PRESENTED BY

NITHISH REDDY
CONTENTS
• DEFINITION
• CLASSIFICATION
• PATHOPHYSIOLOGY
• CAUSES
• HEMATOLOGICAL INVESTIGATIONS
• SHOCK IN ORAL AND MAXILLOFACIAL SURGERY
DEFINITION

Shock is the clinical condition of organ

dysfunction resulting from an imbalance
between cellular oxygen supply and demand
CLASSIFICATION
HINSHAW AND COX 1972
• DISTRIBUTIVE
• CARDIOGENIC
• OBSTRUCTIVE
• HYPOVOLEMIC
ALSO CLASSIFIED INTO
 VASOCONSTRICTIVE
 TRAUMA,BLEEDING,BURNING,ILEUS
 PULMONARY EMBOLISM(impaired cardiac filling)
 MYOCARDIAL INFARCTION
 VASODILATIVE
 ANAPHYLAXIS,SEPSIS
 SPINAL MEDULLARY INJURY
 HYPOTHERMIA
CLASSIFICATION
• DISTRIBUTIVE
o SEPTIC SHOCK
o PANCREATITIS
o ANAPHYLACTIC SHOCK
o NEUROGENIC SHOCK
o ENDOCRINE SHOCK
o ADRENAL CRISIS
• CARDIOGENIC
o MYOCARDIAL INFARCTION
o MYOCARDITIS
o ARRHYTHMIA
o VALVULAR
• OBSTRUCTIVE
o Tension pneumothorax
o Cardiac tamponade
o Restrictive pericarditis
o Pulmonary embolism
o Aortic dissection
• Hypovolemic
o Hemorrhagic
o GI losses
o Burns
o Polyuria
• i. Diabetic ketoacidosis
• ii. Diabetes insipidus
PATHOPHYSIOLOGY
• The cellular oxygen imbalance of shock is most commonly related to
impaired oxygen delivery in the setting of circulatory failure.
• Shock can also develop during states of increased oxygen consumption or
impaired oxygen utilization
• In the setting of insufficient oxygen supply, the cell is no longer able to
support aerobic metabolism.
• With adequate oxygen, the cell metabolizes glucose to pyruvate, which then
enters the mitochondria where ATP is generated via oxidative
phosphorylation. Without sufficient oxygen supply, the cell is forced into
anaerobic metabolism, in which pyruvate is metabolized to lactate with
much less ATP generation (per mole of glucose).
• Maintenance of the homeostatic environment of the cell is dependent on an
adequate supply of ATP. ATP-dependent ion pumping systems, such as the
Na+/K+ ATPase, consume 20–80% of the cell’s energy.
• Inadequate oxygen delivery and subsequent decreased ATP disrupt the cell’s
ability to maintain osmotic, ionic, and intracellular pH homeostasis.
• Influx of calcium can lead to activation of calcium-dependent phospholipases
and proteases, causing cellular swelling and death.
• In addition to direct cell death, cellular hypoxia can cause damage at the
organ system level via leakage of the intracellular contents into the
extracellular space activating inflammatory cascades and altering the
microvascular circulation
 STAGES OF SHOCK
• There are four stages of shock
INITIAL
COMPENSATORY
PROGRESSIVE
REFRACTORY

Taha M, Elbaih A. Pathophysiology and management of

different types of shock. Narayana Med J. 2017;6:14-39.
HEMODYNAMIC CHARACTERISTICS OF DIFFERENT
TYPES OF SHOCK
TYPE OF SHOCK CVP PCWP CARDIAC SYSTEMIC VASCULAR
RESISTANCE
OUTPUT
Distributive ↓ ↓ ↑ ↓

Cardiogenic ↑ ↑ ↓ ↑

Obstructive ↑ ↓↑ ↓ ↑

Hypovolemic ↓ ↓ ↓ ↑

CVP- central venous pressure , PCWP - pulmonary capillary wedge pressure

Central venous pressure is the blood pressure in the venae cavae, near the right atrium of
the heart. CVP reflects the amount of blood returning to the heart and the ability of the heart to
pump the blood back into the arterial system
Pulmonary capillary wedge pressure provides an indirect estimate of left atrial pressure
INITIAL PHASE
• During this stage, the state of hypoperfusion causes hypoxia.
• Due to the lack of oxygen, the cells perform lactic acid fermentation.
Since oxygen, the terminal electron acceptor in the electron transport
chain, is not abundant, this slows down entry of pyruvate into the
Krebs cycle, resulting in its accumulation.
• Accumulating pyruvate is converted to lactate by lactate
dehydrogenase and hence lactate accumulates
COMPENSATORY PHASE
• This stage is characterised by the body employing physiological
mechanisms, including neural, hormonal and bio-chemical
mechanisms in an attempt to reverse the condition.
• As a result of the acidosis, the person will begin to hyperventilate in
order to rid the body of carbon dioxide (CO2)
• In this phase the body is experiencing a state of low blood volume but
is still able to maintain low blood pressure and organ perfusion by
increasing heart rate and constricting blood vessels
symptoms:
Agitation restless and anxiety
Altered mental status ,tachycardia or tachypnoea
Weak ,thready or absent pulse
PROGRESSIVE PHASE
• Shock will enter into progressive phase as the compensatory mechanism fails
• Due to the decreased perfusion of the cells, sodium ions build up within while
potassium ions leak out.
• As anaerobic metabolism continues, increasing the body's metabolic acidosis,
the arteriolar smooth muscle and precapillary sphincters relax such that blood
remains in the capillaries.
• Due to this, the hydrostatic pressure will increase and, combined with
histamine release, this will lead to leakage of fluid and protein into the
surrounding tissues.
• As this fluid is lost, the blood concentration and viscosity increase, causing
sludging of the microcirculation. The prolonged vasoconstriction will also
cause the vital organs to be compromised due to reduced perfusion.
• If the bowel becomes sufficiently ischemic, bacteria may enter the blood
stream, resulting in the increased complication of endotoxic shock.
REFRACTORY OR IRREVERSIBLE
• At this stage, the vital organs have failed and the shock can no longer be
reversed.
• . Brain damage and cell death are occurring, and death will occur
imminently.
• One of the primary reasons that shock is irreversible at this point is that
much cellular ATP has been degraded into adenosine in the absence of
oxygen as an electron receptor in the mitochondrial matrix.
• Adenosine easily perfuses out of cellular membranes into extracellular
fluid, furthering capillary vasodilation, and then is transformed into uric
acid.
• Because cells can only produce adenosine at a rate of about 2% of the
cell's total need per hour, even restoring oxygen is futile at this point
because there is no adenosine to phosphorylate into ATP.
 DETERMINANTS OF OXYGEN DELIVERY
• Disease processes affecting any of the components of oxygen delivery have the
potential to lead to the development of shock.
• Disturbances to key determinants of oxygen delivery form the basis of
SHOCK ,They are
o Cardiac output
o Arterial oxygen content
• The two components of CARDIAC OUTPUT are
o Heart rate
o Stroke volume
• The determinants of STROKE VOLUME are
o Preload
o Systemic vascular resistance
o contractility
DISTRIBUTIVE SHOCK
• Distributive shock is the condition of reduced oxygen delivery where
the primary physiologic disturbance is a reduction in Systemic
vascular resistance
The most common cause of distributive shock is sepsis
• Sepsis has recently been redefined as the dysregulated host response
to infection resulting in life-threatening organ dysfunction mainly
gram negative septicaemia
• When this process is accompanied by persistent hypotension
requiring vasopressor support, it is classified as septic shock.
• In early cases of septic shock cardiac output increases ,but vascular
resistance decreases due to dilated cutaneous arteriovenous shunts
• In late stages vascular permeability increases so that blood volume decreases
leading to hypovolaemia
• In further advanced cases the cardiac function is damaged due to toxins liberated
by the organisms
CLINICAL FEATURES
EARLY WARM SHOCK- Increased pulse rate, decreased systemic arterial pressure
associated with intermittent spikes of fever alternating with bouts of cold
LATE COLD SHOCK – Reduced left heart filling and cardiac output with an existing
septic focus
ANAPHYLACTIC SHOCK
• Anaphylactic shock results from a cardiovascular
collapse due to severe vasodilation, increased
capillary permeability and loss of plasma from the
circulation into the body tissues.
• Vasodilation and capillary permeability is a direct
result of the released chemicals due to the
anaphylactic or anaphylactoid reaction.
• With such vasodilation occurring throughout the
body, the normal redistribution mechanism
collapses and the balance between the capacity of
circulation and total blood volume is disrupted, less
blood returns to the heart and the cardiac output is
reduced.
• A fall in the arterial blood pressure is a natural
consequence of the reduced cardiac output
• Anaphylaxis is predominantly an IgE-mediated
allergic reaction that can rapidly develop after
exposure to an allergen (food, medication, or insect
bite), in which there is a profound distributive type
of shock possibly mediated through histamine
release
• Anaphylaxis is a severe, life-threatening,
generalized or systemic hypersensitivity reaction.
Characterized by rapidly developing lifethreatening
airway and or breathing and or circulation problems
usually associated with skin and mucosal changes.
• Other processes that manifest as cellular hypoxia
related to a primary reduction of Systemic vascular
resistance include pancreatitis, severe burns, and
liver failure.

skin and mucosal changes with

anaphylaxis
Neurogenic shock
• Neurogenic shock is defined as the injury to the spinal cord with associated
autonomic dysregulation.
• Association and the International Spinal Cord Society proposed the definition of a
neurogenic shock to be general autonomic nervous system dysfunction that also
includes symptoms such as orthostatic hypotension, autonomic dysreflexia,
temperature dysregulation.
• This dysregulation is due to a loss of sympathetic tone and an unopposed
parasympathetic response. Consequently, patients suffer from instability in blood
pressure, heart rate, and temperature regulation.
• Neurogenic shock is most commonly a consequence of traumatic spinal cord
injuries.
• Bradyarrhythmia, hypotension, flushed warm skin are the classic signs associated
with neurogenic shock.
Taylor MP, Wrenn P, O'Donnell AD. Presentation of neurogenic shock within the emergency
department. Emerg Med J. 2017 Mar;34(3):157-162.
Endocrine shock
• ENDOCRINE AND METABOLIC CAUSES OF SHOCK
• Adrenal insufficiency
• Hypothyroidism-reduces cardiac output and can lead to hypotension
and respiratory insufficiency
• Thyrotoxicois-may induce reversible cardiomyopathy
• Diabetic ketoacidosis
• Severe acidosis/ alkalosis and electrolyte disturbances (e.g.
hypocalcemia)
• Adrenal insufficiency has been observed in 30% to 70 % of septic shock
cases
• The clinical diagnosis of adrenal insufficiency lacks specificity during septic
shock.
• Observed symptoms include fever, abdominal pain, persistent
hypotension, vomiting, and altered consciousness.
• Thyroid storm may be the initial presentation of thyrotoxicosis in
undiagnosed children, particularly in neonates.
• The clinical presentation includes fever, tachycardia, hypertension, and
neurological and GI abnormalities. Hypertension may be followed by 
congestive heart failure that is associated with hypotension and shock
Adrenal Insufficiency in Septic Shock Virginie Maxime, MDa , Olivier Lesur, MD, PhDb , Djillali
Annane, MD, PhD
Thyroid Storm
•Author: Madhusmita Misra, MD, MPH; Chief Editor: Robert P Hoffman, MD
CARDIOGENIC SHOCK

• Cardiogenic shock is characterized by reduced oxygen delivery related

to a reduction in Cardiac output owing to a primary cardiac problem
• In cardiogenic shock, the Stroke volume may be reduced by processes
that affect
• Myocardial contractility -Myocardial infarction
Ischemic cardiomyopathies
Primary myocarditis
• Mechanical valvular disease -Acute mitral insufficiency
Aortic insufficiency.
• CS is a low cardiac output state resulting in life-threatening end-organ
hypoperfusion and hypoxia
PATHOPHYSIOLOGY
• The primary insult is a reduction in myocardial contractility resulting in
diminished cardiac output, hypotension, systemic vasoconstriction, and cardiac
ischemia.
• The hallmark is peripheral vasoconstriction and vital end‐organ damage, which
stems from ineffective stroke volume and insufficient circulatory
compensation.
• Compensatory peripheral vasoconstriction may initially improve coronary and
peripheral perfusion, however it contributes to increased cardiac afterload that
overburdens damaged myocardium.
• This results in diminished oxygenated blood flow to peripheral tissue and,
ultimately, the heart.
Vahdatpour C, Collins D, Goldberg S. Cardiogenic shock. Journal of the
American Heart Association. 2019 Apr 16;8(8):e011991.
CLINICAL FINDINGS

• The clinical presentation is typically characterized by persistent

hypotension (<90 mmHg systolic blood pressure[BP]) unresponsive to
volume replacement and is accompanied by clinical features of
peripheral hypoperfusion, such as elevated arterial lactate
• Most patients initially are dyspneic, appear pale, apprehensive, and
diaphoretic, and mental status may be altered.
• The pulse is typically weak and rapid or occasionally severe
bradycardia due to high-grade heart block may be present.
OBSTRUCTIVE SHOCK
• Obstructive shock is also characterized by a reduction in oxygen
delivery related to reduced CARDIAC OUTPUT, but in this case the
etiology of the reduced CARDIAC OUTPUT is an extracardiac processes
impairing blood flow.
• Processes that can impede venous return to the heart and reduce
CARDIAC OUTPUT include tension pneumothorax (PTX), cardiac
tamponade, and restrictive pericarditis.
• Similarly processes that obstruct cardiac outflow, such as
Pulmonary embolism (right heart)
Aortic dissection (left heart)
HYPOVOLEMIC SHOCK
• This is the most common type of shock and is caused by insufficient
circulating volume.
• Its primary cause is hemorrhage (internal and/or external), or loss of
fluid from the circulation.
• Vomiting and diarrhea are the most common cause in children.
• With other causes including burns, environmental exposure and
excess urine loss due to diabetic ketoacidosis and diabetes insipidus
DIAGNOSIS
• SWAN-GANZ CATHETER-This catheter is used to get valuable
information about the precise diagnosis and circulatory derangements
of shock
Flow in the cardiovascular system
Accurate measurement of blood gases in mixed venous blood
Filling pressure of both right and left sides
COMPENSATORY MECHANISMS
CVP – CENTRAL VENOUS PRESSURE
CO – CARDIAC OUTPUT
SVR – SYSTEMIC VASCULAR
RESISTANCE
CRUSH SYNDROME
• IT is a symptom complex in which a portion of ther body becomes
crushed due to a heavy weight falling on that portion of body
• This type is seen in injury due to earthquakes ,mine injuries, air raids,
use of torniquet for longer period
• In this syndrome ,oligaemic shock occurs due to extravasation of
blood into the muscles in the affected portion of the body
• As it is confined within a tough deep fascia in the inferior extremity
and superior extremity, tension develops within the fascia which
endangers circulation and causes ischaemic damage
SHOCK IN ORAL AND
MAXILLOFACIAL SURGERY
Stevens described three phases of STSS: phase
I, which involves an influenza-like prodrome
followed by hypotension; phase II, which
involves tachycardia, tachypnea, increasing
pain, and persistent fever; and phase III, which
involves sudden shock, organ failure, and gross
cutaneous necrosis
Case report A 64-year-old white female presented to an
outside hospital (OSH) with the chief complaint of right-sided
facial pain, palsy, and anesthesia following a ground-level
mechanical fall with impact to the right side of her face. She
was diagnosed with a minimally displaced lateral orbital wall
fracture and instructed to follow up with the surgeon on call.
Her past medical history was significant for hypertension,
hypothyroidism, diabetes mellitus, Sjo¨gren’s syndrome, and
fibromyalgia, and she had a history of smoking. Forty-eight
hours after her initial presentation, she went to her primary
care provider complaining of insomnia due to increasing pain
and swelling, nausea, vomiting, and diarrhea, in addition to
palsy and loss of sensation of the right face. Based upon her
symptoms, she was sent to the emergency department of a
second OSH and was evaluated for a stroke versus facial nerve
palsy.
HEMORRHAGIC SHOCK
IN A CASE OF
FRACTURED ZYGOMA
THANK YOU