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1. SHOCK
Definition:
Shock is a condition in which circulation fails to meet the
nutritional needs of the cells and at the same time fails to remove
the metabolic waste products.
Or
Shock may be defined as an acute, generalized inadequate
perfusion of critical organs that, if continued will produce serious
pathophysiologic consequences.
Stages of Shock:
Divided into 3 stages :-
a) Early, "compensated shock".
b) Progressive, "decompensated shock".
c) Irreversible shock.
Early or Compensated Shock:
Is due to minor deficiency in the circulating blood volume
such as compensatory mechanisms. Eg.
- Constriction of the arteriolar bed.
- Augmentation of heart rate.
- Increase secretion of ADH (Adenosinedihydrogenase).
The Progressive, "Decompensated Shock" :
This stage of shock appears with persistence of shock,
especially when an additional stress is imposed on an individual in
"compensated shock". In this stage there is :-
- Intense arteriolar constriction.
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2. - Increase heart rate.
- Decline in BP and cardiac output.
- Techypnea is common (Hurried or Laboured Breathing)
Irreversible Shock:
This is marked by :-
- Progressive reduction in the cardiac output.
- Progressive fall in B.P.
- Worsening of metabolic acidosis.
The reduced blood flow to the brain, heart and kidneys leads
to ischemic cell death in these organs with progressive deepening,
coma, progressive renal failure and uremia (Increase blood urea).
Classification of Shock:
1) Hypovolaemic shock or Haematogenic shock.
2) Cardiogenic shock.
3) Traumatic shock
4) Neurogenic shock
5) Pyschogenic shock
6) Septic shock
7) Miscellaneous types
- Anaphylactic shock.
- Insulin shock.
1) Hypovolaemic Shock or Haematogenic Shock :
Most common type seen in patients with maxillofacial
trauma. This is due to reduction in the amount of fluid pumped
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3. through the vascular bed. Example, blood loss, plasma or body
water, electrolytes, vomiting, diarrhea and dehydration.
This is clinically manifested by :-
- Low cardiac output.
- Tachycardia (increase pulse rate >70)
- Low blood pressure &
- Vasoconstriction.
Clinical Features: Depends on the degree of loss of blood volume
and on the duration of shock.
Depending on this it is classified as :
a) Mild
b) Moderate
c) Severe shock
Mild Shock : Loss of less than 20% of the blood volume.
Clinical Features:
 Constriction of B.V. in the skin.
 Collapse of subcutaneous veins in extremities, particularly the
feet become pale and cool.
 Sweating in forehead, hands and feet due to adrenergic
discharge.
 The patient feels thirsty and cold.
Moderate Shock : Loss of blood volume from 20-40%.
Clinical Features : Along with the above findings there will be-
- Oliguria (decrease urine output).
- Pulse rate is increase but less than 100 per minute.
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4. Severe Shock: Loss of blood volume more than 40% usually leads
to severe shock.
Clinical Features:
- There is pallor (skin or extremities become pale)
- Low urinary output
- Rapid pulse
- Low B.P.
Treatment:
1) Resuscitation : This should be started immediately as the
patient is admitted with hypovolumic shock. This starts with -
- Establishment of clear air way.
- Maintaining adequate ventilation.
- Oxygenation.
- Patient should be in 15° trendlenberg position.
Care should be taken when lowering the head to support the
jaws to prevent airway obstruction, and this will improve venous
return preventing stasis of blood in the muscles and legs
preventing oedema.
2) Immediate control of Bleeding: This is very important in case of
haemorrhagic shock.
3) Extracellular fluid replacement: Fluid replacement should be
started immediately after the control of bleeding.
4) Drugs :
a) Sedatives : Commonly used to alleviate pain.
Eg. Morphine should be given I.V. or S.C.
It is contraindicated in –
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5. - Children
- Patient with head injury.
For children  Barbiturates are preferred.
Morphine dose : Inj morphine 100 mgIm. Morphine produces relief
of pain and does not alter the other functions of CNS like slurred
speech or motor in co-ordination.
b) Chronotropic agents: In patients with decrease heart rate
chronotropic agents are used which primarily increase heart
rate.
Eg. Atropine is most widely used in this group.
Dose : Inj Atropine sulphate 0.65mg is diluted in 5ml of distilled
water and this solution is given slowly through IV route followed
by another 0.5ml if radial pulse is not clearly palpable.
c) Vasoconstrictions : The main role of this drug is that it –
- Increase B.P.
- Increase perfusion pressure for coronary circulation.
The most commonly used drugs are :-
- Phenylephrine
- Metaraminol
d) Beta-Blockers: This drug increases efficiency of ventricular
contraction.
Eg. Propranolal is most widely used drug in this group.
3) Traumatic Shock:
This type of shock is caused by major injuries like –
- Fractures
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6. - Crush injuries
- Burns
- Extensive soft tissue injuries.
In this type of shock there is hypovolaemia due to bleeding
both externally such as lacerations or from internal sources.
- GIT bleeding (eg. ulcer).
- Femoral fractures.
- Crush injuries.
- Ruptured internal organs (eg. liver and spleen).
Clinical Features: Similar to hypovolemic shock.
The differentiating features from hypovoleamic shock are :-
a) Presence of peripheral and pulmonary oedema. Infusion of large
volumes of fluid which may be adequate for pure hypovolaemic
shock and is usually inadequate for traumatic shock.
Treatment:
1. Resuscitation: In this type of shock mechanical ventilators
support is more needful.
2. Local treatment of trauma.
3. Control of bleeding and surgical debridement of ischemic and
dead tissues.
4. Immobilisation of fractures may be required.
5. Fluid replacement.
Cardiogenic Shock:
Results from intrinsic injury to the heart. Most common
cause – left ventricular failure secondary to Myocardial infarction,
cardiac arrhythmias or cardiac failure.
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7. Clinical Features:
- In the early stages the skin is pale and cool.
- Urine output is low.
- Rapid pulse.
- Arterial blood pressure becomes low.
In case of L.V.F the patient has :-
- Decrease cardiac output.
- Increased pulmonary artery occlusion pressure and
pulmonary oedema.
- Increased systemic vascular resistance.
- Patient has bronchial rales.
- 3rd
heart sound is heard.
In case of R.V.F the :-
- Neck veins becomes distended.
- Liver may also be enlarged.
- Peripheral oedema.
Treatment:
- Airway must be clear.
- Adequate oxygenation.
- If patient complains of pain- It should be treated with
adequate sedative
- Pulmonary oedema should be treated with a diuretic.
Cardiogenic shock may also be due to :-
- Cardiac dysarhythmias.
- Mitral regurgitation
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8. - Acute aortic regurgitation or stenosis.
- Acute viral myocarditis.
Neurogenic Shock:
This is caused by –
- Paraplegia
- Quadriplegia
- Trauma to the spinal cord
- Spinal anaesthesia.
This is due to blockage of sympathetic nervous system
resulting in loss of arterial and venous tone with pooling of blood in
the dilated peripheral venous system.
Clinical Features:
The peculiar feature is that :-
- The skin remains warm, pink and well perfused in
contradistinction to hypovolaemic shock.
- Urine output may be normal.
- Heart rate is rapid.
- B.P. is low.
Vasovagol or Vasogenic Shock: Is a part of neurogenic shock in
which there is pooling of blood due to dilatation of peripheral
vascular system.
Caused due to :
- Decrease venous return to the heart leading to low cardiac
output and bradycardia.
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9. Pyschogenic Shock:
- Caused by sudden fright from unexpected bad news.
- Sight of accident etc.
Its effect may vary in intensity from unconsciousness to sudden
death.
Treatment of Neurogenic Shock:
1) Elevation of legs is effective in treating patients with neurogenic
shock. Trendelenburg position (i.e, head end of the bed is
lowered). This position displaces blood from the systemic
venules and small veins and thus increases cardiac output.
2) Administering of fluids : This increases filling of the right heart
which in turn increase cardiac output.
3) Vasoconstrictor drug : Because its action is to restore venous
tone and thus restoring cardiac output. Its prompt action saves
the patient from sudden fall in B.P. and decrease cardiac output
and from damage to brain, heart and kidneys.
Septic Shock:
This type of shock is most often due to –
- Gram negative septicaemia. This may occur in cases of I)Severe
septicaemia, ii)Peritonitis, iii)Meningitis.
Gram negative organisms  Coli & Bacteroids.
- Gram positive organisms which cause these types of shock are
I)Stephylococcus, ii)Streptococcus and iii)Pneumococcus.
Clinical Features:
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10. - Initially there is development of chills and cold and increase
temperature above 100°F.
- Increase cardiac output.
- In late cases vascular permeability increase. So that the blood
volume decreases leading to hypovolaemia.
- In advanced cases cardiac function is damaged due to toxins
liberated by organisms.
Treatment: Divided into 2 groups :-
a) Treatment of infection by early surgical debridement or drainage
and use of antibiotics.
b) Treatment of Shock – includes fluid replacement, steroid
administration, use of vasoactive drugs.
Antibiotics : Depending on culture and sensitivity test.
c) Fluid replacement is very important. This will provide sufficient
blood volume to the vital organs.
Miscellaneous Types : Include –
a) Anaphylactic shock.
b) Insulin shock.
Anaphylactic shock : Commonly seen after penicillin
administration Such type of shock is said to be due to increase
release of histamine and slow release substance (SRS) of
anaphylaxis by combination of antigen with 1gE on the mast cells
and basophils.
Anaphylactic Shock:
Anaphylaxis : This is the classical immediate hypersensitivity
reaction. The term anaphylaxis (ana-without, phylaxis-protection)
was coined by Richet 1902.
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11. Clinical Features : The clinical features of anaphylaxis are the
some with any antigen, but are different in different species. The
clinical features are due to smooth muscle contraction and
increased vascular permeability.
The organs affected vary with the species. The tissues or
organs predominantly involved in anaphylaxis reaction are known
as "target tissues" or 'shock organs".
The other changes seen in anaphylaxis are oedema,
decreased coagulability of blood, fall in blood pressure and
temperature, leucopenia and thrombocytopenia.
Signs and Symptoms of Anaphylactic shock:
Begin with itching of the scalp of tongue. There may be
nausea, vomiting, abdominal pain and diarrhoea, sometimes with
blood in the stool, acute hypotension, loss of consciousness and
death follow.
Anaphylaxis commonly associated with heterogeneous serum
therapy is now seen mostly following antibiotic injections. Insect
stings can also cause anaphylaxis in man. Prompt treatment with
adrenaline can be lifesaving. Adrenaline is to be administered,
0.5ml of a 1 in 1000 solution, sub-cuteneously or intramuscularly,
the dose being replaced upto a total of 2.0ml over 15 minutes if
necessary.
Cutaneous Anaphylaxis : When a small shocking dose of an
antigen is administered intradermally to a sensitized host, there
will be a local 'wheal and flare' response (local anaphylaxis). The
wheal is a pale, central area of puffiness due to oedema, which is
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12. surrounded by a flare caused by hyperaemia and subsequent
erythema.
Cutaneous anaphylaxis (skin test for type I hypersensitivity)
is useful in testing for hypersensitivity and in identifying the
allergen responsible in atropic diseases. In highly sensitized
individuals even the skin test may lead to serious and even fatal
reactions. Hence, a syringe loaded with adrelalin should always be
kept ready whenever a skin test is performed to detect anaphylactic
hypersensitivity.
Passive cutaneous anaphylaxis (PCA) : This test developed by
Ovary (1952) is an extremely sensitive in-vivo method for detection
of antibodies. A small volume of the antibody is injected
intradermally into a normal animal. If the antigen, along with a
dye such as evans blue, is injected intravenously 4-24 hours
afterwards, there will be an immediate blueing at the site of
intradermal injection due to vasodilation and increased capillary
permeability (wheal and flare reaction). PCA can be used to detect
human IgG antibody which is 'heterocytotropic' (capable of fixing to
cells, of other species), but not IgE which is 'homocytotropic'
(capable of fixing to cells of homologous species only).
Anaphlaxis in-vitro : Isolated tissues, such as intestinal or
uterine muscle strips from sensitized guinea pigs, held in a bath of
rings solution will contract vigorously on addition of the specific
antigens to the bath. This is known as Schultz-Dale Phenomenon.
The reaction is specific and will be elicited only by the antigen to
which the animal is sensitive.
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13. Mechanism of Anaphylaxis : Anaphylactic hypersensitivity can
be passively transferred from a sensitive donar to a normal
recipient by injection of serum. This passive sensitization
establishes that the reaction is determined by circulating antibody.
Homocytotropic IgE antibody is the major antibody responsible for
anaphylactic hypersensitivity. To a lesser extent heterocytotropic
IgG may be responsible.
IgG molecules are bound to surface receptors on mast cells in
tissues and basophils in circulation. Following exposure to the
shocking dose, the antigen molecules combine with the cell bound
IgE, bridging the gap between adjacent antibody molecules. This
cross linking increases the permeability of the cells to calcium ions
and leads to degranulation with release of biologically active
substances contained in the granules.
The manifestations of anaphylaxis are due to pharmacological
mediators, which are of 2 kinds :-
- The primary mediators which are the preformed contents of
mast cells and basophil granules, (histamine, serotonin,
easinophil chemotactic factor of anaphylaxis, neutrophil
chematoctic factor, heparin and various proteolytic enzymes).
- The secondary mediators which are newly formed upon
stimulation by mast cells, basophils and other leukocytes (slow
reacting substance of anaphylaxis, prostaglandins and platelet
activating factors).
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14. I) Primary Mediators of Anaphylaxis:
Histamine : This is the most important vasoactive amine in
human anaphylaxis. Histamine is formed by the decarboxylation
of histidine found in the granules of mast cells, basophils and in
platelets. Released into the skin, histamine stimulates sensory
nerves, producing burning and itching sensations. It causes
vasodilation and hyperaemia by an axon reflex (flare effect) and
edema by increasing capillary permeability (wheal effect).
Histamine induces smooth muscle contraction in diverse
tissues and organs, including vasculature, intestines, uterus and
especially the bronchioles. It also stimulates secreations
(secretogogue effect).
Serotonin (5-hydroxy tryptamine) : This is a base derived by
decarboxylation of tryptophas. It is found in the intestinal mucosa,
brain tissues and platelets. It causes smooth muscle contraction,
increased capillary permeability and vasoconstruction. It is
important in anaphylaxis in rats and mice, but its role in man is
uncertain.
Chemotactic factors : The eosinophil chemotactic factors of
anaphylaxis (ECF-A) are acidic tetrapeptides released from mast
cell granules which are strongly chemotactic for eosinophils. These
probably contribute to the eosinophilic accompanying many
hypersensitivity states. A high molecular weight chemotactic factor
has been identified, which attracts neutrophils.
Heparin is an acidic mucopolysaccharide. It contributes to
anaphylaxis in dogs, but apparently not in man.
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15. II] Secondary Mediators of Anaphylaxis :
1) Slow reacting substance of anaphylaxis (SRS-A) : This is so
called because of the slow but stained contraction of the smooth
muscles that it causes. It is produced by leukocytes, mainly in
lungs.
They act on the smooth muscles of the larger blood vessels
and of the bronchi and may be responsible for the prolonged
respiration distress in asthma. They are much more potent
bronchoconstrictors than histamine and are not inhibited by
antihistaminics.
Prostaglandins and Leukotrienes : They are derived by two
different pathways from arachidonic acid, which is formed from
disrupted cell membranes of mast cells and other leukocytes. The
lipoxygenase pathway leads to the formation of leukotrienes, while
the cyclo-oxygenase pathway leads to prostaglandins and
thromboxane. Prostaglandin F2a and thromboxone A2 are
powerful, but transient, bronchoconstrictors. Prostaglandin E2 is
a bronchodilator.
Prosthaglandins also effect secreation of mucous glands,
platelet adhesion, permeability and dilation of capillaries and the
pain threshold.
Platelet activating factors (PAF) : Is a low molecular weight lipid
release from basophils during immediate hypersensitivity. If
causes aggregation of platelets and release of their vasoactive
amines.
Other Mediators of Anaphylaxis:
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16. Resides the products of mast cells and other leukocytes,
several other biologically active substances have been implicated in
anaphylaxis. These include the anaphylatoxins released by
complement activation and bradykinin and other kinins formed
from plasma kininogens.
Anaphylactoid reaction : Intravenous injection of pentone,
trypsin and certain other substances provokes a clinical reaction
resembling anaphylactic shock. This is termed 'anaphylactoid
reaction'. The clinical resemblance participating in both the
reactions. The only immunological basis and is a non-specific
mechanism involving the activation of complement and the release
of anaphylatoxins.
Management of Shock in Dental Clinic:
Shock can be more easily prevented than treated. In
prosthodontics at times neurogenic, anaphylactic and septicaemic
shock may be seen. Treatment should be aimed at determination
of the cause for shock for better management.
It can be caused due to :-
- Anxiety
- Drugs (local anesthesia)
- Surgery (placement of implants).
General Principles in Management of Shock:
1. Best treatment of shock is prevention. If shock cannot be
prevented one should concentrate on limiting its depth and
duration.
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17. 2. Detect the underlying cause of shock, eg. If shock is due to
volume loss, the cause of volume loss must be stopped and
immediate volume replacement instituted. If problem is due to
sepsis underlying site of infection, causative organism should be
isolated and treated with appropriate antibiotics.
3. The patient condition and severity of shock should be measured
at regular intervals.
4. Frequent monitoring especially of ventilation, acid-base balance,
fluids and electrolytes should be done.
A clinical state which is most commonly seen in a dental
clinic which may be seen in the form of shock is syncope.
Syncope : Is defined as a sudden, transient loss of consciousness,
usually secondary to cerebral ischemia.
Predisposing Factors: Factors that can precipitate syncope may be
divided into 2 groups:
Phychogenic factors Non-phychogenic factors
- Fright - Hunger
- Anxiety - Exhaustion
- Emotional stress - Poor physical condition
- Unwelcome news - Hot, humid, crowded
environment
- Pain / sudden, unexpected.
- Sight of surgery and other dental
instruments.
Clinical Manifestations : May be grouped into three phases.
- Presyncope.
- Syncope
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18. - Postsyncope (recovery period).
Early :
- Feeling of warmth in neck and face.
- Loss of color, pale or ashen-gray skin tone.
- Heavy perspiration
- Complains of feeling faint
- Nausea
- B.P. approximately baseline
- Rapid heart rate (eg. 120 per minute).
Late :
- Pupillary dilation
- Yawning
- Hyperpnea
- Coldness in hands and feet
- Hypotension
- Bradycardia
- Dizziness
- Vascular disturbances
- Loss of consciousness
Management of Syncope:
Step 1: Place patient in supine position with feet slightly elevated.
Step 2 : - Establish patient airway.
- Head tilt chin lift method
- Check breathing
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19. - Jaw thrust maneuver if necessary.
- Check circulation.
Step 3 : - Monitor vital signs
- B.P.
- Heart rate
- Respiratory rate.
Support Patient
- Ammonia vaporole crushed under nose of patient.
- Blankets if cold or shivering
- Reassure patient.
Step 4 : Maintain your composure
Step 5 : Follow-up treatment.
- Determine factors causing unconsciousness.
- Prevent recurrence of syncope.
- Arrange for patient to be taken home by friend or
relative.
- No further dental treatment for 24 hours.
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