MEDICAL EMERGENCIES

LEVELS OF CONSCIOUSNESS
GLASGOW-COMA SCALE
NEUROLOGIC ASSESSMENT

BEHAVIORABLE, OBSERVABLE,
ASSESS AND REASSESS THE PATIENT

CATEGORIES:
I. Eyes open
II. Best verbal
III. Best motor
 I. Eyes Open

–Never 1
–To pain 2
–To verbal stimuli 3
–Spontaneously 4
 II. Best Verbal Response
– No response 1
– Incomprehensible sounds 2
– Inappropriate words 3
– Converses but disoriented 4
– Converses and oriented 5
 III. Best motor response
– No response 1
– Extension 2
– Flexion, abnormal 3
– Flexion withdrawal 4
– Localizes pain 5
– Obeys 6
 Level of Consciousness
The comatose patient lies with the eyes closed
and cannot be aroused.

Patients who can be aroused, but only with great

effort, are called stuporous.

If more easily arousable, lethargic.

 SHOCK:
I.V. FLUIDS USED:

CRYSTALLOID SOLUTIONS: Most used is Lactated

Ringer’s solution (electrolyte solution) will diffuse into
interstitial cellular spaces.

COLLOID SOLUTIONS: Most used for hemorrhagic

shock. Are whole blood products (plasma or serum
albumin).

Replace blood and fluid loss.

 SHOCK
Eyes vacant

Breathing Shallow/irregular

Skin: Pale, cold, moist

Nausea

Pulse: Weak or absent

 SHOCK
What is it?
Bodily reaction to illness, trauma, severe
emotional disturbance.

Interruption of blood flow to vital organs.

A decreased ability of body tissue to use oxygen

and other nutrients.
 SHOCK SIGNS AND SYMPTOMS
Onset: Suddenly Hypotension

Not only to seriously ill pts. Cyanosis

Decreased temperature Apathetic, confused,

comatose.
Weak thready pulse

Rapid shallow respiration Restlessness, anxiety

HYPOVOLEMIC SHOCK What is it?

Low volume of circulating blood.

Internal or external hemorrhage.

Loss of plasma ( liquid part of blood ) due to burns.

Fluid loss: vomiting, diarrhea, heat prostration.

Trauma that causes blood loss into a body cavity or

obvious hemorrhage.
 HYPOVOLEMIC SHOCK
SIGNS AND SYMPTOMS
Restlessness, thirst, cold, clammy skin.

Pallor; sweating; cyanosis.

Rapid pulse, heart beats to try and compensate

for low B/P.

Rapid respiration, weakness, lethargy.

Systolic B/P low HYPOTENSIVE 60-90 mm

HYPOVOLEMIC SHOCK
ACTIONS
Stop exam.
Vitals every 5 minutes.
Get help.
Glove:
Maintain Airway
Assist: oxygen , I.V., meds.
Don’t overheat.
No fluids.
Don’t leave patient.
 SEPTIC SHOCK: What is it?

Severe systemic infections and bacteremia

(bacteria in blood stream)

SIGNS AND SYMPTOMS

Early: skin warm and dry, flushed.
Late: skin cold, clammy.
Abrupt decrease in LOC.
Tachycardia (rapid heartbeat) VIDEO

Tachypnea (rapid respiration)

Seizures, circulatory collapse and cardiorespiratory
failure
SEPTIC SHOCK: ACTIONS
Stop procedure. Call for help.

Patient flat, supine.

Cover with sheet.

Vitals every 5 min.

Help with oxygen . I.V.

CARDIOGENIC SHOCK: What is it?

Failure of the heart to pump adequate

amount of blood to
vital organs causing inadequate tissue
perfusion (passing of a fluid through spaces)

Sudden onset.

May follow open heart surgery or Myocardial

Infarct.
CARDIOGENIC SHOCK:
SIGNS AND SYMPTOMS
Chest pain: radiate to jaws and arms.

Dizziness. Restless and anxious.

Decreased B/P

Decreased pulse pressure;

NEXT SLIDE
 PULSE PRESSURE
Difference between systolic and diastolic blood
pressures

Normal pulse pressure

Range: 30-40 mmHg

mmHg=Abbreviation for millimetres of mercury to

measure the partial pressure of a gas.
 CARDIOGENIC SHOCK:
ACTIONS

Get Code Cart.

Patient Semi Fowlers position

Keep warm and quiet.

Vitals.

Prepare for CPR.

No food or drink.
NEUROGENIC SHOCK: What is it?

Concussion, spinal cord injury, psychic

trauma, spinal anesthesia.

Abnormal dilation of peripheral blood

vessels.

B/P decreases as blood pools in veins=

reduced cardiac output.
http://www.patrol.org/
NEUROGENIC SHOCK:
SIGNS AND SYMPTOMS

Hypotention Systolic less than 90 mmHg.

Bradycardia Pulse less than 60 bpm.

Skin warm and dry, subnormal body temp.

Poor tissue perfusion:

cool extremities
diminishing
peripheral pulses
NEUROGENIC SHOCK: ACTIONS

Pt. Flat

Vitals

Do not move pt. with spinal cord injuries

Oxygen, I.V.
ANAPHALACTIC SHOCK
What is it?

Exaggerated hypersensitivity reaction to an

antigen that was previously encountered by
the body’s immune system.
 ANAPHALACTIC SHOCK
SIGNS AND SYMPTOMS

HISTAMINE IS RELEASED CAUSING:

Vasodilatation

Peripheral pooling of blood

Contraction of nonvascular smooth

muscles of the Respiratory system

Respiratory failure and death within

minutes.
 ANAPHALACTIC SHOCK
CAUSATIVE AGENTS:
Drugs.
Iodinated contrast agents.
Foods.
Anesthetics.
Insects.
ENTRY TO SYSTEM:
Skin.
Respiratory tract.
Gastrointestinal tract.
 ANAPHALACTIC SHOCK
SYMPTOMS
EARLY
Tightness in the chest.
Itching at site or eyes and nose.
Nasal congestion, sneezing, coughing.
Apprehension.
Nausea, vomiting.
 ANAPHALACTIC SHOCK
SYMPTOMS
LATE
Decreased B/P Nasal congestion,
sneezing, coughing
Dilated pupils
Apprehension
Change in LOC
Nausea, vomiting
Itching at site or eyes
and nose
 ANAPHALACTIC SHOCK
SYMPTOMS
LATE
Urticaria ( hives).

Angioneurotic edema- swelling of subcutaneous

tissues and mucus membranes.

Choking, wheezing, dyspnea, cyanosis.

 ANAPHYLACTIC SHOCK:
ACTIONS

Call 911 or hospital code

Monitor vital signs.

Document in chart and all records

 ANAPHYLACTIC SHOCK:
MEDICATIONS GIVEN:
Epinephrine: Vasoconstrictor ( constricts blood
vessels, prevent diffusion into system) Relaxes
bronchioles. ( helps breathing )

Diphenhydramine: Benedryl. Antihistamine-

prevents but does not reverse histamine
response.

Hydrocortisone: Decreases inflammation.

Suppresses the immune system.

Aminophyline: Bronchodilator- relief of

bronchospasm.
http://www.patrol.org/instructor/index.htm
 DIABETES:
Glucose intolerance, Chronic
CAUSE:
Disturbance in production, action or utilization of
insulin (hormone secreted by the islands of
Langerhans located in the pancreas.)

Diagnosed by lab measurements of blood glucose

levels.
Normal level: 80-115 mg/dl.
Symptoms of diabetes
Frequent urination

Excessive thirst

Extreme hunger

Unusual weight loss

Increased fatigue

Irritability

Blurry vision
 DIABETES

TYPE I INSULIN DEPENDENT

Usually occurs in children and young

adults.

Genetic.

Little or no production of insulin.

 DIABETES
TYPE II NON INSULIN DEPENDENT
Age 30 or older.

Obesity, hereditary factors, environmental

conditions.

Decrease in insulin production, insufficient

to meet needs of the body.

Controlled by diet, weight loss, or oral

hypoglycemic agents.
HYPOGLYCEMIA: INSULIN SHOCK

Blood glucose level below 50-60 mg/dl.

Excess insulin in blood.

Hyperfunction of the islets of Langerhans.

Excessive injection of insulin.

Inadequate food intake to utilize insulin.

Rapid onset.
 HYPOGLYCEMIA SYMPTOMS:
MILD
Tremor, sweating, tachycardia, nervousness.
MODERATE
Dizzy, headache, confusion, numbness of
lips or extremities. Cold, clammy skin.
Slurred speech.
SEVERE
Disorientation. Seizure. Coma.
Give sugar. Unconscious, under tongue.
INSULIN DEFICIENCY DIABETIC COMA

Not enough insulin in the body.

Missed dose of insulin.

Glucose decreased-liver produces more

glucose = hyperglycemia (increase of blood
sugar)

Kidneys compensate: excrete glucose with

water and electrolytes = dehydration and
electrolyte imbalance.
 QUESTIONS FOR ALL DIABETICS:

Have you eaten? Have you taken your insulin?

INSULIN SHOCK… IF PATIENT HAS TAKEN INSULIN

AND NOT EATEN = brain damage if sugar not given.

DIABETIC COMA… IF PATIENT HAS EATEN AND NOT

TAKEN INSULIN = sugar will rise glucose level but can be
corrected when ER care arrives.

LESSER OF TWO EVILS: IF UNSURE AS TO INSULIN

SHOCK OR DIABETIC COMA GIVE SUGAR.
 PULMONARY EMBOLISM:
Occlusion of one or more pulmonary
arteries by a thrombus (Blood clot)

Trauma that results in venous stasis

(stagnation of normal flow of blood
caused by venous congestion)

Usually trauma to long bones, leg, arm,

femur, humerus, tib.-fib.
 PULMONARY EMBOLISM:
Pulmonary thromboembolism is not a disease in
and of itself.
A fatal complication of underlying venous
thrombosis.
PE occurs when these propagating clots break
loose and embolize to block pulmonary blood
vessels.
Embolism: (A clot formed by platelets or leucocytes that blocks a
blood vessel)
.
 PULMONARY EMBOLISM:
PE can arise from Deep Vein Thrombosis
(DVT) anywhere in the body.

Fatal PE often results from thrombus that

originates in the axillary or subclavian veins
(deep veins of the arm or shoulder) or in
veins of the pelvis.

Thrombus that forms around indwelling

central venous catheters is a common
cause of fatal PE.
 PULMONARY EMBOLISM:
Studies show that acute DVT may be
demonstrated in any of the following:

– General medical patients placed at bed rest

for a week (10-13%)
– Patients in medical intensive care units (29-
33%)
– Patients with pulmonary disease kept in bed
for 3 or more days (20-26%)
– Patients admitted to a coronary care unit after
myocardial infarction (27-33%)
 PULMONARY EMBOLISM:
Massive PE is one of the most common
causes of unexpected death, being
second only to coronary artery disease as
a cause of sudden unexpected natural
death at any age.
PULMONARY EMBOLISM
SYMPTOMS
Sudden onset.

Chest pain- substernal, severity depends on

size of embolus.

Rapid, weak pulse.

 PULMONARY EMBOLISM
SYMPTOMS

Dyspnea- air hunger, labored difficult breathing.

Tachypnea- rapid respirations.

Hemoptysis- expectoration of blood.

Diaphoresis- profuse sweating.

 PULMONARY EMBOLISM
SYMPTOMS
Syncope = dizzy.

Arterial hypoxemia insufficient oxygenation of the

blood.

Shock.

Coma, deep stupor.

Sudden death.
 PULMONARY EMBOLISM:
ACTIONS:
Stop procedure.

Call for help.

Code cart.

Monitor vitals.

Reassure patient.
 STROKE:
CVA Cerebrovascular accident

TIA Mild stroke=

trans ischemic attack (TIA)
– Temporary interference with blood supply to the brain.
– May last few moments or hours.
– No residual brain damage or neurological damage
remains.
 STROKE:
CAUSE:
Occlusion or
rupture of
cerebral arteries
directly into the
subarachnoid
space

Subarachnoid: covering of the brain between the arachnoid membrane and

the pia matter of the covering of the brain)
 STROKE:
SYMPTOMS:
Severe headache. Dizziness.
Muscle weakness, flaccidity of face or extremities,
usually one sided.
Eye deviation, one sided, may lose vision.
Dysphasia = difficult speech.
Aphasia = no speech.
Ataxia =defective muscle coordination, esp. voluntary
movement.
Stiff neck, nausea, vomiting. Loss of consciousness
SYNCOPE:
Insufficiency in the supply of
blood to the brain.
CAUSES:
Heart disease.
Hunger.
Poor ventilation.
Fatigue.
Emotional shock.
 SYNCOPE:
SYMPTOMS:
Always preceded by symptoms. Observe patient.
Never leave unrestrained or uanttended
Pale, dizzy.
Nausea.
Diaphoretic.
Hy perp ne’ a = Increased respiratory
rate or deeper breaths.
Tachycardia. Cold, clammy skin.
 SYNCOPE:
ACTIONS:
Lay patient down.

Head lower than body.

Trendelenberg

Ammonia inhalant.
CONVULSIVE SEIZURES:

Sudden brief attack of altered

consciousness, motor activity or sensory
phenomena.

Little or no warning.

Lasts seconds or minutes.

CONVULSIVE SEIZURES:
CAUSE:

Infectious disease.

High fever.

Stress.

Head trauma.

Brain tumor.
CONVULSIVE SEIZURES:

GRAND MAL:
Whole body convulses.
Pt. Loses consciousness.
Muscles rigid.
Eyes wide open.
Jerky body movements.
Rapid, irregular respirations.
Froth or blood streaked saliva.
Incontinence.
Sleeps after.
CONVULSIVE SEIZURES:

PARTIAL SEIZURE
SIMPLE:
– Consciousness maintained.
COMPLEX:
1. Lasts 1-4 minutes.
2. Pt. not responsive but appears awake.
3. Lip smacking, chewing and face grimacing.
4. Swallowing movements.
5. Patting and pinching or rubbing oneself or
clothing.
6. Confusion for several minutes post
seizure.
CONVULSIVE SEIZURES:

PETIT MAL:
Brief; may not know one has occurred.
Rare in adults.
Brief loss of awareness accompanied by
blank stare.
Eyes seem not to focus.
Total return to consciousness.
Eyes blinking- mild body movement.
Sudden loss of muscle tone, may fall.
 ACTIONS for ALL:
CONVULSIVE SEIZURES:

Code cart.
Prevent injury, stay with patient.
No insertion of objects into mouth.
Document in chart.
Report to physician/nurse.
Do not proceed with exam until Dr. Orders.
After seizure: Position to prevent choking.
Put pt. On side or prone.
Restrain gently, hold.
 TRAUMA
PREPARE ROOMS AT BEGINNING OF SHIFT:

ASSESS PATIENT:
Continuously monitor LOC (level of consciousness)

Watch for symptoms of shock (especially ER patients)

Sequence exams for least amount of movement

AP,Lat, Obls

Combine studies: spine AP's first

 GENERAL TRAUMA GUIDELINES
Do not remove:
Dressings or splints

Backboards or
C-collars until cleared

Do not disturb impaled objects

Get assistance to move

Patients
 HEAD INJURIES
CLOSED: Blunt injury
Brain may swell= pressure causes extensive brain injury
Signs:
Unequal pupil dilation
Seizures
Vomiting
Hemiparesis
Drowsiness, confusion, irritability, stupor, coma
Loss of reflexes
Change in vital signs
Headache, dizziness, giddiness
Gait abnormalities
 HEAD INJURIES
OPEN:

Brain vulnerable to damage

and infection because protective
skull or meninges has been broken

Signs:
Abrasions, contusions, lacerations visible
Penetration in skull apparent by inspection
or seen on radiograph
Varying LOC
 BASAL SKULL FRACTURE:
Fracture at the base of the skull at occiput
May not be seen on x-ray

Signs:
Leakage of cerebral spinal from ears, nose or post
nasal drip

HALO sign: Blood on sheet or dressing surrounded

by a yellow stain
 BASAL SKULL FRACTURE
Assess patient:
LOC changes

Hypoxia = decreases oxygen in inspired air

Check vital signs frequently

Airway obstruction due to relaxation of tongue, absence

of gag reflex, blood drainage in throat

Be prepared to assist with suction equipment

http://www.patrol.org/
 IMPLICATIONS:
Don't leave patient alone
Keep head and neck immobilized:
Do not remove c-collar, sandbags or
dressing
Wear gloves even if you have no plans to
touch patient
Use sterile gloves if applying sterile
dressings...watch for pressure....may
depress skull fx
 FACIAL INJURIES
SIGNS:
Malalignment of face and teeth

Ecchymosis of mouth and buccal mucosa

( cheek )

Lack of facial symmetry

Inability to close jaw

Loss of sensation on injured side

 FACIAL INJURIES
Diplopia- double vision

Epistaxis- nosebleed

Signs of head injury

 IMPLICATIONS:

Glove: sterile if in contact with wound

Observe for airway obstruction
Noisy or labored respirations
Signs of shock
No suction through nasal passages
LOC assessment
 SPINAL CORD INJURIES
SPINAL CORD:
Carries messages from brain to peripheral nervous
system

Housed in vertebral canal, protected by fluid in the

canal and vertebra ( looses protection if injury to
vertebra )

Has little healing power

SPINAL CORD INJURIES

PARTIAL TRANSECTION
Asymmetrical flaccid paralysis below the
level of injury

Asymmetrical loss of reflexes

Some sensory retention: pain, temp.,

pressure, touch
SPINAL CORD INJURIES

COMPLETE TRANSECTION
Loss of all sensation below the site of injury

Flaccid paralysis of skeletal muscles below injury

Absence of somatic sensations ( structures of the

body wall like skeletal muscles) below site

Absence of visceral sensations ( pert. to organs)

below site

Incontinence...bowel and bladder

 SPINAL COLUMN:
Most injuries to cervical or lumbar: most mobile

Injury may compress spinal cord

Physician supervises any moves

Do not move head or neck even if in

awkward position

Do not move any support

At least 6 assisting for log roll

Monitor vitals
 IMPLICATIONS
Usually portable with ER Dr. attending
Physician supervises any moves
Do not move head or neck even if in
awkward position
Do not move any support
At least 6 assisting for log roll
Monitor vitals
 IMPLICATIONS
Maintain airway..listen for noisy or labored
breathing

Observe for shock

Prepare to assist with CPR