Nursing care of Clients in

Emergency Situation - 2
Triage and Severity Indices
Triage

• derived from Old French

word “trier” which means
“to sort”
• the process of determining
the priority of patients’
treatments based on the severity of their condition.
• sorting injured people into groups based on their need for an
immediate medical treatment
Triage
NOTE: Before performing a triage
✓Evaluate every situation before acting
✓perform quick incident scene survey
✓Determine scene hazards
✓Use appropriate PPE
✓Remain in appropriate zone
Triage
Casualty – a person severely affected by an event or situation, victim
• Multiple – number of victims is < 100
• Mass – number of victims is > 100 - MCI (Mass Causality Incident) is
an event that exceeds the health care capabilities of the response
• Direct Victim – an individual who is immediately affected by the event
• Indirect Victim – may be a family member or friend of the victim or a
first responder
• Displaced – those who have to evacuate their home, school or business
as a result of the disaster
• Refugees – a group of people who have fled their home or even their
country as a result of famine, drought, natural disaster, war or civil
unrest
Disaster Triage Methods
1. M.A.S.S. – Move, Assess, Sort, Send
- Starts the process by clearing the ‘walking wounded’
using verbal instructions
- moving, evaluating, classifying and transferring.
- has four tags: red, yellow, green and black

2. S.A.L.T. – Sort, Assess, Life-threatening interventions, Treat

and Transport
Disaster Triage Methods
3. S.T.A.R.T.
– Simple Triage and Rapid Treatment (Jump START for Pediatrics)
- Rapid approach to triaging large numbers of causalities
- Fast, easy to use and to remember
- Allows the most good for the most patients with the least amount
of resources
- RPM = 30-2-Can Do
Triage Tagging
1. Black = expectant (deceased)
2. Red = immediate – client needs
immediate treatment within the
hour but has a chance of survival
3. Yellow = delayed – client not in
immediate danger; treatment may
be delayed for an hour
4. Green = minor – minimal
“walking wounded”
Emergency Severity Rating Systems
• Emergency department triage has several functions:
1. Identification of patients who should not wait to be seen
2. Prioritization of incoming patients

• Accomplished by determining the patient’s illness/injury severity

or acuity
• Assess the degree to which the patient’s condition is life- or limb-
threatening and whether immediate treatment is needed to
alleviate symptoms
• Means of scoring an individual’s severity of condition
Characteristics: Validity & Reliability Systems
2-5-level triaging

➢ 2-level = sick / not sick

➢ 3-level = Emergent/Urgent/Non-urgent
➢ 4-level = life-threatening/Emergent/Urgent/Non-urgent
➢ 5-level = most acute/Emergent/Urgent/Non-urgent /least acute
Emergency Severity Index (ESI)
➢ A – intubated, pulseless, apneic, unresponsive = unstable
➢ B – high risk situation (confused, lethargic, or disoriented; in
severe pain or distress) = threatened = stable in less than 60
minutes
➢ C – number of resources needed = could be delayed
➢ D – danger zone = reclassify based on vital signs
Quick Assessment Components

A. For Adults (AMPLE)

- Allergies
- Medications taken
- Past medical history
- Last mealtime
- Event/environment
Quick Assessment Components
B. For Pediatric Clients (CIAMPEDS)
• Chief complaint
• Immunizations
• Allergies
• Medications taken
• Past medical history
• Event/environment
• Diet and diapers
• Signs and symptoms present (include onset)
Heat Stroke

• is an acute medical emergency caused by

failure of the heat-regulating mechanisms of
the body.
• It usually occurs during extended heat waves,
especially when they are accompanied by
high humidity.
• This is due to exposure to elevated ambient
temperature or excessive exercise during
extreme heat.
Heat Stroke: symptoms
1. profound central nervous system (CNS) dysfunction
a. confusion
b. delirium
c. bizarre behavior
d. coma
2. elevated body temperature
a. (40.6°C [105°F] or higher)
b. hot, dry skin
c. anhidrosis (absence of sweating)
d. tachypnea, hypotension, and tachycardia.
Management
• The primary goal is to reduce the high
temperature as quickly as possible

• treatment focuses on stabilizing

oxygenation using the ABCs of basic life
support.

• During cooling, the patient is massaged to

promote circulation and maintain
cutaneous vasodilation.
Near-Drowning
• is survival for at least 24 hours after submersion.
• The most common consequence is hypoxemia.
• Drowning is one of the leading causes of unintentional death in
children younger than 14 years of age.
• Factors associated with drowning and near-drowning include:
1. alcohol ingestion
2. inability to swim
3. diving injuries
4. hypothermia
5. exhaustion.
Management
• Immediate cardiopulmonary
resuscitation
• Therapeutic goals include:
a) maintaining cerebral perfusion
b) adequate oxygenation to prevent
damage to vital organs.
c) prevention of hypoxia and improve
ventilation which helps to correct
respiratory acidosis.
Snake Bites

• Children between the ages of 1 and 9

years are the most likely victims.
• The greatest number of bites occur
through the daylight hours into early
evening during summer months.
• The most frequent poisonous snakebite
occurs from pit vipers.
• The most common site is the upper
extremity.
Snake Bites
• Venomous snake bites are medical emergencies and nurses should
be familiar with the types of snakes.

• Snake venom consists primarily of

proteins with a broad range of
physiologic effects.

• Multiple organ systems, especially the neurologic, cardiovascular,

and respiratory systems, may be affected.
Snake Bites: Management

• Initial first aid at the site of the snake bite includes having the
victim lie down
• removing constrictive items such as rings
• providing warmth
• cleansing the wound
• covering the wound with a light sterile dressing
• immobilizing the injured body part below the level of the heart.
• Ice or a tourniquet is not applied.
Snake Bites: Management
• Initial evaluation in the ED is performed quickly and includes
information about the following:

• Whether the snake was venomous or nonvenomous;

if the snake is dead, it should be
transported to the ED with the
patient for identification

• Where and when the bite

occurred and the circumstances
of the bite
Snake Bites: Management
• Sequence of events, signs and symptoms (fang punctures, pain,
edema, and erythema of the bite and nearby tissues)
• Severity of poisonous effects
• Vital signs
• Circumference of the bitten extremity or area at several points; the
circumference of the extremity that was bitten is compared with the
circumference of the opposite extremity
• Laboratory data (complete blood count, urinalysis, and clotting
studies)
Snake Bites: Management
There is no one specific protocol for treatment of snake bites.
Generally:
1. Ice
2. Tourniquets
3. Heparin
4. Corticosteroids are not used during the acute stage = contraindicated in
the first 6 to 8 hours after the bite, because they may depress antibody
production and hinder the action of antivenin (antitoxin manufactured
from the snake venom and used to treat snake bites).
5. Parenteral fluids may be used to treat hypotension.
6. Vasopressors are used to treat hypotension - use for short-term
7. Close observation for at least 6 hours = patient is never left unattended.
Administration Of Antivenin (Antitoxin)
1. An assessment of progressive signs and symptoms which is most
effective if administered within 12 hours after the snake bite.
Children may require more antivenin than adults because their
smaller bodies are more susceptible to toxic effects of venom.
2. A skin or eye test should be performed
before the initial dose to detect allergy to
the antivenin.
3. Before administering antivenin and
every 15 minutes thereafter, the
circumference of the affected part
is measured proximally.
Administration Of Antivenin (Antitoxin)
4. Premedication with diphenhydramine and cimetidine decreases
the allergic response to antivenin.
5. Antivenin is administered as an intravenous infusion whenever
possible, although intramuscular administration can be used.
6. The antivenin is diluted in 500 to 1000 mL of normal saline
solution; the fluid volume may be reduced for children.
7. The infusion is started slowly, and the rate is increased after 10
minutes if there is no reaction.
Administration Of Antivenin (Antitoxin)

8. The total dose should be infused during the first 4 to 6 hours after
poisoning.
9. The initial dose is repeated until symptoms decrease. After the
symptoms decrease, the circumference of the affected part
should be measured every 30 to 60 minutes for the next 48 hours
to detect symptoms of compartment syndrome (swelling, loss of
pulse, increased pain, and paresthesias).
10. The most common cause of allergic reaction to the antivenin is
its too-rapid infusion
Administration Of Antivenin (Antitoxin)
11. Reactions may consist of a feeling of fullness in the face,
urticaria, pruritus, malaise, and apprehension followed by
tachycardia, shortness of breath, hypotension, and shock.
12. Intravenous diphenhydramine (Benadryl)
13. Vasopressors are used for patients in shock
14. Resuscitation equipment must be on standby while antivenin is
infusing.
Poisoning
• is any substance that, when ingested,
inhaled, absorbed, applied to the skin, or
produced within the body in relatively
small amounts, injures the body by its
chemical action.

• Poisoning constitutes a major health

hazard and emergency situation.
Poisoning
Goals of Emergency treatment
• To remove or inactivate the poison before it is absorbed
• To provide supportive care in maintaining vital organ systems
• To administer a specific antidote to neutralize a specific poison
• To implement treatment that hastens the elimination of the
absorbed poison
Ingested (Swallowed) Poisons
• Corrosive poisons include alkaline and acid agents that can cause
tissue destruction after coming in contact with mucous membranes
1. Alkaline agents = Lye, drain cleaners, toilet bowl cleaners,
bleach, non phosphate detergents, oven cleaners, and button
batteries (batteries used to power watches, calculators, or
cameras)
2. Acid products = toilet bowl cleaners, pool cleaners, metal
cleaners, rust removers, battery acid.
Ingested (Swallowed) Poisons: Management
• Stabilize cardiovascular and other body functions to
prevent shock
• ECG, vital signs, and neurologic status are monitored
closely
• Indwelling urinary catheter is inserted to monitor renal
function.
• Blood specimens to test for concentration of drug or
poison.
• determine what substance was taken;
✓the amount
✓time since ingestion
Ingested (Swallowed) Poisons: Management

signs and symptoms

➢pain or burning sensations

➢evidence of redness or burn in the mouth or throat
➢pain on swallowing or an inability to swallow,
➢vomiting, or drooling
Ingested (Swallowed) Poisons: Management
• Measures are instituted to remove the toxin or decrease its
absorption.

• The patient who has ingested a corrosive poison is given water or

milk to drink for dilution

• However, dilution is not attempted if the patient has acute airway

edema or obstruction or if there is clinical evidence of esophageal,
gastric, or intestinal burn or perforation.
Ingested (Swallowed) Poisons: Management
• Gastric emptying procedures may be used as
prescribed:
✓Syrup of ipecac to induce vomiting in the alert patient
✓Gastric lavage for the obtunded patient
✓Gastric aspirate is saved and sent to the laboratory for
testing (toxicology screens)
✓Activated charcoal administration if poison is one
that is absorbed by charcoal
✓Cathartic, when appropriate
Inhaled Poisons: Carbon Monoxide Poisoning

• may occur as a result of industrial or household incidents or

attempted suicide
• exerts its toxic effect by binding to circulating hemoglobin and
thereby reducing the oxygen-carrying capacity of the blood.
• Exposure to carbon monoxide requires immediate treatment
Clinical Manifestations:
1. Appears intoxicated (from cerebral hypoxia)
2. Headache
3. muscular weakness
4. palpitation
5. dizziness
6. confusion
7. coma
Management: Goals
• to reverse cerebral and myocardial hypoxia and to hasten
elimination of carbon monoxide.
• general measures apply:
➢ Carry the patient to fresh air immediately
➢ Open all doors and windows.
➢ Loosen all tight clothing
➢ Initiate cardiopulmonary resuscitation if required; administer O2
➢ Prevent chilling; wrap the patient in blankets
➢ Keep the patient as quiet as possible
Management: Goals
➢Do not give alcohol in any form
➢100% oxygen is administered at atmospheric or hyperbaric
pressures to reverse hypoxia and accelerate the elimination of
carbon monoxide
➢Oxygen is administered until the carboxyhemoglobin level is less
than 5%.
➢Psychoses, spastic paralysis, ataxia, visual disturbances, and
deterioration of mental status and behavior may persist after
resuscitation and may be symptoms of permanent brain damage.
Skin Contamination Poisoning (Chemical
Burns)

• Exposure to chemicals are challenging

because of the large number of offending
agents with diverse actions and metabolic
effects.
• The severity of a chemical burn is
determined by the mechanism of action, the
penetrating strength and concentration, and
the amount and duration of exposure of the
skin to the chemical.
Management

1. The skin should be drenched immediately with running water

from a shower, hose, or faucet.
2. The skin of health care personnel assisting the patient should be
appropriately protected if the burn is extensive or if the agent is
significantly toxic or is still present.
3. Prolonged lavage with generous amounts of tepid water is
important.
4. Identity and characterize chemical agent for future treatment
Management

5. Antimicrobial treatment
6. Debridement
7. Tetanus prophylaxis
8. Plastic surgery for further wound management
9. The patient is instructed to have the affected area reexamined at
24 and 72 hours and in 7 days because of the risk for
underestimating the extent and depth of these types of injuries.
FOOD POISONING
• a sudden illness that occurs after ingestion of contaminated food or
drink.
• Botulism is a serious form of food poisoning that requires
continual surveillance.
Management
• The key to treatment is determining the source and type of food
poisoning.
• If possible, the suspected food should be brought to the medical
facility and a history obtained from the patient or family.
FOOD POISONING
Specimen for examination
1. Food
2. Gastric contents
3. Vomitus
4. Serum
5. Feces
FOOD POISONING
Monitoring
1. Respirations
2. Blood Pressure
3. Sensorium
4. CVP (if indicated)
5. Muscular activity
6. Fluid and electrolyte balance
a. Severe vomiting produces alkalosis
b. Severe diarrhea produces acidosis.
FOOD POISONING: Treatment
1. Antiemetic medication
2. Mild nausea, take sips of;
✓weak tea
✓carbonated drinks
✓tap water
✓After nausea and vomiting subside, clear liquids are usually
prescribed 12 to 24 hours
✓Diet progressed to a low-residue, bland diet
Nursing care of Clients in
Emergency Situation - 1
Airway, Breathing, Circulation
(ABC)
Airway Obstruction
• is a life-threatening medical emergency.
• The airway may be partially or completely occluded.
• If the airway is completely obstructed,
permanent brain damage or death will
occur within 3 to 5 minutes secondary
to hypoxia.
• Partial obstruction of the airway can
lead to progressive hypoxia, hypercarbia,
and respiratory and cardiac arrest.
Pathophysiology Upper airway obstruction
• aspiration of foreign bodies

• anaphylaxis, viral or bacterial infection, trauma, and

inhalation or chemical burns.

• In adults, aspiration of a bolus of meat is the most

common cause of airway obstruction.

• In children, small toys, buttons, coins, and other

objects are commonly aspirated in addition to food.
Clinical Manifestations
• Choking • flaring nostrils
• apprehensive appearance • increasing anxiety, restlessness,
• inspiratory and expiratory and confusion.
stridor • Cyanosis
• labored breathing • loss of consciousness develop as
• use of accessory muscles hypoxia worsens.
(suprasternal and intercostal
retraction)
Assessment and Diagnostic Findings

• Assessment - asking the person whether he or

she is choking and requires help.
• If the person is unconscious - inspection of the
oropharynx may reveal the offending object.
• X-rays
• Laryngoscopy
• bronchoscopy also may be performed.
Management
• repositioning the patient’s head to prevent the tongue from
obstructing the pharynx.
• Alternatively, other maneuvers, such as abdominal thrusts
• the head-tilt–chin-lift maneuver
• the jaw-thrust maneuver
Management
• insertion of specialized equipment may be needed to open the
airway
• remove a foreign body
• maintain the airway.
• In all maneuvers, the cervical spine
must be protected from injury.
Head-tilt–chin-lift Maneuver
• The patient is placed supine on a firm, flat surface.
• one hand is placed on the victim’s forehead, and firm backward
pressure is applied with the palm to tilt the head back.
• The fingers of the other hand
are placed under the bony part
of the lower jaw near the chin
and lifted up.
• The chin and the teeth are
brought forward almost to occlusion to support the jaw.
Jaw-Thrust Maneuver
• After one hand is placed on each side of the patient’s jaw, the
angles of the victim’s lower jaw are grasped and lifted, displacing the
mandible forward.
• This is a safe approach to opening
the airway of a victim with suspected
neck injury because it can be
accomplished without extending
the neck.
Pulmonary Injury
• Damage to the lung tissue due to inhalation of
the chemical by- products of combustion
causes significant damage to the lower
airways, resulting in atelectasis, reduced ciliary
clearance, and loss of surfactant.

• Intensive care treatment is required and is

mainly supportive, aimed at preventing
hypoxia, infection, and atelectasis
Anaphylaxis

• is an acute systemic hypersensitivity reaction that occurs within

seconds or minutes after exposure to certain foreign substances,
such as;
1. medications (eg, penicillin, iodinated contrast material)
2. agents, such as insect stings (eg, bee, wasp, yellow jacket, hornet)
3. foods (eg, eggs, peanuts).
4. repeated administration of parenteral or oral therapeutic agents
(eg, repeated exposures to penicillin)
ANAPHYLAXIS
• the antibody immunoglobulin E (IgE) is responsible for most of the
immediate type of human allergic responses.
• The individual becomes sensitive to a particular antigen after
production of IgE to that antigen.
• A second exposure to the same antigen
results in a more severe and more
rapid response.
Clinical manifestations
Management with an anaphylactic reaction
• establishing a patent airway and ventilation is essential.
1. Epinephrine = Intramuscular
2. Antihistamine to block further histamine binding at target cells
3. Aminophylline by slow intravenous infusion for severe
bronchospasm and wheezing refractory
4. Early endotracheal tube intubation = essential to avoid loss of
the airway, and oropharyngeal suction may be necessary to
remove excessive secretions.
Management with an anaphylactic reaction
5. Resuscitative measures are used, especially for patients with
stridor and progressive pulmonary edema.
6. Cricothyroidotomy - is used to provide an airway if glottal
edema occurs

• Additional treatments:
a. Antihistamines to block further histamine binding at target cells
b. Aminophylline by slow intravenous infusion for severe
bronchospasm and wheezing refractory to other treatment
Management with an anaphylactic reaction

c. Albuterol inhalers or humidified treatments to decrease

bronchoconstriction; crystalloids, colloids, or vasopressors to treat
prolonged hypotension
d. Isoproterenol or dopamine for reduced cardiac output; oxygen to
enhance tissue perfusion
e. Intravenous benzodiazepines for control of seizures, and
corticosteroids for prolonged reaction with persistent hypotension or
bronchospasm
Cardiac Arrest
Cardiac Arrest
• The heart stops functioning in three main ways:
1. Failure of the oxygen supply causes asystole (or extreme
bradycardia). There is no electrical activity and no pumping.
2. Failure of electrical control causes ventricular fibrillation (VF) or
pulseless ventricular tachycardia (VT). There is no effective
electrical activity and no effective pumping.
3. Failure of the pump mechanism causes pulseless electrical
activity (PEA) (formerly known as electromechanical
dissociation or EMD). There is electrical activity but no
pumping.
Causes of the three arrest rhythms
1. Asystole
• similar to any other pump, the heart slows and stops when
deprived of its power supply.
• This results from:
➢hypoxia
➢a condition leading to hypoxia (e.g. hypovolemia) Tachycardia
during hypoxia is the result of the influence of the autonomic
nervous system.
➢Left to its own devices, the hypoxic heart contracts more slowly
(terminal bradycardia) and then arrests in asystole
2. Ventricular fibrillation
• is caused by direct damage or ✓hypothermia and near drowning
irritation of the heart. ✓electrocution
• This may be because of: ✓penetrating trauma
✓myocardial ischemia or ✓iatrogenic causes (e.g.
infarction cardioversion and cardiac
✓poisoning catheterization).
✓gross electrolyte imbalance
3. Pulseless electrical activity
• is that state when the pump (the myocardium) is unable to function
despite a relatively normal electrical stimulus (the ECG signal).
• This can be because of primary damage to the cardiac muscle
including:
✓extensive myocardial infarction
✓ruptured cardiac aneurysm
✓papillary muscle rupture
✓tension pneumothorax
✓cardiac tamponade
✓pulmonary embolism (PE)
Causes of cardiac arrest
• The commonest cause of adult cardiac arrest is thrombo-emboli
(AMI/ PE), but the ‘four Hs and four Ts’ should be considered in
all cardiac arrests.
• These cause cardiac arrest, and not just non- VT/ VF, as it is
possible to have a tension pneumothorax presenting in VF.
The four H’s and four T’s in cardiac arrest
• Hypoxia • Tension pneumothorax
• Hypovolemia • Tamponade
• Hyperkalemia or • Toxins
hypokalemia/metabolic disorder • Thrombosis (coronary or
• Hypothermia pulmonary)
Poisoning/overdose

• May be accidental or deliberate.

• Consider the agent. Some are toxic to the
rescuer (e.g. cyanides, organophosphates).
• The ABCDE approach should be followed to
prevent cardiopulmonary arrest.
Poisoning/overdose
• Effective compressions and ventilations (early intubation) are the
principal treatments during resuscitation 2° to poisoning.
• Success following a prolonged cardiac arrest is reported, regardless
of the presenting rhythm, utilizing the ‘four Hs and four Ts’
approach.
• Identification of the poison may enable
the use of an appropriate antidote
(e.g. naloxone for opioids).
Trauma
• Cardiac arrest 2° to blunt trauma has a poor outcome.
• Use the normal ABCDE approach with aggressive and prompt
treatment of injuries.
• These may encompass intubation, bilateral needle decompression
and bilateral chest drain placement, fluid bolus (± O negative
blood), with compressions supported by adrenaline.
• Thoracotomy should be considered where there is a history of
penetrating trauma
Asthma
• Cardiac arrest as a result of a severe asthma attack is often a
terminal event.
• It is linked to bronchospasm, mucus plugging, tension
pneumothorax, and arrhythmias.
• The ABCDE/ early defibrillation
approach should be followed, using
the four Hs and four Ts to guide
management.
• Early intubation assists with oxygenation
Hemorrhage
• Stopping bleeding is essential to the care and survival of patients in
an emergency or disaster situation.
• Hemorrhage that results in the reduction of circulating blood
volume is a primary cause of shock.
• Minor bleeding, which is usually venous, generally stops
spontaneously unless the patient has a bleeding disorder or has
been taking anticoagulants.
Hemorrhage
• Assessed for signs and symptoms of shock:
a. cool, moist skin (resulting from poor peripheral perfusion)
b. falling blood pressure
c. increasing heart rate
d. delayed capillary refill
e. decreasing urine volume (a late sign).
Hemorrhage
• The goals of emergency management:
a. to control the bleeding
b. maintain an adequately circulating blood volume for tissue
oxygenation
c. prevent shock.
Management of Hemorrhage
• Fluid Replacement - fluid replacement is imperative to maintain
circulation
—a loss of circulating blood results in a fluid volume deficit and
decreased cardiac output.
- two large-bore intravenous canulae are inserted to provide a
means for fluid and blood replacement
- blood samples are obtained for analysis, typing, and cross-
matching.
Management of Hemorrhage
• Replacement fluids may include:
1. Isotonic electrolyte solutions (lactated Ringer’s, normal saline)
2. Colloid
3. Blood component therapy = packed red blood cells are infused
when there is massive blood loss.

• Control of External Hemorrhage

• Pressure points to control bleeding
Head Injury
Skull fractures
• The brain is well protected by the skull, CSF, and meninges, and it
takes a significant trauma to cause a skull fracture and cerebral
contusion.
• Skull fractures are usually classified as linear, depressed, or base
of skull.
1. A linear skull fracture is a simple fracture that may be seen in
the occipital, temporal– parietal, or midline areas of the skull.
• These fractures are caused by a significant trauma to the skull and
may cause an underlying hematoma.
HEAD INJURY
2. A depressed skull fracture is more complicated and may be
associated with a scalp laceration.
• The depressed segment may be evident on examination, and
neurosurgical intervention may be required to elevate the segment
to prevent further damage to neural tissue.
3. A fracture of the basilar bone of the skull occurs in the floor of
the skull.
• Fractures in this bone can cause tears in the sac compartments that
hold the brain, resulting in leakage of CSF and thus exposing the
cranial vault to the outside environment and potential infection.
• Prophylactic antibiotics may be considered.
HEAD INJURY
Signs of a basilar skull fracture may include:
• eye bruising (‘raccoon eyes’);
• bruising around the mastoid process (Battle’s sign);
• blood in the ear canals or behind the tympanic membrane (TM).
Patients may complain of:
• visual disturbance • facial muscle weakness;
• loss of hearing • balance problems
• altered facial sensation • loss of sense of smell
• nasal drip caused by leaking CSF
Complications of head injury
Intracranial hematoma
• Deteriorating level of consciousness after a head injury may be due
to an intracranial hematoma.

• Accurate observation and monitoring are essential for identifying

and the need for surgical intervention may be lifesaving.

• Patients on anticoagulants or those with bleeding disorders are at

high risk of developing an intracranial hematoma after a head
injury.
Complications of head injury
Extradural hematoma
• results from rupture of one of the meningeal arteries that run
between the dura and the skull.
• The most common cause is the linear fracture of the temporo–
parietal bone, with associated injury to the middle meningeal
artery.
• The patient may be unconscious
• Signs and symptoms will be due to rising ICP.
• The need for accurate neurological assessment and consistent
monitoring.
Complications of head injury
Subdural hematoma
• It is a blood clot that forms beneath the dura mater.
• This type of venous bleed is usually caused by trauma such as a
fall, an assault, or the acceleration– deceleration patterns
associated with a road traffic accident.
• Two main types of subdural hematoma:
1. Acute— develops within 24h of the initial trauma and is
associated with severe brain insult;
2. Chronic— develops over a period of several days after the initial
trauma and often occurs in the elderly or in alcoholics.
Complications of head injury
Diffuse axonal injury
• This is a severe brain injury, often caused by rapid deceleration,
and it is the commonest cause of coma and subsequent disability.
• Patients with diffuse axonal injury are often in a deep coma
immediately after injury, despite an initially normal ICP and
normal CT scan.
STROKE
• Stroke occurs when the blood supply to part of your brain is
interrupted or reduced, preventing brain tissue from getting oxygen
and nutrients.
• Around 80% of strokes are due to occlusion of an artery that
carries blood to the brain.
• Stroke is a medical emergency, and there should be no time delays
in assessing these patients to specific treatments.
STROKE
Stroke may be caused by:
1. cerebral thrombosis, as a result of atherosclerosis or hypertension
2. cerebral embolism, as a result of atrial fibrillation (AF), MI, or
valve disease.
3. intracerebral hemorrhage, when a blood vessel ruptures within
the brain
4. subarachnoid hemorrhage, when a blood vessel on the surface of
the brain bleeds into the subarachnoid space
5. carotid artery dissection.
Risk factors of stroke Signs/Symptoms
❑ Hypertension ❑ Varying levels of consciousness
❑ Age >70y ❑ Motor weakness (opposite side
❑ Trauma to cerebrovascular accident
❑ Hyper or hypo coagulable state ❑ Incontinence
❑ Smoking ❑ Speech deficits
❑ AF or MI ❑ Facial drooping and/ or loss
of tongue control
❑ Diabetes
❑ CN involvement (same side as
❑ Oral contraceptives CVA)
❑ Ethnicity.
STROKE
The Face Arm Speech Test (FAST)
• The FAST was developed in Newcastle, UK, in 1998 and consists
of three key elements
✓facial weakness
✓arm weakness
✓speech disturbances.

• FAST was designed for assessment of a seated subject, and so does

not assess leg weakness.
STROKE
Immediate management of non-hemorrhagic stroke
• For suspected stroke, should be assessed for thrombolysis
treatment.
• If clinically indicated, there must be no delay in administering the
treatment
• admit the patient directly to a specialist acute stroke unit.
• Brain imaging should ideally be performed immediately
STROKE
Immediate management of intracerebral hemorrhage
• These patients should be closely monitored for deterioration in
consciousness by specialists in a neurosurgical or stroke care unit.

Immediate nursing interventions

• Assess and resuscitate the patient, as needed.
• Position the patient to avoid aspiration, and establish IV access.
• Collect blood samples, and ensure that these are sent to the
laboratory.
• Record CBG levels, and correct them if blood glucose
concentration is
STROKE
• Record an ECG, and request a chest X- ray (CXR).
• An NG tube may be indicated, but a urinary catheter should not be
routinely sited.
• provide reassurance to the patient throughout any procedure.
• Ensure personal hygiene and pressure area care
• keep the patient’s mouth clean and moist
Assessment of Critically ill
clients with Shock and
MODS
Terminologies
Distributive shock – this is also called circulatory shock, the
primary cause of decreasing BP is massive vasodilation of blood
into the peripheral vessels. Anaphylactic, Septic and Neurogenic
shock are distributive shock
MODS – Multiorgan dysfunction syndrome
Shock – inadequate tissue perfusion
Systemic Inflammatory Response Syndrome (SIRS) – is the body’s
response to an infectious or noninfectious insult affecting the whole
body
Shock
Classification of Shock according to Cause
Types of Shock

1. Hypovolemic Shock - caused by little blood volume

2. Cardiogenic Shock - caused by heart illness
3. Anaphylactic Shock - caused by allergic reaction
4. Neurogenic Shock - caused by damage to the nervous
system
5. Septic Shock - due to infections.
Hypovolemic shock
Hypovolemic shock - the most common form of shock
• caused by an inadequate circulating blood volume in the
intravascular bed.
• The circulating oxygenated blood flow to the body organs
decreases.
• This lack of oxygenated blood leads to inadequate tissue perfusion,
causing cellular hypoxia, organ failure, and death
Hypovolemic shock
The causes of hypovolemic shock can be divided into two
categories:
1. Absolute hypovolemia - occurs as a result of fluid loss from the
intravascular space (external fluid loss, internal fluid shifting,
called third spacing).
2. Relative hypovolemia occurs as a result of vasodilation and an
increase in vascular capacitance in comparison to the amount of
circulating volume
Cardiogenic Shock
Cardiogenic shock is a special kind of shock during which the heart
does not adequately pump enough blood to the body’s tissues.
• When the heart does not contract adequately, blood flow to tissues
decreases and oxygen delivery falls.
• When oxygen delivery falls below critical levels, tissues fail to
function and eventually break down (cellular destruction) and die.
• When enough tissues die, the entire body dies.
• The most common cause of cardiogenic shock is a heart attack
(myocardial infarction) that can damage 40% or more of the
ventricle.
Patients at risk for developing cardiogenic shock
• Acute MI (STEMI) • Myocarditis
• Atrial thrombus • Open heart surgery
• Cardiac contusion • Pheochromocytoma
• Cardiac tamponade • Pneumothorax
• Cardiac tumor • Pulmonary embolus
• Cardiomyopathy • Septic shock
• Cardiopulmonary arrest •Ventricular aneurysm
• Dysrhythmias • Valvular dysfunction (mitral or
• Endocarditis aortic regurgitation, mitral
stenosis)
Anaphylactic Shock
Anaphylactic shock is a rare but severe allergic reaction that can be
deadly if don't treat it right away.
• It's most often caused by an allergy to food,
insect bites, or certain medications.
• A shot of epinephrine
is needed immediately
Neurogenic shock
Neurogenic shock is a combination of
both primary and secondary injuries
that lead to loss of sympathetic tone
and thus unopposed parasympathetic
response driven by the vagus nerve.
• Consequently, patients suffer from
instability in blood pressure, heart rate,
and temperature regulation.
Septic Shock

• Septic shock is an inflammatory response.

• The septic process is initiated by the launch of immune mediators
that are part of the inflammatory reaction.
• Eventually the immune system is overwhelmed, and the process
actually harms the body.
• Systemic inflammatory response syndrome (SIRS) refers to a host’s
response to a variety of clinical insults, both infectious and
noninfectious, and is part of the acute sepsis process.
Septic Shock
• The patient in septic shock can exhibit skin lesions that are most
often located on the lower extremities.
• These lesions can be associated with the development of
disseminated intravascular coagulation (DIC), which is another
complication of septic shock; the lesions can also be associated
with the causative bacteria.
• Hyperglycemia can be the first indicator of sepsis in the patient
with diabetes.
Septic Shock

• Septic shock is a distributive shock characterized by tachycardia,

hyperthermia or hypothermia, and hypotension caused by
decreased SVR.
• A decline in SVR is one of the first indications of shock.
• The blood volume is adequate but misplaced.
• fluid is lost in the interstitial space.
• Renal involvement during sepsis can vary from a minor proteinuria
to acute tubular necrosis (ATN) in septic shock.
Patients at the greatest risk for septic shock

• Very young children

• Older adults
• Immunocompromised individuals
• Chronically ill patients
• Patients with malignancies
Compensatory Mechanisms
Compensatory Mechanisms
the compensatory which leads to
organ ischemia
mechanisms are irreversible shock
and failure
short lived. and cell death

metabolic
As the patient’s
acidosis and and eventually
compensatory
hypoxia are death.
mechanisms fail
produced

as the patient’s
shock progresses clinical condition
deteriorates
Clinical Manifestations
General Management and strategies in Shock
General Management and strategies in Shock

• Identify the cause of shock

• Fluid replacement
• Medication therapy
• Maintain adequate tissue
perfusion
Fluid resuscitation
Medication therapy
Medication Desired Action in Shock
Inotropic Agents
• Dobutamine (Dobutrex) • Improve contractility, increase
• Dopamine stroke volume, increase cardiac
output
• Epinephrine (Adrenalin)
• Milrinone
Vasodilators
• Reduce preload and afterload.
• Nitroglycerine Reduce oxygen demand in the
• Nitroprusside heart
Medication therapy
Medication Desired action in shock
Vasopressor agents
• Norepinephrine (Levophed) • Increase blood pressure by
• Dopamine vasoconstriction
• Phenylephrine
• Vasopressin
Monitoring tissue perfusion
Nutritional support
Managing Hypovolemic Shock
Treatment of the underlying Blood transfusions
cause
• Fluid resuscitation or blood • Basis of BT
replacement
• Lack of response to fluid
• Restore intravascular volume resuscitation
• Administer fluids that will • Volume of blood lost
remain in the intravascular
compartment to avoid fluid shifts • Need for hemoglobin
from intravascular to intracellular • Correct coagulopathy
Managing Hypovolemic Shock
Managing Hypovolemic Shock
Managing Cardiogenic shock
Managing Cardiogenic shock
Managing Anaphylactic shock
Systemic Inflammatory Response Syndrome
SIRS is the body’s response to an infectious or
noninfectious insult affecting the whole body.

Criteria of SIRS: at least two of the following:

➢ Temperature : hyperthermia > 38 C or hypothermia < 36.0 C
➢ Heart Rate : tachycardia > 90 beats/minute
➢ Respiratory Rate : tachypnea > 20 breaths/min
➢ White Blood Cells : leukocytosis > 12X109 /l
or leucopenia < 4x 109 /l
Multiorgan Dysfunction Syndrome
• Multiorgan dysfunction syndrome (MODS) is the progressive
dysfunction of more than one organ in patients who are critically
ill or injured.
• It is the leading cause of death in ICU.
Causes including, but not limited to:
• extensive burns
• trauma
• cardiorespiratory failure
• multiple blood transfusions
• systemic infection - most common
Patients at greatest risk for developing MODS

• Patients with systemic infection

(particularly, a gram-negative • Cardiogenic shock
sepsis)
• Human immunodeficiency virus
• Extensive burns (HIV)
• End-organ failure • Aspiration
• Pancreatitis • Multiple blood transfusions
• Hypovolemia • Trauma
Prognosis
• Mortality is high with MODS
• Potential for recovery depends on:
- the severity of illness or injury
- underlying organ reserve
- the speed of instituting effective treatment
- the adequacy of treatment
- and the number and severity of subsequent injuries and
complications.
• If treatment is unsuccessful, death usually occurs between 21 and
28 days after the initial insult.
Nursing Care of Clients
with Altered Perception
Traumatic Brain Injury
TRAUMATIC BRAIN INJURY
TBI - is physical injury to brain tissue that temporarily or
permanently impairs brain function.
Etiology:
1. Falls
2. Vehicular-related collisions
3. Violence – gunshot wound,
child abuse.
4. Sports injuries – soccer,
boxing, football or
any extreme sports
 TBI

Severity Occurrence Location

Mild
Primary Focal
Moderate
Secondary Diffuse
Severe
Classification according to Severity
TBI is graded as mild, moderate or severe on the basis of the level of
consciousness or Glasgow coma scale.
Signs and symptoms of Mild TBI
• Loss of consciousness for a few seconds to a few minutes
• Memory or concentration problems
• Headaches
• Dizziness or loss of balance
• Nausea or vomiting
• Difficulty sleeping
Signs and symptoms of Moderate to severe TBI
• Loss of consciousness from several minutes to hours
• Slurred speech
• Inability to awaken from sleep
• Weakness or numbness in fingers and toes
• Loss of coordination
• Persistent headache or headache that worsens
Presentation of TBI

Cognitive problems –
fogginess concentration, Mood disruptions –
memory deficits, cognitive irritability, sadness, anxiety
fatigue

Physical changes – spasticity,

Sleep dysregulation – trouble
paralysis, light/noise
falling asleep, overnight
sensitivity, loss of stamina,
awakening, too much or too
uncontrolled bowel and
little sleep
bladder
Classification according to Occurrence
1. Primary injury
= is the initial damage to the brain that results from the
traumatic event.
= may include contusions, lacerations, and torn blood vessels
from impact, acceleration/deceleration, or foreign object
penetration

2. Secondary injury
= may occur hours or even days after the initial injury and is
due primarily to brain swelling or ongoing bleeding
Classification according to Occurrence
Pathophysiology of TBI
Classification according to Location
1. Focal brain injury – usually due to contact and causing
scalp injury, it might present as skull fracture, contusions
and or intracranial hemorrhage.
Classification according to Location
2. Diffuse brain Injury
– usually due to acceleration
and concussion resulting in
diffuse axonal injury and brain
swelling. The tearing of the
nerve tissue disrupts the brain’s
regular communication
metabolic processes.
Types of TBI
1. Closed Brain injury – without the skull being broken or
penetrated and the brain has not been exposed.
Ex: rapid movement of the head
backward and forward causes the
brain to move inside the skull and
slam against its
inner bone
Types of TBI
2. Open brain injury – open or penetrating head injury
- a TBI can be focal or diffuse,
meaning damage maybe isolated to one
specific area of the brain in focal injuries
or widespread in the
case of diffuse
injuries.
Brain Injury
The most important consideration in any head injury
• Even seemingly minor injury can cause significant brain damage
due to obstructed blood flow and decreased tissue perfusion.
• The brain cannot store oxygen and glucose to any significant
degree.
• The cerebral cells need an uninterrupted blood supply to obtain
nutrients
• irreversible brain damage and cell death occur when the blood
supply is interrupted for even a few minutes.
Cerebral Contusion
• Is a more severe injury in which the brain is bruised, with possible
surface hemorrhage.
• The patient is unconscious for more than a few seconds or minutes.
• Clinical signs and symptoms depend on the size of the contusion
and the amount of associated cerebral edema.
• Often there is involuntary evacuation of the bowels and the
bladder.
• The patient may lie motionless, v/s are subnormal, cool, pale skin
and the picture is somewhat similar to shock.
• Contusion is any injury that causes blood to collect under the skin.
Cerebral Concussion
• Is a temporary loss of neurologic function which involves period of
unconsciousness lasting from a few seconds to a few minutes.
• A concussions are specific to injuries that affect the brain and may
not involve visible bruises or any apparent structural damage.
• Concussion effects varied depending on its location and severity.
• If the brain tissue in the frontal lobe is affected, the patient may
exhibit bizarre irrational behavior
• Temporal lobe involvement can produce temporary amnesia or
disorientation.
Intracranial Hemorrhage/Hematomas
• Is the most serious brain injuries, most common cause of death
and clinical deterioration after TBI

• A hematoma (collections of blood) may be;

a. epidural (above the dura)
b. subdural (below the dura)
c. intracerebral (within the brain)

• Major symptoms are frequently delayed until the hematoma is

large enough to cause distortion of the brain and increased ICP.
Epidural Hematoma
• Extradural Hematoma or Hemorrhage
• After a head injury, blood may collect in the epidural (extradural)
space between the skull and the dura.
• This can result from a skull fracture that causes a rupture or
laceration of the middle meningeal artery, the artery that runs
between the dura and the skull inferior to a thin portion of
temporal bone.
• Hemorrhage from this artery causes rapid pressure on the brain.
Subdural Hematoma
• A subdural hematoma is a collection of blood between the dura
and the brain, a space normally occupied by a thin cushion of
fluid.
• The most common cause of subdural hematoma is trauma, but it
may also occur from coagulopathies or rupture of an aneurysm.
• A subdural hematoma may be acute, subacute, or chronic,
depending on the size of the involved vessel and the amount of
bleeding present.
Management of Brain Injuries
• Assessment and diagnosis of the extent of injury are accomplished
by the initial physical and neurologic examinations.
• CT Scan, MRI and Positron emission tomography (PET scan)
• Any individual with a head injury is presumed to have a cervical
spine injury until proven otherwise.
• From the scene of the injury, the patient is transported on a board
with the head and neck maintained in alignment with the axis of
the body.
• A cervical collar should be applied and maintained until cervical
spine x-rays have been obtained
Treatment of Increased Intracranial Pressure
• As the damaged brain swells with edema, a rise in ICP occurs and
requires aggressive treatment.
• Initial management is based on the principle of preventing
secondary injury and maintaining adequate cerebral oxygenation.
• ICP; if increased - elevate the head of the bed, and maintaining
normal blood volume.
• Devices to monitor ICP or drain CSF can be inserted during
surgery or at the bedside using aseptic technique.
• The patient is cared for in the ICU, where expert nursing care and
medical treatment are readily available.
Treatment of Increased Intracranial Pressure
Surgical Management:
➢Surgery is required for evacuation of blood clots, debridement and
elevation of depressed fractures of the skull, and suture of severe
scalp lacerations.
Medications:
➢Diuretics – given IV to reduce intracranial pressure.
➢Anti-seizure drugs – given during first week to avoid any
additional brain damage might caused by seizure.
➢Coma-inducing drugs – sometimes use this drugs to put people
into temporary comas because comatose brain needs less oxygen to
function.
Nursing Management
Goal of Nursing Care:

• Maintain normal physiologic parameters

• Prevent secondary brain injury
• Provide emotional and psychological support to
patient and families
• maximize recovery and rehabilitative outcomes
Nursing Management
Assessment /Monitoring:
History
• Mechanism of injury
• Pre-existing Medical condition
• Medications

Physical Exam
• Reflexes
• Signs of fracture
Nursing Management
Assessment /Monitoring:
• Level of consciousness
Nursing Management
Assessment /Monitoring:
• Pupils size and reactivity
Nursing Management
Assessment /Monitoring:
• Muscle tone and Posturing
Nursing Management
Assessment /Monitoring:
• Vital Signs
- BP – target SBP > 100mmHg
- CVP – (8-10cm H20)
- ICP – target is (< 20mmHg)
- CPP – target 60 – 70mmHg

• Intake and Output monitoring

- Use of Indwelling catheters
Nursing Management
Respiratory care:
• Target ABG values
- PaO2 > 60mmHg
- PaCO2 35 – 45mmHg
- pH 7.35 – 7.45
• Suctioning
• Use of PEEP
• Aspiration precautions
Nursing Management
Hemodynamic/Fluid Management
• Avoid Hypotension
- Use of Isotonic fluids
- Use of Vasoactive drugs
• Osmotherapy
- Use of Mannitol
- Use of hypertonic Saline
• Monitoring of volume status
• Maintain electrolyte Balance
Nursing Management
Maintain normothermia and Analgesia
• Temperature – 35 to 37℃
- Sponge bath
- Cooling blanket
- Cold saline solution
• Anti-pyretic medications
- Analgesic to avoid increase ICP
-Kept at minimum requirement to allow
neurologic exam
Nursing Management
Positioning and Nutrition:
• Elevate heat of bed at 30 ͦ
• Head and neck in neutral alignment
• Ensure ET tube ties, cervical collar do not
compress the neck
• Enteral feeding should be initiated within 72hrs
of injury or as prescribed
• Full caloric requirement must be given
• Maintain normal blood glucose level
Nursing Management
Prevention of Complications:
• Seizure precaution and management
• Minimize noxious stimuli
• Prevent secondary Infections
- VAP/HAP
• Prevent pressure injuries
- Good skin care and pressure reduction
• DVT precautions
- ROM exercise
Nursing Management
Rehabilitation and Family Support:
• Physical Therapy
• Occupational therapy
• Speech therapy
• Cognitive therapy
• Social worker referral
• Religious and spiritual support
ACUTE ISCHEMIC STROKE
Etiology, Risk Factors, and Pathophysiology
• Stroke is the layman's term for a cerebrovascular accident.

• This refers to brain dysfunction

that is caused by brain cell damage
and death as a result of inadequate
blood flow to the brain.

• Stroke - is a leading cause of

death and disability world-wide.
Etiology, Risk Factors, and Pathophysiology
Ischemic Stroke
• The blood clot formation are usually the cause of blockage in
blood vessel to the brain that causes ischemic stroke.
• The affected part no longer receives enough blood or oxygen.
• Because the brain cannot store oxygen or glucose and therefore
requires a constant flow of blood to supply these nutrients.
• That part of the brain without blood flow dies.
 Arterial CVA

Hemorrhagic
Ischemic CVA
CVA

Embolism Thrombosis Hypoperfusion

Low Flow Thromboembolism

Etiology, Risk Factors, and Pathophysiology

• The blood supply to the brain can be altered through several

different processes:
a. Embolism or thrombus formation accounts for approximately
85% of all ischemic strokes.
b. Thrombosis
c. Hemorrhage
d. Compression or spasm of the vessels
Etiology, Risk Factors, and Pathophysiology
• Edema occurs in the area of ischemic or infarcted tissue and
contributes to further neuronal cell death.
• If ischemia is not reversed, neuronal cell death and infarction of
brain tissue occurs.
• The penumbra is an area of tissue that
surrounds the core ischemic area.
• The penumbra receives some blood
flow from adjacent vessels but
perfusion is marginal.
• If CBF is improved, the penumbra
may recover.
Risk factors:
1. Hypertension 3. Diabetes
2. Cardiac disease 4. Increased age
a. coronary artery disease 5. Male gender
b. heart failure 6. Prior stroke
c. atrial fibrillation 7. Hypercoagulability
d. endocarditis a. cancer
e. patent foramen ovale b. pregnancy
f. myocardial infarction c. high RBCs,
g. carotid artery disease d. sickle cell
Risk factors:
8. Family history
9. Dyslipidemia
10. Race (African American)
11. Smoking
12. Obesity
13. Physical inactivity
14. Alcohol or illicit drugs
15. Hormone therapy.
Transient ischemic attack (TIA)
• This is an important warning sign for stroke.

• The patient develops stroke symptoms

that resolve without tissue infarction.

• The pathophysiology of stroke varies

based on the precipitating event.

• Thrombosis and embolism formation

result in acute ischemic stroke.
Thrombosis
• It is the most common cause of ischemic stroke and is usually due
to atherosclerosis and the formation of plaque within an artery.
• Thrombotic comes from thrombus,
which is a blood clot
• A thrombus then forms at the site
of the plaque and causes brain tissue
ischemia along the course of the
affected vessel, which results in infarct
if not quickly reversed.
Thrombosis
• Edema often develops, further increasing ischemia by compressing
areas surrounding the infarct.
• Patients with a history of atherosclerosis or arteritis are at highest
risk for thrombotic strokes.
• Thrombotic strokes tend to
develop during periods of sleep
or inactivity, or
when blood flow is less brisk.
Embolism
• It refers to the occlusion of a cerebral vessel, most often by a blood
clot but also by infectious particles, fat, air, or tumor fragments.

• Embolism is often associated with heart

disease that results in bacterial vegetations
or blood clots that are easily detached from
the wall or valves of the heart and then
travel to the brain, lodging in a cerebral
vessel.
Embolism
• Chronic atrial fibrillation, valvular disease, prosthetic valves,
cardiomyopathy, and atherosclerotic lesions of the proximal aorta
are common causes of embolism.
• The fragmented substance easily
lodges at the bifurcation of the
middle cerebral artery, breaking
apart and traveling further into the
cerebral vascular system.
• The onset of an embolic occlusion
is rapid, with symptoms that develop without warning.
Clinical Presentation Symptoms of stroke
• Common signs and symptoms include:
1. weakness in an extremity or on one side of the body
2. sensory changes
3. difficulty speaking or understanding speech
4. facial droop
5. headache
6. visual changes.
• Clinical presentation of stroke varies based on the area of
ischemia or infarction.
Diagnostic Tests
• The goal of initial diagnostic testing in acute stroke is to rule out
intracranial hemorrhage (ICH), because treatments for
hemorrhagic and ischemic stroke differ significantly.
• Non-contrast head CT scan
➢available at most hospitals, can be
performed quickly, and is an excellent
tool for detecting intracranial bleeding
➢evidence of ischemia may not appear
or may be very subtle on standard CT
scanning until 12 to 24 hours after symptom onset.
Diagnostic Tests
• Specialized MRI scans
➢(diffusion-weighted imaging, perfusion-weighted imaging) can
detect areas of ischemia before they are apparent on CT.
Diagnostic Tests
• MRA - detects areas of vascular abnormality, as might be seen
with clot owing to arterial dissection.
a. Cerebral angiography and carotid UTZ
b. Transthoracic or transesophageal ECG
- used to assess cardiac causes of stroke.
c. ECG
- are placed on cardiac monitoring for at least 24 hours
d. Cardiac biomarkers
- there is a correlation between cerebrovascular and
cardiovascular disease
Management of Acute Ischemic Stroke
• Stroke is a medical emergency and is treated with the same
urgency as acute myocardial infarction.
• Just as “time is muscle” when the heart is ischemic,
“time is brain” when cerebral ischemia occurs.
• The goals of treatment are to restore
circulation to the brain when possible,
stop the ongoing ischemic process, and
prevent secondary complications.
Management principles include the following:

1. Evaluation of Conditions - that Mimic Acute Ischemic Stroke

➢ hypoglycemia may cause stroke-like symptoms and is easily
detected by using a bedside monitor to check blood glucose
➢ toxic or metabolic disorders
➢ migraines
➢ seizures
➢ mass lesions such as brain tumors or abscesses
➢ psychological disorders
Management principles include the following:
2. Fibrinolytic Therapy
➢ is administered to restore perfusion to the affected area
➢ IV administration of rtPA can be treated within 3 hours of the
onset of symptoms
➢ recommended dose for rtPA is 0.9 mg/kg, with 10% of the total
dose given as a bolus over 1 to 2 minutes followed by the
remainder of the dose as an infusion over 1 hour
➢ Vital signs and neurologic checks are done every 15 minutes for
the first 2 hours, then every 30 minutes for 6 hours, and then
hourly until 24 hours following initial treatment
Management principles

3. Endovascular Treatment
4. Blood pressure management
5. Management of increase intracranial pressure
6. Glucose management
7. Preventing and treating secondary complications
8. Preventing recurrent stroke
TERMINOLOGIES
• Increased ICP – the pressure inside the skull increases; it is a
medical emergency when this occurs suddenly

• Autonomic dysreflexia - a life-threatening emergency in spinal

cord injury patients that causes a hypertensive emergency; also
called autonomic hyperreflexia

• Brain injury - an injury to the skull or brain that is severe enough

to interfere with normal functioning
Brain injury
• Brain injury, closed (blunt) - occurs when the head accelerates and
then rapidly decelerates or collides with another object and brain
tissue is damaged, but there is no opening through the skull and
dura
• Brain injury, open - occurs when an object penetrates the skull,
enters the brain, and damages the soft brain tissue in its path
(penetrating injury), or when blunt trauma to the head is so severe
that it opens the scalp, skull, and dura to expose the brain
• Concussion - a temporary loss of neurologic function with no
apparent structural damage to the brain
Brain injury
• Contusion - bruising of the brain surface
• Transient ischemic attack – a warning sign of stroke
• Penumbra is an area of tissue that surrounds the core ischemic
area
• Thrombus is a formation of plaque within an artery
• Embolus refers to the occlusion of a cerebral vessel, most often by
a blood clot
Spinal Cord Injury (SCI)
Spinal Cord Injury
• occurs when a force is exerted on
the vertebral column, resulting in
damage to the spinal cord.

• Damage to any part of the spinal

cord or nerves at the end of the spinal
canal often causes permanent changes
in strength, sensation and other body
functions below the site of the injury.
SCIs can be separated into two categories:
1. Primary injuries - are the result
of the initial insult or trauma and
are usually permanent.

2. Secondary injuries - are usually

the result of a contusion or tear injury,
in which the nerve fibers begin to swell
and disintegrate.
 - ischemia, hypoxia,
Primary Secondary edema, hemorrhagic
lesions, which in turn
injuries injuries result in destruction of
myelin and axons

These secondary reactions, believed to be the

principal causes of spinal cord degeneration
at the level of injury, are now thought to be
reversible 4 to 6 hours after injury
• traumatic blow to the spine causing fractures, dislocation, crushing
or compression of one or more of the vertebrae
• Penetrating gunshot or knife wound
• Diseases/Conditions: Arthritis, cancer, inflammation, infections
or disk degeneration of the spine
Severity Classification:
1. Complete – if all sensory and
all motor functions are lost below
the spinal cord injury
2. Incomplete – if some motor or
sensory functions below the affected
area are still present; there are
varying degrees of incomplete
injury.
IMPORTANT!
• For suspected back or neck injury, DO NOT move the injured
person (permanent paralysis and other serious complications may
result).
• Keep the person still.
• Place heavy towels on
both sides of the neck to
prevent from moving
Emergency signs and symptoms
1. Extreme back pain or pressure in your neck, head or back
2. Weakness, incoordination or paralysis in any part of your body
3. Numbness, tingling or loss of sensation in your hands, fingers,
feet or toes
4. Loss of bladder or bowel control
5. Difficulty with balance and walking
6. Impaired breathing after injury
7. An oddly positioned or twisted neck or back
Seizure

• a sudden, abnormal,
excessive discharge of
electrical activity within the
brain that disrupts the brain’s
usual system for nerve
conduction
Classification of Seizure
1. Absence (petit mal) - An absence seizure causes an individual
to blank out or stare into space for a few seconds.
• They can also be called petit mal seizures.
• Absence seizures are most common in
children and typically don’t cause any
long-term problems.

Petit mal
Classification of Seizure

2. Atonic - are a type of seizure that

causes sudden loss of muscle strength.
• These seizures are also called
akinetic seizures drop attacks
or drop seizures.

Atonic
Classification of Seizure
3. Myoclonic - are brief shock-like jerks of a muscle or group of
muscles.
• They occur in a variety of
epilepsy syndromes that have
different characteristics.
• During a myoclonic seizure,
the person is usually awake and
able to think clearly.
Classification of Seizure
4. Clonic - means sustained rhythmical jerking.
• During a clonic seizure, jerking of the body or parts of the body
are the main symptom.
• They can begin in one area
(focal motor) or affect both sides
of the brain (generalized clonic).
• Clonic seizure movements
cannot be stopped by
restraining the person.
Classification of Seizure

5. Idiopathic (unclassified seizures) - Epileptic seizures are defined

as transient signs due abnormal excessive or synchronous neuronal
activity in the brain, and epilepsy refers to at least two unprovoked
seizures more than 24 hours apart.
• The term idiopathic means a disease of unknown cause.
Diagnostics:
1. Electroencephalography (EEG) – definitive test to diagnose
seizure activity
2. SPECT scan – scan of choice for a diagnostic evaluation of
certain types of CNS disorders
Treatment:
1. Medication therapy – hallmark of seizure management
2. Surgery – respective procedures or palliative corpus callosotomy
3. Seizure precautions
4. Oxygen and suction equipment at bedside
5. Re-orient client upon waking
Status Epilepticus
• potential complication of all types of seizures.
• This is a seizure that lasts longer than 5 minutes, or more than 1
seizure within a 5-minute period, without returning to normal level
of consciousness between episodes.
• Hence, this is a medical emergency that may lead to permanent
brain damage or death.
Status Epilepticus

Causes: Diagnostic:
• Stroke • EEG
• Low blood glucose levels • CT
• Too much alcohol, • MRI
withdrawal symptoms • LP
Status Epilepticus
Principle of Management:
• Goal: control seizure as quickly as possible, preventing recurrence,
maintaining patient safety and identifying the underlying cause.
Medications:
1. Lorazepam (Ativan) – induces respiratory depression
2. Flumazenil (Romazicon) – decrease respiratory depression
3. Phenytoin via central venous line
4. Phenobarbital (Luminal)
Patient education on DOs
✓Ease the person to the floor.
✓Turn the person gently onto one side. This will help the person
breathe.
✓Clear the area around the person of anything hard or sharp. This
can prevent injury.
✓Put something soft and flat, like
a folded jacket, under his or her head.
✓Remove eyeglasses.
✓Loosen ties or anything around the
neck that may make it hard to breathe.
✓Time the seizure.
Patient education on DON’Ts

1. Do not hold the person down or try to stop his or her

movements.
2. Do not put anything in the person’s mouth. This can injure teeth
or the jaw. A person having a seizure cannot swallow his or her
tongue.
3. Do not try to give mouth-to-mouth breaths (like CPR). People
usually start breathing again on their own after a seizure.
4. Do not offer the person water or food until he or she is fully alert
mlg