Hemorrhage ,Shock & Unconsciousness PPT

HEMORRHAGE &
SHOCK
UNCONSCIOUSNES
SMATHEW VARGHESE V
MSN(RAK),FHNP (CMC Vellore),CPEPC
Nursing officer-AIIMS Delhi
1mathewvmaths@yahoo.co.in

HEMORRHAGE

HEMORRHAGE
Definition of Hemorrhage
According to medical dictionary
It is the copious and heavy discharge of blood
from blood vessels or circulatory system.

Classification of Hemorrhage
Depending on the source of bleeding:
• External Hemorrhage: When bleeding is
revealed and seen outside, e.g. epistaxis.
• Internal Hemorrhage: Bleeding is
concealed and not seen outside, e.g.
intracranial hematoma

Depending on the Nature of Bleeding Vessel:
• Arterial Hemorrhage: Bright red in color.
Blood emitted as a jet with each heartbeat
• Venous Hemorrhage: Dark red in color.
Blood flow is steady.
• Capillary Hemorrhage: Bright red in color.
Generalized ooze of blood instead of blood
flow.

Depending upon Time of Hemorrhage:
• Primary Hemorrhage: Occurs at the time of
trauma or surgery.
• Reactionary Hemorrhage: Occurs within 24
hours of trauma or operation.
• Secondary Hemorrhage: Occurs after 7 –
14 days of trauma or operation.

Depending upon volume of blood loss:
• Mild Hemorrhage: Blood loss ≤ 500 mL.
• Moderate Hemorrhage: Blood loss 500 –
1000 mL.
• Severe Hemorrhage: Blood loss ≥ 1 L.

Depending upon speed of blood loss:
• Acute Hemorrhage: Massive bleeding in
short span of time.
• Chronic Hemorrhage: Slow bleeding small
in quantity for long time.

• Depending Upon Percentage of Blood Loss
:( American college of surgeons )
• Class I: Up to 15%.
• Class II: Between 15 – 30%.
• Class III: Between 30 – 40%.
• Class IV: More than 40 %

Common Causes of Bleeding
1. Traumatic bleeding
Common types of traumatic injury include:
• Abrasions or grazes that do not penetrate
below the skin
• hematoma or bruises
• Lacerations or incisions
• Puncture wounds from items like needles
or knives
• Crushing injuries
• Gunshot wounds

2. Medical conditions
There are also some medical conditions that can
cause bleeding. It is called medical bleeding
• Intravascular injury :Changes of blood within
the vessels e.g. Increased blood pressure and
deficiency of clotting factors
• Intra mural changes: Changes arising within
the walls of blood vessels E.g. Aneurysm,
Dissections .
• Extra mural Changes: Changes arising outside
the blood vessels E.g. H. Pylori Infection , brain
abscess, brain tumor

Medical conditions
• Leukemia
• Liver disease
• Menorrhagia, heavy or prolonged menstrual
bleeding
• Thrombocytopenia, low blood platelet count
• Von Willebrand disease
• Vitamin K deficiency
• Bowel obstruction
• Lung cancer
• Acute bronchitis
• Severe hypothermia
• Endometriosis

3. Medicines
• Anticoagulants
• Antibiotics, when used on a long-term basis
• Chemotherapy
• Aspirin

Pathophysiology
• Bleeding → Hypovolaemia → Hypo perfusion →
Cellular anaerobic metabolism + lactic acidosis →
decreases level of coag.proteases → coagulopathy
& Hemorrhage → decreased tissue perfusion &
decreased Blood Supply to gut & muscle
• Underperfused muscle →unable to generate heat →
Hypothermia →. Hemorrhage→ Hypo perfusion →
Acidosis→ DEATH

Clinical Features
According to origin
• Mouth & GIT: Hematemesis,Hemoptysis,
Gastric and esophageal bleeding
• Rectum :Hematochezia
• Urinary tract: Heamturia
• Head : ICH,SAH,SDH,EDH
• Lung : Pulmonary Hemorrhage
• Gynecological : PPH,Ovarian and Vaginal
bleeding

Clinical Features
• Anxiety
• Blue lips and fingernails
(Cyanosis)
• Low or no urine output (Oliguria)
• Profuse (excessive) sweating
• Shallow breathing
• Dizziness
• Confusion
• Pallor
• Thirsty
• Tachycardia (Rapid thready&
Weak pulse)
• Tachypnoea
• Cold clammy skin due to
vasoconstriction
• Dry face
• Dry mouth
• Goose skin appearance
• Chest pain
• Loss of consciousness
• Low blood pressure (Hypotension)
• Rapid heart rate

Clinical Features
Signs of internal hemorrhaging include:
• Abdominal pain
• Blood in the stool
• Blood in the urine
• Vaginal bleeding (heavy, usually outside of
normal menstruation)
• Vomiting blood
• Chest pain
• Abdominal swelling

How Bleeding Stops?
Primary Hemostasis
• Vasoconstriction
• Platelet plug formation
Secondary Hemostasis.
• Clotting cascade activated to form fibrin
clot

How Bleeding Stops?

Clotting factors - 13
• Factor I - Fibrinogen
• Factor II - Prothrombin
• Factor III - Tissue Thromboplastin (Tissue Factor)
• Factor IV - Ionized calcium ( Ca++ )
• Factor V - Labile factor or Proaccelerin
• Factor VI – Unassigned (Un Known)
• Factor VII - Stable factor or Proconvertin
• Factor VIII - Antihemophilic factor
• Factor IX - Plasma thromboplastin component, Christmas
factor
• Factor X - Stuart-Prower factor
• Factor XI - Plasma thromboplastin antecedent (PTA)
• Factor XII - Hageman factor
• Factor XIII - Fibrin-stabilizing factor

Clotting Cascade
1. Intrinsic Pathway – Initiated by
Endothelial surface injury
2. Extrinsic Pathway – Trauma
3. Common Pathway

Clotting Cascade

Laboratory Tests
Bleeding Time (BT):
• Patients with BT more than 10 minutes
have increased risk of bleeding.
BT is prolonged in thrombocytopenia, Von –
Willebrand’s disease and platelet
dysfunction.
Platelet count:
• Normal count: 1.5 – 4.5 lakhs per cu mm of
blood.

Laboratory Tests
• Prothrombin Time (PT):
Normal PT is usually 12 – 14 seconds.
Prolonged in patients on warfarin
anticoagulant therapy, vitamin K deficiency
or deficiency of factor V, VII, X, prothrombin
or fibrinogen.
• Partial Thromboplastin Time (PTT):
• Prolonged in hemophilia.
Normal PTT is less than 45 seconds.

Methods of Achieving Hemostasis
• Mechanical Methods
– Pressure.
• Hemostat.
An instrument for preventing blood flow by
compression of a blood vessel.
• Sutures and Ligation

Chemical Methods
Local Agents:
• Adrenaline
• Thrombin
Helps in converting fibrinogen into fibrous clot
• Surgicel- Oxidized cellulose polymer
It coagulates the plasma proteins to form a
black or brown sticky gelatinous clot.

Chemical Methods
• Other Agents
• Gelatine Sponge.
• Micro fibrillar Collagen.
• Fibrous Glue.
• Natural Collagen Sponge
• Bone Wax.

.
Chemical Methods
Systemic Agents:
 Whole Blood
 Platelet Rich Plasma.
 Fresh Frozen Plasma.
 Cryoprecipitate.- Fibrinogen,CF8 &13

Thermal Agents
• Electrocautery
• Lasers.
• Cryosurgery.
Extreme cooling has been used for
Hemostasis.
Temperature ranging from -20°C to -180°C
are used.

Specific measures to stop external
bleeding
• RED
1. REST
2. ELEVATION
3. DIRECT PRESSURE & DRESSING

Specific measures for internal
hemorrhage
• Give whole blood or plasma expanders at
the rate of blood loss
• Prepare the patient immediately for
surgical intervention to identify and control
bleeding
• Monitor client’s hemodynamic status
• Maintain client on supine position till
hemodynamic parameters improve
• Apply pneumatic anti shock garment if
available

Anti shock Garments
• There are 2 types of Anti shock Garments
• Pneumatic and Non Pneumatic
• Non Pneumatic garment is a low technology
first aid device used to treat hypovoleumic
shock.
• Pneumatic Garments are used to treat severe
blood loss situation e.g in Military Set up
• How it works?
When patient in shock, the brain, heart and lungs
are deprived of oxygen and blood. The anti
shock garments reverse shock by increasing
blood flow to the vital organs by increasing
peripheral vascular resistance .

Fluid replacement
• Insert large bore IV canula to provide fluid
and blood replacement
• With draw blood sample for necessary
investigations
• Give fluid replacement including balanced
electrolyte solution
• Give Whole blood as per the patient’s
requirement
• Rate of infusion is based on the severity of
blood loss and chemical evidence of
hypoxia

RATE OF FLUID REPLACEMENT
• Initial phase
For Severe Hypovolaemia
• Rapid infusion of 1-2 L of isotonic NS as rapidly as possible to
restore tissue perfusion
Mild to Moderate Fluid loss
• Infuse at the rate of 50-100 ml/hr depending up on the
estimated fluid loss
• To estimate fluid volume deficit, we need to assess following
parameters
– Urine Output (Hourly)
– CVP
– Blood pressure
– Urine sodium concentration

RATE OF FLUID REPLACEMENT
• Maintenance Phase
• Follow 4/2/1 Rule
• 4ml/kg/hr for first 10 kg
• 2ml/kg/hr for next 10 kg
• 1ml/kg/hr for rest of the body weight

SHOCK

Shock - Definition
• Shock is defined as a state of cellular
and tissue hypoxia due to reduced
oxygen delivery and/or increased oxygen
consumption or inadequate oxygen
utilization.
• This most commonly occurs when there is circulatory
failure manifested as hypotension (i.e., reduced tissue
perfusion).
• Shock is initially reversible, but must be recognized and
treated immediately to prevent progression to
irreversible organ dysfunction.

Causes
• Hemorrhage
• Burns
• Dehydration
• Myocardial Infarction
• Anaphylaxis
• Neurogenic Condition
• Sepsis
• Vascular insufficiency and cardiac dysfunction
• Obstructive condition
• Diarrhea and dysentery

Pathophysiology
Decreased tissue perfusion
Decreased Cardiac Output
Hemorrhage or other fluid loss causes
decreased intravascular space

Pathophysiology
Increased Blood Volume
ADH Released
Increased HR & Systemic Vascular
Resistance
Intracellular fluid shift to IVS
Compensatory mechanism are activated
Epinephrine & Nor-Epinephrine
Renin – Angiotensin Aldostreone
Stimulation

Pathophysiology
Decreased Cardiac output
Compensatory mechanism Fails
Increased Cardiac Output

Pathophysiology
MODS
Decreased perfusion of vital organ
Decreased BP

Stages of Shock:
1. Initial stage
2. Compensatory stage
3. Progressive stage
(Decompansatory Stage)
4. Refractory stage - Irreversible

Initial stage
Main activities in this stage are as follows
• Cells deprived of O2
• Mitochondria cannot produce ATP
• Anaerobic respiration
• Lactic acid builds up
• Metabolic acidosis
• Harmful to cells

Compensatory stage:
• Body’s physiological response to overcome shock
• Hyperventilation to correct acidosis
• Hypotension detected by baroreceptors in carotid
arch and aortic sinus
• Release of adrenaline & noradrenaline
• Vasoconstriction
• Increase BP & HR
• Vasoconstriction of skin, kidneys, GI tract & other
organs
• Increase Blood supply to the heart and brain
(selfish organs)
• Decrease blood to kidneys
• Oliguria

Progressive (Decompansating) stage
• Compensatory mechanism fails
• Decrease Perfusion of cells
• Anaerobic metabolism continues
• Metabolic acidosis
• Arteriolar and capillary sphincter constriction
• Pooling of blood in capillaries
• Increase in hydrostatic pressure
• Leakage of fluid and protein to surrounding
tissue
• Prolonged vasoconstriction
• Decrease perfusion
• vital organs compromised

Refractory stage (Irreversible stage)
• Vital organ failure
• Brain damage
• Cell death
• Death

Types of shock
1. Hypovolemic shock
2. Cardiogenic shock
3. Obstructive Shock
4. Distributive Shock
• Septic Shock
• Anaphylatic Shock
• Neuroenic Shock
5. Dissociative Shock

HYPOVOLEMIC SHOCK:
• A medical or surgical condition in
which rapid fluid loss results in
multiple organ failure due to
inadequate circulating volume
and subsequent inadequate
perfusion.

Etiology:
• Loss of blood (Hemorrhagic shock)
• External hemorrhage: Trauma
• Internal hemorrhage: Hematoma,
Hemothorax, Hemoperitoneum
• Exteriorisation of internal bleeding:
Hematemesis, Melena, Epistaxis,
Hemoptysis

Non- hemorrhagic:
• Digestive losses: Diarrhea, Vomiting,
Nasogastric suction
• Renal losses: Diabetes indipidus, Diuretic
overdose, Polyuric phase of acute renal
failure
• Skin losses: Profuse diaphoresis, Burns
• Third space losses: Ascites, Pleural
effusions, Edema, Intestinal obstruction,
Pancreatitis

GOALS OF MANAGEMENT:
• Maximize oxygen delivery - completed by
ensuring adequacy of ventilation, increasing
oxygen saturation of the blood, and
restoring blood flow
• Control further blood loss
• Fluid resuscitation

Maximizing oxygen delivery:
• ABCs
• Assess patency of airway
• Assess rate and depth of respiration
• Administer high-flow supplemental oxygen
or ventilatory support if needed
• Establish 2 large bore IV cannula 16 gauge
or a central line
• Elevate the foot end of the bed by 6-12
inches

Controlling further blood loss
• Determine the cause of bleeding
• Control external bleeding with direct
pressure, elevation of affected limb above
level of heart and applying tourniquet
• Internal bleeding may require surgical
intervention
• Blood transfusion
• H2 blockers : For GI bleeding
• Inj.Tranexamic acid 500mg or Etamsylate
500 mg IV

Fluid resuscitation
• Initial fluid resuscitation with an isotonic
crystalloid, such as lactated Ringer solution or
normal saline. An initial bolus of 1-2 L is given
in an adult (20 mL/kg in a pediatric patient)
over 15-30 minutes
• After initial therapy, colloids like albumin,
gelatins, dextran, or hydroxyethyl
starches are given
• In hemorrhagic shock and burns, transfuse
whole blood or plasma or plasma substitute
like dextran
• Avoid Hydroxyethyl starches (HES) in patients
with severe sepsis or risk of acute kidney injury

CARDIOGENIC SHOCK:
• Persistent hypotension
(systolic blood pressure <90
mm Hg, cardiac index <2.2
L/min/m2 )and tissue hypo
perfusion due to cardiac
dysfunction in the presence of
adequate left ventricular filling
pressure

ETIOLOGY:
• Systolic dysfunction:
• Myocardial infarction/ Ischemia
• Myocardial depressant drugs (eg: beta blockers,
calcium-channel blockers, and antiarrhythmics)
• Metabolic derangements (eg: acidosis,
hypophosphatemia, and hypocalcemia)
• Severe myocarditis
• Cardiomyopathy (Hypertrophic)
• Cardiotoxic drugs (eg: doxorubicin]
• Ventricular tachyarrhythmias
• Mechanical defect:
• Ventricular septal defect/rupture
• Mitral regurgitation

PATHOPHYSIOLOGY:

Clinical features
• Jugular venous distention
• Crackles in the lungs
• Third and fourth heart sounds may be present
• Narrowed pulse pressure
• Tachycardia
• Altered mental status
• Decreased urine output
• Cool skin and mottled extremities
• Peripheral edema
• Cyanosis

MANAGEMENT:
• ABCs
• Oxygen supplementation
• Treat arrhythmias
• Close hemodynamic monitoring: Insert Arterial
line, central venous(Swan-Ganz) catheter,
urinary catheter
• Perform ECG, ABG, serum electrolytes,
Troponin, CBC, Echocardiogram
• Fluid resuscitation to correct hypovolemia and
hypotension, unless pulmonary edema is
present
• Aspirin and heparin: In MI or acute coronary
syndrome (ACS)

OBSTRUCTIVE SHOCK:
• Reduced cardiac output
due to obstruction of
outflow of blood during
systole or obstruction of
ventricular filling during
diastole

ETIOLOGY:
• Obstruction in the outflow:
• Aortic stenosis
• Aortic outflow tract obstruction
• Coarctation of the aorta
• Pulmonary embolism
• Malignant hypertension
• Obstruction in ventricular filling
• Cardiac tamponade
• Constrictive pericarditis
• Tension pneumothorax
• Restrictive cardiomyopathy

Clinical features:
• Dyspnea, cough
• Chest pain
• Jugular venous distension
• Peripheral edema, Anasarca
• Decreased level of consciousness
• Cardiomegaly
• Hypotension
• Tachycardia
• Oliguria

Management:
• ABCs
• Relieve obstruction
• Needle thoracostomy for tension
pneumothorax
• Valvuloplasty for aortic stenosis
• Pericardiocentesis for cadiac tamponade
• Thrombolytic therapy for pulmonary
embolism

DISTRIBUTIVE SHOCK:
• Hypotension and tissue hypoperfusion due
to loss of peripheral vascular smooth
muscle tone resulting in excessive
vasodilation and peripheral pooling of
blood

ETIOLOGY:
• Sepsis (most common)
• Systemic Inflammatory Response
syndromes due to non-infectious conditions
such as pancreatitis, burns or trauma
• Toxic Shock Syndrome
• Anaphylaxis
• Adrenal insufficiency
• Reactions to drugs or toxins
• Hepatic insufficiency
• Neurogenic shock

Types:
• Neurogenic shock: Spinal cord injury, toxic
or drug effect, affecting the ability of
sympathetic nervous system to maintain
the vascular tone Vasodilation
• Anaphylactic shock: Generalised
anaphylactic reaction releases chemiacal
mediators from mast cells Peripheral
vasodilation and increased vascular
permeability
• Septic shock: Generalised inflammatory
reaction resulting from systemic infection
releases cytokines Vasodilation

Clinical features:
• Change in mental status
• Tachycardia, Tachypnea , Hypotension (SBP< 90
mmHg)
• Extremities: Frequently warm with bounding
pulses and increased pulse pressure in early
shock; Late shock may present as multi organ
dysfunction and cold and clammy skin,
cyanosis
• Hyperthermia: Core body temperature>38.30 C
or Hypothermia (Core body temperature<360C)
• Oliguria

Septic shock
• Symptoms of underlying infection:
• Pneumonia: Dullness to percussion,Rhonchi,
Crackles, Bronchial breath sounds
• Urinary tract infection: Costovertebral angle
tenderness, Suprapubic tenderness, Dysuria
and Polyuria
• Intra-abdominal infection or acute abdomen:
Focal or diffuse tenderness to palpation,
diminished or absent bowel sounds, Rebound
tenderness
• Gangrene or soft tissue infection: Pain, Skin
discolouration, Ulceration

Anaphylactic shock:
Symptoms of anaphylaxis:
• Respiratory distress
• Wheezing
• Urticarial rash
• Angioedema

Neurogenic Shock
• Hypotension
• Bradycardia
• Cool, moist, pale skin above spinal cord
injury
• Warm, dry, flushed skin below spinal cord
injury
• Loss of motor and sensory function below
the level of injury
• Bowel and bladder areflexia

Management:
• MONITORING:
• Vital signs
• Fluid intake and output, Daily weights
• Adequate intravascular access, Urinary
catheter
• Oxygen or mechanical ventilation
• EARLY FLUID RESUSCITATION:
• Using crystalloids or colloids for first 6
hours

Management:
• VASOPRESSORS
• Norepinephrine 0.02-0.25 mcg/kg/min or
Dopamine >10 mcg/kg/mt: First line
treatment
• If fails to increase MAP >60 mm Hg or if
excessive tachycardia or tachyarrhythmias
present with dopamine ,phenylephrine
(0.2-2.5 mcg/kg/min) or vasopressin (0.10-
0.40 U/min) or epinephrine 0.06-0.4
mcg/kg/min may be added to or
substituted for dopamine

Antimicrobial Treatment
(For septic shock)
• Blood and urine cultures : Prior to empiric antibiotic
therapy
• At least 2 blood cultures : Percutaneously as well as
from any vascular access site.
• Cultures from suspected site of infection
• Because initial therapy must be empiric, antimicrobial
coverage should be broad spectrum (duration 7-10 days
usually)
• Avoid antibiotics recently received by the patient.
• Antifungals if fungal infection suspected
• Removal of devices such as intravenous or urinary
catheters and prostheses.
• Surgical drainage or debridement in intra-abdominal
abscess or necrotizing fasciitis

MANAGEMENT OF ANAPHYLACTIC
SHOCK
• Epinephrine :
• 0.2-0.5 mL subcutaneous of 1:1000 every
20 minutes as needed
• Continuous infusion of 30-60 mL/h of
1:10,000 dilution in severe reaction
• Diphenhydramine :
• 50-80 mg IM or IV for urticaria or
angioedema
• Inhaled bronchodilators or intravenous
steroids can be administered for
bronchospasm

MANAGEMENT OF NEUROGENIC
SHOCK:
• ABCs
• Airway control with spinal immobilization
• Crystalloid IV fluids to maintain a mean
arterial blood pressure above 70mmHg.
• If hypotension persists, Norepinephrine
0.02-0.25 mcg/kg/min, phenylephrine (0.2-
2.5 mcg/kg/min)
• Epinephrine 0.06-0.4 mcg/kg/min in
refractory hypotension

MANAGEMENT OF NEUROGENIC
SHOCK
• Severe bradycardia :Atropine 0.5 to 1.0 mg
IV (every 5 min for a total dose of 3.0 mg)
or with a pacemaker.
• Neurologic deficits: High-dose
methylprednisolone therapy within 8 h of
injury.
• 30 mg/kg bolus over 15 min followed by a
continuous infusion of 5.4 mg/kg per h for
the next 23 h.
• Trauma surgery, neurosurgery, and
orthopedic consultation

DISSOCIATIVE SHOCK
• Inability of hemoglobin molecule to give up
the oxygen to tissues
• Tissue perfusion is adequate but oxygen
release to tissue is abnormal

Etiology:
• Carbon monoxide poisoning
• Methemoglobinemia
• Dyshemoglobinemias
• Cyanide poisoning
• Severe anaemia

Management of dissociative shock
• Early recognition and treatment of cause is the
main therapy
• 100% oxygen therapy until the patient is
asymptomatic and HbCO levels are below 10%
• Hyperbaric oxygen therapy for patients with HbCO
levels > 40% or cardiovascular or neurologic
impairment
• Serial neurologic examinations, including
funduscopy, CT scans to detect cerebral edema.
• Sodium thiosulfate 12.5 g intravenously for
combined intoxications of cyanide and CO to
prevent the leftward shift.
• Evaluate acid-base status

Nursing management:
• Ineffective tissue perfusion related to
decreased stroke volume as evidenced by cool,
clammy skin, pale color
• Assess for signs of decreased tissue perfusion such
as pallor, cyanosis, cool or clammy skin
• Monitor vital signs, assess capillary refill,
skin color / mucous membranes, nails
• Assess the client’s ECG for dysrhythmias
• Assess the central and peripheral pulses
• Use pulse oximetry to monitor oxygen saturation
and pulse rate and arterial blood gases
• Provide oxygen therapy if indicated.
• Administer IV fluids, blood, blood products and
ionotropes as ordered.

Nursing management:
• Decreased cardiac output related to alterations in heart
rate and rhythm as evidenced by change in level of
consciousness, Decreased blood pressure
• Assess the client’s HR and BP, including peripheral
pulses.
• Assess the client’s ECG for dysrhythmias.
• Assess for any changes in the level of consciousness
• Monitor the client’s central venous pressure (CVP),
pulmonary artery diastolic pressure (PADP), pulmonary
capillary wedge pressure, and cardiac output/cardiac
index.
• Provide electrolyte replacement as prescribed.
• If the client’s condition progressively deteriorates,
initiate cardiopulmonary resuscitation or other
lifesaving measures according to Advanced Cardiac Life
Support guidelines, as indicated.

Nursing management:
• Fluid volume deficit related to blood loss, diarrhea,
diuresis or abnormal drainage as evidenced by
decreased skin turgor, dizziness, dry mucous
membranes, increased thirst, narrowing of pulse
pressure, tachycardia
• Assess the client’s HR, BP, and pulse pressure
• Monitor BP for orthostatic changes
• Monitor for possible sources of fluid loss
• Assess the client’s skin turgor and mucous membranes
for signs of dehydration
• Monitor the client’s intake and output
• Initiate IV therapy. Start two shorter, large-bore
peripheral IV lines.
• Control the external source of bleeding by applying
direct pressure to the bleeding site.

Nursing management:
• Impaired gas exchange related to interference
with oxygen delivery
• Assess respiratory rate, depth, and effort, including
use of accessory muscles, nasal flaring, and
abnormal breathing patterns.
• Observe for nail beds, cyanosis in skin; especially
note color of tongue and oral mucous membranes
• Monitor patient’s behavior and mental status for
onset of restlessness, agitation, confusion, and (in
the late stages) extreme lethargy
• Monitor oxygen saturation continuously, using
pulse oximeter.
• Administer oxygen to maintain oxygen saturation
at 90% or greater.

Nursing management:
• Anxiety related to change in health status as
evidenced by apprehension
• Assess the client’s level of anxiety
• Assess previous coping mechanism used
• Encourage the client to verbalized his or her
feelings.
• Reduce unnecessary external stimuli by
maintaining a quite environment.
• Explain all procedures as appropriate
• Maintain a confident, assured manner while
interacting with the client.
• Assure the client and significant others of close,
continuous monitoring that will ensure prompt
intervention

Nursing management:
• Other Nursing Diagnoses includes
• Ineffective breathing pattern R/T
inadequate oxygenation
• Impaired skin integrity R/T edema
• Altered Nutrition less than body
requirement R/T anorexia

Conclusion
• Shock can present as a consequence of
multiple causes & affect the body at
cellular, visceral & systemic levels.
• Regardless of source, the fundamental
primary treatment of shock remains
recognition & prompt fluid replacement.
• The search for the underlying cause of the
shock is only initiated after stabilization

UNCONSCIOUSNESS

Introduction
• Consciousness is defined as the state of
awareness of self and the environment.
• Another way of describing it is a condition
for which a person is capable of perceiving
stimuli from the environment and
responding appropriately.
• It has three important aspects i.e;
wakefulness, awareness of self, awareness
of environment and time.

REVIEW OF ANATOMY & PHYSIOLOGY

• RAS (Reticular Activating System)

Reticular activating system
• The reticular activating system, or RAS, is a
piece of the brain that starts close to the top
of the spinal column and extends upwards
around two inches.
• It has a diameter slightly larger than a pencil.
• All of your senses are wired directly to this
bundle of neurons that's about the size of
your little finger.
• Often, the RAS is compared to a filter or a
nightclub bouncer that works for your brain.

Reticular activating system
• While it may be a fairly small part of your
brain, the RAS has a very important role: it's
the gatekeeper of information that is let
into the conscious mind.
• It makes sure your brain doesn't have to
deal with more information than it can
handle. Thus, the reticular activating
system plays a big role in the sensory
information you perceive daily.

Unconsciousness - Definition
• Unconsciousness is a condition in which the
patient is unresponsive and unaware of
environmental stimuli.
• It is an abnormal state where the client is
unarousable and unresponsive. Coma is a
deepest state of unconsciousness.
• Unconsciousness is a symptom rather than a
disease.
• Degrees of unconsciousness that vary in length
and severity. If it is brief it’s called fainting and
its Prolonged called as deep coma

Etiology
Classification I
• Structural or Surgical Unconsciousness
– Trauma
– Epidural / Subdural hematoma
– Brain contusion
– Hydrocephalus
– Stroke
– Tumor
• Metabolic or Medical Unconsciousness
– Infection
– Meningitis
– Encephalitis
– Hypo/hyperglycemia
– Heptic encephalopathy
– Hyponatremia
– Drug /alcohol overdose
– Poisoning /intoxication

Etiology
Classification II
• Intra cranial causes
• Head Trauma
• SAH.
• Cerebral infarction
• Intra cranial Neoplasm.
• CNS infection.
• Epilepsy
•

Etiology
Classification II
• Extra Cranial Causes
• Metabolic causes: Hepatic failure, uraemia,
hypoglycaemia/ hyperglycaemia.
• Respiratory insufficiency: Hypoventilation, anaemia,
hypoxia, hypercapnia.
• Decreased cardiac output: MI, cardiacarrthymia, blood
loss.
• Endocrine causes: Diabetes-hyperglycaemia,
hypopituitarism, adrenal crisis,
hypo/hyperparathyroidism, and hypothyroidism.
• Drug abuse (drug poisoning): Sedatives, hypnotics,
anti- depressants, anticonvulsants, anaesthetic agents.
• Toxins: Alcohol, carbon monoxide
• Psychogenic causes: Hysteria (Psychoneurosis.)

Pathophysoiology
UNCONSCIOUSNESS
Blocks the signal to the RAS (Reticular activating system)
Diffused damage to the cerebral tissues
Increased ICP
Inflammation, edema and hemorrhage
Damage to the brain and skull

Clinical Manifestations
• Respiratory system – Stridor, rales, rhonchi,
progressive cyanosis, cheyne stokes
respiration, asymmetrical chest wall
movements, decreased respiratory rate,
decreased depth.
• Cardiovascular system – bradycardia,
hypotension, ventricular tachycardia, atrial
fibrillation, hyperkalemia, arrhythmias,
decreased cardiac output.

Clinical Manifestations
• Neurological system – Asterexis, myoclonus
seizures, cranial nerve palsies, lethargy, and
unequal pupillary dilation, absent deep
tendon reflexes, absent doll’s eye reflex.
• Gastrointestinal system - Due to the
disruption of CN -10th (vagus) function,
abdominal distension, decreased bowel
sounds, constipation, ascites,
hyperlipidemia.
• Urinary system - Urinary incontinence, high
creatinine index, oliguria, ketonuria, urinary
tract infections, pyuria.

Effects of Altered LOC or Coma:
• Full recovery with no Long term residual
effects
• Recovery with residual damage (learning
deficits, emotional difficulties, impaired
judgment)
• Persistent vegetative state (cerebral death
or brain death)

How to approach an unconscious client
• Assess the level of responsiveness

Maintain respect for the patient & demonstrate care
while performing these maneuvers.

GCS Score Classification
• BEST RESPONSE - 15/15
• GCS ≤ 8 – SEVERE BRAIN INJURY
• GCS 9 – 12 - MODERATE BRAIN INJURY
• GCS ≥ 13 – MILD BRAIN INJURY
• TOTALLY UNRESPONSIVE- 3/15

Immediate management
1. Manage airway & cervical spine
• Note presence of vomitus in mouth.
• Look for evidence of upper airway obstruction (e.g.
Stridor).
• Check for gag reflex.
• Check whether patient’s decreased LOC is
profound enough to require active airway control
such as ET intubation.
• Rule out any cervical spine injury. If injury is
present take precaution to protect the cervical
spine.
• Any trauma with GCS <8 with signs of increased ICP
requires active airway management.
• Agents that may increase the ICP must be avoided.

2. Breathing
• After securing the airway, breathing is
assessed
• In case patient is spontaneously breathing,
then pattern of breathing can be the clue of
the problem.
• Apnea, bradycardia can be seen in c/o drug
overdose
• Kussumaul pattern of respiration is
classically seen in diabetic ketoacidosis.

• Cheyne-stokes respiration is
often seen in CHF, raised ICP,
brain injury
• Apneustic breathing seen in
patients with pontine lesion
• Biot’sbreathing is associated
with meningitis.
• Agonal breathing are seen just
before death 114mathewvmaths@yahoo.co.in

Note the respiratory pattern and smell
of the breath
• Smell the breath for sweet acetone for
diabetic ketoacidosis or odor of alcohol.
• These two smell can be similar so to be sure
check serum glucose level also and breath
analyzer for alcohol.
• Uriniferous odour can be present in uremic
coma.
• Musty smell can be present in hepatic
coma.

3.Circulation
• To assess circulation, evaluate pulses &
capillary refill time.
• Another team member can simultaneously
assess other vital signs.
• Establish IV line.
• Attach patient to cardiac monitor.
• Withdraw blood for lab analysis.
• Notify any abnormality in circulation and
continue the workup.

DON’T
• In patients with h/o alcoholism or those who
appear malnourished, inj. Thiamine 100 mg IV
should be administered. This treatment my
reverse an acute Wernicke syndrome.
• If the patient shows one or more of the
following criteria: pinpoint pupil, respiration <
12 or suspicion of narcotic use administration
of naloxone 2mg should be considered.
• So four vital interventions are important as “
DON’T forget these- Dextrose, Oxygen,
Naloxone, Thiamine

History
• It is difficult to obtain accurate history from patients
with altered mental status.
• Interrogate the attendants, paramedics from the
ambulance, patient’s private physician.
• Check patient’s pocket, wallet, and previous records for
information.
• Inquire about medication use & allergy & drug or
alcohol abuse.
• Ask about medical history – DM, metabolic or
endocrine, kidney, neurological, seizures, cancer, and
psychiatric disorders.
• Ask if patient has been recently ill or previous infection,
headaches or other pain.
• Ask for suicidal thoughts or transient neurological
complaints.

Physical examination
• Check vital sign
• Examine the eyes and head
Fundoscopy-increased ICP - Papilledema
Assessment of pupillary reactions
• For patients in coma or whose cervical
spine is not injured, oculocephalogyric
(or Doll’s eye) maneuver can be
tested.

Doll’s eye
• It is based on the vestibulo ocular reflex which
helps to stabilize our eyes.
• In order to test for Doll’s eye reflex, the head is
elevated about 30 degrees and is rapidly
rotated from side to side with eyes kept open.
• In a positive / normal doll’s eye reflex, the eyes
move in the direction opposite to that of the
head movement.
• A negative response is said to occur if the eyes
move in the direction of the head movement.
• A negative doll’s eye reflex signifies severe
brain damage or brain death.

In c/o cervical injury, we can do cold
caloric test.
• Caloric reflex test (sometimes termed 'vestibular caloric
stimulation') is a test of the vestibulo-ocular reflex that
involves irrigating cold or warm water or air into
the external auditory canal.
• Ice cold or warm water is irrigated into the external
auditory canal, usually using a syringe.
• The temperature difference between the body and the
injected water creates a convective current in
the endolymph of the nearby horizontal semicircular
canal.
• Hot and cold water produce currents in opposite
directions and therefore a horizontal nystagmus in
opposite directions in patients with an intact brainstem:
• Absent reactive eye movement suggests vestibular
weakness of the horizontal semicircular canal of the
side being stimulated

COWS: Cold Opposite, Warm Same.
• Cold water = FAST phase of nystagmus to the
side Opposite from the cold water filled ear
Warm water = FAST phase of nystagmus to
the Same side as the warm water filled ear
• Look for raccoon’s eye
• Raccoon eye/eyes (also known in the United
Kingdom and Ireland as panda eyes) or
periorbital ecchymosis is a sign of basal skull
fracture or subgaleal hematoma, a craniotomy
that ruptured the meninges, or (rarely) certain
cancers.

Raccoon’s eye

Examine the ear
• Look for battle sign.
• Battle's sign, also mastoid ecchymosis, is an
indication of fracture of middle cranial fossa
of the skull, and may suggest underlying
brain trauma.

Examine the skin
• Cyanosis can be seen in hypoxia.
• Bullous lesion of barbiturate intoxication
• Cherry-red spot in c/o CO poisoning
• Puffy face→ myxoedema
• ↑sweating→ hypoglycemia, shock
• Dry skin→ diabetic ketosis, uremia
• ↓Skin turgor →dehydration
• Watch for any injection marks to rule out
drug addiction.

• Perform neurological examination
• Diagnostic Tests
• Blood tests
• Urinalysis
• ABG analysis
• Toxicology test to screen drug abuse
• ECG
• Chest X ray ,skull X ray
• CT scan
• MRI.
• PET - if available
• EEG

Surgical Management
• Hematomas – Surgical evacuation
• Hemorrhage ,tumor, cerebral abscess-
Surgical decompression/ Partial or total
resection
• Cerebral aneurysm - surgically clipping or
endovascular coiling

Nursing Management
• Nursing diagnosis:
• Ineffective airway clearance
• Ineffective cerebral tissue perfusion
• Risk for increased ICP
• Imbalanced fluid volume
• Impaired skin integrity
• Self care deficit
• Imbalanced nutrition
• Incontinence : bowel and /or bladder
• Risk for aspiration
• Risk for contractures
• Altered family process

CONCLUSION
• An unconscious patient is fully dependent
on others for recovery so it is our
responsibility to always think critically
before intervening.
• The more the knowledge we have the
greater the difference we can make to life
of unconscious patients.

DISCUSSION TIME

References
• Dave S, Cho JJ. Shock, Neurogenic. In: StatPearls [Internet].
Treasure Island (FL): StatPearls Publishing; 2018 [cited 2018
Mar 18]. Available from:
http://www.ncbi.nlm.nih.gov/books/NBK45936
• Hypovolemic Shock: Background, Pathophysiology [Internet].
[cited 2018 Apr 2]. Available from:
https://emedicine.medscape.com/article/760145-overview
• Carbon Monoxide Toxicity Treatment & Management:
Prehospital Care, Emergency Department Care, Hyperbaric
Oxygen Therapy [Internet]. [cited 2018 Apr 2]. Available
from: https://emedicine.medscape.com/article/819987-
treatment
• Hemorrhagic Shock in Emergency Medicine: Background,
Pathophysiology, Epidemiology. 2017 Jan 7 [cited 2018 Apr
2]; Available from:
https://emedicine.medscape.com/article/827930-overview
• http://a.umed.pl/anestezja/dokumenty/shock.pdf.

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