Good

Morning

Haemorrhage

&

esented by : Dr. Himanshu Jatania

derated by: Dr. V.K. Joshi

Shock

Dr. Venkatesh Anehosur

Contents
1. Definition
2. Classification
3. Normal physiology of hemostasis
4. Clinical features
5. The Surgical patient & Risk of Haemorrhage
6. Methods of determining blood loss.
7. Haemorrhage control - Mechanical, Thermal & Chemical means
8. Local & Systemic Hemostatic Agents
9. Fluid Replacement
10. Special Clinical Considerations
11. Conclusion
12. References

Definition
- the flow of blood from a ruptured blood vessel (normally due to
injury)
- escape of blood from the circulatory system
- a heavy release of blood within or from the body

The term "haemorrhage" comes from the

Greek "haima" blood + rhegnumai" to break forth = a free and
forceful escape
of blood.

Classification
Source Arterial, venous or capillary
External

Appearance

Internal or concealed
Primary
Time of appearance
Secondary

Reactionary

Arterial
Bright red, spurting as jet with each systole.

Venous
Dark red, steady and copious
E.g. Varicose veins, oesophageal varices in portal
hypertension.

Capillary
Bright red, often rapid can be can be serious in
haemophilia.

* Primary haemorrhage
-

At the time of injury or operation

* Reactionary haemorrhage
Follows primary haemorrhage within 4 to 6 hours. Causes (1) Slipping of
ligature (2) Dislodgement of clot (3) Cessation of reflex vasospasm.
Raise in BP, restlessness

* Secondary haemorrhage
Occurs in 7 to 14 days because of infection and sloughing of vessel wall
(usually artery).
Predisposing factors are pressure of a draining tube, the presence of a
fragment of bone, a ligature in an infected area

Acute

Mild haemorrhage

Blood loss is less than 500ml. E.g.

Onset

minor oral surgical procedure.

Chronic

Moderate haemorrhage

Loss is upto 2L. Initially BP falls

Mild

but is restored by increased PR.

Severity

Moderate

Severe

Severe haemorrhage

Could be more than 2L. Due to

positive feed back mechanism BP
falls significantly hence is lethal.

Hemostasis
Normal hemostasis is dependent upon the complex
interaction of plasma coagulation and fibrinolytic
proteins, platelets, and the blood vasculature
Haemostasis consists of 3 phases:
Vascular phase
Primary Hemostasis
(Platelet Plug)
Platelet phase
Coagulation phase Secondary Hemostasis (Fibrin)

Vascular Phase
Local control - Vasoconstrictors such as thromboxane are released at the site
of the injury.
Systemic control - Epinephrine released by the adrenal glands stimulates
general vasoconstriction.

Platelet Phase

The administration of heparin does not interfere with this reaction and that
fact explains why haemostasis can occur in the heparinized patient

Clotting Factors

Coagulation Phase
Liquid blood -> semi solid gel

Thrombin : How ? Why ?

Inhibition of Excessive Clotting

Clotting factors are rapidly inactivated enzymes in the blood -> inactivate clotting factors.
Fibrin fibers inhibit the activity of thrombin fibrin fibres have an inhibitory effect on activity of thrombin ->
negative feedback loop

Clot Removal

Inhibitors Of Hemostasis
Primary Hemostasis : 1) Prostacyclin
2) Nitric oxide

Secondary Hemostasis: 1) Antithrombin (AT)

2) Heparin cofactor II
3) PROTEIN C
4) PROTEIN S
5) Thrombomodulin

clinical features

Pallor
Tachycardia
Tachypnoea
Rapid thready pulse
Hypotension
Oliguria
Cold clammy skin due to vasoconstriction
Dry face, dry mouth and goose skin appearance
Thirst
Anxiety, confusion and unconsciousness

The Surgical patient & Risk of Haemorrhage

Major Risk Factors
1.

Obstetric Bleeding

Minor Risk Factors

1. History of unusual
bleeding

2. Liver Disease
3.

Renal Disease

4.

Known hereditary diseases

2. Frequent episodes of
epistaxis
3. Unusual mucosal
bleeding

5. History of abnormal blood count

4.
6.

Medications

Abuse of illicit drugs

Low-Risk Patients
No history of bleeding
from previous surgery

Moderate-Risk
Patients

High-Risk Patients

No family H/O
coagulopathies

H/O abnormal bleeding

Patient is known to have
following tooth extraction a coagulopathy
or other minor surgery
Documented family
history of
bleeding
A family H/O bleeding

No H/O excessive
bleeding

Abnormal bruising
without trauma

No H/O liver disease

H/O liver disease

No H/O heavy alcohol

usage

Alcoholic
History of malabsorption

Not taking any

medication known to
cause bleeding

Long term antibiotic

usage

Patient taking warfarin

or heparin (within 4
hours)

Risk Category
Low-risk patient

Action Required

Proceed with surgery. No further investigation or

laboratory testing is required.

A more detailed history should be obtained and

the potential risk assessed.
Laboratory testing: Bleeding profile, bleeding time,
and platelet count. Consult with physician if
necessary.
Optimize patient preoperative: the treatment to
optimize the patient will depend on the results of
the findings that contribute to the risk factors.

Moderate-risk patient

High-risk patient

Consult with a hematologist. Laboratory testing:

Bleeding profile, bleeding time, and platelet count.
Management of bleeding problems before surgery.
Postoperative management.

Methods of determining blood loss

Blood clot: A clot size of a clenched fist is roughly equal to

500ml.

Swelling in closed fractures: Moderate swelling in closed

fracture of the tibia equals 500-1500ml of blood loss.

Moderate swelling in a fractured shaft of femur equals 500-2000ml

of blood loss.

Swab weighing
Blood loss = Weight of swab after use dry weight of swab.
To this add blood collected by suction or in drainage
bottle.1gm=1ml

Multiply this value by 1 to compensate for the water lost from

the plasma by evaporation ( in major surgeries)

Prime task is to stop bleeding

LOCAL HAEMOSTASIS
- Mechanical
- Thermal
- Chemical

Mechanical
Digital Pressure: Finger -> least traumatic
vascular hemostat
Haemostat -> temporary mechanical device to
stem bleeding.

LIGATION
In general, a ligature replaces the haemostat as a
permanent method of effecting haemostasis in a single
vessel.
When a vessel is transected, a simple ligature usually is
sufficient.
For larger arteries with pulsation and longitudinal motion,
transfixation suture to prevent slipping is indicated.
The adventitia and media constitute the major holding
forces within the walls of large vessels, and therefore
multiple fine sutures are preferable to fewer larger
sutures .

Ligation of common carotid artery

It is done at level of hyoid bone where very few
structures
pass across them.

They are middle

thyroid vein
and artery and
internal jugular
vein and
superficial arteries.

Ligation of ECA

Ligation of Lingual Artery

The artery is usually ligated beneath the hyoglossus muscle in
the second part of its course
Ligation of deep lingual artery is by placing an incision on
lateral part of floor
of mouth where it just lies beneath the mucosa and ligated as it
emerges from hyoglossus.

For unilateral operations on tongue - ligate

the artery of that side and for tip operations
both the arteries have to be ligated.

Ligation of maxillary artery

Ligation of maxillary artery is required in many instances in

maxillofacial surgeries, e.g. TMJ surgeries, primary haemorrhage
during maxillary osteotomies or during maxillectomies.

It is done through transantral approach where we can visualize

the first part of artery in the pterygomaxillary fissure and ligate

Ligation of facial artery

As it branches from the ECA and enters into the submandibular

triangle above the stylohyoid muscle
As it emerges onto the face along the anterior border of the
masseter muscle.

Embolization
It involves the selective occlusion of blood vessels by purposely
introducing emboli.
Interventional radiologist and Interventional neuroradiologists.
Indicated in haemangiomas, A-V malformations and epistaxis.
Position of the correct artery or vein supplying the pathology in
question is located by Digital Substraction Angiography [DSA]
Advantages
Disadvantages
Minimally invasive
User dependent success rate
No scarring
Risk of emboli reaching healthy
Minimal risk of infection
tissue
No or rare use of general anaestheticNot suitable for everyone
Faster recovery time
Recurrence more likely
High success rate compared to other
procedures

Thermal
Cauters

The procedure was simple: a piece of metal was heated over fire
and applied to the wound. This would cause tissues and blood to
heat rapidly to extreme temperatures in turn causing coagulation of
the blood thus controlling the bleeding, at the cost of extensive
tissue damage.

Heat achieves haemostasis by denaturation of protein,

which results in coagulation of large areas of tissues.

In cauterization heat is transmitted from the instrument by

conduction directly to the tissues.

Electrocautery has replaced direct heat application.

Electrocautery works by a process of induction from an

alternative current source.

Argon beam coagulator

It represent a new form of electrocautery, more effective

than standard electrocautery

In this coagulator, monopolar current is transmitted to

tissues through the flow of argon gas.

This allows bleeding from vessels that are smaller than 3mm in
diameter to be controlled without the use of haemostats or
ligatures.

There is possibility of gas embolism, as there is stream of gas in

direct contact with tissues.

Cryosurgery

At the other end of the thermal spectrum,

cooling has been applied to control bleeding.

Direct cooling with iced saline is effective and acts by increasing

the local intravascular haematocrit and decreasing blood flow by
vasoconstriction.

Temperature ranging between -20C to -180C are used and

freezing occurs
around the tip of the cannula within 5 sec.

Chemical
In1909, fibrin was used for the first time forhemostaticpurposes
byBergel.
In1911,Cushingused fragments of raw muscle and solidified blood
clots forhemostasis
and noted no adverse effects.
Characteristics of an Ideal hemostatic agent:
(1)capability to stop arterial or venous bleeding within 2 min of
application when applied to an actively bleeding wound
(2) no requirement for mixing or pre-application preparation
(3) simplicity of application
(4) light weight and durable
(5) long shelf life
(6) safe to use with no risk of injury to tissues or transmission of

Gelatin foam
(absorbable gelatin sponge)

Commercially known as Surgifoam.

Introduced in 1940s by Dr. Gray.
It is the porous, pliable sponge made from dried and sterilized porcine
skin gelatin.
It does absorb approximately 45 times its weight in blood and can
expand to
approximately 200% of its initial volume.
Absorbed in approximately four to six weeks

Bone wax

It is a sterile mixture of bees wax, paraffin and isopropyl palmitate.

It is useful when bleeding is from a visualized local vascular channel

within bone, bone bleeder, this occurs commonly during the
extraction of mandibular third molars.

The wax is pliable enough to be placed within a vascular channel,

immediately tamponading the vascular source.

It is non resorbable and due to its possible adverse effect on

osteogenesis caution should be used where regeneration of bone is
expected.

Oxidized regenerated
cellulose
/ Oxycel}
It is {Surgicel
a resorbable
oxidized cellulose material.
After it is fully absorbed with blood, it swells into a
brownish or black gelatinous mass that aids in clotting.
Relatively acidic and is thought to cause some small
vessel contraction.
Relatively bacteriostatic when compared to other
hemostatic agents.
Needs to be applied dry and absorbs within four to
eight weeks.
On post-op imaging surgicel sometimes causes a ringenhancing lesion which can be mistaken for an abscess

Microfibrillar collagen (MFC)

Commercially known as Avitene
This is collagen, which is derived from bovine skin.
Binds tightly to blood surfaces, so a relatively dry field is not
necessary for application.
Works slightly different because in addition to being collagen and
causing
contact activation, it does somehow directly activate platelets.
It is absorbed in three months.

Hemostatic
Gauze

A styptic or hemostatic pencil is

a short stick ofmedication,
usuallyanhydrous aluminium
sulfate,potassium alum (both are
types ofalum) ortitanium
dioxidewhich is used for
stanchingbloodby causingblood
vesselsto contract at the site of
the wound.
Anastringent substance is a chemical compound that tends to shrink
or constrictbody tissues, usually locally aftertopical medicinal
application.
Agents- Tannins [wines & tea]
Alum
Oatmeal
Banana skins
Calamine lotion

Fibrin Glue

Fibrin glueis a synthetic substance used to create afibrinclot.It is

made up offibrinogenandthrombinthat areinjectedthrough one
head into the site of a fibrin tear. Thrombin acts as anenzyme and
converts the fibrinogen into fibrin between 10 and 60 seconds and
acts as atissue adhesive.

Adrenaline
Adrenaline is added in concentration of 1:80,000 in
xylocaine.
It is used for hemostatic purposes because it;
- causes vasoconstriction
- reduces capillary haemorrhage
Side effect of adrenaline is, it produces undesirable
cardiac arrhythmias.
Also has the disadvantage of producing local tissue
cyanosis and acidity.
The use of adrenaline as a local hemostatic agent
is controversial as it may cause rebound

Newer Products
1. CHITOSAN
Chitosan hemostats are topical agents composed of chitosan and its
salts.
Chitosan bonds with platelets and red blood cells to form a gel like
clot which seals a bleeding vessel.
Unlike other hemostat technologies its action does not require the
normal
hemostatic pathway and therefore continues to function even when
anticoagulants like heparin are present.
Chitosan is used in some emergency hemostats which are designed
to stop traumatic life threatening bleeding.
2. ZEOLITE

Systemic agents
Adrenochrome monosemicarbazone - obtained by theoxidationofadrenaline.
Reduces capillary fragility

Controls oozing from raw surfaces

Prevents microvascular bleeding
Ethamsylate - 250-500 mg 4-6 hrly as needed
increasescapillaryendothelialresistance
promotesplateletadhesion
Antifibrinolytics
Tranexamic acid - 1-1.5 g 2-4 times/day
competitively inhibits breakdown of fibrin clots. It blocks binding of plasminogen and
plasmin to fibrin, thereby preventing haemostatic plug dissolution.

Botropase
(Aqueous solution of HAEMOCOAGULOSE isolated from VENOM OF
BOTHROPS JARARACA , containing 0.9% of NaCl)
MOA - Botropase acts on fibrinogen to produce a fibrin monomer that
can be converted by thrombin to a fibrin clot. The action of Botropase
in this way is similar to that of thrombin.
1. The action of thrombin may be inhibited by the antithrombin normally
existing in the blood, whereas the action of Botropase continues, even
when antithrombin is present.
2. By the action of either thrombin or Botropase, the terminal amino acids in
the fibrin clots consist of tyrosine and glycine; however, the ratio is of 1:2,
in the former and in the latter it is 1:1.
3. Unlike thrombin, Botropase is not absorbed by the fibrin clots and is
therefore not neutralised by that mechanism, as occurs with thrombin.
ADULTS :- 1ML I.M. SOS UPTO 2-3 TIMES A DAY.
CHILDREN :- 0.5 -0.7 ML ACCORDING TO THE AGE AND SERIOUSNESS OF
HAEMORRHAGE.

Fluid replacement
Colloids
Crystalloids
Isotonic crystalloids
- Human plasma
- Ringers lactate
- Albumin: 5%, 25%
- 0.9% NaCl

- Dextran Expands
plasma volume
Hypertonic saline solutions
up to 24 hours
- 3% NaCl
- Degraded gelatin
- 7% NaCl
( 3.5% )
Haemaccel
Hypotonic solution
- 0.45% NaCl
- Poly vinyl pyrrolidine (
3.5% )

Blood & Blood Substitutes

Indications
Trauma with severe blood loss. E.g. long bone fractures, liver & spleen lacerations
Major operative procedures in which a certain amount of blood loss is inevitable. E.g.
head and neck cancer surgeries
Following severe burns in which, there is associated haemolysis.
Preoperatively in cases of chronic anemia in which surgery is indicated urgently .
To arrest haemorrhage, or as a prophylactic measure prior to surgery; in a patient with a
haemorrhagic state such as thrombocytopenia, haemophilia or liver disease

Fresh whole blood

This term refers to blood i.e. administered within 24 hr of its donation.
Packed red cells
Packed red cells is the product of choice for most clinical situations.
Essentially it provides oxygen carrying capacity.
Others
Fresh Frozen Plasma, Cryoprecipitate, Platelets, Autologous
Transfusion.

Haemorrhage In Oral & Maxillofacial Surger

Bleeding from a tooth socket
Most common post op haemorrhage encountered by the dental
surgeon.
Most common cause of persistent primary haemorrhage
preexisting local inflammation at the site of wound.

is

Small puncture wounds in the sulcus opposite an upper canine or a

lower second molar due to a slip with an instrument can damage the
upper labial artery or the facial artery and can be cause of profuse,
persistent haemorrhage which may be thought mistakenly to be
coming from the socket.
Secondary haemorrhage is fortunately a rare complication of tooth
extraction.

Treatment
Soft Tissue

Hard

Tissue
Pressure packs
Agents
Suturing
e.g. Figure of 8
Hemostatic Agents
Electrocautery
Ligation of main vessel

Hemostatic
Stay sutures

aemorrhage in orbit
Some degree of retrobulbar haemorrhage is common in orbital
trauma and is recognizable on CT imaging as patchy areas of
increased attenuation.

Cadaver experiments in the young show that the orbital

septum can withstand pressures between 70-100mm Hg
before rupture.

In the elderly the septum is weaker and as little as 1015mm Hg pressure may be enough to cause rupture.

Nose blowing can cause intranasal pressure as high as

114mm Hg and if there is a wall defect in the orbit,
air can be transmitted into the orbit.

Unfortunately retinal vessels and the optic nerve cannot

withstand pressures of 65-70mm Hg for long and

Signs of Retrobulbar Haemorrhage

tense or expanding proptosis
ophthalmoplegia
increased intraocular pressure
loss of pupillary reflexes
optic disc or retinal pallor.

Treatment
Mannitol 20%, 2gm / kg IV over 5 min.
Megadose steroid therapy
Acetazolamide 500mg I.V. and then 1000mg orally over 24 hrs.
Surgical decompression remains the most certain option lateral canthotomy with cantholysis
If visual acuity is deteriorating a four wall decompression
under LA is required to prevent a permanent loss of vision.

emorrhage in cancer patients

Carotid artery blowout

Etiology: carotid artery blowout may occur after a
radical neck dissection.

Slough or skin flaps

Pre-op and /or post-op radiotherapy.
Fistula
Infection

Prevention

Administer pre op, intra op and post op antibiotics.

Cover arteries with viable muscle (E.g. levator scapulae muscle flap)
or PMM.

Do not use preoperative radiotherapy.

Allow no dead space over vessels (e.g. in the supraclavicular area

or in the submandibular area), especially near the angle of the jaw.

Close all intraoral defects in a water tight manner.

Do not perform vascular reconstruction in the presence of infection

Haemorrhage after rhinoplasty

The incidence of excessive bleeding following

septorhinoplasty is approximately 2% - 4%.

But can be as high as 10% when simultaneous turbinate

surgery is performed.

The anterior ethmoid and sphenopalatine vessels are

usually involved.

One of the prime concern with intranasal bleeding is that

an unrecognized and untreated septal haematoma can
lead to saddle nose deformity.

Epistaxis(or anosebleed) is the relatively common occurrence

ofhaemorrhage from thenose.

Management
Initial management of epistaxis includes compression of the
nostrils and plugging of the affected nostril with gauze or cotton
that has been soaked in a topical decongestant.
Complications of nasal packing procedures include septal
hematomas and abscesses, sinusitis, and pressure necrosis .

Anterior nasal pack

Posterior
nasal pack

aemorrhage during TMJ surgery

The vessels at risk during TMJ surgery are the

superficial temporal artery and vein, the maxillary artery,
and the middle meningeal artery.

If the vessels are encountered, ligation may be

necessary to ensure haemostasis.

At the level of the lateral capsule, a vein is usually

encountered, which also must be cauterized or ligated to
ensure haemostasis.

Site
Management
Primary Haemorrhage
Temporalis muscle
(Raytec gauze)
Squamous temporal bone
and/or diathermy
Periarticular
bleeding points
Maxillary/ Mandibular
repositioning of retractors
artery
hypertensive

Type

Venous
Venous
Venous
Arterial

Dry gauze
Horselys bone wax
Oversew the
Firm packing Check whether pt. is
Secure bleeder with

hemostat followed
by Weck arterial clip

morrhage during Orthognathic surgery

Source of bleeding
Maxillary

Pterygoid plexus,
Greater palatine vessel,
Nasopalatine vessels and
maxillary artery.

Mandibular

Maxillary artery,
Facial artery,
Inferior alveolar vessels
Retromolar vessels and
pterygoid plexus.

Prevention

Careful cutting of lateral wall of antrum & avoid resecting

descending palatine artery.
Osteotomy cut should be as low as possible.

Maxillary artery is at risk during disjunction of

pterygoid, large
curved osteotome may cause damage to maxillary
artery hence
swan neck osteotome must be used.

Conclusion
A surgeon, in his daily practice, comes across numerous patients
presenting with haemorrhage due to a variety of causes and should
be adept in measures to be used in the management of such cases.
Apart from achieving hemostasis, one should carefully
monitor the patient to assess the quantity of blood loss and should
perform adequate replacement therapy in the form of administration
of blood, blood products or substitutes, as indicated in individual
cases.
Also, one should be aware of the potential complications of
such therapy upon the occurrence of which ideal treatment should be
instituted.

References
1. Bailey and Loves - Short Practice of Surgery
2. Schwartz Shires Spencer - Principles of Surgery
3. Concise text book of surgery - S. Das
4. Sreenivasan B. - Textbook of Oral and Maxillofacial Surgery
5. Essentials of Pharmacology - K.D. Tripathi
6. Rowe & Williams - Maxillofacial Injuries Vol. I
7. The Internet

Next Week....

Shock

Good
Morning

Haemorrhage in Maxillofacial
Trauma

AIRWAY

ook
fee isten

Maxillofacial injuries that compromise the airway

Blood clot, saliva, bone, teeth or parts
of dentures
Backward displacement of the tongue.
Downward and backward
displacement of a fractured maxilla

Haemorrhage in Maxillofacial
Trauma

BREATHING

Stridor - upper airway obstruction

Gurgling - presence of clot
Wheezing - lower airway obstruction

All patients who have sustained major trauma above levels of

clavicles must be assumed to have sustained a C-spine injury until
proven otherwise

Haemorrhage in Maxillofacial
Trauma

CIRCULATION

ASSESSMENT:
1. Heart rate
2. Systolic BP and Pulse pressure
3. Peripheral pulses
4. Skin condition/perfusion/Capillary
refill
5. Sensorium

 Maxillofacial bleeding
Direct pressure.
Avoid blind clamping in wounds.

Nasal bleeding:
Direct pressure.
Anterior and posterior packing.

Pharyngeal bleeding:
Packing of the pharynx around ET tube.

intubated, with 2 transnasal Foley

catheters and a pulse oxymeter on
his upper lip.

2 transnasal Foley catheters, placed

under traction to provide maxillofacial

Despite recognition of a post traumatic syndrome by Greek physicians

such as Hippocrates and Galen, the origin of the term shock is
generally credited to the French surgeon Henri Francois Le Dran, who in
1737 defined the same in A treatise of reflections drawn from
experience with gunshot wounds and coined the term choc to indicate
a severe impact or jolt.
An inappropriate translation by the English physician Clare, in 1743,
led to the introduction of the word shock to the English language to
indicate the sudden deterioration of a patients condition when major
trauma has occurred.
It was Edwin A. Moses, who began to popularize the term, using it in
his article A practical treatise on shock after operations and injuries

a rude unhinging of the machinery of life

the collapse and progressive failure of the cardiovascular system
Shock is defined as the presence of inadequate organ
perfusion and tissue hypoxia
resulting in end organ damage.
[ Fonseca, 2nd Ed. Vol. II ]
Shock is the clinical syndrome that results from inadequate
tissue perfusion
[ Harrisons Internal Medicine, 17th Ed. Vol. II ]
Simply stated, shock results from inadequate perfusion of the bodys
cells with oxygenated blood.

CLASSIFICATION OF SHOCK ACCORDING TO HINSHAW AND CO

[1972]
Hypovolemic shock
Cardiogenic shock
Distributive shock
Obstructive shock
CLASSIFICATION OF SHOCK ACCORDING TO BLALOCK
Haematogenic
Neurogenic
Cardiogenic
Vasogenic
CLASSIFICATION OF SHOCK ACCORDING TO CAUSE
Inadequate circulatory blood volume
Loss of autonomic control of vasculature
Impaired cardiac function

Symptoms of shock
Increase heart rate as a result of the baroreflex:

1.

2.

Shock will decrease the volume of blood pumped

from the heart and the blood flow to the brain. That
will activate the baroreceptors in the carotid bodies
to increase HR trying to supply enough blood to the
vital organs.

Pale skin:

As a result of vasoconstriction of the peripheral vessels, because

the skin is the least priority tissue for blood flow

3.

Cold and clammy skin : As a result of vasoconstriction.

Shock decreases the skin surface temperature as a result of

vasodilatation, which will increase the internal body temperature.
Because the skin plays a major role in controlling body
temperature, as it will help in exchanging heat with the external
environment.

There are two mechanisms to get red of the excess heat:

Hyperventilation ( Minimal effect in humans)
Vasodilatation of the vessels
flow to the skin)
BP

Flush ( Increase blood

Real shock

Stages of Shock
Initial stage - tissues are underperfused, anaerobic metabolism,
lactic acid building
Compensatory stage -Hyperventilation, Baroreceptors, Renin
angiotensin axis, vasopressin
Progressive stage - Failing compensatory mechanisms: profound
vasoconstriction ISCHEMIA; Lactic acid production is high
metabolic acidosis
Irreversible/ refractory stage brain damage , cell death, Multiple
Organ Dysfunction Syndrome.

Etiology

Hypovolemic Shock
Classification of hemorrhagic shock by American College of surgeons committee
on trauma (1984)
Class I

Acute blood loss 15 % of total blood volume. Pulse

& respiration increased. BP not significantly affected.

Class II

Acute blood loss of 20 25 % of total

blood volume. Increased pulse & respiration.
Decreased BP. No decrease in urine output.

Class III

Blood loss of 30 40 % of total blood volume.

Increased pulse & respiration. Decreased BP
& Urine output.

Class IV

40 50 % loss of total blood volume. Lack of vital signs.

Decreased urine output. Obtunded mental status.

Hypovolemic Shock
Class I

Class II

Class III

Class IV

Blood Loss

750 ml

750 - 1500

1500 - 2000

2000 or more

% loss

15 %

15 30 %

30 40 %

40 % or more

Pulse rate

< 100

> 100

> 120

140 or higher

BP

Normal

normal

decreased

Decreased

Pulse pressure
(mm Hg)
Capillary blanch
test

Normal or
increased

decreased

decreased

decreased

Normal

positive

positive

positive

Respiratory rate

14 20

20 30

30 - 40

> 35

Urine output (ml /

hr )

30 or more

20- 30

5 - 15

Negligible

Anxious and
confused
Crystalloid +
blood

Confused &
lethargic
Crystalloid +
blood

CNS mental status Slightly anxious

Fluid replacement
(3:1 rule )

Crystalloid

Mild anxious
crystalloid

There are three basic compensatory reactions:

adrenergic reaction
Catecholamines

plasma refill
Albumin

acidosis

Hypovolemic Shock
Other related compensatory mechanisms are related system wise, and
are:

he hematologic system
the cardiovascular system
the renal system

the neuroendocrine syste

Decompensated shock
I.e. compensatory mechanisms are no longer able to maintain brain perfusion.
The patient is progressively confused, sleepy, and then comatose, as the brain
perfusion drops.
Blood pressure is below normal, heart rate is above normal, and radial artery
pulse is absent
Skin is pale, cold, patient is covered in cold sweat, core body temperature is
decreased, nail bed capillary refill is absent, and patient is anuric.

Diagnosis of Hypovolemic Shock

History
Clinical
Laboratory Tests
Imaging

Management

A-B-C
Active measures to control
bleeding
Intravenous Access
Fluid Replacement
Drug Therapy - Adrenergic
drugs

Fluid Therapy
RECOMMENDED - AN INITIAL BOLUS OF 1-2 L OF RINGERS LACTATE
IS GIVEN.
BLOOD TRANFUSIONS
ARE
IS A
Class
I REQUIRED IF THERE
Class
II LOSS OF > 20 %
OF CIRCULATING VOLUME.
2.5 L
1.5 L
crystalloids
crystalloids
Or
+
1.0 L colloids
1.0 L colloids
Class III
Class IV
1.0 L crystalloids
+ 0.5 L colloids +
1.0 L whole blood
Or
0.1-1.5 L
concentrated red

1.0 L crystalloids
+ 1.0 L colloids +
2.0 L whole blood
Or
2.0 L concentrated
red cells + 2.0 L

Drug Therapy
Cardiac
Agent

Dopamine
Norepinephr
ine
Dobutamine
Phenylephrin
e

Dose

5-10(/kg)/min.
2-20/g/min.
5-10(/kg)/min.
20-200g/min.

Heart rate

Contractil
ity

1+
1+
1-2+
0

1+
2+
3-4+
0

Cardiogenic Shock
Cardiogenic shock is characterized by a decreased pumping ability of
the heart causing a shock-like state with inadequate perfusion to the
tissues.
It occurs most commonly in association with, and as a direct result of,
acute ischemic damage to the myocardium.
Intrinsic

Extrinsic

1. Myocardial
injury

1. Pericardial
tamponade

2. Tachycardia

2. Tension
pneumothorax

3. Bradycardia
4. Valvular defect

3. Large pulmonary
emblous

Cardiogenic Shock
History
Most patients presenting with cardiogenic shock do so in
conjunction with an AMI and, therefore, present with the
constellation of symptoms of acute cardiac ischemia (e.g., Chest
pain, shortness of breath, diaphoresis, nausea and vomiting).
Patients experiencing cardiogenic shock may also present with
pulmonary edema and presyncopal or syncopal symptoms.
Physical examination
will often reveal a patient in the middle of an AMI.
Patients appear in frank extremis, profoundly diaphoretic and
complaining of severe shortness of breath and chest pain.
Neck examination may reveal jugular venous distention. This is
evidence of right
ventricular failure and may be prominent.

Treatment of Cardiogenic Shock

Pulmonary wedge pressure (Swan-Ganz Catheter)
Intra aortic balloon pump - An intra-aortic balloon pump is a support
device which is inserted in the groin and advanced into the aorta.
The purpose is to reduce the workload on the heart.
Preload
Fluid administration
Inotropic agents :- Dopamine(5-10g/kg/min) ,Dobutamine
10g/kg/min), Epinephrine

(5-

Afterload
Vasodilators :- reduce myocardial wall tension and improve myocardial oxygen supply
to demand ratio. Nitroprusside (0.5-5g/kg/min), Nitroglycerine (3 -5 g/kg/min)

Pneumatic Antishock Garment

Obstructive Shock
Obstructive shockis a form ofshockassociated with physical
obstruction of thegreat vesselsor theheartitself.
Pulmonary embolism andcardiac tamponadeare considered forms of
obstructive shock.
Obstructive shock has much in common withcardiogenic shock, and
the two are frequently grouped together.
Pneumothorax or haemothorax is treated by inserting a chest
tube.
Pulmonary embolism requires thrombolysis (to reduce the size of
the clot), or embolectomy (removal of the thrombus).
Tamponade is treated by draining fluid from the pericardial space
through pericardiocentesis

Distributive Shock
Septic

Anaphylactic
Neurogenic

Systemic inflammatory response syndrome :SIRS to a variety of severe clinical insults. 1) temp > 380 C or < 360 C ,
2) HR> 90 beats /min 3) RR > 20 breaths/min . 4) WBC > 12000/cu. mm or <
4000/cu.mm. 5) PaCO2 < 32mm Hg
Sepsis :-SIRS in association with culture proven infection
Septic shock :- sepsis with hypotension despite adequate fluid resuscitation along
with hypoperfusion , lactic acidosis, oliguria, acute alteration in mental status
Multiple organ dysfunction syndrome (MODS) :- presence of altered organ
function in an acutely ill patient such that hemostasis cannot be maintained without
intervention.

Septic Shock
GRAM NEGATIVE
SEPTICEMIA (endotoxic
shock)
E.coli, Klebsiella,
Meningiococci

GRAM POSITIVE
SEPTICEMIA (exotoxic shock)
Staphylococcus
Streptococci (toxic shock
syndrome)

Pseudomonas produces both endotoxin

and exotoxin

Early warm (hyperdynamic) shock

1.
2.
3.
4.
5.
6.

Fever and chills

High respiratory rate
Profound diuresis
High cardiac output
Low peripheral vascular resistance
Arterial blood gas analysis - metabolic
acidosis
7. Tachycardia
8. Warm, Dry skin

Cold (hypodynamic) shock

1. Subnormal temperature
2. Profound Hypotension and
hypoperfusion
3. Reduced Cardiac Output
4. Cold and mottled skin
5. Rapid pulse and respiration
6. Multisystem failure pulmonary edema,
ARDS, liver and kidney failure, DIC
7. Deteriorated mental status

Investigations
1. Urine Analysis
2. Nasal & throat swabs
3. Blood cultures
4. Sputum specimen
5. Pus / wound swabs
6. IV lines/ Indwelling catheter

1) Ensure a patent airway and that the patient is breathing

spontaneously
O2 To improve the oxygenation.
Oral airway -> ET tube -> tracheostomy
2) Ensure and adequate pulse and blood pressure:
Intravenous canulation: volume loading -> inotropes ->
inoconstrictors
3) Look for source of sepsis (cultures); assess background issues that
may
have contributed.
4) Start antimicrobial therapy, guided by cultures, or "best guess
therapy
5) ICU staff personal hygeine, to prevent transmission of resistant
microbes.

Anaphylactic Shock
Definition
An individual response to a specific antigen which is represented
by respiratory distress followed by vascular collapse.
Predisposing factors
-Hormones, Enzymes, Polysaccharides (Dextran), Antibiotics, LA.
Clinical Manifestations
Upper and lower airway obstruction.
Angioedema of epiglottis and larynx
Audible wheeze.
Non pitting edema.
Urticarial eruptions.

Allergic response mediated by IgE antibody

Activation and release of inflammatory

mediators anaphylatoxins, C3a, C5a,
histamines, kinins, prostaglandins and
others.

ALLERGEN

AIRWAY

ADRENALINE 0.5ml[1:1000] i.m.

ANTIHISTAMINE 10-20mg

AMINOPHYLLINE 5-6mg/kg
ADMINISTER O2 AND FLUID
THERAPY

Cricothyrotomy
absolute need for a definitive airway
unable to perform ETT due for structural or
anatomic reasons,
risk of not intubating is > than surgical airway risk
unable to clear an upper airway obstruction,
multiple unsuccessful attempts at ETT,
other methods of ventilation do not allow effective
ventilation and respiration

Contraindications (relative)
Age < 8 years
evidence of # larynx or cricoid cartilage
evidence of tracheal transection

Steroids in Anaphylactic Shock

Administer them early to try to prevent a potential late-phase
reaction (biphasic anaphylaxis)
Used as adjunct after initial treatment with epinephrine.
Glucocorticoids can supplement primary therapy to suppress
manifestations of allergic diseases of a limited duration.
In very severe diseases intravenous methylprednisolone 125mg
every 6 hours
Patients with asthma may receive additional benefit if
corticosteroids are administered to them during anaphylaxis.

Anaphylactoid Reaction
A reaction that resembles anaphylactic shock; probably caused by
the liberation of histamine, serotonin, or other substances as a
consequence of the injection of colloids or finely suspended
material.
Unlike, anaphylaxis it is not IgE mediated.
However, the treatment for both is essentially the same.

Neurogenic Shock
Occurs when sympathetic denervation produces an impairement in vasomotor tone
Etiology

Clinical features

Spinal anesthesia
Brain damage
Sudden onset of pain

Fainting is variation of
neurogenic shock

Hypotension
Bradycardia
Extremities are warm and dry

Pathogenesis
Sympathetic denervation
Impaired vasomotor tone (arterial & venous
system)
systemic vascular resistance
venous return to heart
cardiac output
SHOCK

Management
Morphine 15mg i.m. should be given
Balanced salt solution to increase cardiac output
Vasopressor drugs dopamine 200mg i.v. infusion
mephenteramine 30-60mg i.v.
Body temperature should be monitored

Endocrine Shock
Hypothyroidism, in critically ill patients, reduces
cardiac output and can lead to hypotension and
respiratory insufficiency.
Thyrotoxicosis - may induce a reversible
cardiomyopathy.
Acute adrenal insufficiency (Addisons) is frequently
the result of discontinuing corticosteroid
treatment without tapering the dosage.

Hypoadrenal Shock
Clinical features
Malaise, weakness, wt loss, anorexia, nausea, vomiting, diarrhoea
Abdominal tenderness and fever
Hyperpigmentation
Hypotension
Hyponatraemia
Hyperkalaemia

Initiate therapy as soon

as acute adrenal crisis
is suspected

Correct hypovolaemia
and sodium depletion
with normal saline

Add 5% dextrose
solution if pt is
hypoglycaemic

Administer
hydrocortisone in a
dose of 100 mg 6 hrly
and taper it over 24 to
48 hrs to a
maintenance dose
once the underlying
stress resolves

Prognosis
The prognosis of shock depends on the
underlying cause and the nature and extent of
concurrent problems.
Hypovolemic, anaphylactic and neurogenic
shock are readily treatable and respond well to
medical therapy.
Septic shock however, is a grave condition and
with a mortality rate between 30% and 50%.
The prognosis of cardiogenic shock is even
worse

Conclusion
Shock, whatever the cause, is associated with an imbalance in
oxygen supply and demand.
Early aggressive treatment with oxygen, fluid administration, and
adrenergic agents when needed, combined with methods to
correct the underlying cause, help to limit the damage.
Repeated clinical examination, with appropriate hemodynamic
and oxygenation parameters, is important to monitor the patients
progress and response to treatment.
The development of improved monitoring techniques, including
strategies to visualize and quantify microcirculatory changes, will
enable us to better assess and target regional perfusion; and by
so doing, improve patient outcomes.

References
1. Bailey and Loves - Short Practice of Surgery
2. Harrisons - Principles of Internal Medicine
3. Schwartz Shires Spencer - Principles of Surgery
4. Concise text book of surgery - S. Das
5. Sreenivasan B. - Textbook of Oral and Maxillofacial Surgery
6. Essentials of Pharmacology - K.D. Tripathi
7. Rowe & Williams - Maxillofacial Injuries Vol. I
8. The Internet

Thank
You