Shock and its management is summarized as follows: 1. Shock is a life-threatening condition characterized by inadequate tissue perfusion due to reduced circulating blood volume or cardiac output. 2. Shock is classified as hypovolemic, cardiogenic, septic, traumatic, neurogenic, or hypoadrenal based on etiology. 3. The pathophysiology involves reduced circulating volume, impaired tissue oxygenation, and release of inflammatory mediators, progressing from compensated to decompensated to irreversible stages if left untreated.

1. SUBMITTED BY :
Dr.BIBIN JACOB EMMANUEL
S
SHOCK AND ITS MANAGEMENT
GUIDED BY :
Dr.MANOHAR BHAT
Dr.ABHISHEK KHAIRWA

2.  DEFINITION
 CLASSIFICATION
 PATHOPHYSIOLOGY
 MORPHOLOGIC FEATURES
 CLINICAL FEATURES AND COMPLICATIONS
 ANAPHYLATIC SHOCK And ITS MANAGEMENT
 ESSENTIAL EMERGENCY DRUGS IN DENTAL CLINIC
 MANAGEMENT OF MEDICAL EMERGENCIES
 BASIC LIFE SUPPORT / CPR
CONTENTS

3.  Shock is a life threatening clinical syndrome of cardiovascular
collapsed characterised by :-
An acute reduction of effective circulating blood volume (
hypotension )
An inadequate perfusion of cells and tissues (hypoperfusion)
 If uncompensated these mechanisms may lead to impaired
cellular metabolism and death
DEFINITION

4. • True /secondary shock :- Its a circulatory imbalance between oxygen
supply and oxygen requirement at the cellular level and is also called
as circulatory shock .
• Initial / primary shock :- it is used for transient and usually a benign
vasovagal attack resulting from sudden reduction of venous return to
the heart caused by neurogenic vasodilation and consequent
peripheral pooling of blood .
Eg :- immediately following trauma , severe pain or emotional
overreaction such as due to fear , sorrow or surprise.

5. • HYPOVOLAEMIC SHOCK
 Acute haemorrhage .
 Dehydration from vomiting ,diarrhoea .
 Burn .
 Excessive use of diuretics .
 Acute pancreatis.
.
CLASSIFICATION

6. • CARDIOGENIC SHOCK
 Deficient emptying e.g ;
 Myocardial infaction .
 Cardiomyopathies .
 Cardiac arrhythmias .
 Rupture of the heart ventricles or papillary muscle

7.  Deficient filling e.g ;
 cadiac tamponade from haemopericardium .
 Obstruction to the outflow eg ;
 Pulmonary embolism .
 Ball valve thrombus .
 Tension pneumothorax.
 Dissecting aortic aneurysm .
• SEPTIC SHOCK
 Gram negative septicaemia
 Gram positive septicaemia

8. • OTHER TYPES
TRAUMATIC SHOCK .
Severe injuries .
Surgery with marked blood loss .
Obstetrical trauma.

9. NEUROGENICSHOCK.
 High cervical spinal anaesthesia .
 Accidental high spinal anaesthesia .
 Severe head injury .
HYPOADRENAL SHOCK.
 Administration of high dose of glucocorticoids .
 Secondary adrenal insufficency .
ANAPHYLATIC SHOCK .

10. This form of shock results from inadequate
circulatory blood volume by various etiologic
factors that may be either from the loss of red
cell mass and plasma due to haemorrhage or
from the loss of plasma volume alone .
HYPOVOLAEMIC SHOCK

11. Acute circulatory failure with sudden fall in
cardiac output from acute disease of the
heart without actual reduction of blood
volume [normevolaemia] results in
cardiogenic shock .
CARDIOGENIC SHOCK

12. Severe bacterial infections or septicaemia
induce septic shock. It may be the result of
Gram-negative septicaemia (endotoxic
shock) which is more common, or less often
from Gram-positive septicaemia (exotoxic
shock).
SEPTIC (TOXAEMIC) SHOCK

13. These include following types:
i) Traumatic shock Shock resulting from trauma is
initially due to hypovolaemia, but even after
haemorrhage has been controlled, these patients
continue to suffer loss of plasma volume into the
interstitium of injured tissue .
OTHER TYPES

14. ii) Neurogenic shock Neurogenic shock results
from causes of interruption of sympathetic
vasomotor supply.
iii) Hypoadrenal shock Hypoadrenal shock occurs
from unknown adrenal insufficiency in which the
patient fails to respond normally to the stress of
trauma, surgery or illness.

15. In general, all forms of shock involve following 3
derangements:
i) Reduced effective circulating blood volume.
ii) Reduced supply of oxygen to the cells and tissues with
resultant anoxia.
iii) Inflammatory mediators and toxins released from shock
induced cellular injury.
PATHOGENESIS

16. It may result by either of the following
mechanisms:
i) By actual loss of blood volume as occurs in
hypovolaemic shock .
ii) By decreased cardiac output without actual loss
of blood (normovolaemia) as occurs in cardiogenic
shock and septic shock.
REDUCED EFFECTIVE
CIRCULATING BLOOD VOLUME

17. • Following reduction in the effective circulating
blood volume from either of the above two
mechanisms and from any of the etiologic
agents, there is decreased venous return to the
heart resulting in decreased cardiac output.
• This consequently causes reduced supply of
oxygen to the organs and tissues and hence
tissue anoxia occurs, which sets in cellular
injury.
IMPAIRED TISSUE OXYGENATION

18.  In response to cellular injury, innate immunity of the body gets
activated as a body defense mechanism and causes release of
inflammatory mediators , but eventually these agents themselves
become the cause of cell injury.
 Endotoxins in bacterial wall in septic shock stimulate massive
release of proinflammatory mediators (cytokines) but a similar
process of release of these agents takes place in late stages of shock
from other causes.
 Several proinflammatory mediators are released from
monocytesmacrophages, other leucocytes and other body cells, the
most important being the tumour necrosis factor(TNF)α and
interleukin1 (IL1) cytokines
RELEASE OF INFLAMMATORY
MEDIATORS

19. PATHOGENESIS OF
CIRCULATORY SHOCK

20. RESPONSE OF INFLAMMATORY
MEDIATORS IN SHOCK

21.  Hypovolaemic shock occurs from inadequate circulating blood
volume due to various causes, most often from loss of red cell
mass due to haemorrhage and, therefore, also called as
haemorrhagic shock.
 Major effects in this are due to decreased cardiac output and
low intracardiac pressure.
 Major clinical features are increased heart rate (tachycardia),
low blood pressure (hypotension), low urinary output (oliguria
to anuria) and alteration in mental state (agitated to confused
to lethargic).
PATHOGENESIS OF
HYPOVOLAEMIC SHOCK

22. • Cardiogenic shock results from a severe left
ventricular dysfunction from various causes such
as acute myocardial infarction .
• Resultant decreased cardiac output has its effects
in the form of decreased tissue perfusion and
movement of fluid from pulmonary vascular bed
into pulmonary interstitial space initially
(interstitial pulmonary oedema).
• Later into alveolar spaces (alveolar pulmonary
oedema).
PATHOGENESIS OF
CARDIOGENIC SHOCK

23. • Septic shock results most often from Gramnegative bacteria entering the
body from genitourinary tract, alimentary tract, respiratory tract or skin,
and less often from Grampositive bacteria.
• In septic shock, there is immune system activation and severe systemic
inflammatory response to infection as follows:
1. Activation of macrophage-monocytes
 Lysis of Gramnegative bacteria releases endotoxin, a lipopolysac
charide (LPS), into circulation where it binds to
lipopolysaccharidebinding protein (LBP).
PATHOGENESIS OF SEPTIC
SHOCK

24.  The complex of LPS LBP binds to CD14 molecule on the surface of
the monocyte/macrophages which are stimulated to elaborate
proinflammatory cytokines, the most important ones being TNFα
and IL1.
 The effects of these cytokines are as under:
a) By altering endothelial cell adhesiveness:
This results in recruitment of more neutrophils which liberate free
radicals that cause vascular injury.
b) Promoting nitric oxide synthase:
This stimulates increased synthesis of nitric oxide which is responsible
for vasodilatation and hypotension.

25. II) ACTIVATION OF OTHER INFLAMMATORY
RESPONSES
Microbial infection activates other inflammatory cascades which have
profound effects in triggering septic shock. These are as under:
a) Activation of complement pathway: Endproducts C5a and C3a
induce microemboli and endothelial damage.
b) Activation of mast cells: Histamine is released which increases
capillary permeability.

26. C) ACTIVATION OF COAGULATION SYSTEM:
Enhances development of thrombi.
D) ACTIVATION OF KININ SYSTEM:
Released bradykinin causes vasodilatation and increased capillary
permeability .
Net result of above mechanisms is vasodilatation and increased
vascular permeability in septic shock. Profound peripheral
vasodilatation and pooling of blood causes hyperdynamic
circulation in septic shock, in contrast to hypovolaemic and
cardiogenic shock.

27. Shock has been divided arbitrarily into 3 stages :
1. Compensated (nonprogressive, initial, reversible) shock .
2. Progressive decompensated shock .
3. Irreversible decompensated shock.
PATHOPHYSIOLOGY (STAGES OF SHOCK)

28. Activation of various neurohormonal mechanisms causing wide spread
vasoconstriction and by fluid conservation by the kidney to maintain adequate
cerebral and coro nary blood supply by redistribution of blood so that the vital
organs (brain and heart) are adequately per fused and oxygenated.
I) WIDESPREAD VASOCONSTRICTION
• In response to reduced blood flow (hypotension) and tissue anoxia, the
neural and humoral factors (e.g. baroreceptors, chemo receptors,
catecholamines, renin, and angiotensinII) are activated. All these bring
about vasoconstriction, particularly in the vessels of the skin and
abdominal viscera.
• Wide spread vasoconstriction is a protective mechanism as it causes
increased peripheral resistance, increased heart rate (tachycardia) and
increased blood pressure.
COMPENSATED (NON-PROGRESSIVE,
INITIAL, REVERSIBLE) SHOCK

29. • However, in septic shock, there is initial vasodilatation followed by
vaso constriction.
• Besides, in severe septic shock there is elevated level of
thromboxane A2 which is a potent vasoconstrictor and may augment
the cardiac output along with other sympathetic mechanisms.
• Clinically, cutaneous vasoconstriction is responsible for cool and pale
skin in initial stage of shock.

30. II) FLUID CONSERVATION BY THE KIDNEY
In order to compensate the actual loss of blood volume in hypo
volaemic shock, the following factors may assist in restoring the blood
volume and improve venous return to the heart:
a) Release of aldosterone from hypoxic kidney by activation of renin-
angiotensinaldosterone mechanism.
b) Release of ADH due to decreased effective circulating blood
volume.
c) Reduced glomerular filtration rate (GFR) due to arteriolar
constriction.
d) Shifting of tissue fluids into the plasma due to lowered capillary
hydrostatic pressure (hypotension).

31. III) STIMULATION OF ADRENAL
MEDULLA
In response to low cardiac output, adrenal medulla is
stimulated to release excess of catecholamines (epinephrine
and nonepinephrine) which increase heart rate and try to
increase cardiac output.

32. This is a stage when the patient suffers from some other stress or risk factors
(e.g. preexisting cardiovascular and lung disease) besides persistence of the
shock condition; this causes progressive deterioration.
The effects of resultant tissue hypoperfusion in progres sive decompensated
shock are as under:
I) PULMONARY HYPOPERFUSION
Decompensated shock worsens pulmonary perfusion and increases
vascular permeability resulting in tachyp noea and adult respiratory
distress syndrome (ARDS).
PROGRESSIVE DECOMPENSATED
SHOCK

33. ii) Tissue ischaemia
• Impaired tissue perfusion causes switch from aerobic to anaerobic
glycolysis resulting in metabolic lactic acidosis.
• Lactic acidosis lowers the tissue pH which in turn makes the
vasomotor response ineffective.
• This results in vasodilatation and peripheral pooling of blood.
• Clinically, at this stage the patient develops confusion and worsening
of renal function.

34. When the shock is so severe that in spite of compensatory mechanisms and
despite therapy and control of etiologic agent which caused the shock, no
recovery takes place, it is called decompensated or irreversible shock.
Its effects due to widespread cell injury are as follows:
i) Progressive vasodilatation
During later stages of shock, anoxia damages the capillary and venular wall
while arterioles become unresponsive to vasoconstrictors listed above and
begin to dilate. Vasodilatation results in peripheral pooling of blood which
further deteriorates the effective circulating blood volume.
IRREVERSIBLE DECOMPENSATED
SHOCK

35. II) INCREASED VASCULAR PERMEABILITY
Anoxic damage to tissues releases proinflammatory mediators which cause
increased vascular perme ability. This results in escape of fluid from
circulation into the interstitial tissues thus deteriorating effective circulating
blood volume.
III) MYOCARDIAL DEPRESSANT FACTOR (MDF)
Progressive fall in the blood pressure and persistently reduced blood flow to
myocardium causes coronary insufficiency and myocardial ischaemia due to
release of myocardial depressant factor (MDF). This results in further
depression of cardiac function, reduced cardiac output and decreased blood
flow.

36. IV) WORSENING PULMONARY HYPOPERFUSION
Pulmonary hypoperfusion causes respiratory distress due to pulmonary oedema,
tachypnoea and adult respiratory distress syndrome (ARDS) .
V) ANOXIC DAMAGE TO HEART, KIDNEY AND BRAIN .
• Progressive tissue anoxia causes severe metabolic acidosis due to anaerobic
glycolysis.
• There is release of proinflammatory cytokines and other inflammatory
mediators and generation of free radicals. Since highly specialised cells of the
myocardium, proximal tubular cells of the kidney, and neurons of the CNS are
dependent solely on aerobic respiration for ATP generation, there is ischaemic
cell death in these tissues.

37. VI) HYPERCOAGULABILITY OF BLOOD
• Tissue damage in shock activates coagulation cascade with release of clot
promoting factor, thromboplastin and release of platelet aggregator, ADP,
which contributes to slowing of bloodstream and vascular thrombosis.
• In this way, hypercoagulability of blood with conse quent micro thrombi
impair the blood flow and cause further tissue necrosis.
• Clinically, at this stage the patient has features of coma, worsened heart
function and progressive renal failure due to acute tubular necrosis.

38. STAGE PATHOGENESIS EFFECTS
COMPENSAED SHOCK WIDESPREAD
VASOCONSTRICTION
TACCHYCARDIA
FLUID CONSERVATION
BY KIDNEY
COOL CLAMMY SKIN
STIMULATION OF
ADRENAL MEDULLA
PROGRESSIVE
DECOMPENSATED
SHOCK
Pulmonary
HYPERPERFUSION
CARDIAC OUTPUT
TISSUE ISCHAEMIA MENTAL CONFUSION
URINARY OUTPUT
TACHYPNOEA
IRREVERSIBLE
DECOMPENSAT-ED
SHOCK
Progressive vasodilatation + BRAIN -
HYPOXIC ENCEPHALOPATHY
Increased vascular
permeability
HEART- FOCAL MYOCARDIAL
NECROSIS
Myocardial depressant
factor (MDF)
LUNGS - ARDS
Worsening pulmonary KIDNEY - ATN

39. MORPHOLOGIC FEATURES

40. HYPOXIC ENCEPHALOPATHY
If the blood pressure falls below 50 mmHg
as occurs in systemic hypotension in
prolonged shock and cardiac arrest, brain
suffers from serious ischaemic damage with
loss of cortical functions, coma, and a
vegetative state.
.

41. GROSSLY
the area supplied by the most distal branches of the cerebral
arteries suffers from severe ischaemic necrosis which is
usually the border zone between the anterior and middle
cerebral arteries .
MICROSCOPICALLY
The changes are noticeable if ischaemia is prolonged for 12
to 24 hours. Neurons, particularly Purkinje cells, are more
prone to develop the effects of ischaemia. The cytoplasm of
the affected neurons is intensely eosinophilic and the
nucleus is small pyknotic. Dead and dying nerve cells are
replaced by gliosis .

42. Heart is affected in cardiogenic as well as in other forms of shock.
There are 2 types of morphologic changes in heart in all types of shock:
HAEMORRHAGES AND NECROSIS
There may be small or large ischaemic areas or infarcts, particularly
located in the subepicardial and subendocardial region.
ZONAL LESIONS
These are opaque transverse contrac tion bands in the myocytes near
the intercalated disc.
HEART IN SHOCK

43. Lungs due to dual blood supply are generally not affected by hypovolaemic
shock but in septic shock the morphologic changes in lungs are quite
prominent termed ‘shock lung’.
GROSSLY
The lungs are heavy and wet.
MICROSCOPICALLY
Changes of adult respiratory distress syndrome (ARDS) are seen. Briefly, the
changes include congestion, interstitial and alveolar oedema, interstitial
lymphocytic infiltrate, alveolar hyaline membranes, thickening and fibrosis of
alveolar septa, and fibrin and platelet thrombi in the pulmonary
microvasculature
SHOCK LUNG

44. One of the important complications of shock is irreversible renal injury,
first noted in persons who sustained crush injuries in building collapses in
air raids in World War II. Renal ischaemia following systemic hypotension
is considered responsible for renal changes in shock. The endresult is
generally anuria and death.
GROSSLY
The kidneys are soft and swollen. Sectioned surface shows blurred
architectural markings.
MICROSCOPICALLY
Tubular lesions are seen at all levels of nephron and are referred to as acute
tubular necrosis (ATN) which can occur following other causes besides
shock . If extensive muscle injury or intravascular haemolysis is also
associated, peculiar brown tubular casts are seen.
SHOCK KIDNEY

45. The adrenals show stress response in shock. This includes release of
aldosterone in response to hypoxic kidney, release of glucocorticoids
from adrenal cortex and catecholamines like adrenaline from adrenal
medulla. In severe shock, acute adrenal haemorrhagic necrosis may
occur
ADRENALS IN SHOCK

46. The hypoperfusion of the alimentary tract in conditions such as shock and
cardiac failure may result in mucosal and mural infarction called
haemorrhagic gastroenteropathy . This type of nonocclusive ischaemic
injury of bowel must be distinguished from fullfledged infarction in which
deeper layers of the gut (muscularis and serosa) are also damaged. In
shock due to burns, acute stress ulcers of the stomach or duodenum may
occur and are known as Curling’s ulcers.
GROSSLY
The lesions are multifocal and widely distributed throughout the bowel.
The lesions are super ficial ulcers, reddish purple in colour. The adjoining
bowel mucosa is oedematous and haemorrhagic.
MICROSCOPICALLY
The involved surface of the bowel shows dilated and congested vessels and
haemorrhagic necrosis of the mucosa and sometimes submucosa.
Secondary infec tion may supervene and condition may progress into
pseudomembranous enterocolitis
HAEMORRHAGIC
GASTROENTEROPATHY

47. GROSSLY
Faint nutmeg appearance is seen.
MICROSCOPICALLY
Depending upon the time gap between injury and cell death, ischaemic
shrinkage, hydropic change, focal necrosis, or fatty change may be seen. Liver
function may be impaired
LIVER IN SHOCK

48. Other organs such as lymph nodes, spleen and pancreas may also show
foci of necrosis in shock. In addition, patients who survive acute phase
of shock succumb to overwhelming infections due to altered immune
status and impaired host defense mechanism.
OTHER ORGANS

49. MORPHOLOGIC FEATURES OF
SHOCK.

50. Classical features of decompensated shock are
characterised by depression of 4 vital processes:
i) Very low blood pressure
ii) Subnormal temperature
iii) Feeble and irregular pulse
iv) Shallow and sighing respiration
In addition, the patients in shock have pale face, sunken
eyes, weakness, cold and clammy skin.
.
CLINICAL FEATURES AND
COMPLICATIONS

51. Lifethreatening complications in shock are due to hypoxic
cell injury resulting in immunoinflammatory responses and
activation of various cascades (clotting, complement, kinin).
These include the following:
1. Acute respiratory distress syndrome (ARDS)
2. Disseminated intravascular coagulation (DIC)
3. Acute renal failure (ARF)
4. Multiple organ dysfunction syndrome (MODS)
With progression of the condition, the patient may develop
stupor, coma and death

52. • HOSPITALISATION .
• CARE OF ALL CRITICALLY ILL PATIENTS
BEGIN WITH A, B And C.
• OXYGEN SHOULD BE ADMINISTERED BY
FACE MASK TO ALL PATIENTS WHO ARE
CONSCIOUS AND ARE ABLE TO MAINTAIN
THEIR AIRWAY .
TREATMENT –GENERAL MEASURES

53. • If unconscious endotracheal intubation and ventilation
with oxygen may be necessary .
• Haemorrhage control .
• Intravenous access : urgent administration of ringers
lactate to restore blood volume to normal .
• Investigations : blood collected for routine investigations
aswell as for blood grouping and cross matching

54. • Cross matched blood is usually given . if the
hemorrhage is life threatening uncross matches o-
ve packed cells may be transfused into the patient
• Use of vasoconstrictor and inotropes is not
indicated as they may harm tissue perfusion .
• If inotropes have been started as a life saving
measures , an attempt should be made to wean
them as soon as the volume status is corrected
and the patient is stable .

55. PRESSURE & PACKING
• To control bleeding from scalp .packing using roller
gauze with or without adrenalin to control bleeding
from nose .
• Bleeding from vein during thyroidectomy , lumbar
veins during lumbar
• Sympathectomy can be controlled using pressure
pack for few minutes .
• Senstaken tube is used to control bleeding from
oesophageal varices internal tamponade .
TREATMENT –SPECIFIC
MEASURES

56. • Elevation of the leg controls bleeding from
varicose vein .
• Elevation of the head end reduces venou
bleeding in thyroidectomy anti
trendlenberg position .
• Sedation to relieve anxiety midazolam in
titrated doses of 1-2mg intravenously may
be given .
POSITION & REST

57. INDICATIONS
Reduction of fracture .
Repairs of tendon .
Repairs of nerves .
When a bloodless field is desired during surgery .
CONTRAINDICATIONS
Patients with peripheral vascular disease [The arterial disease may be
aggrevated due to thrombosis resulting in gangrene ]
TOURNIQUETS

58. TYPES
• Pneumatic cuffs with pressure gauge .
• Rubber bandage.
PRECAUTIONS
Too loose a tourniquet doesn’t serve the purpose .
Too tight Arterial thrombosis can occur which may result in gangrene .
Too long [ duration of application ] .
Gangrene of the limb . Hence when a tourniquet is applied the time of
inflation should be noted down and at the end of 45 minutes to an hour
it has to be deflated at least for 10 minute and reinflated only if
necessary .

59. COMPLICATIONS
ISCHAEMI AND GANGRENE .
TOURNIQUET NERVE PALSY.

60. • Application of artery forceps control bleeding from vein
and arteries .
• Application of ligature for bleeding vessels .
• Cauterisation .
• Application of bone wax to control to bleeding from cut
edges of bone .
• Silver clips are used to control bleeding from cerebral
vessels .
SURGICAL METHOD TO CONTROL HAEMORRHAGE

61. • Proper oxyygenation with intubation ,ventilation support
,cardioversion ,Pacing ,antiarrhythmic drugs ,correction of
electrolyte ,avoiding fluid overload ,prevention of pulmonary oedema
as immediate measures .
• Dobutamine is used to raise cardiac output provided there is
adequate preload and intravascular volume .dobutamine is preferred
in patients with hypotension but it may increase peripheral
resistance and heart rate worsening cardiac ischemia often both
dopamine and dobutamine combination may be required .
CARDIOGENIC SHOCK
MANAGEMENT

62. Careful judicial use of epinephrine , norepinephrine ,phosphodiesterase
inhibitors are often needed . Anticoagulant and aspirin are given
.thrombolytics can be used beta blockers nitrates .ACE inhibitors are
also used .
Intra aortic balloon pumb is need to be introduced transfemorally a
mechanically circulatory support to raise cardiac output and coronary
blood flow .
Relief of pain ,preserving of remaining myocardium and its function ,
maintaining adequate preload ,oxygenation , minimizing sympathetic
stimulation ,correction should be the priorities .

67. Allergy is defined as a hypersensitive state acquired through
exposure to a particular allergen, reexposure to which produces a
heightened capacity to react
ANAPHYLATIC SHOCK AND ITS
MANAGEMENT

68. CLASSIFICATION OF ALLERGYS

70. ANTIBIOTICS
The source of haptensis an unstable beta
lactamase ring to which proteins bind to
penicilloyl epitopes that induce allergy
Penicillins Cephalosporins Tetracyclines
Sulfonamides .

71. ANALGESICS
Allergic reaction to aspirin takes the form of
angioedema and bronchospasm
Acetylsalicylic acid (ASA; aspirin)
Nonsteroidal antiinflammatory drugs
(NSAIDs).

72. OPIOIDS
Opioids can activate mast cell degranulation
through direct stimulation and opioid
receptor activations thereby release of
histamine
Fentanyl Morphine Meperidine Codeine

73. ANTIANXIETY DRUGS
Allergy to barbiturates occurs much more
frequently in persons with a history of asthma
,urticaria and angiioedema.
Barbiturates

74. LOCAL ANESTHETICS
Allergy to local anesthetics occurs much more frequently in response to
the ester local anesthetics such as procaine, propoxycaine, benzocaine,
tetracaine, and compounds related to them, such as procaine penicillin
G and procainamide (an antidysrhythmic drug )
When an ester local anesthetic is involved, a true allergic reaction is
frequently elicited; however, with use of an amide local anesthetic, a
purported allergic reaction is frequently shown to be another type of
response (e.g., overdose, idiosyncrasy, or psychogenic).
Esters Procaine Propoxycaine Benzocaine Tetracaine Antioxidant
Sodium (meta)bisulfite Parabens Methylparaben

75. OTHER AGENTS
Heat-cured acrylics are less frequently associated with
allergy because the monomer is used more thoroughly in the
polymerization process. In cold-cured or self-cured acrylics,
it is likely that small amounts of monomer remain
unpolymerized, and it is this that produces the allergic
response in the previously sensitized individual.
Acrylic monomer (methyl methacrylate)

77. CLINICAL MANIFESTATIONS
Clinical manifestations of allergic skin
reactions

78. CLINICAL MANIFESTATIONS OF RESPIRATORY ALLERGIC
REACTIONS

79. CLINICAL MANIFESTATIONS OF ALLERGIC CARDIOVASCULAR
REACTIONS

80. • Generalized anaphylaxis is a most dramatic
and acutely life-threatening allergic
reaction .
• Most deaths from anaphylaxis occur within
the first 30 minutes after antigenic
exposure, although many victims succumb
up to 120 minutes after the onset of the
anaphylactic reaction .
GENERALIZED ANAPHYLAXIS

81. • Four major clinical syndromes are recognized: skin
reactions, smooth muscle spasm (gastrointestinal and
genitourinary tracts and respiratory smooth muscle),
respiratory distress, and cardiovascular collapse .

82. MANAGEMENT

83. MANAGEMENT OF DELAYED-ONSET, ALLERGIC SKIN
REACTION

84. MANAGEMENT OF RAPID-ONSET, ALLERGIC SKIN REACTION

85. MANAGEMENT OF RESPIRATORY ALLERGIC REACTION

86. MANAGEMENT OF LARYNGEAL
EDEMA

87. MANAGEMENT OF GENERALIZED
ANAPHYLAXIS

89. ESSENTIAL EMERGENCY DRUGS IN DENTAL CLINIC

90. EMERGENCY DRUGS IN DENTAL CLINIC

91. MANAGEMENT OF MEDICAL
EMERGENCIES

97. 1. HARSH MOHAN TEXTBOOK OF PATHOLOGY, 7TH
EDITION .
2. MEDICAL EMERGENCIES IN THE DENTAL OFFICE
(2007)
3. MANAGEMENT OF MEDICAL EMERGENCIES IN THE
DENTAL OFfiCE: CONDITIONS IN EACH COUNTRY, THE
EXTENT OF TREATMENT BY THE DENTIST -JDSA
ARTICLE .
4. MANAGEMENT OF MEDICAL EMERGENCIES AND
Basic Life Support/ Cardiopulmonary Resuscitation –
JOURNAL OF PEDIATRIC DENTISTRY 17 - 18
REFERENCES

98. THANKYOU