Hemorrhage and shock

Haemorrhage &
Shock
Guided By-
Dr. Surekha Godbole
Dr. Anjali Bhoyar
Dr. Seema Sathe
Dr. Trupti Dahane
Dr. Sweta Pisulkar Presented By- Rohit Mistry

Learning Objectives
sr.n Core area Aim Significance
1. Hemorrhage, definition and
classification
Cognitive Must know
2. Clinical signs and symptoms of
hemorrhage
Cognitive Must know
3. Pathophysiology of hemorrhage Cognitive Must know
4. Physiologic response to hemorrhage Cognitive Must know
5. General management of hemorrhage Cognitive, Psychomotor Must know
6. Prosthodontic consideration Cognitive, psychomotor Must know

Contents
(Haemorrhage)
• Introduction
• Classification of haemorrhage
• Clinical Signs and symptoms of haemorrhage and related pathophysiology.
• Physiology of haemostasis
• How to measure blood loss
• Conditions Causing Excessive Bleeding
• Management of haemorrhage
• Local Haemostatic Agents
• Prosthodontic Consideration.

Blood
(From Proto-Germanic *blodam that
means to spurt or gush)
Definitions-
The fluid that circulates in the heart, arteries,
capillaries, and veins of a vertebrate animal
carrying nourishment and oxygen to and bringing
away waste products from all parts of the
body.(merriam-webster )
OR
The red liquid that circulates in the arteries and
veins of humans and other vertebrate animals,
carrying oxygen to and carbon dioxide from the
tissues of the body
(oxford dictionary)
Blood is a connective tissue composed of a liquid
matrix called Plasma that dissolves and suspends
various cells and cell fragments.
BLOOD IS A LIQUID CONNECTIVE TISSUE

Key words:
• Stroke volume-The difference between the ventricular end-diastolic volume
(EDV) and the end-systolic volume (ESV). (average is 70ml)
• Heart Rate- The speed at which the heart beats. (average 72 beats/min)
• Cardiac output- The amount of blood the heart pumps through the circulatory
system in one minute. (Q= HR x SV) average is 5.04 lts/min
• Haemostasis -or haemostasis is a process which causes bleeding to stop, meaning
to keep blood within a damaged blood vessel (the opposite of haemostasis is
haemorrhage)

Composition • Plasma(55%)
Water (92%)
Proteins (7-8%)
Inorganic salts(1%)
Glucose(0.1%).
• Corpuscular/Hematocrit(45%)
RBC
(Males-4.7 to 6.1 million/μl,
Females-4.2 to 5.4 million/μl)
WBC(4000-1100/μl)
Granulocytes- Eosinophils, Basophils, Neutrophils
Agranulocytes- Monocytes and Lymphocytes
Platelets (200000-400000/ μl)

Functions of Blood.
Transportation
• Transport of oxygen from
lungs to body
• Transport of carbon-di-
oxide from body to lungs
• Blood provides the cells
with nutrients,
transports hormones and
removes waste products.
Regulation
• Thermostasis (37˚C/98F).
• Acid-Base Regulation with
Ph of 7.35
Protection
• If a blood vessel is
damaged, certain parts of
the blood clot together very
quickly to make sure the
bleeding stops.
• White blood cells and other
messenger substances also
play an important role in
the immune system.
https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0072576/

Haemorrhage
noun hem·or·rhage
• The escape of blood from the vessels.
(According to Dorland's dictionary)
• A copious or heavy discharge of blood from
the blood vessels.
(According to Merriam-Webster Dictionary)
• The escape of large quantities of blood from
a blood vessel; heavy bleeding.
(According to Collins Dictionary)

“The circulation of blood is fundamental in maintaining the constancy of
the composition, volume and temperature of the interstitial fluid. All organs
depend on it for the transport of oxygen and substrates for synthesis and
transfer of energy , for the removal of end products of catabolism for
excretion. Thus homeostasis is seriously deranged when substantial amount
of blood is lost by haemorrhage, the consequent reduction in blood flow
and circulating blood volume having widespread effects which involve
every organ”
Wiggers,1950; Cuthbertson 1960 10
Why to Study Haemorrhage?

Classification of Haemorrhage
• Depending on nature of the vessel involved.
• Depending on the timing of haemorrhage.
• Depending on the of volume of blood lost.
• Depending on the nature of bleeding.
• Depending upon type of Intervention.

Arterial Bleeding
Bright red (as it consists of
well oxygenated blood)
Emitted as spurting jet.
Can lead to severe blood
loss.
Often hard to control.
Venous Bleeding
Darker red.(as it consists of
deoxygenated blood)
Steady and copious flow.
Colour becomes further darker
with oxygen desaturation.
Usually easy to control.
Capillary Bleeding
Bright red.
Slow, even flow.
Blood loss becomes serious if continues for
hours.
Generally minor & easy to control.
shock and blood transfusion, Bailey & Love, a short practice of surgery.

According to the Timing of Haemorrhage.
Primary (immediately):
Haemorrhage occurring
immediately as a result of an
injury (or surgery).
Reactionary(within 24 hours):
Delayed haemorrhage (within
24 hours)
Secondary (occurs 7-14 days
after injury): It usually occurs
7–14 days after injury

Depending on Nature of Haemorhage
Concealed Haemorrhage : It is contained within the body cavity and must be
suspected, actively investigated and controlled.
Revealed Haemorrhage : It is obvious external haemorrhage, such as
exsanguination from an open arterial wound.

Surgical Haemorrhage: It is the
result of injury and amenable to
surgical control.
Non-Surgical Haemorrhage: It is
general ooze from all raw surface
due to coagulopathy, it cannot
be stopped by surgical mean,
require correction of coagulation
abnormalities.
shock and blood transfusion, Bailey & Love, a
short practice of surgery.
Depending upon the Type of Intervention

Depending on the Volume of Blood lost
Rossaint R, Bouillon B, Cerny V, et al. Management of bleeding following major trauma: an updated European guideline. Critical Care. 2010;14(2):R52. doi:10.1186/cc8943.

Pathophysiology of haemorrhage
• The effects of haemorrhage depend partly on the amount of blood lost
,and partly on the rate of loss.
Acute blood loss Chronic blood loss
Poorly tolerated by body Well tolerated by body
There is rapid loss of blood volume which cannot be
compensated
Plasma volume expands in order to compensate for the
volume deficit
Failure to compensate blood loss by haematopoiesis. The Red blood cells production increases to tackle the
cellular deficit
The cardiac output is decreased as the volume is decreased The cardiac output increases to overcome the anaemic
hypoxia
• Intestinal secretions and salivary flow are reduced.
• Urine formation diminishes or ceases.
• The coagulation time of the blood is considerably
shortened.
Appreciated clinically as hyperdynamic circulation
PHYSIOLOGICAL EFFECTS OF HAEMORRHAGE, J Freeman, 1950

The Reactions to Increasingly severe blood loss
can be described in 3 stage
(1) Depletion of venous reservoirs
(2) Failure to maintain systemic blood pressure
(3) Deterioration to death by vicious cycle.

Depletion of Venous Reservoirs
• Contraction of these reservoirs mediated by baroreceptor reflex and sympathetic
activity can compensate for blood volume reductions of upto 10%. without
changes in cardiac output or blood pressure.
• The state of compensated shock is seen at 20% blood loss.
• Blood flow tends to be preserved through the brain and myocardium, circulations
which are relatively independent of reflex vasoconstriction.
Major Venous
Reservoirs
Cutaneous
venous
plexuses
Large veins Splanchnic bed
Pulmonary
vessels and the
heart

Failure to Maintain Blood Pressure
• Systemic blood pressure declines after 20-30%
reductions in blood volume.
• Cardiac output decreases and peripheral resistance falls.
• Fall in blood pressure followed by tachycardia.
• Pulmonary blood flow is reduced.
• Hyperventilation often occurs during rapid haemorrhage,
associated with a temporary increase in arterial pH and
decrease in arterial P 𝐶𝑂2
• The hypoxia results in metabolic acidosis, pyruvates and
lactates accumulate in the blood.
• Catabolism of carbohydrate and proteins increase.
Haemorrhagic
hypotension
Haemorrhagic
hypoxia

Deterioration to death by the vicious cycle
• The imbalance between arterial hypotension and extreme vasoconstriction
initiate a vicious cycle.
Decreased
cardiac
output
Decreased
coronary
flow
Cardiac
arrest
Continued
Haemorrhage
Decreased
Pulmonary
Perfusion
Decreased
oxygen
saturation
Hypoxia &
Cyanosis
DEATH

Signs and symptoms of haemorrhage
Signs
• Dizziness and light-headedness
• Cold Clammy skin
• Shallow breathing with gasping
• Profuse sweating
• Thirst
• Blurred vision
Symptoms
• Weak and Rapid Pulse
• Tachycardia
• Unconsciousness
• Erratic Blood Pressure
• Cyanosis

Physiological Response to haemorrhage
Haemostasis(hemo=blood; sta=remain)
is the stoppage of bleeding, which is vitally important when blood
vessels are damaged.
• Following an injury to blood vessels several actions may help prevent
blood loss
Haemostasis and Blood Coagulation, textbook of medical physiology, Guyton and hall,

There are three stages of clot formation
• Clot formation is when soluble precursor fibrinogen is converted into
insoluble fibrin by activation of thrombin.
• Stage 1
Formation of Prothrombin activator
• Stage 2
Conversion of prothrombin to thrombin
• Stage 3
Conversion of fibrin from fibrinogen.
Note- Calcium is essential for conversion of prothrombin to thrombin

New Model Of Haemostasis
• Initiation Phase
New Models of Hemostasis,Maureen McMichael, 2012

Amplification Phase

Propagation Phase

How to measure Blood Loss?
• There is no definitive method of measuring blood loss
• Following are some methods of arbitrarily estimating blood loss
I. Weighing the blood soaked swabs
II. Measure the amount of blood in the suction
III.Measuring the packed cell volume
IV.Measuring haemoglobin count

Conditions that cause excessive bleeding in
human beings.
• Vitamin k Deficiency
• Platelet Deficiency(Thrombocytopenia)
• Haemophilia

Vitamin K Deficiency
• Causes-
• Malabsorption of fat
• Poor intestinal flora
• Diseased liver
• How is it related to Haemostasis?
Formation of prothrombin, Factor VII, Factor IX, Factor X, and protein C
Management
Vitamin K is injected 4-8 hours in all surgical patients with liver disease or
with obstructed bile ducts before performing the surgical procedure.

Haemophilia
• Haemophilia is a bleeding disease that occurs almost exclusively in males:
• Haemophilia A - Deficiency of Factor VIII
• Haemophilia B – Deficiency of Factor IX
• von Willebrand’s disease- Deficiency of vW factor
Management-
The only therapy that is truly effective is injection of purified Factor
VIII.

Thrombocytopenia(thrombocyte- Platelets penia- deficiency)
• Small punctate haemorrhages occur throughout all the body tissues. The skin of
such a person displays many small, purplish blotches, giving the disease the name
thrombocytopenic purpura.
• Caused by one of the Three mechanism-
I. Decreased Production in Marrow
II. Increased Sequestration in Spleen
III.Accelerated Destruction
• Management-
Relief from bleeding for 1 to 4 days can often be effected in a patient with
thrombocytopenia by giving fresh whole blood transfusions that contain large numbers
of platelets. Also, splenectomy is often helpful

Management Of Haemorrhage
• Identify – Haemorrhage / Hypovolaemia & Shock – clinically
• Resuscitation – O2 / Blood & Fluids
• Identify site of Haemorrhage - U/S, endoscopy, CT scan, DPL, Blood tools etc.
• Control of Haemorrhage – Surgery, endoscopic control, therapeutic embolization.
• Definitive treatment if any
• Use of Local Haemostatic agents
• Sepsis control
• Prevention of coagulopathy
• Critical care management
• End-point resuscitation, fluids & electrolyte management, prevention of organ
failure
Management of bleeding following major trauma:Rolf Rossaint1, Bertil Bouillon2,Critical Care 2010, 14:R52

Local Haemostatic agents
•Passive agents
 Collagen-based products
 Microfibillar collagen (Avitene)
Colla-Cote, Colla-Tape, Colla-
Plug, Helistat.
 Cellulose-based products
 ActCel and Gelitacel
 Gelatin-based products
•Active Agents
 Thrombin
 FloSeal (flowable hemostatic
agent)
 Polysaccharide-based
hemostats
Poly-N-acetyl glucosamine-
based materials, QuikClot
LOCAL HEMOSTATIC AGENTS IN THE MANAGEMENT OF BLEEDING IN ORAL SURGERY, SANTHOSH KUMAR MP*, Asian J Pharm Clin Res, Vol 9, Issue 3, 2016, 35-41

Haemostatic solutions
• Styptics
• Tranexamic acid
• Tannic acid
• Epsilon aminocaproic acid
LOCAL HEMOSTATIC AGENTS IN THE MANAGEMENT OF BLEEDING IN ORAL SURGERY, SANTHOSH KUMAR MP*, Asian J Pharm Clin Res, Vol 9, Issue 3, 2016, 35-41

Prosthodontic Considerations
• Haemorrhage is encountered during:
• Surgical Procedures like Implant Placement and Pre- Prosthetic
Surgical Procedure
• Patients With Coagulopathies
• Patients On Anti-Coagulant Therapy

Haemorrhage during Implant placement
(anatomic factor )
• The cause of bleeding during implant placement in the anterior mandible is
perforation of the lingual cortex, resulting in injury to the terminal branches
of the sublingual or submental artery.
• Moderate or severe maxillary bleeding may result from injury to intraosseous
vessels lying within the walls of the maxilla
Surgical Complications After Implant Placement, Dental Clinics of North America, Volume 59, Issue 1, Pages 57-72

Pre-Prosthetic Surgery
• Promoting haemostasis and favouring the formation of granulation
tissue are two critical steps of the healing process post operatively.
• Bleeding during these surgeries are well tolerated by a healthy patient.

• Management
• Control of the haemorrhage and ABC
• Injection of local anesthesia with a vasoconstrictor through the perforation.
• Pressure packs must be given to attain primary haemostasis followed by
application of surgical pack to avoid further trauma and secondary bleeding.
• Local haemostatic agents are used to stop the haemorrhage
• Collagen Matrix has given excellent clinical results in control of post-operative
haemostasis.
• If there is any doubt about control of bleeding, the airway should be secured in the
dental office or the patient should be transported to the nearest hospital

Patients with Coagulopathies
• Removable Prosthesis are indicated in these patients.
• Proper Case History Recording.
• Estimation of INR levels and BT, CT, platelet counts before surgery.
• International guidelines advise the use of clotting factor replacement therapy for
all invasive surgical interventions in patients with hemophilia
Shastry SP, Kaul R, Baroudi K, Umar D. Hemophilia A: Dental considerations and management. Journal of International Society of Preventive & Community Dentistry. 2014;4(Suppl 3):S147-
S152. doi:10.4103/2231-0762.149022.

Patients on Anti-coagulant therapy
• INR Ratio of 3.5 is ideal for a patient to undergo simple extraction.
• The anti-coagulant dosage must be adjusted to avoid any complication
and physicians consent must be obtained.
• there are no established protocols for managing patients taking these
drugs who are undergoing dento-alveolar surgery.
• Such cases must be treated in stages.

Summary
• The complication which arises from haemorrhage warrants the need
for its study
• The haemodynamic changes which occur during haemorrhage are
subjective to the quantity and the way through which the blood is
lost, the understanding of the same is necessary to decide the
treatment modality
• Formation of blood clot is the ultimate goal of haemostasis which is
to be achieved by all possible means.
• Control of haemorrhage and avoidance of further complications helps
in achieving better health care for the patient.

References
• Functions Of Blood https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0072576/
• Physiological effects of haemorrhage, J Freeman, 1950.
• Shock and blood transfusion, Bailey & Love, a short practice of surgery.
• Advanced Trauma Life Support Manual. Chicago: American College of Surgeons; 1997.
pp. 103–112.
• Haemostasis and Blood Coagulation, textbook of medical physiology, Guyton and hall.
• Management of bleeding following major trauma:Rolf Rossaint1, Bertil Bouillon2,Critical
Care 2010, 14:R52
• Surgical Complications After Implant Placement, Dental Clinics of North America,
Volume 59, Issue 1, Pages 57-72.
• Use of a Collagen Matrix as a Substitute for Free Mucosal Grafts in Pre-Prosthetic
Surgery: 1 Year Results From a Clinical ,The Open Dentistry Journal, 2016, 10, 395-410
Prospective.
• Shastry SP, Kaul R, Baroudi K, Umar D. Hemophilia A: Dental considerations and
management. Journal of International Society of Preventive & Community Dentistry.
2014;4(Suppl 3):S147-S152. doi:10.4103/2231-0762.149022.
• LOCAL HEMOSTATIC AGENTS IN THE MANAGEMENT OF BLEEDING IN ORAL SURGERY,
SANTHOSH KUMAR MP, Asian J Pharm Clin Res, Vol 9, Issue 3, 2016, 35-41

Queries From Part I
• Should Oral Anti Coagulant therapy be stopped during invasive dental
procedure?
A. “No clinically significant increased risk of postoperative bleeding
complications from invasive dental procedures in patients on either
single or dual antiplatelet therapy. These findings support the
recommendation that there is no indication to alter or stop these
drugs, and that local haemostatic measures are sufficient to control
bleeding.”
(Oral SurgOral Med Oral Pathol Oral Radiol 2013;115:491-499)
Madrid C, Sanz M. What influence do anticoagulants have on oral implant therapy? A systematic
review. Clin. Oral Impl. Res. 20 (Suppl. 4), 2009; 96–106.doi: 10.1111/j.1600-0501.2009.01770.x

How to Determine the Volume of blood from
cotton swab?
A. The difference in weights is the weight of blood lost in cotton and
gauze. This is converted into (volume)ml by dividing the weight by
specific gravity, which is 1.0506 at 37˚C

How to diagnose haemophilia in patients
A. Clotting factor tests, also called factor assays, are required to
diagnose a bleeding disorder. This blood test shows the type of
haemophilia and the severity

What happens when the haemorrhage
reverses.
• Definitive management post haemorrhage can only assure the
reversal of deranged physiology back to normal. Fluid resuscitation is
of no actual use unless the haemorrhage has been controlled at site.
• The reverse feedback mechanism reverts the cardiac changes and
establishes normal haemodynamic as the trigger on the carotid
baroreceptors is relieved, this happens when the oxygen saturation
gets back to normal ie p𝑜296% .
• The metabolic acidosis is resolved by the kidneys and lungs by
flushing out carbonate (HCO3) ions.

On the other end (ischaemia Reperfusion
Syndrome)
• IF Extensive injury has occurred once normal circulation is restored to
these tissues. The acid and potassium load that has built up can lead
to direct myocardial depression, vascular dilatation and further
hypotension. The cellular and humoral elements activated by the
hypoxia (complement, neutrophils, microvascular thrombi) are
flushed back into the circulation where they cause further endothelial
injury to organs such as the lungs and kidneys. This leads to acute
lung injury, acute renal injury, multiple organ failure and death.
Reperfusion injury can currently only be attenuated by reducing the
extent and duration of tissue hypo-perfusion.

Haemorrhage &
Shock Part-II
Guided By-
Dr. Surekha Godbole
Dr. Sweta Pisulkar
Presented By- Rohit Mistry

Shock
• Definition
• Pathophysiology of Shock
• Classification Of Shock
• Compensated Shock
• Severity Of Shock
• Empirical Management (The ABCDE Approach and The 2010 CAB guidelines)
• Fluid Resuscitation
• Monitoring Shock
• Shock with Atypical Management
• Vasovagal syncope

Specific Learning Objectives
Sr. n Core area Aim Significance
1. Shock and its classification Cognitive Must know
2. Clinical signs and symptoms of shock
to look out for
Cognitive Must know
3. Pathophysiology of shock and
clinically gauging the severity of
shock
Cognitive Must know
4. Empirical management of shock Cognitive &
Psychomotor
Must know
5. Fluid Resuscitation Cognitive, Psychomotor Must know
6. Monitoring Shock Cognitive, Psychomotor Must know
7. Some atypical shock and their
management
Cognitive an
psychomotor
Must Know

DEFINITION
• Generalized inadequacy of blood flow throughout the body to the extent that the
body tissues are damaged because of too little flow, especially because of too little
delivery of oxygen and other nutrients to the tissue cells.
-Guyton
• Shock is defined as inadequate delivery of oxygen and the nutrients to maintain
normal tissue and cellular function.
-S.Das
• Shock is a systemic state of low tissue perfusion, which is inadequate for normal
cellular respiration. With insufficient delivery of oxygen and glucose, cells switch
from aerobic to anaerobic metabolism. If perfusion is not restored in a timely
fashion, cell death ensues.
- Bailey and Love

Pathophysiology of Shock
• Cellular
• Micro-Vasculature
• Systemic

Cellular Changes
Decreased
oxygen supply
to cell
Anaerobic
respiration
Lactic acid
production
leading to
metabolic
acidosis
Glucose reserve
exhausts and the
cells starve
Loss of function
of cell
Cell Death

Microvascular Changes
Ischemia causes
activation of
coagulation and
immune system
Complement
System is activated
and neutrophils are
released
Free Oxygen
radicals are
produced
Injury to endothelial
cells and leaky
capillaries form
Interstitial oedema
ensues

Systemic Changes
Cardiovascular
System
Baroreceptor
feedback is activated
resulting in
tachycardia and
systemic
vasoconstriction
Respiratory system
The ensuing Acidosis
warrants hyper-
ventilation to flush
away excess Carbon-
di-oxide
Renal system
Reduced Perfusion
causes retention of
water and sodium in
the body and reduces
the GFR

Classification Of Shock
On the basis of initiating Mechanism shock can be classified as
• Hypovolemic
• Cardiogenic
• Obstructive
• Distributive
• Endocrine

Hypovolaemic Shock
Hypovolaemic shock is caused by a reduced circulating volume.
Hypovolaemia may be due to haemorrhagic or non-haemorrhagic
causes.
Non-haemorrhagic causes
• Poor fluid intake (dehydration)
• Excessive fluid loss because of vomiting, diarrhoea,
• Urinary loss (e.g. diabetes),
Hypovolaemia is probably the most common form of shock and is to
some degree a component of all other forms of shock.
Absolute or relative hypovolaemia must be excluded or treated in the
management of the shocked state, regardless of cause.

Cardiogenic Shock
Cardiogenic shock is due to primary failure of the heart to pump blood
to the tissues. Causes of cardiogenic shock include myocardial
infarction, cardiac dysrhythmias, valvular heart disease, blunt
myocardial injury and cardiomyopathy

Obstructive Shock
In obstructive shock there is a reduction in preload because of
mechanical obstruction of cardiac filling. Common causes of obstructive
shock include cardiac tamponade, tension pneumothorax, massive
pulmonary embolus and air embolus. In each case there is reduced
filling of the left and/or right sides of the heart leading to reduced
preload and a fall in cardiac output.

Distributive Shock
Distributive shock describes the pattern of cardiovascular responses characterising a
variety of conditions including septic shock, anaphylaxis and spinal cord injury.
• In anaphylaxis, vasodilatation is caused by histamine release
• In high spinal cord injury there is failure of sympathetic outflow and
adequate vascular tone (neurogenic shock).
• In sepsis is related to the release of bacterial products (endotoxins)
and the activation of cellular and humoral components of the immune
system

Endocrine Shock
Cause
• Hypo- and Hyperthyroidism and adrenal insufficiency.
• Hypothyroidism causes a shock state similar to that of neurogenic
shock as a result of disordered vascular and cardiac responsiveness to
circulating catecholamines. Cardiac output falls because of low
inotropy and bradycardia. There may also be an associated
cardiomyopathy.
• Thyrotoxicosis may cause a high-output cardiac failure.

Compensated shock
• During the initial phases of shock when there is 15% loss of blood the
body tries to compensate
1. By increasing the blood supply to the central organs
2. Reducing peripheral circulation by vasoconstriction
3. Retention of sodium and water by activation of Renin-Angiotensin
Mechanism
Decompensation starts ones the body has lost 30-40% of blood.

Severity Of Shock

Empirical Management
• Immediate resuscitation manoeuvres for patients presenting in shock
are to ensure a patent airway and adequate oxygenation and
ventilation. Once ‘airway’ and ‘breathing’ are assessed and controlled,
attention is directed to cardiovascular resuscitation

ABCDE approach
Initial assessment and treatment with the Airway, Breathing, Circulation, Disability, Exposure (ABCDE) approach, Troels Thim, International Journal of General Medicine 2012:5 117–121

AHA 2010 C-A-B Guidelines
• Why the Change From A-B-C to C-A-B?
In the A-B-C sequence, chest compressions are often delayed while the
responder opens the airway to give mouth-to-mouth breaths, retrieves a
barrier device, or gathers and assembles ventilation equipment. By
changing the sequence to C-A-B, chest compressions will be initiated
sooner and the delay in ventilation should be minimal

Head-tilt and chin-lift to open the airway.
Airway
• Assess
• Airways Voice
• Breath sounds
• Treat
• Head tilt and chin lift
• Oxygen (15 l min-1)
• Suction

Breathing
• Assess
• Respiratory rate
• (12–20 /min)
• Chest wall movements
• Chest percussion
• Lung auscultation
• Pulse oximetry (97%–100%)
• Treat
• Seat comfortably
• Rescue breaths
• Inhaled medications
• Bag-mask ventilation
• Decompress tension
• pneumothorax

Circulation
• Assess
• Skin colour, sweating
• Capillary refill time(2 s)
• Palpate pulse rate(60–100/min)
• Heart auscultation
• Blood pressure (systolic 100–140mmHg)
• Electrocardiography monitoring
• Treat
• Stop bleeding
• Elevate legs
• Intravenous access
• Infuse Fluid

Place your other hand directly on top of
the first hand. Try to keep your fingers off of the chest
by interlacing them or holding them upward.

Disability
• Assess
• Level of consciousness –
• AVPU
• Alert
• Voice responsive
• Pain responsive
• Unresponsive
• Limb movements
• Pupillary light reflexes
• Blood glucose
• Treat
• Treat Airway, Breathing, and
circulation problem
• Recovery position
• Glucose for hypoglycemia

Exposure
• Assess
Expose skin
Temperature
• Treat
Treat suspected cause

Resuscitation
• It is important to determine the cause of shock in order to provide
necessary resuscitation
• When in doubt always assume its hypovolemic shock
• Treat with fluid resuscitation and check response.
• Once the definitive cause is identified start with definitive
management parallel to fluid replacement

Fluid therapy
• In all types of shock regardless of cause hypovolemia and inadequate
preload must be addressed before definitive management.
• Administration of inotropic and chronotropic drugs in order to
increase the preload will prove futile if fluid is not replaced which will
lead to the stage of unresuscitable shock as the myocardium becomes
progressively more ischaemic and unresponsive to resuscitative
attempts.
• Therefore, fluid replacement is the first line of treatment.

Types of Fluid to be uses
• There is continuing debate over which resuscitation fluid is best for
the management of shock
• The two major categories of solutions are crystalloid and colloid
• Crystalloids include normal saline, Hartmann’s solution, Ringer’s
Lactate
• Colloidal solution include Albumin and fresh frozen plasma
• However the ideal Replacement is Blood as colloids and crystalloids
do not have oxygen carrying capacity, patients are put on crystalloids
till blood is made available.

Dynamic Fluid Response
• During the ongoing treatment the patients condition is monitored in
terms of BP, CVP and Heart rate, and are classified as
• Responders- They are not actively losing anymore fluid but
require filling to attain a normal value status.
• Transient Responders- Show an improvement but then revert to
their previous state over the next 10–20 min.
• Non-Responders-severely volume depleted.

Vasopressors and inotropic support
(the second line of treatment)
• Vasopressor agents (phenylephrine, noradrenaline) are indicated in
distributive shock states (sepsis, neurogenic shock)
• When the vasodilatation is resistant to catecholamines, vasopressin
may be used as an alternative vasopressor.
• In cardiogenic shock or when myocardial depression complicates a
shock state (e.g. severe septic shock with low cardiac output),
inotropic therapy may be required to increase cardiac output and,
therefore, oxygen delivery. The ino-dilator dobutamine is the agent of
choice.

Monitoring the status of Shock
• Minimum
• Electrocardiogram
• Pulse oximetry ( Oxygen saturation (SaO2) - 94 - 100% )
• Blood pressure ( Diastolic above 60mmof Hg )
• Urine output ( Adult, >0.5 mL/kg/hr. Child, >1 mL/kg/hr. Neonate, >2 mL/kg/hr )
• Additional modalities
• Central venous pressure
• Invasive blood pressure
• Cardiac output
• Base deficit and serum lactate

Shocks Requiring Atypical management.
• Anaphylaxis
• Hypoglycaemic shock
• Septic shock
Shock, Rajiv Borle, Textbook Of oral and Maxillofacial Surgery

ANAPHYLACTIC SHOCK
(Ana=against Phylactic=protection)
• This type of shock is due to increased release of histamine against a foreign
agent.
Causes
• Drugs
• Insect sting
• Foods
• Medication
• Aeroallergens

Characteristics of Anaphylaxis
• Immediate type of hypersensitivity reaction
• Mediated through Ig-E
• Life threatening
• Needs prompt reaction

Clinical Features
• Flushing
• Urticaria
• Angioedema
• Hypotension
• Tachycardia
• Bronchospasm
• Hypoxia
• Cyanosis
• Metabolic acidosis
• Involuntary defecation
• If not treated within 3-5 min severe life threatening, irreversible brain death.
URTICARIA
Angioedema

Pathophysiology
Acute allergic reaction
vasodilatation
Increase in capillary permeability Marked
Hypovolemia
Release of large quantity of histamine

Management
Nanavati RS, Kumar M, Modi TG, Kale H. Anaphylactic shock management in dental clinics: An overview. J Int Clin Dent Res Organ 2013;5:36-9

HYPOGLYCEMIA
• Normal Blood Glucose 80-120 mg/ dl (fasting)
120-140mg/dl (post prandial)
• Adults Blood glucose < 50 mg/dl
Children Blood glucose < 40 mg/dl

• The brain requires about 70 ml of blood flow per minute/ 100 gms. of
brain matter
• about 3 – 5 ml of oxygen/min/100gms. of brain matter.
• The glucose requirement is about 5 – 7 mg./ min./ 100 gms of brain
matter.

Etiology
• Starvation
• Diabetics
• Long procedures, upright postures
• Hot, humid conditions

Clinical Features
• Feeling of tiredness, fatigue, lethargy
• Blurring of vision
• Bizarre behaviour
• Sleepiness
• Slurring of speech
• Lack of muscle co ordination
• Sweating- warm, moist skin
• Mild tachycardia
• Headache
• Altered level of consciousness/Unconsciousness
• If untreated, coma and death occurs.

Management
CONSCIOUS PATIENT
•Stop the procedure
•supine position
•No crowd
•hypertonic glucose solution orally (70-
100 gm in 50-100ml water)
•Monitor the level of consciousness and
the vital signs.
UN- CONCIOUS PATIENT
•supine position with feet slightly elevated.
•Maintain airway
•IV infusion of 1 -2 ampules of 25%
dextrose.
•Inj glucagon

SEPTIC SHOCK
• It is a condition of a human response to a infection.
• Most common is gram negative bacteria.
• Occurs in elderly and immuno-compromised patients.

Pathophysiology
Micro-organism (infection)
Bacteraemia
Introduction of m/o to the bloodstream
Septicaemia
Systemic Immune Response(SIR)
Leading to Toxic Shock Syndrome
Refractory Septic Shock

Clinical Manifestations
• Start with onset of chills.
• Temperature above 38°C
• Two Phases :
• Early Warm Shock
• Late Cold Shock

Early Warm Shock
Sepsis
Release of toxins
Temperature raise
Cutaneous vasodilation

Late Cold Shock
Increase in vascular permeability
Release of toxins in the circulation
Damage to capillaries
Volume replacement demand increases
Hyper dynamic circulation

Management
• Treatment of infection
• Antibiotic treatment
• Fluid replacement
• Mechanical ventilation
• Vasoactive drugs

Vasovagal syncope (Syncope = “to interrupt”)
(vay-zoh-VAY-gul SING-kuh-pee)
• Vasovagal Syncope is the most common emergency in dental practice
It is defined as a transient loss of consciousness due to reduced blood
supply to the brain.
• It is often caused by anxiety.
• The typical presentation of vasovagal syncope is dizziness
accompanied with sweating, feeling of being light headed, slowed
pulse rate, and loss of consciousness.
• Nausea and/ or vomiting may or may not occur.

Causes of vasovagal syncope
Psychogenic
• Fright
• Anxiety
• Emotional Stress
• Pain
• Sight of blood or surgical dental
instruments
Non-psychogenic
• Sitting In an upright position
• Hunger
• Exhaustion
• Hot and humid Condition
• Male sex
Medical Emergencies in Dental Office Stanley F Malamed

Stages
• Pre- Syncope
• Syncope
• Post-Syncope

Presyncope
• Feeling of warmth Pupillary dilatation
• Loss of colour : pale or ashen skin tone
• Yawning
• Hyperpnea
• Heavy perspiration
• coldness in hands and feet
• Complaint of feeling bad or Hypotension
• Faint Bradycardia
• Nausea
• Visual disturbances

Syncope
• Breathing irregular, gasping
• Pupil dilate
• Death like appears
• Bradycardia
• Pulse weak
• Decreased blood pressure.

Post-Syncope
• Pallor
• Nausea
• Weakness
• sweating from few min. to many hrs.
• Short period of mental confusion
• Disorientation
• Blood pressure and heart rate- normal
Tendency of second attack if allowed to stand or sit too soon

Pathophysiology
Induction Of Stress
Release of
Cathecholamine
Decreased in
peripheral vascular
Resistance
Pooling of blood
causing decrease in
circulatory volume
Decrease in
cerebral blood flow
Syncope.

Precaution
• Controlling the predisposing factors before the patient enters the
treatment area.
• It should be made certain that the patient has eaten recently.
• A comfortable environmental temperature and humidity in the office.
• Stress reduction modalities can be employed.
• Reducing anxiety.
• Proper positioning and receiving supplemental oxygen.
• Sedation through variety of drugs (only if all other measures fail)

Generalized Management
• Positioning: no premature sitting of patient, Trendelenburg position,
and supine preferred, In Pregnancy lateral decubitus preferred.
• Relief from compression on the neck.
• Try to Revive the Person by taping briskly.
• Evaluate and maintain Airway, breathing, circulation. If absent, begin
CPR.
• If the person is breathing, restore blood flow to the brain by raising the
person’s legs above heart level — about 12 inches (30 centimeters) —
if possible.
Management of Syncope in Dental Camps, Gururaju CR, Feb 10 2016 Journal of Oral Health.

• Give supplemental oxygen.
• When consciousness is regained, patient should be kept flat and
reassured. If the person doesn’t regain consciousness within one
minute, call local emergency number.
• Once pulse and blood pressure recover, slowly raise patient to seated
position. Fruit juices or glucose water can be administered orally until
person recovers completely.
• Patients with significant medical problems,or when syncope is
prolonged or complicated by seizure activity, should be transferred to
a hospital environment for further assessment
Management of Syncope in Dental Camps, Gururaju CR, feb 10 2016 Journal of Oral Health.

Summary
• Shock is an anomaly which presents itself unexpectedly, it is
necessary for a clinician to figure out the exact Etiology of shock and
treat it accordingly.
• The Protocol given by the American heart association is the C-A-B
according to the 2010 revision.
• Emergency medical services must be at the disposal of the clinicians
in case the situation goes out of control for the clinician.

References
• Functions Of Blood https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0072576/
• Physiological effects of haemorrhage, J Freeman, 1950.
• Shock and blood transfusion, Bailey & Love, a short practice of surgery.
• Advanced Trauma Life Support Manual. Chicago: American College of Surgeons; 1997. pp. 103–112.
• Haemostasis and Blood Coagulation, textbook of medical physiology, Guyton and hall.
• Management of bleeding following major trauma:Rolf Rossaint1, Bertil Bouillon2,Critical Care 2010, 14:R52
• Initial assessment and treatment with the Airway, Breathing, Circulation, Disability, Exposure (ABCDE) approach,
Troels Thim, International Journal of General Medicine 2012:5 117–121.
• Nanavati RS, Kumar M, Modi TG, Kale H. Anaphylactic shock management in dental clinics: An overview. J Int Clin
Dent Res Organ 2013;5:36-9
• Surgical Complications After Implant Placement, Dental Clinics of North America, Volume 59, Issue 1, Pages 57-72.
• Use of a Collagen Matrix as a Substitute for Free Mucosal Grafts in Pre-Prosthetic Surgery: 1 Year Results From a
Clinical ,The Open Dentistry Journal, 2016, 10, 395-410 Prospective.
• Shastry SP, Kaul R, Baroudi K, Umar D. Hemophilia A: Dental considerations and management. Journal of International
Society of Preventive & Community Dentistry. 2014;4(Suppl 3):S147-S152. doi:10.4103/2231-0762.149022.
• Shock, Rajiv Borle, Textbook Of oral and Maxillofacial Surgery
• Anaphylaxis: an update for dental practitioners NG Maher,* J de Looze,* GR Hoffman*†
• Medical Emergencies in Dental Office Stanley F Malamed.
• Management of Syncope in Dental Camps, Gururaju CR, Journal of Oral Health.

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