Haemorrhage and Shock: Relevance in Periodontal Surgery

IMPORTANT TERMS
 Cardiac Cycle
 The repetitive pumping action that produces pressure
changes that circulate blood throughout the body
 Cardiac Output
 The total amount of blood separately pumped by each
ventricle per minute, usually expressed in liters per
minute

Cardiac Output
 Normal cardiac output = 5 to 6 liters per minute
(LPM)
 Can increase up to 30 LPM in times of stress or
exercise
 Determined by multiplying the heart rate by the
volume of blood ejected by each ventricle during
each beat (stroke volume)
 CO is influenced by:
 Strength of contraction
 Rate of contraction
 Amount of venous return available to the ventricle
(preload)

Circulation
 Systolic Pressure
 Strength and volume of cardiac output
 Diastolic Pressure
 More indicative of the state of constriction of the
arterioles
 Mean Arterial Pressure
 1/3 pulse pressure added to the diastolic pressure
 Tissue perfusion pressure

Starling’s Law of the Heart
 When the rate at which blood flows into the
heart from the veins (venous return) changes,
the heart automatically adjusts its output to
match inflow.
 The more blood the heart receives the more it
pumps…
 Increased end diastolic volume increases
contractility.
 Increases stroke volume.
 Increases cardiac output.
 Starling curves at any end-diastolic volume.
 Increased sympathetic input increases stroke volume.
 Decreased sympathetic input decreases stroke volume.

HAEMORRHAGE
 It is defined as the escape of blood from a blood vessel.
 The bleeding may occur externally or interally into serous
cavities e.g. haemothorax, haemoperitoneum etc into a
hollow viscus.
 Extravasation of blood into the tissues with resultant
swelling is called haematoma.
 Large extravasation of blood into skin and mucous
membrane are called ecchymoses.
 Purpura are small areas of haemorrhages into skin and
mucous membrane.
 Petechiae are minute pin-head sized haemorrhages.

ETIOLOGY
The blood loss may be large or sudden (acute), or small
repeated bleeds may occur over a period of time (chronic).
1. Trauma to the vessel wall e.g. penetrating wound in the
heart or great vessels, during labour etc.
2. Spontaneous haemorrhage e.g. rupture of an aneurysm,
septicaemia, bleeding diathesis, acute leukaemia’s,scurvy.
3. Inflammatory lesions of the vessel wall, e.g. bleeding
from chronic peptic ulcer, typhoid ulcers, syphilitic
involvement of the aorta.
4. Vascular diseases e.g. atherosclerosis.
5. Elevated pressure within the vessels e.g. cerebral and
retinal haemorrhages in systemic hypertension etc.

CLASSIFICATION
According to the source of haemorrhage, it is classified in two
ways:-
A. 1. EXTERNAL HAEMORRHAGE
2. INTERNAL HAEMORRHAGE
B.1. ARTERIAL
2. VENOUS HAEMORRHAGE
3. CAPILLARY HAEMORRHAGE

1.External haemorrhage- is the one that is revealed
outside or can be seen externally.
2.Internal haemorrhage- is one that is not seen
outside, it is a concealed haemorrhage. For e.g.
bleeding peptic ulcer, ruptured ectopic gestation,
fracture of major bones. Sometimes this
haemorrhage may be revealed or can be external .
E.g. melaena from bleeding peptic ulcer.

1. Arterial haemorrhage
It is the extravasation of blood from artery,
Bright red in colour
Spurting as a jet which rises as falls in time with
the pulse.
2. Venous haemorrhage
One which comes from a vein.
Darker red, and the colour darkens still further
from excessive oxygen desaturation when blood
loss is severe or in respiratory depression or
obstruction.
Has a steady, copious flow.

3. Capillary haemorrhage
bright red in colour
Often oozes out rapidly
If continues for many hours, blood loss becomes
serious, as in haemophilia.
Venous haemorrhage whether primary or
reactionary, is exceedingly difficult to bring under
control. Penetrating wounds involving man veins if
the thigh or groin are fatal .

According to the time of appearance of
haemorrhage, it is of following types:-
• It occurs at the time of injury or
operation.
1. PRIMARY
HAEMORRHAG
E
• May follow primary haemorrhage
within 24 hours and is due to
slippage of ligature, dislodgement
of clot, or cessation of reflex
vasospasm.
2.
REACTIONARY
HAEMORRHAG
E
• Occurs after 7-14 days and due to
infection and sloughing of a part of
the wall of an artery.
• Predisposing factors are pressure of
discharge tube, cancer etc.
3. SECONDARY
HAEMORRHAG
E

CLINICAL FEATURES OF HAEMORRHAGE
In case of external haemorrhage, the bleeding is seen from
outside and the diagnosis is confirmed
In case of internal haemorrhage the bleeding is concealed
and is not seen from outside.
A few symptoms and signs usually accompany heavy blood
loss, be it internal or external.
 Increased pulse rate,
 low blood pressure,
 increasing pallor,
 restlessness and
 deep sighing inspiration with in-drawing of the ala nasae
(air hunger).
 Cold and clammy extremities, empty veins are also
characteristically seen when the bleeding is continuing.

ASPECTS OF THE PATHOPHYSIOLOGY OF
HAEMORRHAGE
Low cardiac output is an early feature in shock.
Vasoconstriction occurs in an attempt to maintain perfusion
pressure to the vital organs such as brain, kidney etc.
It pushes more blood into dynamic circulation while tachycardia
helps to maintain a falling cardiac output.
The minute ventilation rises 1-2 times and respiratory rate 2-3 times
maintaining oxygenation except in cardiogenic shock with
pulmonary oedema.
The renal blood flow is reduced with reduction of glomerular
filtration and urine output

The renin-angiotensin mechanism is activated with further
and aldosterone release, causing salt and water retention .
As cardiac output falls, the hypotension and tachycardia
cause poor perfusion of the coronary arteries, and this , in
conjunction with hypoxia, metabolic acidosis and release
of cardiac depressants causes further cardiac depression
and pump failure.
The cells become starved of oxygen and anaerobic
metabolism lead to lactic acidosis. Eventually the cell
membranes cannot pump sodium out of the cells; sodium
enters the cells and potassium leaks out.

Thus the serum potassium is elevated. Calcium leaks into
the cells, lowering the serum calcium.
Furthermore intracellular lysosomes break down and release
powerful enzymes causing further damage. The cells are
sick- ‘ the sick cell syndrome’.
The platelets are activated in shock due to stagnation of
blood in the capillaries. Blood sludging with red cell
aggregation may progress to formation of clots leading to
disseminated intravascular coagulation (DIC).

MEASUREMENT OF ACUTE BLOOD LOSS
It is important to measure how much patient has lost blood.
This amount should always be replaced.
The blood loss detected by the methods is usually less than
the actual loss. This is because a considerable amount of
water is lost via lungs, from the wound and by evaporation
of sweat from skin.
This loss of plasma and water constitutes 20% more than
blood loss detected by various methods.

The best method of detecting is by weighing swabs. The
other methods are as follows:-
1. Blood clot tells the size of a clenched fist is roughly equal
to 500ml.
2. Swelling in closed fractures- Moderate swelling in closed
fracture of tibia is equal to 500-1500 ml blood loss.
Moderate swelling in fractured shaft of femur is 500-
2000ml.
(Ruscoe Clarke)
3. Swab weighing – Blood loss can be measured by weighing
the swabs before and after use and adding the total so
obtained (1g = 1ml) to the volume of blood collected in
the suction or drainage bottles.

 In extensive wounds , the blood loss estimated in this way is
much less than the total amount of blood, plasma and water
actually lost from the vascular system because of loss into the
tissues, evaporation of sweat etc accounting for additional 20%.
4. Haemoglobin level- This is estimated in g/100m normal being
12-16/100ml (12-16 g/dl). There is no immediate change in
haemorrhage, but within few hours the level is lowered by
haemodilution the movement of fluid into the vascular
compartment in order to restore the blood volume.
The degree of dilution can be gauged by haematocrit reading
(PCV) packed cell volume.
PCV is measured on capillary blood and read in mm.
Men- 40-56 %
Women – 35-48 %
5. Measurement of central venous pressure.

THE TREATMENT OF HAEMORRHAGE
Stop the blood loss by Pressure and Packing,
Position and Rest, Operative procedures( ligation, repair
etc).
Restore blood volume by blood
transfusion,Albumin 4-5 %, gelatin, dextran, plasma
infusions.

1. PRESSURE and PACKING
 The first-aid treatment of haemorrhage from a wound is
pressure dressing and it should be bound on tightly.
Sterile pieces of gauze and bandages can be used.
 Packing by means of rolls of wide gauze is an important
standby in operative surgeries.
Tourniquets are to be avoided in first aid. These cannot
stop arterial bleeding, on contrary causes venous
congestion and increases venous bleeding. In modern
surgery place of tourniquet is only restricted in the
operation theatre as a prophylactic measure to control
haemorrhage.

2) POSITION and REST
 Absolute rest is vital so far as the treatment haemorrhage is
concerned. Restlessness causes more blood loss. Some
sedatives and analgesics can be prescribed to the patient.
 Analgesia facilitates rest. Morphine (10-20 mg) relieves
pain, calms restlessness and aids coronary and cerebral
blood flow.
 It is best given intra-muscularly or intravenously. It should
never be given subcutaneously. (?)
 But it is contraindicated in head injuries (?), very young
and very old where pethidine may be preferred.
In case of haemorrhage from thyroidectomy wound, the
head end of the bed is raised (anti-trendelenburg position)
In case of varicose veins, the foot-end is raised. It increases
blood supply to brain and restores blood pressure.

3) BY OPERATIVE METHODS
 During operation haemorrhage is usually stopped by artery
forceps and clips applied to the bleeding vessels. Now the
bleeding vessel is either ligated with catgut or silk
according to size of the vessel.
 When haemorrhage is in the form of oozing, Oxycel or
gelatine may be used to stop such bleeding.This type of
material provides a network upon which fibrin and
platelets are deposited to stop bleeding.
 When actual bleeding vessel cannot be ligated it is
customary to use rolls of gauze for packing of wound for
sometime. After 5 minutes the gauze pack is removed and
slight bleeding from the spurting vessel can be identified
and ligated to stop bleeding.

SHOCK
Shock is a life threatening condition characterized by poor
tissue perfusion with impaired cellular metabolism,
manifested in turn by serious physiological abnormalities.
 The term initial or primary shock is used for transient and
usually a benign vasovagal attack resulting from sudden
reduction of venous return to the heart caused by
neurogenic vasodilatation and peripheral pooling of blood.
 Clinically patients of primary shock suffer from attack
lasting few seconds or minutes and develop brief
unconsciousness, weakness, sinking sensation, pale and
clammy limbs.

CVP
 The central venous pressure (CVP) is the pressure
measured in the central veins close to the heart. It
indicates mean right atrial pressure and is frequently used
as an estimate of right ventricular preload.
 The central venous pressure (CVP) measures the filling
pressure of the right ventricular (RV); it gives an estimate
of the intravascular volume status and is an interplay of the
(1) circulating blood volume (2) venous tone and (3) right
ventricular function.
 Normal range for CVP is 2-8 cm H20 or 2-6 mmHg.
Measured by seldinger technique.
 The response of central venous pressure to a small fluid
challenge (200ml of crystalloid) helps in distinguishing
between cardiogenic and hypovolemic shock.
"Central Venous Catheter Physiology"

PCWP
 The pressure measured by wedging a pulmonary
catheter with an inflated balloon into a small
pulmonary arterial branch.
Because of the large compliance of the pulmonary
circulation, it provides an indirect measure of the left
atrial pressure.
For example, it is considered the gold standard for
determining the cause of acute pulmonary edema. It
has also been used to diagnose severity of left
ventricular failure and mitral stenosis, given that
elevated pulmonary capillary wedge pressure strongly
suggests failure of left ventricular output.
Postgrad. med. J. (August 1969) 45, 506-511.

 Better indicator of both
circulating blood volume
and left ventricular
function obtained by a
pulmonary artery
flotation ballon catheter.
 It is used to differentiate
between left and right
ventricular failure,
pulmonary embolus,
septic shock and ruptured
mitral valve.
 It is used to measure
cardiac output.

CLASSIFICATION AND ETIOLOGY OF SHOCK
1) Hypovolemic shock
 Acute haemorrhage
 Dehydration from vomitings, diarrhoea
 Burns
 Excessive use of diuretics
 Acute pancreatitis
2) CARDIOGENIC SHOCK
1) Deficient emptying
 Myocardial infarction
 Cardiomyopathies
 Rupture of the heart, ventricle, papillary muscle
 Cardiac arrythmias

2) Deficient filling
Cardiac tamponade from haemopericardium
3) Obstruction to the outflow
Pulmonary embolism
Ball valve thrombus
Tension pneumothorax
Dissecting aortic aneurysm
3) SEPTIC SHOCK
1)Gram-negative septicaemia e.g. Infection from E.coli,
Klebsiella, Pseudomonas
2)Gram-positive septicaemia e.g. Infection with
streptococci, pneumococci

4) OTHER TYPES
1) Traumatic shock
 Severe injuries
 Surgery with marked blood loss
 Obstetrical trauma
2) Neurogenic shock
 High cervical spinal cord injury
 Accidental high spinal anaesthesia
 Severe head injury
3) Hypoadrenal shock
 Administration of high doses of glucocorticoids
 Secondary adrenal insufficiency

PATHOGENESIS OF SHOCK
All forms of shock involve following derangements:-
a)Reduced effective circulating blood volume
b) Reduced supply of oxygen to the cells and tissues with
resultant anoxia.
c) Inflammatory mediators and toxins released from
shock induced cellular injury.

TYPES OF SHOCK
1) VASO-VAGAL SHOCK
It is brought about by pooling of blood in larger vascular
reservoirs and by dilatation of the arteriolar bed
causing reduced venous return to the heart, low
cardiac output and reflex bradycardia.
The reduced cerebral perfusion causes cerebral hypoxia
and unconsciousness but prostration and reflex
vasoconstriction increases the venous return and
cardiac output to restore cerebral perfusion and
consciousness.
It must be remembered that if the patient is maintained
in upright position as in a dental chair, it will cause
permanent cerebral damage.

2) HYPOVOLEMIC SHOCK
It is due to loss of intravascular volume by haemorrhage,
dehydration, vomiting and diarrhoea. It mostly occurs
from the systemic venules and small veins which
usually contain about 50% of total blood volume.
Loss of blood causes decreased filling of the right heart.
This causes decrease of filling of pulmonary vasculature.
Decreased filling of the left atrium and ventricle.
Drop in the arterial blood pressure.

COMPENSATORY MECHANISMS
The following compensatory mechanisms come into play:-
a) Adrenergic discharge
It starts within 60 secs after the blood loss.
It causes vasoconstriction of the venules and small veins, increase
heart rate and also constricts the vascular sphincters in the
kidney, skin etc.
This constriction displaces the blood into the right atrium and
ventricle increasing the diastolic pressure in the right ventricle
and also its stroke volume.
This selective vasoconstriction leads to increase in filling in right
heart and cardiac output.
Diverting the blood to the heart and brain.

b) Hyperventilation
This occurs in response to metabolic acidemia which
develops shortly after haemorrhage.
Spontaneous deep breathing sucks blood from
extrathoracic sites to the heart and lungs.
This leads to increase in the filing of left ventricle and
also the stroke volume.
BOTH ADRENERGIC DISCHARGE AND HYPERVENTILATION OCCUR
WITHIN ONE MINUTE OF BLOOD LOSS.

c) Release of vasoactive hormones
 Low perfusion of kidneys leads to release of hormone
known as renin from juxta-glomerular apparatus.
 Renin releases angiotensin I from liver, which is converted
to angiotensin II by the lungs.
 Angiotensin is a potent vasoconstrictorleading to
constriction of vasculature of splachnic organs, kidneys
and skin.
 Another potent vasoactive hormone is epinephrine which
is released from adrenal medulla as a conequence of
discharge of adrenergic nervous system.
d) Collapse
Assumption of recumbent posture due to collapse
automatically displaces blood from the lower part of the
body to the heart and increases the cardiac output.

CLINICAL FEATURES OF HYPOVOLEMIC SHOCK
1) MILD SHOCK
 Loss of less than 20% of blood volume leads to mild
shock.
 The most sensitive clinical finding is due to
adrenergic constriction of blood vessels in the skin.
 The result is the collapse of sub-cutaneous veins of
the extremities, particularly the feet which become
pale and cool.
 There is sweat in the forehead, head and feet due to
adrenergic discharge.
 Urinary output, pulse rate and blood pressure at this
stage are normal. The patient feels thirsty and cold.

2) MODERATE SHOCK
It involves loss of 20-40% of blood volume. Alongwith
the findings mentioned above, there will oliguria.
This oliguria is because of adrenergic discharge
alongwith the effects of circulating aldosterone and
vasopressin.
The pulse rate is increased but is less than 100 beats per
minute.
3) SEVERE SHOCK
Loss of blood volume more than 40% causes severe
shock.
There is pallor, low urinary output, rapid pulse and low
blood pressure.

CLINICAL MONITORING
Once the shock is diagnosed, constant monitoring of the patient is
required to assess the degree of blood loss and hemodynamic
impairment.
1) BLOOD PRESSURE
The diastolic pressure is the main indicator of the degree of
vasoconstriction. The systolic pressure indicates
vasoconstriction with stroke volume and rigidity of vessels.
The pulse pressure indicates the stroke volume and the cardiac
output.
2) RESPIRATION
Hyperventilation is a normal response of an early shock. If the
patient is not hyperventilating , he is surely suffering from
central nervous system or respiratory damage.
Persistent hyperventilation is an ominous sign and indicates
treatment of shock.

3) URINE
Urine output is a good indication of severity of shock. Urine
output is affected quite early even in moderate shock. It is
also a good index of adequacy of replacement therapy.
4) CVP
Measurement of Central Venous Pressure is quite important
in assessing shock. In hypovolemic shock, the blood
volume is decreased, so is the CVP, whereas in cardiogenic
shock there is no depletion of blood volume and the CVP
remains normal.
Technique of measuring CVP
A standard length of 20cm of intravenous catheter is passed
into the right internal jugular vein. This is performed with
full aseptic precautions with the patient head-down
position.

The head-down position is used to distend the vein and to
prevent air being sucked in. The catheter tip is gradually
pushed in to be positioned in the superior vena cava.
The catheter is connected to a saline manometer. By the level
of the saline, one can detect CVP. If the CVP is low,
intravenous infusion is suggested and if the CVP is high
intravenous may not be required.
5) E.C.G.
In severe shock electrocardiogram may show signs of
myocardial ischemia with depression results are less
accurate than the above method.

6) PULMONARY CAPILLARY WEDGE PRESSURE
It is a better indicator of circulating blood volume and left
ventricular function. If the catheter in a portion of the lung
where inflation of the lung occludes the pulmonary
capillaries the end of catheter estimates the pressure in the
alveoli rather than pressure in left atrium.
This catheter is used to differentiate between left and right
ventricular failure, presence of pulmonary embolism and
can also be used as a guide to therapy with fluids.

TREATMENT
1)RESUSCITATION
This should began immediately as the patient shows the
signs of hypovolemic shock. This starts with the
establishment of a clear airway and maintaining
adequate ventilation and oxygenation.
Lowering of head with support of the jaw to prevent airway
obstruction and administration of oxygen are usually all
that are needed.
Lowering of the head will improve venous return preventing
stasis of blood in the muscles of lungs and preventing
oedema.
This also improves the cerebral circulation which is quite
important at this stage.

Many patients in shock, particularly those who are suffering
from traumatic or septic shock require intubation and
positive-pressure ventilation.
Positive pressure ventilation improves the patients
cardiovascular status. Abrupt increase in airway pressure
expands the alveoli, displaces blood from pulmonary
vasculature into left atrium and ventricle.
Both the left ventricular output and systemic arterial
pressure increase.

2) IMMEDIATE CONTROL OF BLEEDING
This can be achieved by raising the foot-end of the bed and
by the compression bandage to tamponade external
haemorrhage.
Operation may be required to stop such bleeding as soon as
resuscitation has been achieved.
3) EXTRACELLULAR FLUID REPLACEMENT
Fluid replacement should be started following the control of
bleeding immediately.
A non-sugar , non-protein crystalloid solution with a sodium
concentration that of plasma is preferable in the initial
stages of fluid replacement.
The solution can be Ringer’s lactate, Ringer’s acetate or
normal saline.

 The solution is run at a speed of 45 minutes between 1000-
2000 ml solution is given intravenously. It is often observed
that the blood pressure will come back to normal and
become stable after infusion of 1 or 2 litres of such solution.
 Resuscitation should always be started with crystalloid
solution even if blood is available. If it is started with
acidotic cold bank blood with potassium concentration,
efficiency of myocardium is tremendously jeopardized.
 3 litres of fluid given over 45 minutes should resuscitate
any patient with arrested haemorrhage.
 The need for more fluid indicates continuation of bleeding
and such haemorrhage should be controlled surgically.

4) DRUGS
Few drugs are used sometimes in different types of shock:-
1) Sedatives
These are used to alleviate pain and some amount of sedation
is always required in any type of shock.
2) Chronotropic drugs
The patients in shock who have slow heart rate benefit from
chronotropic drugs as these increase heart rate.
Atropine is the most widely used drug in this group, followed
by isoproterenol.
These also act as vasodilators of systemic arterial and
capillary sphincters.

3) Ionotropic drugs
These drugs improve the strength of cardiac muscle
contraction.
Patients with cardiogenic and severe septic shock requirethis
drug especially.
The most commonly used are dopamine and dobutamine.
These lower the myocardial contractility and increase the
renal blood flow by dilating the renal vasculature.
4) Vasodilators
The most commonly used are nitroprusside and
nitroglycerine as these are reversible and short acting.
These are used when systemic vascular resistance is too much
raised.

5) β- blockers
Patients in cardiogenic shock with stiff myocardium and
rapid heart rate are benefitted.
The drug increases the efficiency of ventricular contraction.
Propranol is the most widely used drug in this group.
6) Diuretics
These drugs reduce the vascular volume and decrease filling
pressure.
Though oliguria is one of the main clinical manifestations of
hypovlemic shock, yet diuretics will not correct the
underlying cause but will further cause hypovolemia.
These are also not used in septic shock.

TRAUMATIC SHOCK
It is primarily due to hypovolemia from bleeding external and
internal wounds.
The pecularityof this shock is that traumatised tissues
activate the coagulation system and release microthrombi
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
generalised increase in capillary permeability.
This leads to loss of plasma into the interstitial tissues
throughout the body.
This depletes the vascular volume to a great extent.

CLINICAL FEATURES
The traumatic shock are almost similar to those of
hypovolaemic shock. The two differentiating features are:-
1) Presence of peripheral and pulmonary oedema
2) Infusion of large volumes of fluid which may be adequate
for pure hypovolaemic shock is usually inadequate for
traumatic shock.
TREATMENT
1) Resuscitation
In this type mechanical ventilatory support is more needed.
2) Local treatment of trauma and control of bleeding
Same as the hypovolaemic shock. Surgical debridement of
ischaemia and dead tissues and immobilisation of
fractures may be required.

3) Fluid replacement
More fluids are required to bring back the patient to
normalcy.
Role of anti-coagulation has a debatable role.
Increased coagulation consumes clotting factors of the blood
leading to more bleeding.
Moreover obstruction of microvasculature with such
microthrombi leads to ischemia.
Anti-coagulation with doses of heparin is large enough to
fully anticoagulate the patient may reverse the condition.

CARDIOGENIC SHOCK
It occurs when more than 50 percent of the wall of the
ventricle is damaged by infarction.
It is due to primary dysfunction of one ventricle over the
other. Such dysfunction may be due to myocardial
infarction, chronic congestive heart failure, cardiac
arrhythmia's.

PATHOGENESIS
Dysfunction of right ventricle leads to decreased ability of
right heart to pump blood in adequate amounts to blood.
Filling of left heart decreases.
Left ventricular output decreases. Fluid overload leads to
over-distension of the left ventricle, with pump failure.
High filling pressure in right ventricle make fluid leakage of
the pulmonary capillaries causing pulmonary oedema and
hypoxia.
Reduction in pumping efficiency of heart leads to excess
sweating, vomiting, diarrhoea and diminishes cardiac
output.

CLINICAL FEATURES
 In the beginning, cool and the urine output is low, gradually
pulse becomes rapid and arterial blood becomes low.
 In cases of right ventricular dysfunction the neck veins become
distended and liver may also become enlarged.
 In left ventricular dysfunction the patient has bronchials rales
and a third heart sound is heart. Gradually heart becomes
enlarged and right ventricle also fails.
 Distented neck is always.
TREATMENT
 ABC
 In case of right sided failure caused by massive pulmonary
embolus, should be treated with large dose of heparin I.V.
 In case of left sided failure, morphine should be given.
 For fulminant pulmonary oedema, diuretics should be given.

NEUROGENIC SHOCK
It is caused by traumatic or pharmacological blockage of
sympathetic nervous system producing dilatation of
resistance arterioles and capacitance veins, leading relative
hypovolemia and hypotension.
PATHOPHYSIOLOGY
Dilatation of systemic vasculature which lowers the systemic
systemic arterial blood pressure
Blood pools in systemic venules and small veins
Right heart filling and stroke volume decreases.
This decreases the pulmonary blood volume and left
ventricular output decreases.

The discharge of adrenergic nervous system to the innervated
parts of body and release of angiotensin and vasopressin
are compensatory mechanism which fail to restore the
cardiac output to normal though systemic arterial pressure
responds in part.
CLINICAL FEATURES
The peculiar feature is that skin remains warm, and well
perfused in contradistinction to the hypovolemic shock.
Urine output maybe normal but B.P. is low.

TREATMENT
 Elevation of legs
 Assumption of Trendelenburg position displaces blood
from systemic venules and small veins into the right heart
and thus increases cardiac output,
 Left ventricular emptying is quite efficient inspite of
elevated legs as the systemic vascular resistance is low.
 Administration of fluid is important. This increases filling
of right heart which in turn increases cardiac output.
 It can be treated with vasoconstrictor drugs. Its prompt
action saves the patient from sudden low B.P. and low
cardiac output from imminent damage to the more
important organs like brain, heart and kidneys.

SEPTIC SHOCK
This type of shock is most frequently caused by gram-
positive and gram-negative bacteria, though any agent
is capable of causing shock ( including viruses,
parasites, fungi).
The importance of this shock is that it posses a high
mortality rate of about 50%.

The common organisms which are concerned with septic shock
1) E.coli
2) Klebsiella aerobacter
3) Proteus
4) Pseudomonas
5) Bacteriods
In the order of decreasing frequency
Gram-positive sepsis and shock
It is usually caused by dissemination of
a potent exotoxin liberated from gram-
positive bacteria without the evidence
of bacteraemia.
E.g. Clostridium tetani or perfringes
Caused by massive fluid loss
Gram-negative sepsis and shock
Frequent source is the gram-
negative bacteria causing infections.
E.g. esophageal anastomoses or
suppurative conditions.

CLINICAL FEATURES
Septic shock is often recognised initially by the development
of chills and elevated temperature above 100˚ F.
EARLY WARM SHOCK
There is cutaneous vasodilatation. The toxins from the
infected tissues increase the body temperature. To bring
this temperature down, the vasculature of the skin dilates.
The cutaneous vasodilatation decreases the systemic vascular
resistance. So the arterial blood pressure falls, but the
cardiac output increases because the left ventricle has
minimal resistance against it.
Adrenergic discharge further increases cardiac output.

At this stage the skin is warm, pink and well perfused. The
pulse rate becomes high and systemic arterial pressure is
low.
LATE COLD SHOCK
There is increased vascular permeability due to liberation of
toxic products into the centre circulation.
This results in hypovolemia and right heart filling decreases.
There is decrease in flow into pulmonary vasculature, so left
heart filling decreases
Hence cardiac output decreases.

TREATMENT
Treatment can be divided into two groups:-
Treatment of infection by
early surgical
debridement or drainage
and by use of appropriate
antibiotics.
Treatment which includes
fluid replacement, steroid
administration and use of
vaso-active drugs.

STEROIDS
Steroids protect the body cell and its content from the effect
of endotoxin. Larger doses of steroids are known to exert
ionotropic effect on the heart and produce mild peripheral
vasodilatation.
Short term, high dose steroid therapy is recommended in
most cases that donot respond to the other methods of
treatment.
An initial dose of 15 to 30 mg per kg body weight of methyl
prednisolone or equivalent dose of dexamethasone is given
I.V. for 5 to 10 minutes.
The same dose may be repeated within 4 hrs if the beneficial
effects are not attained.

VASOACTIVE DRUGS
 The vasopressure drugs with prominent alpha adrenergic
effects are of limited value in treatment of this type of
shock.
 Vasodilator drugs such as phenoxybenzamine are more
popular particularly when combined with fluid
administration.
 Ionotropic agents eg iso-proterenol or dopamine is ideal
when simple volume replacement and other measures have
failed to restore adequate circulation.

1) Once a case has been diagnosed, the source of infection is
made while treatment of shock is started with fluid
replacement.
 Careful monitoring of central venous pressure,
pulmonary capillary wedge pressure, urine output and
venous blood gases.
 Debridement or drainage of infection should be
performed under local or general anaesthesia as soon as
possible after the initial stability of the patient.
 The use of specific antibiotics based on appropriate
culture and senstivity results .
 Often a combination of antibiotics may be sarted.
Cephaothin (6-8 gm/day I.V. in 4 to 6 divided doses).
 Gemtamycin (5mg/day), clindamycin are the antibiotics
to be started in beginning.

2) Fluid replacement is of great importance to provide
sufficient volume to vital organs.
3) Mechanical ventilation alongwith endotracheal intubation
is needed in treating patients with late septic shock.
Inadequate tissue oxygenation is a consistent feature of shock
and attention to all components of oxygen transport system
is essential.

Blood loss during periodontal flap surgery
Post operative bleeding after oral and periodontal surgery is a common
complication. The surgical procedure presents a challenge to the
body’s haemostatic mechanism.
Following surgical procedures, hemorrhage can range from a minor
leakage or oozing at the site, to extensive or frank bleeding at
surgical site.
The likelihood of this may be attributed to many factors, like the
 tissues of mouth and jaw are highly vascular
 infection
 intrinsic trauma
 presence of foreign bodies
Even after repeated instructions patients tend to play with the area of
surgery with their tongue and dislodge the blood clot, which
initiates secondary bleeding.
The tongue may also cause suction of blood by creating small negative
pressures that cause secondary bleeding. Salivary enzymes may lyse
the blood clot before it gets organized.

 Post operative bleeding may be present immediately
(primary hemorrhage),within 24hrs or as delayed post
operative bleeding (reactionary hemorrhage).
 It can be due to slippage of suture, dislodgement of clots,
cessation of reflex vasospasm, normalization of blood
pressure.
 Hemorrhage occurring after 7-14days is secondary to
trauma or surgery. The attributed cause is infection and
sloughing of blood vessels. Signs and symptoms may
include continuous flow, oozing or expectoration of blood
or copious pink saliva. Bleeding may be accompanied by
pain.
Patients lost an average of 134 ml of blood, with a range of 16 to 592 ml,
during periodontal flap procedures involving an average of 5 1/2 teeth in
posterior sextant.
J. Periodontal. November, 1977

Treatment includes:-
Reassurance, pressure pack, source of bleeding should
be determined.
If bleeding is due to residual granulation tissue or liver
clot type then it should be removed by high speed
suction or curettage.
Bony bleeding can be controlled by crushing the bone
with appropriate instrument.
Soft tissue bleeding may be treated by clamping it with
hemostat, if it still persists vessel ligation with sutures,
laser coagulation or electro-cautery may be necessary.
 Additional haemostatic agents may also be used.
International Journal of Contemporary Medical
Research 2016;3(5):1285-1286

 Surgery has become commonplace in the treatment of the
periodontal patient. A flap approach is commonly used to allow
the exposure and correction of periodontal defects. Although
such surgery may be routine, little attention has been directed to
the extent of hemorrhage occuring during this type of procedure.
 A healthy adult may lose up to 1 liter of blood before developing
hypotension, and many people frequently donate 500 ml to a
blood bank without any apparent adverse consequences.
 However, considering the possibility of postoperative oozing
and blood lost into the tissues during surgery, several
investigators recommend that blood losses greater than 500
ml should be replaced immediately with intravenous fluids
or whole blood.
 Balanced salt solutions do not involve as many hazards as blood
transfusion and should be used for volume replacement when
the loss of volume is less than 1 liter and the hemoglobin
concentration is adequate.

The following procedures are recommended while operating in
large areas of the mouth at one sitting or operating for long time
periods:
 Preoperative and postoperative blood pressures with the patient
sitting should be taken.
 A postoperative standing blood pressure should be recorded to
assess possible orthostatic hypotension resulting from acute
blood loss.
 Patients experiencing a drop in systolic blood pressure in the
standing position of 20 mm Hg, or a drop in diastolic blood
pressure of 10 mm Hg following surgery, should be treated with
balanced salt solutions intravenously until the blood pressure
returns to normal.

 A simple volumetric measurement of blood loss during
periodontal flap surgery should be performed using an
aspirator with a collection reservoir. The volume can be
assessed by using a known volume of irrigating fluids and
subtracting this from the total volume of fluid.
 Intravenous fluid replacement should be performed when the
patient either
(a) experiences orthostatic hypotension, or
(b) loses 500 ml or more of blood.
 Postoperative management of all periodontal surgery patients
should include instructions to drink 1 to 2 liters of fluid the day
of surgery and 2 days following surgery to help prevent
postoperative dehydration.

 The combination of possible postoperative blood loss
with operative haemorrhage suggests that patients
undergoing multiple quadrants of periodontal flap
surgery on the same day may lose as much blood as
patients undergoing a major surgical operation.
 In dentistry there is a need to be more conscious of
the possible sequelae and treatment of hypotension
and dehydration resulting from surgical blood loss.
This is especially true in periodontal surgery, as most
patients are being treated on an outpatient basis.

Haemorrhage and Shock: Relevance in Periodontal Surgery

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