1

SHOCK

DR MEGHA S
1ST YEAR POST GRADUATE
DEPARTMENT OF PUBLIC HEALTH DENTISTRY
CONTENTS 2

 INTRODUCTION
 HISTORY
 CLASSIFICATION
 STAGES OF SHOCK
 PATHOPHYSIOLOGY
 DIAGNOSIS
 MANAGEMENT
 DENTAL CONSIDERATIONS
 CONCLUSION
 REFERENCES
INTRODUCTION 3

 Shock is a life-threatening medical condition as a result of insufficient blood flow

throughout the body.

 often accompanies severe injury or illness.

 can lead to other conditions such as lack of oxygen in the body's tissues

(Hypoxia), Heart attack (Cardiac arrest) or organ damage.

 HISTORICAL ASPECTS 4

 Hippocrates described a ‘‘posttraumatic syndrome’’

 The word shock is derived from the French word choquer, meaning ‘‘to collide with.’’

 The term choc was first used by a French surgeon, Le Dran,

 Fisher suggested ‘‘vasomotor paralysis’’ By the late 1800s

 Maphoter, suggested extravascular leakage of fluids

 a toxic factor was released during shock leading to altered capillary permeability and loss
of blood volume from the intravascular space (1900s Cannon)
CLASSIFICATION 5
ACCORDING TO ETIOLOGY 6

 Septic shock
 Anaphylactic shock
 Cardiogenic shock
 Hypovolemic shock
 Neurogenic shock
STAGES OF SHOCK 7

 Initial
Hypoxia
The cells perform lactic acid fermentation
Slows down entry of pyruvate into the Krebs cycle, resulting in its accumulation.
Pyruvate is converted to lactate by lactate dehydrogenase and hence lactate
accumulates
Lactic acidosis
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Compensatory

 Characterized by the body employing physiological mechanisms

 Neural, hormonal and bio-chemical mechanisms in an attempt to reverse the
condition.
 Hyperventilation in order to rid the body of carbon dioxide
 Attempting to raise the pH of the blood
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 release of epinephrine and norepinephrine

 results in an increase in blood pressure.
 The renin-angiotensin axis is activated, and arginine vasopressin (Anti-diuretic
hormone; ADH) is released to conserve fluid via the kidneys
 vasoconstriction of the kidneys, gastrointestinal tract, and other organs
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 Progressive

 the cause of the crisis not be successfully treated

 compensatory mechanisms begin to fail
 arteriolar smooth muscle and precapillary sphincters relax
 hydrostatic pressure will increase
 lead to leakage of fluid and protein into the surrounding tissues.
 the blood concentration and viscosity increase, causing sludging of the
microcirculation
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 vital organs to be compromised due to reduced perfusion

 bacteria may enter the blood stream, resulting in the increased
complication of endotoxic shock.
 Refractory
12
 vital organs have failed and the shock can no longer be reversed.
 Brain damage and cell death
 cellular ATP has been degraded into adenosine
 Adenosine easily perfuse out of cellular membranes into extracellular fluid,
 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.
PATHOPHYSIOLOGY 13
HYPOVOLEMIC SHOCK 14

 occures from inadequate circulating blood volume

 Major effects are due to decreased cardiac output and low intra cardiac pressure
 Severity of clinical features depends on degree of blood volume lost
 fluid loss (severe burns , persistent vomiting and severe diarrhoea causing
dehydration)
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 Classification
o Hemorrhagic- due to blood loss
o Non- Hemorrhagic shock-burns, ascites, pancreatitis, water loss due to severe
diarrhoea,vomiting
PATHOPHYSIOLOGY 16
Hemorrhage from small venules & vein

Decreased filling of right heart

Decreased filling of pulmonary vascularure

Decreased filling of left atrium & ventricle

Left ventricular stroke volume decreases

Drop in arterial blood pressure & tachycardia

Poor perfusion to pulmonary arteries

Clinical monitoring 17

 Blood pressure
 Respiration
 Urine output
 Central venous pressure
 ECG
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Management-
 Fluid replacement and increased tissue perfusion.
 Volume resuscitation
 Initial resuscitation is done with crystalloids such as normal saline.
 After resuscitation, colloids such as starch solution should be used as they restore
intravascular volume.
 Hypotension in patients with hypovolemic shock should be treated with I.V
fluids.
SEPTIC SHOCK 19

 Severe bacterial infections or septicaemia causes septic shock

 Most often due to gram negative & gram positive septicaemia
 It occurs in cases of severe septicaemia, cholangitis, peritonitis, meningitis etc.
 infection with E.coli, Proteus, Klebsiella, Pseudomonas
 Endotoxins of gram negative bacilli have been implicated as the most important
mediator of septic shock
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 Gram positive sepsis & shock

o Usually caused by dissemination of a potent exotoxin liberated from gram
positive bacteria without evidence of bacteremia.
o Usually seen in Clostridium Tetany or Clostridium Perfringes infection.
o Basically caused due to massive fluid losses.
o Arterial resistance fall but there is no fall in cardiac output
o Urine output usually remains normal.
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 Gram negative sepsis and shock

o the most common cause of this infection is genito-urinary infection.
o Persons who have had operations of the genito-urinary tract are also susceptible.
o It may also be seen in patients who have undergone tracheostomy or those with
gasterointestinal system infections.
o The prognosis is more favorable when the infection is accessible to surgical
drainage.
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MANAGEMENT-

 Early and effective volume replacement

 Adequate oxygen supply to cells
 Control of infection with antibiotic therapy and control of source of infection
 Fluid replacement
 Mechanical ventilation
CARDIOGENIC SHOCK 23

 Acute circulatory failure with sudden fall in cardiac output from acute diseases of
the heart without actual reduction of blood volume
 Causes:
 Deficient emptying - myocardial infarction ,rupture of the heart ,cardiac
arrhythmias
 Obstruction of the outflow-pulmonary embolism
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 Clinical features
o Skin will be pale & urine output is low
o Pulse become rapid and the systemic blood pressure is low
o Right ventricular dysfunction: neck veins are distended & liver is enlarged.
o Left ventricular dysfunction: there are bronchial rales & third heart sound heard.
o Gradually the heart also become enlarged.
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Management-

 Airway must be cleared

 Initial treatment is identifying the cause
 Maintaining adequate systolic B.P , cardiac output, tissue perfusion with volume
expansion.
 Revascularization with either angioplasty or bypass surgery have suggested
improved survival.
TRAUMATIC SHOCK 26

Shock following trauma due to large haemorrhage due to hypovolemia.

 Causes- surgery with marked blood loss ,severe injuries

o Bleeding externally : open wounds, fractures

o Bleeding internally : ruptured liver spleen etc.

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 Clinical features
o Presence of peripheral & pulmonary edema.
o Infusion of large amount of fluid which is adequate in hypovolemic shock is
inadequate here.
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 Management

 resuscitation

 local treatment of trauma and control of bleeding

 surgical debridement of the ischemic& dead tissue

 fluid replacement with ringer’s lactate, ringer’s acetate.

NEUROGENIC SHOCK 29

 May occur as a result of interruption of sympathetic vasomotor input after a high

cervical spinal cord injury, severe head injury.
 Cause- spinal anesthesia, car accidents that cause injury to the nerve, injuries that
causes injury to the spine
 Clinical features- pale gray skin, nausea, warm skin or face, tachycardia,
coldness in hands and feet.
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 Management
o Trendelenburg position displaces blood from systemic venules into right heart &
increases cardiac output.
 Administration of fluids
 Vasoconstrictor drugs-phenylephrine
 Only type of shock safely treated with vasoconstrictor. Its action saves patient
from immediate damage to important organs like brain, heart and kidney
PSYCHOGENIC SHOCK 31

 Part of neurogenic shock

 Occurs following sudden fright from unexpected bad news or at the sight of
horrible accident
 Effect may vary from temporary unconsciousness to even sudden death
ANAPHYLACTIC SHOCK 32

 Most common cause is the use of penicillin

 Other causes include:anaesthesia,consumption of shell fish,serum injections

 Clinical features
o It manifests as bronchospasm, laryngeal edema, respiratory distress, hypoxia,
massive vasodilation, hypotension and shock
o The mortality rate is 10%
o In the dental office this reaction can occur during or immediately following the
administration of penicillin or LA to a previously sensitized patient.
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 Management

 Step 1: position the patient, place the patient in the supine position with legs
elevated
 Step 2 : A-B-C
Open the Airway by tilting the head. Breathing and Circulation should be
established
 Step 3 : Definitive care
As soon as systemic allergy is suspected emergency medical help is sought
EFFECTS OF SHOCK 35

 CARDIOVASCULAR
 Tachycardia
 Vasoconstriction

 RESPIRATORY
 Increased respiratory rate and excretion of carbon dioxide

 RENAL AND ENDOCRINE

 Decrease in urine output
 Increase in sodium and water retention
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 HEART IN SHOCK
• Hemorrhages and Necrosis: located in subepicardial & subendocardial region.
• Zonal Lesion: Opaque transverse contraction bands in a myocyte near an
intercalated disc.
 SHOCK IN LUNG
• Lungs have dual blood supply & generally not affected by hypovolemic shock
• Septic shock : symptoms of ARDS, congestion, edema, lymphocytic infiltrate etc
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 SHOCK IN KIDNEY
• Irreversible renal injury Important complication of shock.
• Renal ischemia following systemic hypotension cause renal changes
• Anuria and even death.

 GIT
• hemorrhagic gastroenteropathy
• Curlings ulcers
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 LIVER
• Focal necrosis, fatty changes
• Impaired liver function

 Brain
• Hypoxic Encephelopathy
• Cerebral ischaemia may produce altered state of consciousness

• If BP falls below 50mmHg in systemic hypotension,prolonged shock and cardiac arrest,brain suffers serious
ischaemic damage with loss of cortical functions,coma and vegetative state
INITIAL ASSESSMENT-ABC 39
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 AIRWAY
 Opening the airway with head tilt and chin lift

 BREATHING
 Look listen and feel for breathing
 If patient is conversing, A and B are fine-place patient on oxygen
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 CIRCULATION
 Perform chest compressions to support circulation
 Vitals (HR and BP)
 IV,start flluids,put on continuos monitor
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 In a trauma,perform ABCDE and not ABC

 DEFICIT or DISABILITY
 Movement of all 4 extremities
 Movement of the pupils

 EXPOSURE
 Loosening of clothing on trauma patients
MANAGEMENT OF SHOCK 43

 History
 Physical exam
 Laboratory investigations
 Other investigations
 Treat the Shock – Start treatment as soon as you suspect Pre-shock
 Monitor
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 HISTORY
• Trauma?
• Pregnant?
• Acute abdominal pain?
• Vomiting or Diarrhea?
• Fever?
• Chest pain?
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 PHYSICAL EXAM
• Vital – HR, BP, Temperature, Respiratory rate, Oxygen saturation
• Capillary blood sugar
• Weight in children
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 In a patient with normal level of consciousness – physical exam can be directed to the
history.
 In a patient with abnormal level of consciousness-
 Primary survey-
• Cardiovascular( murmurs, JVP, muffled heart sounds )
• Respiratory exam( crackles, wheezes)
• Abdominal exam
• Skin and mucous membranes
• Neurologic examination
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 LAB TESTS
• CBC, Creatinine, glucose
• Cardiac enzymes
• Blood culture – from two different sites
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 OTHER INVESTIGATIONS
• ECG
• Urinalysis
• CXR
• Echo
• FAST ( Focused Abdominal Sonography for Trauma )
 Management of hypovolemic shock 49

 Aim : to restore cardiac filling pressure promptly and adequately without inducing
pulmonary edema
 Arresting ongoing blood loss
• External hemorrhage by pressure elevation and tourniquet
• Internal hemorrhage by immediate surgical exploration
 Restoration of circulating blood volume
• Start two large bore IV cannula
 Correction of metabolic acidosis
Management of cardiogenic shock 50

 Three steps
 Initial stabilization
• Establishment of ventilation and oxygenation
• Treatment of pain, arrhythmias and acid base abnormality
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 Evaluation of the patient

• Through history, physical examination and investigations
• ECG
• Chest X-ray
• Echo
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 Definitive therapy

• Pharmacological support : epinephrine, dopamine, dobutamine,

 Surgical interventions : IABP, Angioplasty, Cardiac tansplant

Management of Anaphylactic shock 53

 INITIAL THERAPY
• Maintain adequate ventilation
• Epinephrine : 0.3 – 0.5 mg IV
• Inhaled beta agonists
• Establish adequate venous access
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 SECONDARY THERAPY
• Antihistamines : 25-50mg Hydroxyzine/ Diphenhydramine
• Corticosteroids : 250 mg Hydrocortisone

Observation in the hospital for at least 24 hrs

 Glucagone in patients on beta blockers, they may be resistant to epinephrine.

DENTAL CONSIDERATIONS 55

 The common factors that cause shock in a dental chair are pain and anxiety.
 Patients with allergies and systemic disease should be give more attention during
dental treatments.
 Long treatment procedures can cause shock or syncope.
 TERMINATE DENTAL PROCEDURE
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POSITION THE PATIENT

BASIC LIFE SUPPORT

DEFINITIVE MANAGEMENT

OBSERVE THE PATIENT ADMINISTER ORAL HISTAMINE

MEDICAL CONSULTATION
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TERMINATE DENTAL PROCEDURE

POSITION THE PATIENT IN SUPINE POSITION

BASIC LIFE SUPPORT

SEEK MEDICAL ASSISTANCE

ADMINISTER OXYGEN

MONITOR VITAL SIGNS

DEFINITIVE MANAGEMENT
CONCLUSION 58

 Early recognition of warning signs and diagnosis in the reversible phase is

important for successful management of shock.

 The principle of initial resuscitation is same irrespective of type of shock.

 Some dentists are not aware of this emergency vital clinical condition. Therefore,
dentists should develop their knowledge on this subject of the shock management,
to prevent this life threatening event.
REFERENCES 59

 Mohan H, Mohan S. Essential pathology for dental

students. JP Medical Ltd; 2011 Jun 30.
 Walker BR, Colledge NR. Davidson's principles and
practice of medicine e-book. Elsevier Health Sciences;
2013 Dec 6.
 Bhat S. SRB's Manual of Surgery. JP Medical Ltd; 2019
Jun 30.