Shock and its management final/ dental implant courses

SHOCK AND ITS
MANAGEMENT
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

CONTENTS
DEFINITION
• Causes of shock
• Stages of shock
• Evaluation of shock
• Level of consciousness
• Clinical monitoring
TYPES OF SHOCK AND ITS MANAGEMENT
1. Hypovolemic shock
2. Traumatic shock
3. Vasogenic shock
a. Neurogenic shock
b. Psychogenic shock
c. Vasovagal shock
d. Anaphylactic
4. Cardiogenic
5. Septic shock
6. Insulin shock
7. Hypoadrenal shock
• Crush syndrome
• MODS
• ARTICLES

Shock

DEFINITION
• “ A state of depression of the vital functions of the
body due to inadequate tissue perfusion of the vital
organs, resulting from insufficient microcirculation”
• Inadequate tissue perfusion
• Decreased oxygen supply
• Anaerobic metabolism
• Accumulation metabolic waste

CAUSES OF SHOCK
• Severe or sudden blood loss
• Large drop in body fluids
• Myocardial infarction
• Major infections
• High spinal injuries
• Anaphylaxis
• Extreme heat or cold

Stage 1: Anticipation stage
• The disease has started but remains local.
Parameters are stable and within normal limits.
• There is usually enough time to diagnose and treat the underlying condition.
• This is the best time to prevent shock altogether.

The Pre-Shock Stage
• The disease is now systemic.
• Parameters drift, slip and slide... and start touching the upper or
lower limit of their normal range, but there is no shock yet!
• The absence of shock is due to the fact that compensatory
mechanisms are at play.

COMPENSATED SHOCK
•
Compensated shock can start with low normal blood pressure: a condition called
"normotensive, cryptic shock"
• The proof that a patient is in shock with normal blood pressure is the appearance of metabolic
acidosis due to some organ hypoperfusion.
•
The reason for normotension (or even hypertension in some cases) is that blood pressure is
maintained due to marked activation of many compensatory mechanisms (including the
sympathetic nervous system). However, because organs suffer from inadequate perfusion, it is
already a state of shock.

DECOMPENSATED SHOCK, REVERSIBLE
• This is "SHOCK" because hypotension is always present at this stage.
Normotension can only be restored with intravenous fluid (if indicated) and/or
vasopressors.
If the cause of shock is not diagnosed by this stage, it will be very difficult to treat the
patient. The reason? --- organs now suffer Multiple Organ Dysfunction Syndrome and
acidosis is becoming rapidly more and more severe.
• This systemic suffering worsens shock itself (vicious cycles) and leads to
catastrophic microvascular damage, D.I.C. and
Systemic.Inflammatory.Response.Syndrome

Irreversible stage
• Microvascular and organ damage are now irreversible
(untreatable)
There is often a "last ditch" effort from the ischemic midbrain with
an enormous discharge of endogenous catecholamines and this
can create a last spike of sinus tachycardia (asterix*). We call
stage 5 the "whoops! stage" --- too late to be able to turn things
around.

• In severe shock the microcirculation changes
dramatically.
• Those changes are mainly due to a
"cytokine storm" induced by extremely
severe tissue ischemia or, directly, by a
pathogen:
• (1) the endothelium is activated (vasodilates,
becomes pro-coagulant, expresses adhesion
molecules),
• (2) monocytes are activated (and discharge
numerous cytokines),
• (3) white blood cells obstruct some
capillaries
• (4) disseminated intra-vascular coagulation
and platelet aggregation plug
microcirculation as well.
• When there is so much deterioration to the
microcirculation, perfusion to organs worsens
rapidly....and, as a consequence, systemic
shock also worsens extremely rapidly...

EVALUATION OF SHOCK
• Geneva handshake
• Internal or external hemorrhage
• Underlying cardiac problems
• Sepsis
• Trauma to spinal cord
• Contact with known allergic substance
• History regarding the onset / aggravating event

Geneva Handshake
• When you shakes somebody's hand, you are getting in close contact with two
"great operators": (1) the autonomous nervous system (sympathetic and
parasympathetic nervous systems) and (2) the inflammatory system. This
handshake can be very useful in critically sick patients.

Internal or external hemorrhage
• Determine amount of blood loss;-
Blood clot –clenched fist- 500ml
Moderate swelling in closed fracture-tibia-500-1500ml
-femur-500-2000ml
In operation theatre- weighing the swabs after use and
subtracting the dry weight.

LEVEL OF CONSCIOUSNESS
• Report (from pt) and record
• Alert
• Verbal response to stimuli
• Pain response to stimuli
• Unresponsive to any stimuli

GLASGOW COMA SCALE
1 2 3 4 5 6
Eyes
Does not
open eyes
Opens eyes in response
to painful stimuli
Opens eyes in
response to voice
Opens eyes
spontaneously
N/A N/A
Verbal
Makes no
sounds
Incomprehensible sounds
Utters inappropriate
words
Confused, disoriented
Oriented,
converses normally
N/A
Motor
Makes no
movement
s
Extension to painful
stimuli
Abnormal flexion to
painful stimuli
Flexion / Withdrawal
to painful stimuli
Localizes painful
stimuli
Obeys
Comm
ands
The scale comprises three tests: eye, verbal and motor responses. The three
values separately as well as their sum are considered. The lowest possible GCS
(the sum) is 3 (deep coma or death), whilst the highest is 15 (fully awake person).www.indiandentalacademy.com

CLINICAL MONITORING
1. Blood pressure
2. Respiration
3. Urine
4. CVP
5. E.C.G
6. Pulmonary capillary wedge pressure (Swan-Ganz
catheter)
7. Chest radiograph
8. Other diagnostic tests

Blood pressure
• B.P may be normal in mild shock
• Diastolic pressure- degree of
vasoconstriction
• Systolic pressure- vasoconstriction along
with stroke volume and rigidity of the main
vessels
• Pulse pressure- (S.P- D.P)- the stroke
volume of the heart and cardiac output

RESPIRATION
• Hyperventilation is an important indicator of
shock.
• It is a normal response of early shock
• If the pt is not hyperventilating in shock, he is
probably suffering from central nervous
system or respiratory system damage
• Persistent hyperventilation is an ominous sign
and indicates improper treatment of shock

Urine
• It is a good indicator for the severity of shock
• It is affected quite early even in moderate
shock
• It is also a good index of adequacy of
replacement therapy

CVP
• It is important in assessing shock
• As the blood volume decreases in
hypovolemic shock- CVP also decreases.
• Cardiogenic shock- no depletion in blood
volume and thus the CVP remains normal

Technique for measuring CVP

E.C.G
• In severe shock E.C.G may show signs of
myocardial ischaemia with depression of ST-T
segments.

Swan- Ganz catheter

• a) Flow in the cardiovascular
system
b) sampling of blood from
the pulmonary artery to give
accurate measurements of
blood gases in mixed venous
blood
c) filling pressure of both
right and left sides of the
heart
• Cardiac output
• Mixed venous
oxygen levels
• Vascular pressureswww.indiandentalacademy.com

Other diagnostic tests
• Diagnostic tests and purpose in shock
• • Blood hemoglobin and hematocrit: hypovolemic shock
• • Arterial Blood Gases: identify body compensatory mechanisms, such as
acidosis
• • Electrolytes
• • BUN and creatitine, osmolality: renal function
• • Blood cultures: identify causative organism in septic shock; treatment
• Diagnostic tests and purpose in shock
• • White blood count and differential: septic shock
• • Cardiac enzymes: diagnosis of cardiogenic shock (Cardiac enzymes are:
lactate dehydrogenase (LDH); Creatine phosphokinase (CPK); serum
glutamic-oxaloacetic
• transaminase (SGOT,SGPT):liver function
• Other tests may be ordered

TYPES OF SHOCK
• HYPOVOLEMIC (Oligaemic, Haematogenic) SHOCK
TRAUMATIC shock is a type of Hypovolemic shock.
• SEPTIC- Combination of VASOGENIC & HYPOVOLEMIC
COMPONENTS

I. Haematogenic shock
Causes of hypovolemic shock
• Haemorrhagic i.e. loss of blood
a) Blood lost from injured part- external or internal
b) Blood lost into injured part- major fractures, big
loops of strangulated gut, acute pancreatitis
• Non- Haemmorhagic
a) Loss of plasma and fluid:
from and into the intestine- vomiting , diarrhea, gut
obstruction
b) Into the peritoneal cavity –peritonitis, acute
pancreatitis.

HYPOVOLEMIC SHOCK

CLINICAL FEATURES
% Blood loss
Clinical Signs
< 15 Slightly increased heart rate, bleeding.
15-30 Increased heart rate, increased diastolic
blood pressure, prolonged capillary refill
30-40 Above findings plus: hypotension,
confusion, acidosis, decreased urine
output
> 40 Refractory hypotension, refractory
acidosis, death

Mild shock
• Loss less than 20%
• Adrenergic constriction of blood vessels in the skin
• Collapse of subcutaneous veins of the extremities, which
becomes pale and cool.
• Sweat in the forehead, hand and feet due to adrenergic
discharge.
• Urinary output, pulse rate and blood pressure at this
stage remains normal.
• The patient feels thirsty and cold.

Moderate shock
• 20-40% blood loss
• all the above findings plus oliguria
• The pulse rate-increased but < 100 beats /minute
• The blood pressure remains normal but may fall in the later
stage in more severe group.
• Pulse rate and blood pressure are never the main signs of
shock- shock may be present even with normal pulse rate and
normal blood pressure.

Severe shock
• Loss of blood more than 40% pallor-skin of
extremities becomes pale, low urinary output, rapid
pulse and low blood pressure

TREATMENT
• 1) Resuscitation
• 2) Immediate Control of Bleeding
• 3) Extracellular fluid replacement
• 4) Drugs

Resuscitation
• Clear Airway and maintaining adequate ventilation and
oxygenation.
• Lowering of the head with support of the jaw to prevent
airway obstruction and administration of oxygen.
• Lowering the head will improve venous return preventing
stasis of blood in the muscle of leg and preventing oedema,
also improve cerebral circulation.
• Intratracheal intubation and mechanical ventilation are
required in cases of airway obstruction.

Immediate control of Bleeding
• Raising the foot end of the bed
• Compression bandage to tamponade
external haemorrhage.
• Operation may be required to stop
bleeding as soon as the resuscitation
has been achieved.

Extracellular fluid replacement
• A non sugar, non protein crystalloid solution with a sodium
concentration approximately that of a plasma is preferable in
the initial stage of fluid replacement-
(Ringers lactate, Ringers acetate, or normal saline supplemented
by 1 or 2 ampoules of sodium bicarbonate)
• Solution is run at a rapid speed so that in 45 minutes between
1000 and 2000 ml solution is given intravenously, upto 1 or 2
liters

• Rapid administration of 5% glucose is never
recommended- may induce osmotic diuresis- which
further depletes patients vascular volume.
• Resuscitation should always be started with
crystalloid solution even if blood is available.
• If started with acidotic cold bank blood with
potassium concentration-efficiency of myocardium
is tremendously jeopardized.

Drugs-
Chronotropic agents
• It increases the heart rate
• Drugs should be used selectively to patients with bradycardias
• Atropine is the ,most widely used, followed by Isoproterenol.
Inotropic agents
• These drugs improve the strength of cardiac muscle
contraction.
• Dopamine and Dobutamine are the most commonly used drug
• These drugs in low doses increase myocardial contractility
and selectively increase renal blood flow by dilating the renal
vasculature

Vasoconstrictors
• Are particularly beneficial in neurogenic shock,
seldom used in hypovolemic shock.
• The main role of these drugs in this condition is that
they increase blood pressure and increase blood
perfusion for coronary circulation.
• They also increase myocardial contractility
• Phenlyephrine and Metaraminol.

II. TRAUMATIC SHOCK
• PATHOPHYSIOLOGY
• That traumatized tissue activate the coagulation system and release the
micro thrombi into the circulation.
• These may occlude or constrict parts of pulmonary microvasculature to
increase pulmonary vascular resistance.
• This increases right ventricular diastolic and right atrial pressures.
• Humoral products of these microthrombi induce a generalized increase in
capillary permeability- to loss of plasma into the interstitial tissue
throughout the body.
• This depletes the vascular volume to a great extent

Clinical features
• Similar to hypovolemic shock,
• Two differentiating features are;-
1. Presence of peripheral and pulmonary oedema in
this type of shock
2. Infusion of large volumes of fluid which may be
adequate for pure hypovolemic shock, is usually
inadequate for traumatic shock.

Treatment
• Resuscitation-
Mechanical ventilatory support is more needed.
• Local treatment of trauma and control of bleeding-surgical
debridement of ischaemic and dead tissues and immobilisation
• Fluid replacement- more fluid is required than hypovolemic
shock
• Role of anticoagulation therapy to prevent dessiminated
intravascular coagulation has debateable role.
• One intravenous dose of 10,000 units of Heparin seems to be
effective for this purpose.

III. Vasogenic shock
• The essential cause is pooling of blood in the terminal
arterioles and capacitance veins, leading to gross reduction in
the actively circulating blood volume.
• Neurogenic shock
• Psychogenic shock
• Vasovagal shock
• Anaphylactic shock

A. NEUROGENIC SHOCK
• Cause:
• There is loss of sympathetic control of the peripheral
vasculature
a) Spinal cord injury
b) Spinal anesthesia

Pathophysiology
• There is dilatation of the systemic vasculature which lowers the
systemic arterial pressure. Blood pools in the systemic venules and
small veins.
• The right heart filling and stroke volume decreases
• This decrease pulmonary blood volume and left heart filling so that
left ventricular output decreases.
• Discharge of adrenergic nervous system to the innervated parts of
the body and release of Angiotensin and Vasopressin are the
compensatory mechanisms which fail to restore cardiac output to
normal, though systemic arterial pressure responds in part.

CLINICAL FEATURES
• The peculiar features are the skin remains warm,
pink and well perfused in contradiction to the
hypovolemic shock.
• Urine output may be normal.
• But heart rate is rapid and the blood pressure is low.

TREATMENT
• Elevation of the legs (Trendelenburg position)
• Administration of fluids is important.
• Safely treated with vasoconstrictors drug.
• Though there is some risk as the vasculature above the spinal
cord lesion may also be constricted excessively and may
develop ischaemic necrosis of the fingers, yet its action to
restore venous tone and thus restoring right heart filling and
cardiac output is more important .

B. Psychogenic shock
• Causes;
By loss of sympathetic control:
• Sudden fright, apprehension, grief.
• Acute pain e.g blow to testis
• Pathophysiology:
• A sudden dilation of the blood vessels takes place in
response to an emotional or traumatic situation
• CLINICAL FEATURES
• Signs/Symptoms: Rapid pulse, Normal or low blood
pressure.

Treatment of Psychogenic shock
• Determine duration of unconsciousness
• Record initial vital signs and mental status
If patient is
confused or slow to regain consciousness, suspect head
injury.

C. Vasovagal shock
• Cause:
• Pooling of blood in the large venous reservoirs (limb muscles)
and dilated splanchnic arterioles causing reduced venous
return to the heart, low cardiac output and reflex bradycardia.
• Consequently the reduced cerebral perfusion causes cerebral
hypoxia and unconsciousness, but prostration and reflex
vasoconstriction so increases the venous return and cardiac
output as to restore cerebral perfusion and consciousness.
• If the patient is maintained in an upright or sitting position, for
long e.g. in dental chair, permanent cerebral damage may
occur.
• Most common form of shock in dental setup.www.indiandentalacademy.com

TREATMENT:
Stop the dental procedure
Remove any instruments, gauze or cotton rolls that can be
aspirated or which can obstruct the airway.
• Positioning of the patient- supine position, legs elevated.
• Clothes are loosened
• Vital signs are to be monitored.
• Chills- pts covered with blankets to provide warmth.
• Administration of oxygen.
• Ammonia can be used for inhalation –respiratory stimulant–
direct stimulation of the CNS.
• Administration of atropine,iv –restoration of hemodynamic
state.

D. Anaphylactic shock
• A result of an immediate hypersensitivity reaction that
causes the blood vessels to dilate and the tissues lining the
respiratory system to swell.
Causes:
• Penicillin administration is among the common causes.
• Other causes include anaesthetics, dextrans, serum
injections, stings and consumption of shellfish
• Pathophysiology:
• The antigen combines with IgE on the mast cells and
basophils, releasing large amounts of histamine and slow
release substances of anaphylaxsis (SRS-A)

Signs and symptoms, and treatment of Anaphylactic Shock
• the blood vessels to dilate,
• the tissues lining the respiratory system to swell in a response to the
substance to which the individual is allergic.
• Some signs and symptoms of anaphylactic shock may include:
• it can develop within seconds,
• mild itching, burning skin, vascular dilation, generalized edema,
bronchospasm, laryngeal edema, respiratory distress with hypoxia,
profound coma, rapid death.
• mortality rate is around 10%.
• Treatment of anaphylactic shock
• Supply respiratory assistance
• Assist ventilations
• Determine cause of reaction
• Epinephrine( per doctor’s order)

IV. CARDIOGENIC SHOCK
• Causes
• Intrinsic cardiogenic shock- the myocardial contractility is
grossly impaired e.g. myocardial infarction, myocarditis,
cardiac arrhythmias
• Cardiac compressive shock- there is compression of the
cardiac chambers and /or great veins, e.g, cardiac
tamponade, tension pneumothorax.
• Cardiac obstructive shock- there is obstruction either in the
pulmonary or systemic circulation-
a) Pulmonary embolism, pulmonary vascular disease
b) Mechanical obstruction to aorta, systemic arteriolar
constriction.

Pathophysiology
• It is usually due to primary dysfunction of one ventricle or the other.
Dysfunction-
• myocardial infarction,
• chronic congestive heart failure,
• cardiac arrhythmias,
• pulmonary embolism or systemic arterial hypertension
• When right ventricle is envolved- right heart unable to pump blood in
adequate amounts to the lungs. Filling of the heart decreases. So left
ventricular output decreases.
• When left ventricle is envolved the left ventricle is unable to maintain an
adeqate atroke volume. Left ventricular output and systemic arterial blood
pressure decreases. There is engorgement of the pulmonary vasculature
due to normal right ventricular output, but failure of the left heart.

CLINICAL FEATURES
• The skin is pale and cool
• The urine output is low.
• Gradually the pulse becomes rapid.
• The arterial blood pressure becomes low.
• In right ventricular dysfunction -the neck veins (distented) and the liver
may also be enlarged.
• In left ventricular dysfunction -bronchial rales are present and a third
heart sound is heard.
• Gradually the heart becomes enlarged and when the right ventricle also
fails distended neck veins will be visible.

TREATMENT
• Airway must be clear with adequate oxygenation.
• In case of right sided failure caused by a massive pulmonary embolus
should be treated with large doses of Heparin intravenously.
• If pain is complained of in case of left sided failure proper sedative e.g.
Morphine should be prescribed.
• Fulminant pulmonary oedema should be treated with a diuretic.
• Further treatment of cardiogenic shock is complex and beyond the scope
of this treatise.

V. SEPTIC SHOCK
• The importance of this shock is that it possesses a high
mortality rate of about 50% or more.
• This is a sequela to severe systemic sepsis.
• The common sources of infection:
1. the genito-urinary tract
2. respiratory tract
3. intraabdominal sepsis
4. burns and indwelling monitoring catheters.

Pathophysiology
• The most frequent causative organisms are gram positive and gram
negative bacteria, though any agent capable of producing infection
may cause septic shock.
• Because of effective antibiotic treatment available for the most gram
positive infections, the majority of cases of septic shock are now
caused by gram negative bacteria.

The common organisms are-(in order of decreasing
frequency).
• E.coli,
• Klebsiella serobacter,
• Proteus,
• Pseudomonas and Bacteroids
• Recently Klebsiella group are more isolated in cases of
septic shock.

Gram positive sepsis and shock-
• Caused by dissemination of a potent exotoxin liberated from
gram positive bacteria without the evidence of bacteraemia.
• More noticed in Clostridium tetani and Clostridium perfringes
infection and fulminating infections from Staphylococcus,
Streptococcus or Pneumococcus organisms.
• Basically caused by massive fluid losses.
• Arterial resistence falls, but the peculiar feature is that there
is little or no reduction in cardiac output even with
progressive hypotension.
• Urine output is usually normal.

• Gram negative sepsis and shock –
• The most frequent source of gram negative infections
1. The genitourinary system- the patients often associated had operations or
instrumentations of the urinary track.
2. The respiratory system and the patients have had tracheostomy done.
3. The G.I tract system with disease such as biliary tract infections,
intraabdominal abscesses and peritonitis
• The severity of the shock is considerable.
• There may be mild hypotension following instrumentation of the
genitourinary tract.
• In contrast the patient with multiple intraabdominal abscesses or
necrotizing pneumonia may suffer from fulminating septic shock with poor
prognosis.
• Outlook is more favorable when the source of infection more accessible to
surgical intervention. i.e surgical drainage. e.g. septic abortions

CLINICAL FEATURES
• Development of chills
• Elevated temperature above 100 degree F.
• Two types- Early warm shock
• Late cold shock

In early warm shock
• There is cutaneous vasodilatation. The toxins from the
infected tissue increase the body temperature. To bring this
temperature down, the vasculature of the skin dialates. The
cuatneous vasodilatation decreases systemic vascular
resistence. So the arterial blood pressure falls, but the cardiac
output increases because the left ventricle has minimal
resistance to pump against.
• Adrenergic discharge further increases cardiac output .
• In this stage the skin remains warm, pink and well perfused.
The cutaneous veins remain full. The pulse rate becomes high
and the systemic arterial pressure low. Diagnosis is not
difficult as this condition is associated with intermittent spikes
of fever alternating with bolus of chills.

In late cold shock
• there is increased vascular permeability due to
liberation of toxic products into the center
circulation.
• This results in hypovolemia and right heart filling
decreases. Similarly there is decrease of flow into the
pulmonary vasculature, so left heart filling decreases,
so is the cardiac output.
• Clinically it may be difficult to differentiate this type
of shock from hypovolemic shock or from traumatic
shock, only guide remains is the knowledge of
existence of a septic focus.

TREATMENT
• The only effective way to reduce the
mortality is by prompt diagnosis and
treatment
1. Treatment of infection by early surgical
debridement or drainage and by use of
appropriate antibiotics.
2. Treatment of shock which includes fluid
replacement, steroid administration and use
of vasoactive drugs.

• Cephalothin 6-8 gm/day in 4-6 divided doses,
• Getamicin 5mg/kg/day
• Clindamycin (bacteroids) or chloromycetin
• Fluid replacement
• Mechanical ventilation along with endotracheal
intubation is frequently needed in treating patients
with late septic shock. In adequate tissue oxygenation
is consistent feature of shcok and attention to all
components of oxygen transport system is essential.

• Steroids
• Effectivity questioned
• 15- 30 mg /kg of methylprednisolone or equivalent dose of
dexamethasone is given i.v in 5 to 10 mins
• The same dose may be repeated within 4 hours if the
beneficial effects have not been achieved.
• There is hardly need of more than two doses
• Vasoactive drugs
• The vasopressure drug with prominent alpha adrenergic effect
are of limited value in the treatment of this type of shock. The
use of vasoactive drug with mixed alpha and beta adrenergic
effects e.g. Metaraminol may be indicated

• Vasodilator such as Phenoxybenzamine are more
popular particularly when combined with fluid
replacement and other measures havce failed to
restore adequate circulation
• Isoproterenol has inotropic and chronotropic efefcts
on the heart and produces mild peripheral
vasodilatation. This may cause a slight fall in blood
pressure due to vasodilatation which requires
additional volume replacement

INSULIN SHOCK
• Pt has taken insulin but food intake is insufficient.
• Physical Appearance- very weak
• moist and pale skin.
• Pulse-full and bounding
• Tremors –frequent
• Convulsions in late stage.
Treatment-
If pt is conscious a high sugar drink or orange juice.
If pt is unconscious a glucose paste can be applied to the buccal
mucosa and 5% dextrose iv drip as fast as follows should be
instituted.

HYPOADRENAL SHOCK
• It occurs in settings in which unrecognized adrenal insufficiency
complicates the host adrenal response to the stress induced by acute
illness or major surgery
• Adrenocortical insufficiency may occur as a consequence of the
1. Chronic administration of high doses of exogenous glucocorticoids
2. Trauma
3. Sepsis
• Less commonly adrenal insufficiency secondary to
1. Idiopathic atrophy of adrenal gland
2. TB
3. Metastasis
4. Bilateral hemorrhage
5. Amyloidosis

Treatment consists of
• Dexamethasone sodium phosphate 4mg i.v
Or
• Hydrocortisone 100mg every 6-8hr
• Simultaneous volume resusitation and pressor support
are required.

CRUSH SYNDROME
• It is a symptom complex in which a portion of
the body becomes crushed due to heavy weight
falls on that portion of the body.
• This type of injury is come across after
earthquakes, mine injuries, air raids, collapse
of a building or use of tourniquet for a longer
period

• In this syndrome oligaemic shock occurs due to
extravasation of blood into the muscles in the affected
portion of the body. But the degree of shock has no relation
to the development of the syndrome.
• The muscles become crushed and myohaemoglobin enters
the circulation and may cause acute renal tubular necrosis.
• The crushed muscles swell considerably. As they are
confined within a tough deep fascia in the inferiro ischaemic
damage to the limb.
• At this stage the limb feels tense and the aptient complains of
severe pain in the limb. Urine output is reduced, if ureamia
supervenes the patient may show restlessness, apathy and
mild delirium.

• Treatment
• First aid measure application of tourniquet to the affected limb
above the crush injury is a good method to reduce admission of
deleterious substances into general circulation
• Parallel incisions can be given to relieve tension, through
which the crushed swollen muscles may protrude.
Administration of intravenous fluid is required to combat
hypovolaemic shock, but it should be remembered that in this
condition kidney function is also jeopardized so
administration of fluid should be restricted to 500 ml+ urinary
output.

• Low molecular weight dextran (40000) or Rheomacrodex is particularly
effective in this condition as it prevents sludging of red cells in small blood
vessels and maintains circulation.
• Mannitol is also very effective in this condition-1mg/kg body weight as
20% solution in 12 hours
• This approximately corresponds to three infusions of 100 ml during and
after operation. This restores urinary output and prevents acute renal
failure.
• Catherisation od the bladder should be performed before instituting
mannitol
• Haemodialysis should be used as a life saving procedure in grave
conditions.

ADJUNCTIVE THERAPIES
• Positioning:
Elevating the foot of the bed (i.e. placing the “shock blocks”) and assumption
of the Trendelenburg position without flexion of the knees are effective but
may increase work of breathing and risk of aspiration. Simply elevating
both legs may be an optimal approach.
• Pneumatic AntiShock Garment (PASG):
The PASG and the Military AntiShock Trousers (MAST) are inflatable external
compression devices that can be wrapped around the legs and the abdomen.
The most appropriate use is as a means to tamponade and to prevent
ongoing bleeding and augment hemostasis.
• Rewarming
The infusion of large volumes of refrigerated blood products and room
temperature crytalloid solutions can rapidly drop core temperatures if fluid
is not run through warming devices ---leading to hypothermia– directly
impairs the coagulation pathway, sometimes causing a significant
coagulopathy. www.indiandentalacademy.com

Use of guanylate cyclase inhibitors in the
treatment of shock
US Patent Issued on March 29, 1994
• The invention relates to a method for the treatment of shock states,
comprising the administration of a therapeutically effective amount of a
guanylate cyclase inhibitor to a patient in need thereof.
• wherein said guanylate cyclase inhibitor is selected from the group
consisting of methylene blue, 6-anilino-5,8-guinalinedione (LY83583), N-
methylhydroxylamine, hydroxylamine, ethacrynic acid and retinol.
The invention also relates to the method for treatment of shock, comprising
the administration of a therapeutically effective amount of a redox dye to a
patient in need thereof. Redox dye is selected from the group consisting of
methylene blue, toluidine blue, neutral red, tetrazolium salts, chloranil and
dichlorophenolindophenol

.
The invention also relates to the methods of the invention, wherein said
shock comprises septic shock, cardiogenic shock, hypovolemic shock,
shock resulting from blood flow obstruction, neuropathic shock, and
hypotensive disorders.
The invention also relates to the methods of the invention wherein said
compounds are administered as part of a pharmaceutical composition
comprising a pharmaceutically acceptable carrier.
The invention also relates to the methods of the invention wherein said
pharmaceutical composition is administered to a patient by a route
comprising intravenous, intramuscular, subcutaneous, sublingual, oral,
rectal or aerosol delivery.

Summary
• Life threatening: Early goal directed therapy and regular
monitoring by trained staff will change outcome.
• Early detection : DON’T RELY ON BP
• High index of suspicion
• Monitor casualties susceptible to shock

References
1. http://www.stagesofshock.com/stage1/index.ht
ml
2. Bailey and Love’s Short Practise of Surgery 24th
Edition.
3. Textbook of Oral and Maxillofacial Surgery
Neelima Mallik 2nd
Edition.
4. Jonathan S etal: Treatment of Patients with
Severe Sepsis and Septic Shock:A Retrospective
review of Practice Prior to the Publication of
Sepsis Guidelines: www. Googlesearch.com

• Use of guanylate cyclase inhibitors in the
treatment of shock www.uspatents.com
• Harrison:Principles of Internal
Medicine;17th
edition
• Dental Management of medically
compromised patient,7th
edition, Little and
Falace.
• Medical emergencies in dental office, 6th
edition; Stanley Malamed.

Shock and its management final/ dental implant courses

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (13)

Similar to Shock and its management final/ dental implant courses

Similar to Shock and its management final/ dental implant courses (20)

More from Indian dental academy

More from Indian dental academy (20)

Recently uploaded

Recently uploaded (20)

Shock and its management final/ dental implant courses