bone growth relates to the despite the significant damage to
preservation of circulation to the the physis.
epiphyseal bone fragment;
however, the prognosis is usually
quite favorable
▪ Salter-Harris Type IV Fractures

o In type IV injuries, the fracture line
originates at the articular surface,
extends through the epiphysis and
the entire thickness of the physis, ▪ TORUS FRACTURES
and continues through the o Compressive forces often result in
metaphysis. a bulging or buckling of the
o The risk of growth disturbance periosteum rather than a more
with this type of fracture is complete fracture line. Cortical, or
significant, and reduction must be torus, fractures are so named to
precise. describe prominence or bulging of
the bony cortex, usually involving
the metaphysis. These are also
called buckle fractures.
o A simple torus fracture will not
produce a visible deformity to the
shape of the extremity; however,
there is typically soft tissue
swelling and point tenderness over
the bony injury.
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▪ GREENSTICK FRACTURES o Risk factors include high birth

o A greenstick fracture is weight and shoulder dystocia. The
characterized by cortical infant may demonstrate upper
disruption and periosteal tearing extremity palsy secondary to a
on the convex side of the bone, brachial plexus injury or may have
with an intact periosteum and on “pseudoparalysis” of the extremity
the concave side of the fracture. secondary to pain. Although many
o Greenstick fractures are more clavicle fractures are detected at
stable and somewhat less painful birth, the diagnosis may be
than complete fractures because delayed, especially if the fracture
the area of intact periosteum is non-displaced.
limits bony displacement. o An ED visit may be made when the
newborn is not moving one arm
▪ PLASTIC DEFORMITIES (BOWING OR during the first week of life, or
BENDING FRACTURES) when a parent notices a small
o Plastic deformities, also referred to “lump” or callus at the clavicle
as bowing or bending fractures, during the first 2 to 3 weeks of
are almost exclusively limited to life.
the forearm and lower leg long o Clavicle fractures in the newborn
bones. do not need specific treatment.
o The classic clinical hallmark is pain Pain control and careful handling
out of proportion to physical of the baby are usually all that are
examination findings, and in the required.
forearm, pain is maximal on o Clavicle fractures outside of the
pronation/ supination. newborn period usually result
o The cortex of the diaphysis of the from accidental injury in a mobile
long bone is deformed, but the child.
periosteum along the entire o The most common mechanism of
diaphysis is preserved. injury is either a fall onto an
o Moderate-severe plastic deformity outstretched hand or onto the
is usually obvious clinically, which lateral side of the shoulder. The
should guide the inexperienced clavicle may fracture in three
clinician who may think that in the general sites: the diaphysis, medial
absence of an obvious fracture the end, or lateral end.
radiograph appearances are
normal. a. FRACTURES OF THE MIDDLE THIRD
OF THE CLAVICLE
▪ CLAVICLE FRACTURE - are the most common of all
o Clavicle fractures occur during two clavicle fractures. Most of these
distinct time frames: the newborn injuries can be treated with
period and childhood. analgesics, support of the injury
o Fractures of the clavicle in the with a broad arm sling for 3 to 4
newborn usually result from birth weeks, and follow-up with the
injury. primary care physician.
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b. FRACTURES OF THE MEDIAL relative imbalance between glutamate

CLAVICLE and γ-aminobutyric acid with
- Fractures at the medial end of paradoxical excitation from γ-
the clavicle are uncommon. Given aminobutyric acid makes younger
the strong ligamentous children more susceptible to seizures.
attachment of the clavicle to the (Complete myelination of sheet by 18
sternum, injuries to this area are months)
usually epiphyseal disruptions. • Seizures can be primary (unprovoked) or
Orthopedic consultation is secondary (provoked). Primary seizures
recommended for these injuries. are often idiopathic or may be caused by
congenital developmental abnormalities,
c. FRACTURES OF THE DISTAL in utero CNS insult (e.g., infection, infarct),
CLAVICLE or genetic factors. (or no evident cause
- Fractures of the distal end of the can be defined)
clavicle are also uncommon in • Secondary seizures may result from
children and again more likely to trauma or injury, infection, metabolic
be epiphyseal disruptions. abnormalities (e.g., hypoglycemia,
Minimally displaced distal clavicle electrolyte abnormalities, inborn errors of
fractures only need immobilization metabolism), toxins, or systemic illness
with a sling or equivalent. Surgical • Electrical stimulation of the brain,
reduction may be needed for more convulsant potentiating drugs, profound
displaced fractures. metabolic disturbances, or significant
head trauma all may cause reactive
seizures in otherwise normal individuals.
SEIZURES Reactive seizures are generally self-
PATHOPHYSIOLOGY: limited and not considered to be a seizure
disorder or epilepsy.
• Seizures represent abnormal, excessive,
paroxysmal neuronal activity in the brain, Seizure – neurons are synchronously active
primarily the cerebral cortex. The way ions flow control the two
• Glutamate released from firing neurons neurotransmitters:
✓ If neurotransmitters bind to the
activates N-methyl-D-aspartic acid
receptors, they tell the cells to open
receptors that subsequently initiate and the ion channels and relay the electrical
propagate seizure activity. message – EXCITATORY
• Seizures are inhibited by γ-aminobutyric neurotransmitters
acid (inhibitory), and failure of this ✓ If neurotransmitters bind to the
receptors, they tell the cells to close
inhibition facilitates seizure spread.
the ion channels and stop the relay of
• A seizure results when a sudden electrical message – INHIBITORY
imbalance occurs between the excitatory neurotransmitters
and inhibitory forces within the network
of cortical neurons in favor of a sudden- During a seizure, clusters of neurons in the
onset net excitation. brain become temporarily impaired and starts
sending out a ton of excitatory signal
• Incomplete myelination of the brain repeatedly, sometimes called as “paroxysmal”.
may limit secondary generalization of
seizure activity in young infants, and a
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Paroxysmal may happen if there is too much hallucinations, memory disturbances,

excitation or too little inhibition. distorted perception, and affective
disorders.
Main excitatory neurotransmitter in the brain
is glutamate and NMDA is the primary receptor
that responds to the glutamate by opening ion GENERALIZED SEIZURE – both hemispheres of
channels (Calcium comes in – positive ion) the brain are affected and patients either lose
consciousness briefly or for a long period then
Main inhibitory neurotransmitter is GABA with usually followed by a period of postictal
binds to the GABA receptor to inhibit the signal
drowsiness. It may start as a partial and then
by opening channels (Chloride comes in –
negative ion) quickly develop in to a secondary generalized
✓ Symptoms depend on neurons affected seizure (because a partial came before it and was
the primary event)
TYPES OF SEIZURES: - thought to be caused by near simultaneous
PARTIAL OR FOCAL SEIZURE – when the affected activation of the entire cerebral cortex, perhaps
area is limited to one hemisphere or a single lobe. caused by an electrical discharge originating deep
- are due to electrical discharges beginning in a in the brain and spreading outward.
localized region of the cerebral cortex.
▪ Tonic Seizure – muscles all of a sudden
- Focal seizures are more likely to be secondary to become stiff and flexed which causes the
a localized structural lesion of the brain. patient to fall often backwards;
▪ This is divided into two: If remains ▪ Atonic Seizure – muscles suddenly relax
conscious – simple partial seizure; if loses
and become floppy which causes the
consciousness – complex partial seizure patient to fall forward (sudden loss of
▪ Simple partial seizure affect a small area muscle tone with a sudden “drop” to the
of the brain – may experience strange floor)
sensations, jerking movements in specific ▪ Clonic Seizure – have violent muscle
muscle groups that the neurons contractions (aka. convulsions)
controlling those muscles are affected, ▪ Tonic - Clonic Seizure – are the most
usually know what’s happening and common generalized seizure where
remember the seizure afterwards; It is patient experience a tonic phase where
possible to deduce the likely location of the muscles suddenly tense up followed
the initial cortical discharge from the by a clonic phase where muscles rapidly
clinical features at the onset of the attack.
contract and relax; aka. grand mal;
▪ If jerking activity starts in specific muscle - Are the most familiar and dramatic of
group and then spreads to surrounding the generalized seizures; in a typical
muscle group as more neurons are attack, the patient suddenly becomes
affected, it is called the jacksonian march
rigid (tonic phase), trunk and extremities
▪ Complex partial seizures involves losing are extended, and the patient falls to the
consciousness completely or having ground.
impaired awareness or responsiveness, - Patients are often apneic during this
may not remember what happened; period and may be cyanotic, often urinate
commonly misdiagnosed as psychiatric and may vomit
problems because symptoms can be so - As the attack ends, the patient is left
bizarre. Symptoms may include flaccid and unconscious, often with deep,
automatisms, visceral symptoms, rapid breathing; Consciousness returns
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gradually, and postictal confusion, (life threatening if not treated

myalgias, and fatigue may persist for immediately)
several hours. ▪ due to severity patients are often treated
- Lasts from 60 – 90 seconds with benzodiazepines which helps
▪ Myoclonic Seizure – are short muscle enhance the effect of the inhibitory
twitches sometimes a single twitch or neurotransmitter - GABA
many in a short amount of time ▪ Refractory status epilepticus is a
▪ Absence Seizure – patient lose prolonged seizure that cannot be
consciousness and then quickly regain controlled with two or more doses of
consciousness (brief episode of staring standard treatment; is persistent seizure
without a postictal state); aka. petit mal activity despite the IV administration of
- Very brief, generally lasting only a few adequate amounts of two antiepileptic
seconds agents.
- Patients suddenly develop altered ▪ Nonconvulsive status epilepticus may
consciousness but no change in postural present as a prolonged postictal state and
tone. They appear confused or detached, must be considered in any patient with
and current activity ceases. altered mental status
- They may not respond to voice or to ▪ If a seizure persists after two doses of a
other stimulation, exhibit voluntary benzodiazepine have been given,
movements, or lose continence. fosphenytoin, levetiracetam, or valproic
- Classic absence seizures occur in school- acid are preferred second-line treatment
aged children; attacks can occur as choices.
frequently as 100 or more times daily and ▪ Status epilepticus can occur in patients
may result in poor school performance; with a history of seizures or can be a first
usually resolve as the child matures. epileptic event. The most common causes
of status epilepticus include sub
- note: Similar attacks in adults are more therapeutic antiepileptic levels;
likely to be minor complex partial seizures preexisting neurologic conditions, such as
prior CNS infection, trauma, or stroke;
IMPORTANT NOTE: Any “prolonged” seizure or
acute stroke; anoxia or hypoxia; metabolic
recurrent seizures lasting longer than 5
abnormalities; and alcohol or drug
minutes without return to full consciousness
are considered --- status epilepticus intoxication or withdrawal.
TREATMENT:
STATUS EPILEPTICUS
➢ Early recognition and treatment of status
▪ seizure longer than 5 minutes of ongoing epilepticus are critically important.
seizure or seizure without returning to Mortality dramatically increases with
normal state in between; usually tonic - delayed diagnosis or initiation of
clonic subtype seizure but can also include treatment, particularly with non-
other subtypes that do not involve convulsive status epilepticus, age greater
convulsions than 60 years, and in patients with no
▪ considered as a MEDICAL EMERGENCY documented seizure disorder.
and rapid termination is important to ➢ The goal of treatment is seizure control as
prevent irreversible neuronal damage. soon as possible and within 30 minutes of
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presentation. Examination, identification temporarily control the seizures until more

of potential causes, application of the specific agents can be given.
ABCs (airway, breathing, and circulation),
IV lorazepam (2 to 4 milligrams) and IV diazepam
and treatment all begin simultaneously
(5 to 10 milligrams) have equal efficacy in
➢ Establish large-bore IV access and
controlling status epilepticus
determine a bedside glucose. Administer
normal saline, avoiding IV fluids Compared to diazepam, lorazepam has a slightly
containing glucose as phenytoin is not slower onset (3 vs. 2 minutes) but a significantly
compatible with glucose-containing longer duration of action (12 to 24 hours vs. 15 to
solutions. Place the patient on oxygen, a 60 minutes) and is associated with fewer seizure
cardiac monitor, pulse oximeter, and end- recurrences
tidal capnography.
IV lorazepam is still considered the initial agent of
➢ In established status epilepticus, consider
choice if IV access is available. Lorazepam is also
endotracheal intubation for airway
more effective than phenytoin or phenobarbital
protection, oxygenation, and ventilation.
as a first-line agent. Respiratory depression and
Use a short-acting paralytic agent in order
hypotension may occur, especially in young
not to mask ongoing seizure activity.
children and in patients taking alcohol,
Arrange for continuous EEG monitoring as
barbiturates, narcotics, or other sedatives.
soon as possible after paralytic agents
have been used. In patients with difficult IV access and emergent
➢ Initial laboratory evaluation includes need for seizure control, there may be a role for
blood glucose, a metabolic panel including rectal diazepam gel or buccal midazolam.
calcium and magnesium, lactate, and if
In established status epilepticus, follow
appropriate, a pregnancy test, a
benzodiazepines with longeracting antiepileptic
toxicology screen, and anticonvulsant
agents: fosphenytoin or phenytoin;
levels. Administer glucose IV if
levetiracetam; valproate; or lacosamide. One of
hypoglycemia is suspected or confirmed.
these antiepileptic agents should be started
Monitor temperature continuously, and
within 20 minutes of diagnosis.
treat hyperthermia with passive cooling.
➢ Place a urinary catheter to monitor urine REFRACTORY STATUS EPILEPTICUS
output and insert a nasogastric tube to
Refractory status epilepticus is defined as
help prevent aspiration.
persistent seizure activity despite the IV
➢ If toxic ingestion is suspected as the cause
administration of adequate amounts of two
of seizures, proceed with GI
antiepileptic agents and usually exceeds 60
decontamination (as appropriate). Do not
minutes
attempt lumbar puncture during status
epilepticus. Overall, there are few controlled trials that
strongly support a single agent or combination of
The drugs most often used in the therapy of
agents. Recommendations include propofol,
status epilepticus are the benzodiazepines
midazolam, and barbiturates such as
(lorazepam, midazolam, or if not available,
phenobarbital or pentobarbital given as infusions
diazepam) and phenytoin or fosphenytoin.
All of these agents can lead to hypotension,
Benzodiazepines are used in patients with
sometimes requiring concomitant vasopressor
continuous or very frequent seizures to
use, and frequently require intubation. Ideally,
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treatment is in consultation with a neurologist unrecognized seizures, history of recent or

and in an intensive care setting, as advanced remote head injury, Persistent, severe, or
respiratory support, cardiovascular support, and sudden headache suggests intracranial
EEG monitoring are all needed. pathology, Pregnancy or recent delivery
raises the possibility of eclampsia, A
CLINICAL FEATURES
history of metabolic or electrolyte
HISTORY abnormalities, hypoxia, systemic illness
(especially cancer), coagulopathy or
FOR ADULTS:
anticoagulation, exposure to industrial or
1. First Step: Determine if the episode is environmental toxins, drug ingestion or
really a seizure withdrawal, and alcohol use may point to
2. Obtain careful history of the details of the predisposing factors.
attack from the patient and the
bystanders or witness of the attack
FOR PEDIATRICS:
3. Inquire about the physical description of
the attack, as witnesses may mislabel the
activity and mistake non-seizure activity
as a seizure (which includes: presence of a
preceding aura, abrupt or gradual onset,
progression of motor activity, loss of
bowel or bladder control, presence of oral
injury, and whether the activity was
localized, generalized, symmetric, or
asymmetric)
4. Ask about the duration of the episode,
and determine the presence of postictal
confusion or lethargy.
5. Determine the clinical context of the
episode. If the patient is a known
epileptic, clarify the baseline seizure
pattern. If the attack is consistent with the
previous seizure pattern, identify
precipitating factors of the current
seizure. (Common precipitating factors
include missed doses of antiepileptic
medications; recent alterations in
medication, including dosage change or
conversion from brand name; sleep
deprivation; increased strenuous activity;
infection; electrolyte disturbances; and
alcohol or substance use or withdrawal.)
6. If no previous history, then a more
detailed history taking like symptoms such
as unexplained injuries, nocturnal tongue
biting, or enuresis suggest previous
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PHYSICAL EXAMINATION • Abrupt onset and termination. Some

focal seizures are preceded by auras
✓ Immediately obtain a complete set of vital
that can last 20 to 30 seconds, but
signs and a point-of-care glucose.
most attacks begin abruptly.
✓ In the post seizure setting, focus the initial
• Episodes reported to develop over
exam on checking for injuries, especially
several minutes or longer should be
head or spine trauma, as a result of the
regarded with suspicion. Most
seizure.
seizures last only 1 or 2 minutes,
✓ A posterior shoulder dislocation is an
unless the patient is in status
injury that is easy to overlook.
epilepticus.
✓ Lacerations of the tongue and mouth,
• Lack of recall. Except for simple partial
dental fracture, and pulmonary aspiration
seizures, patients usually cannot recall
are also frequent sequelae. Lateral tongue
the details of an attack.
biting was found to have a specificity of
100% and a sensitivity of 24% for the • Purposeless movements or behavior
occurrence of a seizure. during the attack.
✓ Perform a directed, complete neurologic • Most seizures are followed by a period
examination and subsequent serial of postictal confusion and lethargy
examinations.
✓ Follow the patient’s level of consciousness DIFFERENTIAL DIAGNOSIS
and mentation closely to avoid missing FOR PEDIATRICS:
nonconvulsant status epilepticus • Syncope is the most common condition
✓ Todd’s Paralysis - a transient focal deficit that may be mistaken for seizures;
following a simple or complex focal however, there are many differentiating
seizure; typically resolves within 48 hours features. Syncope is commonly preceded
(weakness of a limb, such as your hand, by dizziness, weakness, tunnel vision,
arm, or leg, numbness, slurred speech, pallor, and diaphoresis (presyncopal
disorientation) – resulted because of aura). It is also associated with a brief loss
temporary or severe suppression of of consciousness and a quick recovery
seizure-affected area with no postictal state
✓ Primary survey: ABCs, vital signs, bedside • In infants, myoclonic jerks, sleep
glucose level, basic mental status, and myoclonus, shudder attacks, and
pupillary symmetry and reactivity - Signs Sandifer’s syndrome (gastroesophageal
of toxidromes (sympathomimetic) - reflux) are common. In toddlers, breath-
Trauma (abrasions, contusions, fractures) holding spells become more prevalent.
- Increased intracranial pressure Self-stimulation and night terrors should
(papilledema or Cushing reflex) - Any focal be considered in preschool and young
neurologic abnormality that would school-age children, whereas tic disorders
indicate a secondary cause of seizure typically begin in older children.
Psychogenic non-epileptic seizures may
DIAGNOSIS present in adolescents with and without
epilepsy.
Clinical features that help to distinguish seizures
from other non-seizure attacks include the
following:
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FOR ADULTS: part of your vision); active movement

• Syncope usually presents with prodromal disorders are inconsistent with migraine.
symptoms, such as lightheadedness,
diaphoresis, nausea, and “tunnel vision.” PARACLINICAL DIAGNOSIS
Syncope may be associated with injury,
FOR PEDIATRICS:
incontinence, or even brief tonic-clonic
• Check bedside glucose on all seizing or
activity. Recovery is usually rapid, with no
postictal patients – glucose is an
postictal-like symptoms. (same with
important energy source during seizure
pediatrics)
• If indicated by the history and
• Pseudoseizures can be difficult to
examination, labs that may be helpful
distinguish from true seizures and may
include electrolytes (including calcium),
occur in a patient who also has a
serum antiepileptic medication levels,
documented seizure disorder. Suspect this
toxicologic testing, and spinal fluid for
diagnosis when seizures occur in response
evaluation of possible CNS infection in the
to emotional upset or occur only with
appropriate setting.
witnesses present. Pseudoseizures are
• Urine culture and analysis may be
often bizarre and highly variable. Patients
indicated in the evaluation of febrile
often are able to protect themselves from
seizures in the child with fever and no
noxious stimuli during the attack.
identifiable source.
Incontinence and injury are uncommon,
• When trauma is suspected, in infants less
and there is usually no postictal confusion.
than a year old (inflicted injury), or in the
Patients will often stop the seizure-like
setting of focal deficits, obtain a head CT.
activity on command.
• It may be impossible to distinguish Todd’s
• Hyperventilation syndrome can be
paralysis from stroke or hemorrhage, and
misdiagnosed as a seizure disorder. A
emergent imaging should be considered.
careful history will reveal the gradual
onset of the attacks with shortness of • Consider obtaining an ECG for evaluation
breath, anxiety, and perioral numbness. of syncope with seizure activity to rule out
Such attacks may progress to involuntary arrhythmia.
spasm (especially carpopedal) of the • Emergent electroencephalogram
extremities and even loss of monitoring may be required for patients
consciousness, although postictal with refractory status epilepticus
symptoms are rare. Asking the patient to (especially those requiring rapid-sequence
hyperventilate often reproduces the intubation with a paralytic) or concern for
episodes. nonconvulsive status epilepticus
FOR ADULTS:
• Movement disorders, such as dystonia,
chorea, myoclonic jerks, tremors, or tics, • In a patient with a well-documented
may occur in a variety of neurologic seizure disorder who has had a single
conditions. unprovoked seizure, the only tests that
• Migraine headaches may be preceded by may be needed are a glucose level and
an aura similar to that seen in some pertinent anticonvulsant medication
partial seizures. The most common levels.
migraine aura is the scintillating scotoma • Obtain serum glucose, basic metabolic
(is an aura or blind spot that obstructs panel, lactate, calcium, magnesium, a
pregnancy test, and toxicology studies.
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• Obtain a CT scan of the head in the ED for is no evidence of increased intracranial pressure,
patients with a first-ever seizure or a perform a lumbar puncture to exclude CNS
change in established seizure patterns to infection. If no explanation for seizures is found,
evaluate for a structural lesion. (A non- then obtain a contrast-enhanced head CT or MRI.
contrast CT is an appropriate screening
tool.) ▪ NEUROCYSTICERCOSIS
• Obtain a CT scan if there is any concern Neurocysticercosis is caused by a CNS infection
for an acute intracranial process based on with the larval stage of the tapeworm Taenia
history, comorbidities, or findings on solium and is the most common cause of
physical examination. Concern for an provoked (secondary) seizures in the developing
acute intracranial process is an important world. The most common form of disease is
indication for obtaining CT imaging, even parasitic invasion of brain parenchyma and cyst
if there is a coexistent metabolic process. formation. Over 1 to 2 years, the cyst
• Lumbar puncture in the setting of an degenerates and becomes fibrotic, leaving a focal
acute seizure is indicated if the patient is area of scar and calcification. Seizures are the
febrile or immunocompromised or if most common clinical manifestation of
subarachnoid hemorrhage is suspected neurocysticercosis and most frequently occur as
and the non-contrast head CT is normal. the parasite is degenerating. In 80% to 90% of
• Although EEG is helpful, it is often not cases, the lesions resolve within 3 to 6 months,
readily available in most EDs. Emergent leaving the patient free of seizures. Up to 20% of
EEG can be considered in the evaluation patients will continue to have seizures and
of a patient with persistent, unexplained require ongoing therapy with antiepileptic
altered mental status to evaluate for medications. In most cases, neuroimaging in
nonconvulsive status epilepticus, subtle neurocysticercosis is nondiagnostic. CT or MRI
status epilepticus, paroxysmal attack may demonstrate a 1- to 2-cm cystic lesion with
when a seizure is suspected, or ongoing thin walls and a 1- to 3-mm mural nodule (the
status epilepticus after chemical paralysis parasite), a localized area of ring-like
for intubation enhancement with surrounding edema, a
calcified lesion, or hydrocephalus. Definitive
diagnosis relies on a combination of the patient’s
PLS CHECK YOUR OTHER HANDOUT FOR
clinical picture, exposure history, serologic
TREATMENTS CONCERNING STATUS testing, and neuroimaging. Seizures in
EPILEPTICUS, SEIZURES IN BOTH ADULS neurocysticercosis are typically controlled by
AND PEDIATRICS. antiepileptic monotherapy. Definitive treatment
of neurocysticercosis is controversial and highly
SPECIAL CONSIDERATIONS (ADULTS) variable, depending on the number, location, and
viability of the parasites within the CNS.
▪ HUMAN IMMUNODEFICIENCY VIRUS Antiparasitics (praziquantel and albendazole) and
Mass lesions, encephalopathy, herpes zoster, steroids are best initiated in consultation with an
toxoplasmosis, Cryptococcus, neurosyphilis, and infectious disease specialist or neurologist.
meningitis are all seen more frequently in this
population and can all provoke seizure activity. ▪ PREGNANCY
Perform an extensive investigation for the cause The management of seizures (or control of
of the seizure. If no space-occupying lesion is epilepsy) during pregnancy requires a
identified on noncontrast head CT scan and there multidisciplinary approach. Most seizures in
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pregnancy are not first-time seizures, and initial disruption of blood flow or nutrient
evaluation is generally as discussed above, with delivery to both cerebral cortices or to the
the addition of an obstetric evaluation to brainstem reticular activating system, or
determine gestational age and fetal well-being. reduction of cerebral perfusion by 35% to
When a woman beyond 20 weeks of gestation 50%.
develops seizures in the setting of hypertension, ▪ Most commonly, an inciting event causes
edema, and proteinuria, the diagnosis is a drop in cardiac output, which decreases
eclampsia. Magnesium sulfate is the treatment. oxygen and substrate delivery to the
In eclampsia, magnesium sulfate infusion brain.
compared to diazepam and phenytoin resulted in ▪ Cerebral perfusion and consciousness are
a >50% reduction in recurrence of seizures and a restored by the supine position, the
lower incidence of pneumonia, intensive care response of autonomic autoregulatory
unit admission, and assisted ventilation. centers, or restoration of a perfusing
cardiac rhythm.
▪ ALCOHOL ABUSE
Seizures and alcohol use are associated through DEFINITION OF TERMS:
missed doses of medication, sleep deprivation as ▪ Syncope ⎯ A transient loss of
an epileptogenic trigger, increased propensity for consciousness with an inability to
head injury, toxic coingestions, electrolyte maintain postural tone.
abnormalities, and withdrawal seizures. ⎯Occurs secondary to impaired blood flow
Benzodiazepines in doses sufficient to manage to either the reticular activating system or
withdrawal symptoms will usually afford the bilateral cerebral hemispheres.
adequate protection from acute seizures. These ▪ Neurally Mediated (Reflex) Syncope ⎯
doses are often very large and need to be given in Occurs because of an excessive
an escalating fashion. Evaluate and treat the parasympathetic output in response to a
alcohol-abusing patient with a first seizure as any stressful event.
other patient with a first-time seizure a. Vasovagal Syncope – orthostatic,
or emotional
LOSS OF CONSIOUSNESS/SYNCOPE o Dx: Prodrome: Pallor, sweating,
nausea
Syncope or fainting is a symptom complex b. Situational Syncope – defecation,
consisting of a brief loss of consciousness swallowing, coughing
associated with an inability to maintain postural o Dx: Pattern –follows a specific
tone that spontaneously resolves without trigger
medical intervention with the person returning to c. Carotid Sinus Syndrome –
their baseline neurologic condition. baroreceptors react too strongly to
detecting an increased pressure
Near syncope, a premonition of fainting without
leading to an excessive drop in
loss of consciousness, shares the same basic
blood pressure, and therefore,
pathophysiologic process as syncope and carries
syncope
the same risks.
▪ Orthostatic Syncope ⎯ Occurs because of
PATHOPHYSIOLOGY transient arterial hypotension after a
▪ The final common pathway of syncope is positional change to either sitting upright
the same regardless of the underlying or standing.
cause: about 10 seconds of complete
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⎯ Underlying mechanism depends on Delirium May not remember who they

either significant volume depletion are, or may have delusions
(bleeding, dehydration) or intrinsic and hallucinations, may also
autonomic dysfunction. become frowsy or less alert at
- Symptom onset is usually within the first times
3 minutes after assuming the upright Obtundation Often sleeps much more than
usual, and when awakened,
posture, but may be more delayed in
remains drowsy and confused
some patients.
Stupor Unresponsiveness from which
- When a person assumes an upright
a person can be aroused only
posture, gravity shifts blood to the lower by a vigorous and repeated
part of the body, and cardiac output painful stimulation.
drops. This change triggers the healthy Coma Appears to be asleep but
autonomic nervous system to increase cannot be awakened; reflexes
sympathetic output and decrease are absent; legs and arms may
parasympathetic output, increasing heart be rigid; RR slow
rate and peripheral vascular resistance,
and thus increasing cardiac output and
❖ The Glasgow Coma Scale may be used to
blood pressure.
assess a patient LOC quickly.
▪ Cerebrovascular syncope ⎯ Rarely the
cause of syncope GLASGOW COMA SCALE
⎯Loss of consciousness can occur after a
Eye Opening Response
subarachnoid hemorrhage when the
intracranial pressure rises suddenly and ▪ Spontaneous--open with blinking at
the cerebral perfusion is transiently baseline - 4 points
lowered. ▪ To verbal stimuli, command, speech - 3
▪ Cardiac syncope ⎯ Occurs when either points
structural heart defects or cardiac ▪ To pain only (not applied to face) -2 points
dysrhythmias transiently impair cardiac ▪ No response - 1 point
output.
Verbal Response
⎯Tends to have the worst prognosis, with
1 -year mortality rates of 18-33%. ▪ Oriented - 5 points
▪ Medication-induced Syncope ⎯Can be a ▪ Confused conversation, but able to
common complication of answer questions - 4 points
pharmacotherapy. ▪ Inappropriate words - 3 points
⎯ Because of poor autonomic responses ▪ Incomprehensible speech - 2 points
and multiple medications, the elderly is ▪ No response - 1 point
particularly prone to syncope as a side
Motor Response
effect of medication use.
▪ Obeys commands for movement - 6
LEVELS OF CONSIOUSNESS
points
Confusion Cannot properly process all ▪ Purposeful movement to painful stimulus
information from their - 5 points
surrounding; especially to ▪ Withdraws in response to pain - 4 points
time, unable to carry out more ▪ Flexion in response to pain (decorticate
than a few simple demands posturing) - 3 points
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▪ Extension response in response to pain o Abdominal or back pain – to

(decerebrate posturing) - 2 points consider a Ruptured Abdominal
▪ No response - 1 point Aortic Aneurysm [AAA] or Ectopic
Pregnancy
▪ Review current medications
▪ Antecedent dizziness, nausea, and
diaphoresis →Benign Vasovagal Syncope
▪ Moving from a recumbent or sitting to
upright position→ Orthostatic Syncope
Sudden occurrence, without prodrome
but with physical activity →T/C
Arrhythmia or structural heart disease
▪ Prolonged recovery period after syncope
indicates a cerebrovascular etiology
(stroke, seizure, SAH)
PHYSICAL EXAMINATION
• Signs of trauma without defensive injuries

to the hands or knees may be due to a
sudden event without warning, such as a
dysrhythmia.
• Focus the physical examination on the
HEAD INJURY CLASSIFICATION: cardiovascular and neurologic systems.
• A GCS of 8 or less is the accepted • Obtain blood pressure measurements in
definition of the comatose patient. Thus, both arms.
severe head injury is associated with a • Consider aortic dissection or subclavian
GCS less than or equal to 8. steal if blood pressures are unequal.
• Moderate head injury a GCS of 9 to 12 • Take orthostatic blood pressures after 5
• Mild head injury a GCS of 13 to 15. minutes in the supine position. Repeat
measurements after 1 and 3 minutes of
standing. A symptomatic decrease of >20
HISTORY mm Hg in the systolic pressure is
considered abnormal, as is a decrease in
Ask a comprehensive history: pressure.
▪ Clarify all of the events immediately TREATMENT
preceding, during, and after the episode
▪ Inquire about any concerning prodromal 1. Place pt in a supine position w/ lower
symptoms including: extremities slightly elevated or w/ head tilted –
o Headache – to consider this will increase cerebral perfusion
Subarachnoid Hemorrhage 2. Jaw thrust maneuver should be done if spine
o Chest pain – to consider injury is speculated.
Myocardial Infarction, aortic 3. No injury –> do head-tilt-chin-lift maneuver –
dissection this will help maximize cerebral blood flow, offer
protection from trauma and secure the airway.
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4. Loosen any tight clothing esp around the neck cells), which are important
and waist effectors of type I hypersensitivity.
5. Peripheral stimulation: sprinkling water in face o IL-13 -- enhances IgE production
may help and acts on epithelial cells to
6. Assess pulse and direct cardiac auscultation to stimulate mucus secretion.
determine if it is associated with bradycardia or ▪ IgE (cytotropic antibodies) attaches to
tachycardia mast cells through the Fce receptors
7. Do not give anything by mouth or permit to ▪ In addition, TH2 cells (as well as mast cells
rise unless physical weakness has passed. and epithelial cells) produce chemokines
8. Direct cause of syncope should be determined that attract more TH2 cells, as well as
to properly give treatment and address the other leukocytes, to the reaction site.
underlying cause
EARLY
ANAPHYLAXIS ▪ When a mast cell, armed with IgE

antibodies previously produced in
Anaphylaxis is a serious allergic reaction, with a response to an antigen, is exposed to the
rapid onset; it may cause death and requires same antigen, the cell is activated, leading
emergent diagnosis and treatment. Consensus eventually to the release of an arsenal of
clinical criteria provide consistency for diagnosis. powerful mediators responsible for the
clinical features of immediate
PATHOPHYSIOLOGY:
hypersensitivity reactions. Mast cells
SENSITIZED degranulates the antigen, as a result
producing more pro-inflammatory
▪ Presentation of the antigen, the dendritic
mediators (histamines)
cells and/or macrophages captures the
▪ Histamine binds with H1 receptors causes:
antigen from the point of entry and
o smooth muscles of the bronchi to
present it to the naive CD4+ helper T cells
contract (constricts aiways)
▪ In response to antigen and other stimuli,
o blood vessels to dilate and
the T cells differentiate into TH2 cells; TH2
increase permeability
cells produce a number of cytokines
(edema/swelling and
(Interleukins 4,5 and 13) upon subsequent
urticaria/hives )
encounter with the antigen
▪ This cytokines acts on B cells to stimulate LATE
class switching to IgE and promotes the
▪ In the late-phase reaction, leukocytes are
development of additional TH2 cells.
recruited that amplify and sustain the
o IL-4 -- acts on B cells to stimulate
inflammatory response without additional
class switching to IgE and
exposure to the triggering antigen
promotes the development of
▪ Eosinophils are recruited to sites of
additional TH2 cells.
immediate hypersensitivity by
o IL-5 -- is involved in the
chemokines, such as eotaxin, and others
development and activation of
that may be produced by epithelial cells,
eosinophils (degranulates /
TH2 cells, and mast cells.
releases toxins that damage
▪ Upon activation, eosinophils liberate
invading cells and surrounding
proteolytic enzymes as well as two unique
proteins called major basic protein and
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eosinophil cationic protein, which damage cardiovascular collapse or respiratory

tissues. (Tx in the late phase requires the failure, respectively.
use of broad spectrum anti-inflammatory ✓ 80-90% of anaphylactic episodes are
drugs such as steroids.) uniphasicand 10-20% of cases are
biphasic,in which anaphylactic symptoms
Anaphylaxis is highly likely when any ONE of the
return about anhour or longer
three criteria occurs:
afterresolution ofinitial symptoms.
1. Acute onset of an illness (minutes to ✓ There may be upper and/or lower airway
several hours) with involvement of the obstruction
skin and/or mucosal tissue (e.g., ✓ Asthmatics are predisposed to severe
hives/urticaria, pruritus, flushing, swollen involvement of the lower airways and
lips, tongue, or uvula) associated with at increased mortality.
least one of the following: ✓ Laryngeal edema= “lump” in throat,
o Respiratory compromise (e.g., hoarseness, or stridor
dyspnea, wheeze, stridor, etc.) ✓ Bronchial obstruction= feeling of tightness
o Reduced blood pressure in the chest and/or audible wheezing.
o Associated symptoms of organ o Lungs show marked hyperinflation
dysfunction (e.g., hypotonia, on gross andmicroscopic
syncope, incontinence, etc.) examination.
2. Two or more of the following that occur ✓ GI: nausea, vomiting, crampy abdominal
rapidly after exposure to a likely allergen pain, and/or fecal incontinence.
for that patient (minutes to several Angioedema of the bowel wall may also
hours): cause sufficient intravascular volume
o Involvement of the skin and/or depletion to precipitate cardiovascular
mucosal tissue. collapse.
o Respiratory compromise ✓ Cutaneous: the most common
o Reduced blood pressure or presentations of anaphylaxis (>90% of
associated symptoms cases).Symptoms include urticarial
o Persistent GI symptoms (e.g., eruptions, flushing with diffuse erythema,
cramps, vomiting) and/or a feeling of generalized warmth.
3. Anaphylaxis should be suspected when Urticarial eruptions are intensely pruritic
patients are exposed to a known allergen and may be localized or disseminated.
and develop hypotension. They may coalesce to form giant hives but
seldom persist beyond 48hrs.
CLINICAL MANIFESTATION:
✓ In the vast majority of patients, signs and
✓ The clinical signs of systemic allergic symptoms begin suddenly, often within 60
reactions include diffuse urticaria and minutes of exposure. In general, the
angioedema. faster the onset of symptoms, the more
✓ Anaphylaxis is the most severe life- severe the reaction, as evidenced by the
threatening form of a systemic allergic fact that one half of anaphylactic fatalities
reaction, often involving respiratory or occur within the first hour.
cardiovascular compromise.
DIAGNOSIS:
✓ Dangerous when hypotension or hypoxia
occurs, leading potentially to ➢ The diagnosis of anaphylaxis is clinical;
diagnosis is easily made if there is a clear
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historyof exposure, such as a bee sting, First line Therapy:

shortly followed by the multisystem signs
▪ The first-line therapies for anaphylaxis
and symptoms
(epinephrine, IV fluids, and oxygen) have
➢ Unfortunately, diagnosis is not always
immediate effect during the acute stage
easy or clear, because symptom onset
of anaphylaxis.
may be delayed, symptoms mimic other
▪ Vital signs, IV access, oxygen
presentations (e.g., syncope,
administration, cardiac monitoring, and
gastroenteritis, and anxiety), or
pulse oximetry measurements should be
anaphylaxis may be a component of other
initiated immediately.
diseases (e.g., asthma).
▪ Airway and Oxygenation
➢ Because the diagnosis of anaphylaxis is
o SECURING THE AIRWAY IS THE
made clinically, laboratory investigations
FIRST PRIORITY.
have a limited role to play.
o Examined for signs and symptoms
➢ ** Histamine levels, elevated for 5 to 30
of angioedema (e.g., uvula edema
minutes post reaction, are unhelpful
or hydrops, audible stridor,
because they decline by presentation to
respiratory distress, hypoxia).
the ED. **
o IF ANGIOEDEMA IS PRODUCING
➢ Tryptase is a neutral protease of unknown
RESPIRATORY DISTRESS,
function in anaphylaxis that is found only
intubation should be completed
in mast cell granules and is released with
early, as delay may result in
degranulation. Serum tryptase levels are
complete airway obstruction
elevated for several hours and have been
secondary to progression of
proposed for later confirmation of a
angioedema.
suspected anaphylactic episode, but these
o O2 therapy to maintain arterial
tests are rarely useful or collected in
oxygen saturation >90%.
clinical emergency practice.
▪ Decontamination
Treatment: o Identify causative agent and
terminate exposure However,
Emergency Treatment:
GASTRIC LAVAGE is NOT
▪ Emergency management starts with the RECOMMENDED for food-borne
ABCs (airway, breathing, circulation) of allergens
resuscitation.
Epinephrine
▪ ALL acute allergic reactions require triage
Epinephrine is a mixed α1-and β2-
AT THE HIGHEST LEVEL OF URGENCY, due receptoragent
to its possible development of life- ▪ α1 receptoractivation reduces
threatening complications; must be mucosal edema and membrane
rapidly assessed and treated. leakage and treats hypotension.
▪ Anaphylaxis, as defined by airway ▪ β2-receptoractivation provides
compromise or hypotension, is obviously bronchodilation and controls
a true medical emergency mediator release
▪ With suspected anaphylaxis, the single IS THE DRUG OF CHOICE AND THE
MOST IMPORTANT step in treatment is FIRST DRUG THAT SHOULD BE
ADMINISTERED IN ACUTE
the rapid administration of epinephrine.
ANAPHYLAXIS.
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DOSE: vary by both the age of the victim and the

anatomic location exposed.
If no cardiovascular compromise or collapse:
▪ Thermal injury results in a spectrum of
▪ IM epinephrine can be administered; 0.3 local and systemic homeostatic disorders
to 0.5 milligram (0.3 to 0.5 mL of the that contribute to burn shock. These
1:1000 dilution) include disruption of normal cell
▪ Repeated every 5 to 10 minutes according membrane function, hormonal
to response or relapse. (5-20 min interval alterations, acid-base disturbance,
harrisons) hemodynamic changes, and hematologic
▪ For convenience, patient safety, and derangement.
accurate dosing, many EDs have adopted ▪ The fluid and electrolyte abnormalities
the use of EpiPen seen in burn shock are largely the result of
alterations of cell membrane potential
If refractory to treatment despite repeated IM
causing intracellular influx of water and
epinephrine, or with signs of cardiovascular
sodium and extracellular migration of
compromise or collapse
potassium, secondary to dysfunction of
▪ Institute an IV infusion of epinephrine. the sodium pump. In patients with burns
Initially, 100 micrograms (0.1 milligram) >60% of total body surface area,
IV, should be given as a 1:100,000 depression of cardiac output results in a
dilution. (done by placing epinephrine, 0.1 lack of response to aggressive volume
milligram (0.1 mL of the 1:1000 dilution), resuscitation
in 10 mL of normal saline (NS) solution ▪ Thermal injury is progressive. Local effects
and infusing it over 5 to 10 minutes(a rate of thermal injury include the liberation of
of 1 to 2 mL/min). vasoactive substances, disruption of
cellular function, and formation of edema.
Epinephrine can further accelerate empty
▪ Although many factors may influence
heart syndrome due to its chronotropic effects.
prognosis, the severity of the burn, the
For this reason, it is recommended that
patients who suffer from anaphylaxis be placed presence of inhalation injury, associated
in the supine position before receiving injuries, the patient’s age, comorbid
epinephrine. conditions, and acute organ system failure
are most important
BURNS BURN SIZE

Burn size determines fluid resuscitation needs
THERMAL BURNS and the majority of decisions for hospital
ANATOMY: transfer. Burn injury size is quantified as the
percentage of body surface area involved.
▪ Skin consists of two layers: the epidermis
and the dermis. ▪ The Rule of Nines is a simple and
▪ Skin thickness varies both by age and commonly used method to calculate burn
anatomic location: It is relatively thinner size
at extremes of age, whereas it is thicker
on the palms, soles, and upper back. Thus,
the depth and severity of thermal injury
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▪ A superficial burn involves only the

epidermal layer of skin. Sunburn is
frequently given as an example, even
though it is caused by ultraviolet light
instead of thermal injury. The burned skin
is red, painful, and tender without blister
formation. Superficial burns usually heal
▪ The depth of a burn has historically been in about 7 days without scarring and
described in degrees: first, second, third, require only symptomatic treatment
and fourth. However, a classification of ▪ Partial-thickness burns extend into the
burn depth according to the need for dermis and are subdivided into superficial
surgical intervention has become the partial-thickness and deep partial
accepted approach in burn treatment thickness burns.
centers: superficial partial-thickness, deep ▪ In superficial partial-thickness burns, the
partial-thickness, and full-thickness burns epidermis and the superfcial dermis
(papillary layer) are injured, while the
deeper layers of the dermis, hair follicles,
and sweat and sebaceous glands are
spared. Superficial partial-thickness
burns are often caused by hot water
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scalding. The skin is blistered, and the

exposed dermis is red and moist. These
wounds are exceedingly painful to touch.
The dermis is well-perfused with intact
capillary refill. Healing typically occurs in
14 to 21 days, scarring is usually minimal,
and there is full return of function.
▪ Deep partial-thickness burns extend into
the deep dermis (reticular layer). Hair
follicles and sweat and sebaceous glands
are damaged, but their deeper portions
usually survive. Hot liquids (e.g., oil or
grease), steam, or flame usually cause
this type of injury. The skin may be
blistered, and the exposed dermis is pale
white to yellow in color. The burned area
does not blanch; it has absent capillary
refill and absent pain sensation. Deep
partial-thickness burns may be difficult to
distinguish from full-thickness burns.
Healing takes 3 weeks to 2 months;
scarring is common and related to the The American Burn Association provides
depth of the dermal injury. Surgical guidelines for referral to a burn center, in
debridement and skin grafting may be addition to indications based on burn depth.
necessary to obtain maximum function. Children < 10 ears of age and adults >50 years are
▪ Full-thickness burns involve the entire considered high-risk patients. Patients with
thickness of the skin. All epidermal and significant comorbidities, such as heart disease,
dermal structures are destroyed. These diabetes, or chronic pulmonary disease, are also
injuries are typically caused by flame, hot likely to require prolonged care and should be
oil, steam, or contact with hot objects. considered for transfer to a burn unit.
The skin is charred, pale, painless, and
leathery. Surgical repair and skin grafting INHALATION INJURY:
are necessary; significant scarring is the • As treatment of burn shock and sepsis has
norm improved, inhalation injury has become
▪ Fourth-degree burns are those that the main cause of mortality in burn
extend through the skin to the patients. Most fire-related deaths are due
subcutaneous fat, muscle, and even to smoke inhalation
bone. These are devastating, life- • Inhalation injury is associated with closed-
threatening injuries. Amputation or space fires and conditions that decrease
extensive reconstruction is sometimes mentation, such as overdose, alcohol
required. intoxication, drug abuse, and head injury.
Exposure to smoke includes exposure to
heat, particulate matter, and toxic gases
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• Direct thermal injury is usually limited to Therefore, when inhalation injury is present,
the upper airway; thermal injuries below careful fluid resuscitation guided by
the level of the vocal cords can occur in hemodynamic monitoring can help avoid
cases of steam inhalation. pulmonary edema and acute respiratory
• Smoke contains particulate matter, distress syndrome.
usually <0.5 µm in size, which is formed
from incomplete combustion of organic The initial diagnosis of smoke inhalation is made
material. from a history of exposure to fire in an enclosed
• Small particles may reach the terminal space and physical signs that include facial burns,
bronchioles, where they can initiate an singed nasal hair, soot in the mouth or nose,
inflammatory reaction that leads to hoarseness, carbonaceous sputum, and
bronchospasm and edema. expiratory wheezing
• Toxic inhalants are divided into three
Control of the upper airway is achieved by
large groups: tissue asphyxiants,
prompt endotracheal intubation.
pulmonary irritants, and systemic toxins.
Indications for intubation include
The two major tissue asphyxiants are 1. full-thickness burns of the face
carbon monoxide and hydrogen cyanide. or perioral region,
• Carbon monoxide poisoning is a well- 2. circumferential neck burns,
known consequence of smoke inhalation 3. acute respiratory distress,
injury. Severe carbon monoxide poisoning 4. progressive hoarseness or air
produces brain hypoxia and coma. hunger,
Comatose patients lose airway protective 5. respiratory depression or
mechanisms, which may result in altered mental status, and
aspiration and further pulmonary injury. 6. supraglottic edema and
inflammation on bronchoscopy.
• All patients with suspected carbon
monoxide exposure should receive 100%
oxygen by non-rebreather mask and The management of patients with moderate to
should be evaluated for hyperbaric major burns can be divided into three phases:
oxygen therapy
o prehospital care,
• Inhalation injury damages endothelial
o ED resuscitation and stabilization,
cells, produces mucosal edema of the
and
small airways, and decreases alveolar
o admission or transfer to a
surfactant activity, resulting in
specialized burn center
bronchospasm, airflow obstruction, and
atelectasis. Although lower airway edema PRE-HOSPITAL:
may not be clinically evident for up to 24
The basis of prehospital care of the burn-injured
hours, upper airway edema can occur
patient consists of the following:
rapidly.
• Over time, tracheal and bronchial epithelial (1) stop the burning process;
sloughing occurs. Approximately half of (2) assess and, if necessary, secure the airway;
intubated burn patients admitted to burn (3) initiate fluid resuscitation;
centers develop acute respiratory distress (4) relieve pain;
syndrome
(5) protect the burn wound; and
(6) transport the patient to an appropriate facility
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neck, burns inside the mouth, or

wheezing, perform early
On-site assessment of a burned patient is divided
endotracheal intubation.
into primary and secondary surveys. In the
g. Assess the adequacy of circulation
primary survey, identify and treat immediately
by noting the blood pressure,
life-threatening conditions. Initial management of
pulse rate, capillary refill time,
the burn-injured patient is similar to that of any
mental status, and urinary output,
other trauma patient: airway, breathing,
keeping in mind that due to the
circulation, and cervical spine immobilization
catecholamine response
where appropriate. During the secondary survey,
associated with burn injury, a
perform a thorough head-to-toe evaluation.
heart rate of 100 to 120 beats/min
NOTE: Pay close attention to the airway: rapid is considered within normal limits
deterioration may occur even when the initial for adults.
assessment judges the airway to be acceptable. h. Insert IV lines in unburned areas,
but when this is not possible, a
EMERGENCY MANAGEMENT: burned area can be used and
resuscitation started according to
a. Obtain a directed history from the a burn fluid resuscitation formula.
patient and EMS personnel to i. Routine laboratory tests, including
determine the burning agent(s), a CBC and measurement of
involvement of chemicals, the electrolyte, BUN, creatinine, and
duration of exposure, and if the glucose levels, should be
injury was sustained in an open or performed
enclosed space. j. Burn injury in the pregnant woman
b. Assess for loss of consciousness, is associated with significant
risk of blast injury from explosion, morbidity to mother and child. The
contact with electricity, or other outcome of the pregnancy is
trauma. determined by the extent of injury
c. Assess the adequacy of, or need to the mother.
for, cervical immobilization.
d. Obtain the general history, FLUID RESUSCITATION
including past medical and surgical
illnesses, chronic disease, allergies,
medications, and tetanus
immunization status.
e. Quickly assess the patient’s
respiration and circulation and
initiate stabilization
f. Examine the patient for signs of
inhalation injury, as evidenced by
respiratory distress, facial burns,
carbonaceous sputum, singed
nasal hair, and soot in the mouth.
If there is any evidence of airway
compromise with swelling of the
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WOUND CARE Dressings should ideally be changed twice daily,

gently removing residual ointment, for as long as
▪ Initially, wounds are best covered with a
the wounds continue to weep, then daily until
clean, dry sheet. Later, small burns can be
healing is complete.
covered with a moist saline-soaked
dressing while the patient is awaiting Wounds are cleansed and debrided prior to
admission or transfer. application of these dressings.
▪ The soothing effect of cooling on burns is
The goal is for the dressing to act as artificial skin.
most likely due to local vasoconstriction.
Wounds should be reevaluated at 24 to 48 hours
▪ Escharotomy
o Patients with circumferential deep Reassess burn wounds at 24 to 48 hours for
burns of the limbs may develop depth and extent of burn. Explain the follow-up
compromise of the distal visit schedule and prescribe analgesics. Discharge
circulation, particularly after instructions should include home burn care, pain
initiation of resuscitation control, and the symptoms and signs of infection.
o The distal vascular status of such Burned extremities should be elevated for 24 to
patients must be monitored 48 hours to prevent edema. Advise patients to
closely, including pulses, capillary return to the ED with signs or symptoms of
refill, pulse oximetry, and skin infection or if pain is inadequately controlled.
temperature
CHEMICAL BURNS
o The eschar is incised with a scalpel
to the level of the fat on the mid- ▪ Most chemicals produce tissue damage by
lateral portion of the limb, using their chemical reaction rather than by
care to avoid incising the fascia thermal injury. Certainly, some chemicals
(i.e., fasciotomy). Elevated produce significant heat by means of an
compartment pressures can be exothermic reaction. However, most skin
clinically evident. damage is the result of the chemical’s
unique characteristics
▪ Unlike thermal burns, chemical burn
injuries require tailored evaluations and
treatments based on the specific agent
involved.
▪ Most chemical burns are caused by acids
or alkalis. At similar volumes and manner
of contact, alkalis usually produce far
more tissue damage than acids.
▪ Acids tend to cause coagulation necrosis
Do not use silver sulfadiazine on the face because with protein precipitation forming a
it can stain the skin gray. Silver sulfadiazine tough leathery eschar. The eschar
should not be used in infants less than 2 months typically limits deeper penetration of the
of age. agent. Alkalis produce liquefaction
For the face or other small minor burns, necrosis and saponification of lipids. The
recommended topical agents include bacitracin result is a poor barrier to chemical
and triple-antibiotic (neomycin, polymyxin B, and penetration allowing deeper burns and
bacitracin zinc) ointments persistent tissue injury
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▪ Death early after severe chemical burns is decrease the rate and intensity of the
usually related to hypotension, acute chemical reaction and dissipate the heat
renal failure, and hypovolemic shock. 9. Continue irrigation at a gentle flow to
However, systemic toxicity and avoid continued skin contact with
subsequent morbidity and mortality may chemicals. After irrigation and
also occur if chemicals are absorbed debridement of remaining particles and
devitalized tissue, apply topical
GENERAL APPROACH TO CHEMICAL BURNS
antimicrobial agents to affected areas,
1. The initial goal of treatment is to remove and provide tetanus immunization as
the patient from the exposure and needed
prevent any further chemical contact 10. Aggressive fluid replacement is needed if
2. If not performed prior to arrival, remove extensive chemical burns are sustained.
all exposed clothing immediately. With Analgesics may be needed, and in the case
few exceptions, aggressive large-volume of allergic responses to chemicals,
irrigation with water is the cornerstone of epinephrine, antihistamines, and steroids
initial treatment may be required.
3. Chemical agents will continue to damage
ACID BURNS
tissue until they are removed or
inactivated. Perform a complete examination of a patient
4. Dry chemical particles such as lime should with a significant chemical acid burn to the skin
be brushed away before irrigation. because acids may also cause respiratory and
Sodium metal and related compounds mucous membrane irritation. Furthermore, skin
should be initially covered with mineral oil absorption of some compounds may occur and
or excised, because water can cause a result in systemic illness.
severe exothermic reaction. Dilution of
Contact time with the skin is the most important
phenol (carbolic acid) with water may
chemical burn feature that healthcare
enhance penetration.
professionals may alter. For example,
5. For the most part, however, use of water
instantaneous skin decontamination of 18M
or saline to irrigate a chemical burn
sulfuric acid will cause no burn, but a 1-minute
should not be delayed while searching
exposure can cause full-thickness skin damage
for other treatment agents and should
ideally begin immediately at the scene of • ACETIC ACID
the accident o The most common cause of
6. Almost universally, earlier irrigation chemical burns to the scalp in
means a better prognosis women. Prolonged contact,
7. Use pH indicator paper to determine especially with an already
continued presence of alkali or acid in damaged scalp, can cause a
burn wounds and possible need for partial-thickness burn that heals
further irrigation. Irrigation should slowly and is prone to infection.
continue until pH is neutral or near Initial treatment is copious water
neutral. irrigation. Oral antibiotics should
8. Although thermal energy is produced in be prescribed if the scalp burn has
an exothermic reaction when using water created open skin lesion.
irrigation, copious amounts of water will
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• CARBOLIC ACID (PHENOL) method for prevention of systemic

o Phenol (carbolic acid), a corrosive effects because depth of the burn
organic acid used widely in is difficult to determine and
industry and medicine, denatures absorption of chromium may
proteins and causes chemical continue after irrigation
burns characterized by a relatively • FORMIC ACID
painless white or brown coagulum o Formic acid in 60% solution is used
o Coagulation necrosis of the by acrylate glue makers, cellulose
involved area is common. Necrotic formate workers, and tanning
tissue may delay absorption workers.
temporarily, but phenol may o Treatment includes immediate
become entrapped under the decontamination and irrigation
eschar. with water. Systemic toxicity may
o Remove contaminated clothing require IV sodium bicarbonate for
and begin water irrigation the metabolic acidosis or exchange
immediately. Water lavage alone transfusions for severe hemolysis
may not be totally effective, • HYDROCHLORIC AND SULFURIC ACIDS
because the necrotic coagulum o The dermal toxicity of hydrochloric
inhibits water penetration to the acid and sulfuric acid is so well
deeper layers. recognized that early
o Decontamination is more effective decontamination and water
using an undiluted polyethylene irrigation usually prevent severe
glycol solution of molecular weight burns to the skin
200 to 400 or by a gentle wash • HYDROFLUORIC ACID
with isopropyl alcohol. An o Hydrofluoric acid is used in the
isopropyl alcohol rinse is production of high-octane fuel,
equivalent to polyethylene glycol glass etching, semiconductors,
in removing phenol microelectronics/micro
• CHROMIC ACID instruments, germicides, dyes,
o The chromate ion in chromic acid plastics, tanning, and fireproofing
produces a chronic penetrating material and is used in cleaning
ulcerating lesion of the skin. stone and brick buildings. It is also
Generalized exposure to a very effective rust remover.
powdered chromic acid can result o Unlike other acids, hydrofluoric
in conjunctivitis, lacrimation, and acid penetrates deeply and will
ulceration of the nasal septum. cause progressive tissue loss. It
Systemic chromium toxicity can produces burns in two ways.
cause liver or renal failure, GI o First, hydrogen ions cause direct
bleeding, coagulopathy, and CNS cellular damage as other acids do
disturbances through protein denaturation.
o Any acute skin exposure to o Second, free fluoride ions
chromic acid should be treated scavenge intracellular cations,
with copious water irrigation and such as calcium and magnesium,
observation for systemic effects. disrupt cellular membranes, and
Aggressive excision is the best
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inhibit the OCULAR BURNS

sodium/potassium/ATPase
✓ After the hands, the eyes are the second
o TREATMENT:
most common site of chemical burns
documented in a national insurance
database in Asia. Chemical burns to the
eyes are ocular emergencies requiring
immediate treatment.
✓ If the nature of the chemical is not known,
use pH paper to determine the presence
of acid or alkali. Acid quickly precipitates
the superficial tissue proteins of the eye,
• METHACRYLIC ACID producing the typical “ground glass”
o Methacrylic acid, found in many appearance of the cornea. Damage
artificial nail cosmetic products, sustained secondary to acid burns is, in
can produce severe dermal burns, most cases, immediate and limited to the
usually in preschoolers. Emergency area of contact.
treatment is copious water ✓ Alkali burns are generally more severe
irrigation. than acid burns, frequently with unsightly
• NITRIC ACID and disastrous results. In a short period of
o Nitric acid is used in industry for time, strong alkalis can penetrate the
casting iron and steel, cornea, anterior chamber, and retina,
electroplating, engraving, and with destruction of all sensory elements,
fertilizer manufacturing. Upon thus causing complete blindness
contact with skin, nitric acid can ▪ Begin with 1 to 2 L of normal saline
produce tissue damage by for each eye for 30-minute
oxidation and may turn the skin continuous irrigation as the
yellowish as it is burned. minimum treatment. Do not use
Emergency treatment consists of neutralizing substances.
copious water irrigation and ▪ Check the pH in the conjunctival
standard burn care sac to see whether it has returned
• OXALIC ACID to 7.0-7.3 to determine the need
o Oxalic acid is used for leather for further irrigation. Many liters
tanning and blueprint paper. may be needed for irrigation.
Oxalic acid binds calcium and However, extended 2- to 3-hour
prevents muscle contraction. The irrigation, despite apparent
wounds should be irrigated with conjunctival pH correction, is
water, and IV calcium may be recommended in the setting of
required. Serum electrolytes and strong alkaline or hydrofluoric
renal function should be acid burns with obvious
evaluated, and cardiac monitoring examination abnormality, to
should be instituted after serious correct anterior chamber pH as
dermal exposure. well as conjunctival pH.
▪ During irrigation, the eyelid may
have to be held open manually or
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with retractors due to severe survival than those who did not have or
orbicularis spasm require any of these
▪ The eyelids should be everted.
TREATMENT
Sweep the fornices with a wet
cotton applicator to remove any PREHOSPITAL CARE:
particulate matter, especially if the
❖ Rapid resuscitation of a drowning victim
pH is not responding well to
(quickly restoring ventilation and
irrigation
oxygenation) optimizes outcome. After
DROWNING safe removal of the victim from the water,
CPR should be initiated as quickly as
Drowning is submersion in a liquid medium possible.
resulting in respiratory difficulty or arrest. ❖ Administer high-flow oxygen by facemask
if the patient is breathing or by positive-
Drowning incidence peaks in three age groups:
pressure bag-valve-mask ventilation if the
The highest is in children <5 years old,2,3 the
patient is not breathing. For patients who
second peak is in those aged 15 to 24 years,2,3
do not recover spontaneous respiratory
and the third peak is in the elderly.
effort, endotracheal intubation and
Toddlers drown primarily after falling into positive-pressure ventilation are
swimming pools or open water, but they also necessary.
drown in bathtubs and buckets in the home.
PRIMARY ED TREATMENT:
PATHOPHYSIOLOGY:
▪ Upon the patient’s arrival at the ED,
▪ After submersion, the degree of hypoxic assess and secure the airway, provide
insult to the CNS determines the ultimate oxygen, determine core temperature, and
outcome. It was previously thought that assist ventilation as necessary.
parasympathetic activation of the diving ▪ If the patient is hypothermic, administer
reflex (i.e., bradycardia, apnea, peripheral warmed isotonic IV fluids and apply
vasoconstriction, and central shunting of warming adjuncts (e.g., blankets,
blood flow) provided transient protection overhead warmers, warming devices).
during submersion. However, in most ▪ Address any associated injuries.
cases, the diving reflex is overwhelmed by ▪ Patients who present to the ED with a
the stimulation of the sympathetic Glasgow Coma Scale score of >13 and an
nervous system, yielding no meaningful oxygen saturation of ≥95% are at low risk
protection for complications and should be observed
▪ Cerebral protection in cold water for 4 to 6 hours
submersions most likely results from rapid ▪ The patient should be told to return if
CNS cooling before significant hypoxic fever, mental status changes, or
damage occurs. pulmonary symptoms occur. If, after 4 to
▪ Patients who had a low Glasgow Coma 6 hours, the patient develops an oxygen
Scale score upon arrival to the ED requirement, the findings on pulmonary
(average of 3.2 for nonsurvivors vs. 11.6 examination are abnormal (rales, rhonchi,
for survivors), who required CPR, who wheeze, retractions, etc.), or the patient’s
were intubated, or for whom presser condition deteriorates, reassessment and
support was initiated all had a lower
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admission or transfer to a monitored bed ▪ SYMPTOMATIC DROWNING

are needed o Because submersion duration is
▪ Patients who present to the ED with a frequently unknown or only
Glasgow Coma Scale score of <13 should estimated, the extent of required
be maintained on supplemental oxygen resuscitation is often the most
and ventilatory support as needed. objective measure of the degree of
anoxic or ischemic insult
SECONDARY TREATMENT
o Details of initial presentation and
▪ Most patients demonstrate rapid resuscitation are frequently strong
improvement in oxygenation in the first prognostic indicators. For patients
24 hours. Patients presenting with a who require hospital admission, if
significant aspiration pattern or the submersion victim does not
cardiovascular collapse are predisposed to require cardiopulmonary
develop acute respiratory distress resuscitation at the scene or in the
syndrome. ED, complete recovery within 48
▪ For patients who have been resuscitated hours is expected.
from cardiac arrest, the hemodynamic
Victims undergoing CPR in the ED have a poor
response to exogenously administered
prognosis. Prolonged (>30 minutes) CPR in
epinephrine is frequently short lived, and
drowning victims indicates significant anoxic or
most require a continuous infusion of
ischemic insult to the heart, brain, and other vital
dopamine or epinephrine in the ED or
organs.
intensive care unit
▪ Hemodynamic recovery, when it occurs,
can be expected within 48 hours. Patients
demonstrating no hemodynamic recovery
after 48 hours may slowly improve over
the first week but are more likely to have
long-term neurologic damage
PROGNOSIS, DISPOSITION, AND FOLLOW-UP
▪ ASYMPTOMATIC DROWNING
o Drowning victims who are
asymptomatic or mildly
symptomatic can be observed for
4 to 6 hours. If the findings of
pulmonary examination and
oxygen saturation on room air
remain normal, patients can be
discharged home. If deterioration
is going to occur, it will do so
within the 4- to 6-hour observation
period
َ ‫ْت‬
ََّ ‫شئ‬

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ًَّ‫س ْهال‬

MEDICAL EMERGENCIES 2. Compression rate should be 100 to 120

breathing normally, and Pulse Check: Adult/Child

Patient Rescuers How to

Electrical cardioversion defibrillators will require an operator to manually

just below the patient’s right o Chest compression fraction >80%

contrast to earlier recommendations, a

Component of High-Quality CPR: (SPAMGA)

CHEST THRUSTS 2. with infant’s torso positioned

▪ Maintain continuous compressions during

and addressing the reasons for the

Note: Low BP does not equal shock.

CATEGORIES OF NON-TRAUMATIC SHOCK o Compensatory responses to

o Dysrhythmia are another common

▪ Obstructive shock CATEGORIES OF TRAUMATIC SHOCK

o Cerebral hypoperfusion causes more severe hypothermia, the patient

Note: Between hypothermia, coagulopathy Orthopedic injuries to these structures

ANATOMY: Subluxation: Partial disruption of a joint, in

Ligament: A bundle of connective tissue Sprain: A tearing injury to one or more

forces, torque (twisting stress), or a - Damage to the epiphyseal plate during a

affected joint may become

Splints HISTORY TAKING

Palpation to a minimum or at least halting its

▪ Any rotational deformity should be ▪ The purposes of debridement and

ANATOMY (CHILDREN): TYPES OF FRACTURES (CHILDREN):

▪ Salter-Harris Type III Fractures ▪ Salter-Harris Type V Fractures

▪ Salter-Harris Type IV Fractures

▪ GREENSTICK FRACTURES o Risk factors include high birth

b. FRACTURES OF THE MEDIAL relative imbalance between glutamate

Paroxysmal may happen if there is too much hallucinations, memory disturbances,

gradually, and postictal confusion, (life threatening if not treated

presentation. Examination, identification temporarily control the seizures until more

treatment is in consultation with a neurologist unrecognized seizures, history of recent or

PHYSICAL EXAMINATION • Abrupt onset and termination. Some

FOR ADULTS: part of your vision); active movement

⎯ Underlying mechanism depends on Delirium May not remember who they

▪ Extension response in response to pain o Abdominal or back pain – to

• Signs of trauma without defensive injuries

ANAPHYLAXIS ▪ When a mast cell, armed with IgE

eosinophil cationic protein, which damage cardiovascular collapse or respiratory

historyof exposure, such as a bee sting, First line Therapy:

DOSE: vary by both the age of the victim and the

BURNS BURN SIZE

▪ A superficial burn involves only the

scalding. The skin is blistered, and the

neck, burns inside the mouth, or

WOUND CARE Dressings should ideally be changed twice daily,

• CARBOLIC ACID (PHENOL) method for prevention of systemic

inhibit the OCULAR BURNS

admission or transfer to a monitored bed ▪ SYMPTOMATIC DROWNING

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