Haemorrhage & shock*

by;
Dr.tawfeeq jasim
2022-2023
Introduction;
 Shock is the most common cause of death of surgical patients.
 Shock is a systemic state of low tissue perfusion which is inadequate
to meet the metabolic needs of the cells.
 Shock requires immediate treatment and can get worse very rapidly. As
many 1 in 5 people who suffer shock will die from it.
 With insufficient delivery of oxygen and glucose, cells switch from
aerobic to anaerobic metabolism.
 The initial cellular injury that occurs is reversible; however, the injury
will become irreversible(multiple organ failure) if tissue perfusion is
prolonged or severe enough such that, compensation is no longer
possible. and cell death ensues.
 The heart rate divided by systolic blood pressure, known as the shock
index(SI). SI of greater than 0.8 supports the diagnosis more than low
blood pressure or a fast heart rate in isolation
.Signs common to most forms of shock
 Pallor, mottled skin, cold extremities, sweating
and thirst.
 Rapid and weak pulse often only detected on major
arteries (femoral or carotid).
 Low blood pressure (BP), narrow pulse pressure,
BP sometimes undetectable.
 Capillary refill time (CRT) > 3 seconds.
 Cyanosis, dyspnoea, tachypnoea are often present
in varying degrees depending on the mechanism.
 Consciousness usually maintained, but anxiety,
confusion, agitation or apathy are common.
 Oliguria or anuria.
Signs specific to the mechanism of shock.

Hypovolaemic shock;
The common signs of shock listed above are typical of hypovolaemic shock.
Signs of shock may not become evident until a 50% loss of blood volume

Anaphylactic shock;
– Frequent cutaneous signs: rash, urticaria, angioedema
– Respiratory signs: dyspnoea, bronchospasm

Septic shock;
– High fever or hypothermia (< 36 °C), rigors, confusion
– BP may be initially maintained, but rapidly, same pattern as for
hypovolaemic shock.

Cardiogenic shock;
– Respiratory signs of left ventricular failure (acute pulmonary oedema)
are dominant: tachypnoea, crepitations on auscultation.
– Signs of right ventricular failure: raised jugular venous pressure,
hepatojugular reflux,
PATHOPHYSIOLOGY OF SHOCK;
;Cellular and metabolic response
 Regardless of etiology , the imbalance between cellular supply and
demand leads to neuroendocrine and inflammatory responses,
 Cellular metabolism is based primarily on the hydrolysis of adenosine
triphosphate (ATP). The majority of ATP is generated in our bodies
through aerobic metabolism . This process is dependent on the
availability of O2
 As O2 tension within a cell decreases, the generation of ATP slows.
 Therby,, the cells shift from aerobic to anaerobic metabolism and
glycolysis to generate ATP. This occurs via the breakdown of cellular
glycogen stores .
 The product of anaerobic respiration is not carbon dioxide but pyruvate
and, under hypoxic conditions , pyruvate is converted into lactate .The
accumulation of lactic acid in the blood produces a systemic metabolic
acidosis
;Microvascular response
Damaged endothelium loses its integrity and becomes ‘leaky’. Spaces
,between endothelial cells allow fluid to leak out and tissue oedema ensues
stages of shock;
As it is a complex and continuous condition there is no sudden transition from one
stage to the next.
I. Compensatory stage( Non-progressive phase);
As shock progresses, the compensatory responses reduce flow to non-essential
organs to preserve preload and flow to the kidneys,lungs and brain.
Systemic response;
Cardiovascular;
 As preload and afterload( venous return and cardiac output) decrease, there is
a compensatory baroreceptor response resulting in increased sympathetic
activity and release of catecholamines (epinephrine and norepinephrine) into the
circulation.
 This results in increased heart rate and contractility, as well as venous and
arterial vasoconstriction (except in sepsis). ; the combined effect results in an
increase in blood pressure
 The arterial vasoconstriction is not uniform; with blood shunted away from less
essential organ beds such as the intestine, muscles and skin. In contrast, the
brain and heart have autoregulatory mechanisms that attempt to preserve their
blood flow despite a global decrease in cardiac output.
 Catecholamine effects on peripheral tissues include
stimulation of hepatic glycogenolysis and gluconeogenesis to
increase circulating glucose availability to peripheral tissues,
an increase in skeletal muscle glycogenolysis, suppression of
insulin release, and increased glucagon release
Respiratory;
 The metabolic acidosis and increased sympathetic response
result in an increased respiratory rate(hyperventilate) and
minute ventilation to increase the excretion of CO2.
 CO2 indirectly acts to acidify the blood and by removing it the
body is attempting to raise the pH of the blood. (and so
produce a compensatory respiratory alkalosis).
Renal;
 Decreased perfusion pressure in the kidney leads to reduced
filtration at the glomerulus and a decreased urine output. The
renin–angiotensin–aldosterone axis is stimulated, resulting in
further vasoconstriction and increased sodium and water
reabsorption by the kidney.
Endocrine;
 Shock stimulates the hypothalamus to release corticotropin-
releasing hormone (CRH), which results in the release of
adrenocorticotropic hormone (ACTH) by the pituitary. ACTH
subsequently stimulates the adrenal cortex to release cortisol.
 Cortisol acts synergistically with epinephrine and glucagon to induce
a catabolic state.
 Cortisol stimulates gluconeogenesis and insulin resistance, resulting
in hyperglycemia as well as muscle cell protein breakdown and
lipolysis to provide substrates for hepatic gluconeogenesis.
 Cortisol causes retention of sodium and water by the kidney.
 The pituitary also releases vasopressin(ADH) in response to
hypovolemia, ADH acts on the distal tubule and collecting duct of
the nephron to increase water permeability, decrease water and
sodium losses, and preserve intravascular volume.,
 ADH acts as a potent mesenteric vasoconstrictor, shunting
circulating blood away from the splanchnic organs during
hypovolemia.
 Vasopressin also increases hepatic gluconeogenesis and increases
2. Progressive phase;
 Should the cause of the crisis not be successfully treated, the shock will proceed to
the progressive stage and the compensatory mechanisms begin to fail.
 Due to the decreased perfusion of the cells, sodium ions build up within
while potassium ions leak out.
 anaerobic metabolism continues, increasing the body's metabolic
acidosis, the arteriolar smooth muscle and precapillary sphincters relax
such that blood remains in the capillaries.
 Due to this, the hydrostatic pressure will increase and, combined
with histamine release, this will lead to leakage of fluid and protein into
the surrounding tissues.
 As this fluid is lost, the blood concentration and viscosity increase,
causing sludging of the micro-circulation (DIC).
 The prolonged vasoconstriction will also cause the vital organs to be
compromised due to reduced perfusion.
 If the bowel becomes sufficiently ischemic , bacteria may enter the
blood stream, resulting in the increased complication of endotoxic shock.
 cerebral hypoperfusion result in altered mental status
3.stage of decompensation (Irreversible phase) ;
 the ability of the body to compensate is lost.

Patients who are in profound shock for a prolonged

period of time become ‘unresuscitatable’.

Cell death follows from cellular ischaemia

the vital organs have failed and the shock can no
longer be reversed.
There is myocardial depression and loss of
responsiveness to fluid or inotropic therapy.
Brain damage and cell death are occurring,
Death is the inevitable result.
Multiple organ failure;
Multiple organ failure is defined as two or more failed organ
systems
 CNS: stroke, hypoxic brain damage
 Heart: reduced coronary perfusion → acute coronary
syndrome, myocardial depression
 Kidneys: acute tubular necrosis → acute kidney failure
 Liver: necrosis that begins around the
hepatic veins → acute hepatic failure
 Lungs: acute respiratory distress syndrome
 Coagulation system: disseminated intravascular coagulation
 Intestine: ischemic colitis → paralytic ileus
 Adrenals: hypocortisolism, hypoglycemia
 Skin and soft tissue: necrosis, gangrene, myositis,
and necrotizing fasciitis
*Classification of shock;
compensated mild moderate
severe
lactic acidosis + ++ ++ +++

urine output normal normal reduced

anuric

conscious level normal mild anxiety drowsy

comatose

respiratory rate normal increased increased

laboured

pulse rate mild increase increased increased

increased

blood pressure normal normal mild hypotension sever

hypotensione
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 with a
mortality rate between 30% and 50%.
 The prognosis of cardiogenic shock is even worse
with a mortality rate between 70% and 90%
Classification of shock;
 Shock is divided into four main types based on
the underlying cause:
I. Hypovolaemic shock(low volume)
II. Cardiogenic shock
III. Obstructive shock
IV. Distributive shock (septic shock)

A few additional classifications are occasionally

used including:
endocrine shock.
Hypovolaemic/Hemorrhagic shock;
 Hypovolemic shock is the most common type of shock and is caused by
insufficient circulating volume.
 Hypovolaemia may be haemorrhagic( internal or external hemorrhage ), or non-
haemorrhagic causes.

Non-haemorrhagic causes include;

 poor fluid intake (dehydration),

 excessive fluid loss due to vomiting,

 diarrhoea,

 excess urine loss due to diabetic ketoacidosis and diabetes insipidus,

 evaporation,

 ‘third-spacing’ where fluid is lost into the gastrointestinal tract and interstitial
spaces, as for example in bowel obstruction or pancreatitis.
 Hypovolaemia is probably the most common form of shock,
 Shock in a trauma patient and postoperative patient should be
presumed to be due to hemorrhage until proven otherwise
 In general, loss of around 15 per cent of the circulating blood
volume(700 to 750 mL for a 70-kg patient) is within normal
compensatory mechanisms and may produce little in terms of obvious
symptoms,
 Young healthy patients with vigorous compensatory mechanisms may
tolerate larger volumes of blood loss while manifesting fewer clinical
signs despite the presence of significant peripheral hypoperfusion.
 Elderly patients may be taking medications that either promote
bleeding (e.g., warfarin or aspirin), or mask the compensatory responses
to bleeding (e.g., beta blockers).
 In addition, atherosclerotic vascular disease, diminishing cardiac
compliance with age, inability to elevate heart rate or cardiac
contractility in response to hemorrhage, and overall decline in
physiologic reserve decrease the elderly patient's ability to tolerate
hemorrhage.
 Classification of Hemorrhage

Class I II III IV

Blood loss )750ml( 15% < 30%–15 40%–30 40% >

)750-1500( )1500-2000 2000 >

Heart rate 100 < 120–100 140–120 140 >

Systolic blood Normal Normal ↓ ↓

pressure

Pulse pressure ↑ Normal or ↓ ↓ ↓

Respiratory rate 20–14 30–20 40–30 35 >

output Urine mL/hr 30 > mL/hr 30–20 mL/hr 15–5 Absent

Mental status Anxious Mildly anxious Anxious, Confused,

confused lethargic
Signs and symptoms;
 A rapid, weak, thready pulse due to decreased blood flow
combined with tachycardia
 Cool, clammy skin due to vasoconstriction and stimulation of
vasoconstriction
 Rapid and shallow breathing due to sympathetic nervous
system stimulation and acidosis
 Hypotension with narrow pulse pressure in the
decompensated stage
 Hypothermia due to decreased perfusion and evaporation of
sweat
 Thirst and dry mouth, due to fluid depletion
 Cold and mottled skin (Livedo reticularis), especially
extremities, due to insufficient perfusion of the skin
 Specific symptoms corresponding to the cause
* DIAGNOSIS
- Identifying the sources of blood loss in patients with
penetrating wounds is relatively simple.
- Each pleural cavity can hold 2 to 3 L of blood and can
therefore be a site of significant blood loss.
- Diagnostic and therapeutic tube thoracostomy may be indicate
- chest radiograph may be obtained.
- Major retroperitoneal hemorrhage typically occurs in
association with pelvic fractures, which is confirmed by pelvic
radiography.
- Intraperitoneal hemorrhage is probably the most common
source of blood loss inducing shock.may be rapidly identified by
diagnostic ultrasound or diagnostic peritoneal lavage.
- computed tomography scans may be needed to assess for head,
chest, and/or abdominal bleeding.
- Serum lactate and base deficit are measurements that are
helpful
- Substantial blood loss externally may be suspected from
prehospital medical reports
A patient can bleed and yet show a
“normal” hemoglobin value (hyperacute bleeding
without the compensatory “dilution effect”);

 in the case of hemorrhage, hemoglobin value will

only start to drop after 8–12 hours, when
the interstitial fluid shifts into the plasma.

Continuous monitoring of the blood pressure and

the heart rate is, therefore, more important in the
acute setting!
TREATMENT;
 Control of ongoing hemorrhage is an essential component of the
resuscitation of the patient in shock.
 treatment of hemorrhagic shock is instituted concurrently with
diagnostic evaluation to identify a source
 The appropriate priorities in these patients are
(a) secure the airway,
(b) control the source of blood loss, and
(c) IV volume resuscitation.
 So that diagnostic laparotomy or thoracotomy may be indicated.
 Initial resuscitation is limited to keep SBP around 90 mmHg. This
prevents renewed bleeding from recently clotted vessels.
 Resuscitation and intravascular volume resuscitation is accomplished
with blood products and limited crystalloids,
 Patients who fail to respond to initial resuscitative or those
who respond to initial resuscitative effort but then
deteriorate hemodynamically frequently have ongoing
bleeding for which some form of intervention (i.e.,
operation or interventional radiology) is required.

 Additional resuscitative adjuncts in patients with

hemorrhagic shock include minimization of heat loss and
maintaining normothermia.

 The development of hypothermia in the bleeding patient is

associated with acidosis, hypotension, and coagulopathy.
Type of fluids;
 In most studies of shock resuscitation there is no overt
difference in response or outcome between crystalloid
solutions (normal saline, Hartmann’s solution, Ringer’s
lactate) or colloids (albumin or commercially available
products).
 Most importantly, the oxygen carrying capacity of
crystalloids and colloids is zero.
 If blood is being lost, the ideal replacement fluid is blood,
although crystalloid therapy may be required while awaiting
blood products.
 Hypotonic solutions (dextrose etc.) are poor volume
expanders and should not be used in the treatment of shock
unless the deficit is free water loss (eg. diabetes insipidus)
or patients are sodium overloaded (eg. cirrhosis).
Cardiogenic shock;
 Cardiogenic shock is defined clinically as circulatory pump failure
leading to diminished forward flow and subsequent tissue hypoxia, in
the setting of adequate intravascular volume.
 Mortality rates for cardiogenic shock are 50 to 80%.
 Causes of cardiogenic shock include damage to the heart muscle, most
often from a large myocardial infarction myocardial infarction, cardiac
dysrhythmias, cardiomyopathy/myocarditis congestive heart failure
valvular heart disease(Acute mitral regurgitation Aortic stenosis Mitral
stenosis Acute aortic insufficiency ) ventricular septal defect, Left
atrial myxoma,Pericardial tamponade,,and blunt myocardial injury.,
Left atrial myxoma
 Acute, extensive MI is the most common cause of cardiogenic shock;
 Cardiogenic shock complicates 5 to 10% of acute MIs. Usually within 24
hours after onset of infarction
Symptoms of cardiogenic shock:
 Weak pulse, tachycardia,Pulsus paradoxus in case of
tamponade
 Cold, clammy extremities, poor capillary refill
 Dyspnea, fine basal crepitations
 Elevated JVP and distended neck veins
 Hypotension with a narrow pulse pressure in the
decompensated stage
 Other clinical features related to the underlying
disease: chest pain, abnormal auscultatory findings (e.g., S3,
S4)
DIAGNOSIS;
 Signs of circulatory shock include hypotension, cool and
mottled skin, depressed mental status, tachycardia,
 Confirmation of a cardiac source for the shock requires
electrocardiogram and urgent echocardiography.
 Other useful diagnostic tests include chest radiograph,
arterial blood gases, electrolytes, complete blood count,
and cardiac enzymes.
TREATMENT;
 Ensuring adequate oxygenation, sufficient ventilation,
 judicious volume restoration,
 minimizing sympathetic discharge through adequate relief
of pain, and
 correcting electrolyte imbalances
 Anticoagulation and aspirin are given for acute MI.
 Intubation and mechanical ventilation often are required,
 Significant dysrhythmias and heart block must be treated
with antiarrhythmic drugs, pacing, or cardioversion, if
necessary.
 When profound cardiac dysfunction exists, inotropic
support may be indicated to improve cardiac contractility
and cardiac output. Epinephrine stimulates alpha and beta
receptors and may increase cardiac contractility and heart
Obstructive shock;
 Obstructive shock is a form of cardiogenic shock that results from
mechanical impediment to circulation rather than primary cardiac failure.
 Common causes of obstructive shock include cardiac tamponade, tension
pneumothorax, massive pulmonary embolus or air embolus.
 Pulmonary embolism is the result of a thromboembolic incident in the blood
vessels of the lungs and hinders the return of blood to the heart
 Other causes IVC obstruction Aortic stenosis hinders circulation by
obstructing the ventricular outflow tract ,Deep venous thrombosis, Neoplasm.
 Cardiac tamponade occurs when sufficient fluid has accumulated in the
pericardial sac prevents inflow of blood into the heart..
 Acutely, the pericardium does not distend; thus small volumes of blood may
produce cardiac tamponade. If the effusion accumulates slowly (e.g., in the
setting of uremia, heart failure, or malignant effusion), the quantity of
fluid producing cardiac tamponade may reach 2000 mL.
 With either cardiac tamponade or tension pneumothorax, reduced filling of
the right side of the heart from either increased intrapleural pressure
secondary to air accumulation (tension pneumothorax) or increased
intrapericardial
DIAGNOSIS AND TREATMENT
 Diagnosis of tension pneumothorax should be made on clinical
examination.
Respiratory embaresment ,hypotension, diminished breath sounds over
one hemithorax, hyperresonance to percussion, jugular venous distention,
and shift of mediastinal structures to the unaffected side with tracheal
deviation.
 Chest x-ray findings that may be visualized include deviation of
mediastinal structures, depression of the hemidiaphragm, and hypo-
opacification with absent lung markings.
 Cardiac tamponade results from the accumulation of blood within the
pericardial sac, usually from penetrating trauma or chronic medical
conditions such as heart failure or uremia.
total circulatory collapse and cardiac arrest,. dyspnea, orthopnea,
cough, peripheral edema, chest pain, tachycardia, muffled heart tones,
jugular venous distention, and elevated central venous pressure
 emergency pericardial decompression, usually through a left
thoracotomy.
 Chest radiographs, ultrasonography, Echocardiography
 Pericardiocentesis under ultrasound guidance to diagnose pericardial
blood and potentially relieve tamponade may be used.
Distributive shock;
 Distributive shock is low blood pressure due to a dilation of blood vessels within
the body (due to loss of muscle tone in the arteries or inflammation and dilation
of the capillaries). This can be caused by
 systemic infection (septic shock)
 severe allergic reaction (anaphylaxis)
 spinal cord injury (neurogenic shock).
 Inadequate organ perfusion is accompanied by vascular dilatation with
hypotension, low systemic vascular resistance, inadequate afterload and a
resulting abnormally high cardiac output.

 In anaphylaxis, vasodilatation is due to histamine release, while in high spinal

cord injury there is failure of sympathetic outflow and adequate vascular tone
(neurogenic shock).

 The cause in sepsis is less clear but is related to the release of bacterial
products (endotoxin) and the activation of cellular and humoral components of
the immune system.
Septic Shock (Vasodilatory Shock);
 Caused by an overwhelming systemic infection resulting in failure of the
vascular smooth muscle to constrict appropriately secondary to
circulating inflammatory mediators and cells( vasodilation )
 Main manifestations are produced due to massive release
of histamine which causes intense dilation of the blood vessels
 Septic shock can be caused by Gram negative bacteria such as
Escherichia coli, Proteus species, Klebsiella pneumoniae , other Gram-
positive cocci, such as pneumococci and streptococi, and certain fungi as
well as Gram-positive bacterial toxins.
 Vasodilatory shock is characterized by peripheral vasodilation with
resultant hypotension and resistance to treatment with vasopressors.
Despite the hypotension, plasma catecholamine levels are elevated, and
the renin-angiotensin system is activated in vasodilatory shock.
 the mortality rate for severe sepsis remains at 30 to 50
DIAGNOSIS;
 Patients with sepsis have evidence of an infection, as well
as systemic signs of inflammation (e.g., fever,
leukocytosis, and tachycardia).

 Positive blood cultures

 evidence of tissue hypoperfusion (such as confusion,

malaise, oliguria), and systemic hypotension

 These should prompt an aggressive search for infection,

including a thorough physical examination, inspection of all
wounds, evaluation of catheters or other foreign bodies,
obtaining appropriate cultures, and adjunctive imaging
studies, as needed.
TREATMENT;
 early recognition of symptoms, and early administration of
broad spectrum and organism specific antibiotics
 assessment of the adequacy of their airway and
ventilation. fluid resuscitation and restoration of
circulatory volume with balanced salt solutions is essential.
 vasopressors
 Empiric antibiotics must be chosen carefully based on the
most likely pathogens
 IV antibiotics will be insufficient to adequately treat the
infectious episode in the settings of infected fluid
collections, infected foreign bodies, and devitalized
tissue. This situation necessate percutaneous drainage
and operative management to target a focus of infection
Anaphylactic shock;
 Anaphylactic shock(type I hypersensitivity reaction) or anaphylactoid
reactions is caused by a severe anaphylactic reaction to
an allergen, antigen,Bee sting, drug,contrast medium allergy or foreign protein
causing degranulation of mast cells with massive histamine release which
causes widespread vasodilation, leading to hypotension and increased capillary
permeability

Clinical features
Tachycardia, tachypnea,Hypotension with a narrow pulse pressure, Flushed,
itchy skin, Bronchospasm, laryngeal edema →
wheeze, stridor, cyanosis,Angioedema,Vomiting, diarrhea

Treatment
Epinephrine
Airway support (e.g., intubation, nebulization with albuterol)
Glucocorticoids (e.g., hydrocortisone
Neurogenic Shock;
 Neurogenic shock is usually secondary to spinal cord injuries
from vertebral body fractures of the cervical or high
thoracic region that disrupt sympathetic regulation of
peripheral vascular

 The classic symptoms include a slow heart rate due to loss

of cardiac sympathetic tone and warm skin due to dilation
of the peripheral blood vessels.

 This term can be confused with spinal shock which is a

recoverable loss of function of the spinal cord after injury
and does not refer to the haemodynamic instability per se.)
 Other causes of neurogenic shock are Spinal cord
neoplasm,Spinal/epidural anesthetic
DIAGNOSIS;
 The classic description of neurogenic shock consists of
decreased blood pressure associated with bradycardia,
flushed warm extremities (loss of peripheral
vasoconstriction), motor and sensory deficits indicative of
a spinal cord injury,
 radiographic evidence of a vertebral column fracture.

TREATMENT;
 After the airway is secured and ventilation is adequate, fluid
resuscitation and restoration of intravascular volume often
will improve perfusion in neurogenic shock .
 If the patient's blood pressure has not responded to what
is felt to be adequate volume resuscitation, dopamine may be
used first.
Endocrine shock;
 Causes of endocrine shock include hypo- and
hyperthyroidism and adrenal insufficiency.
 Hypothyroidism causes a shock state similar to that of
neuro- genic shock Cardiac output falls due to low inotropy
and bradycardia. There may also be an associated
cardiomyopathy.
 Thyrotoxicosis may cause a high-output cardiac failure.
 Adrenal insufficiency may be acute or relative
 Acute adrenal insufficiency is frequently the result of
discontinuing corticosteroid treatment without tapering
the dosage.
 Relative adrenal insufficiency in critically ill patients where
present hormone levels are insufficient to meet the higher
demands
Monitoring for patients in shock;
 Monitor the following parameters continuously:
 Heart rate and blood pressure
 Check skin color and capillary refill time (CRT)
 Shock index = pulse rate / systolic blood pressure. Shock index greater than
1 (positive shock index) may indicate the presence of shock
 Oxygen saturation by pulse oximetry
 Catheterize the bladder to assess the urine output.
 The level of consciousness is an important marker of cerebral perfusion,
 ECG,
 Additional modalities includes; CVP, invasive BP.

 The following investigations must be performed frequently

 Renal function tests:
 Arterial blood gas analysis: lactic acidosis
 Clotting parameters:
 Liver function tests: hyperbilirubinemia,
 Electrolytes (especially sodium, potassium, and calcium)
 central venous pressure
 Pulmonary artery catheterization: to measure hemodynamic parameters
(see cardiac catheterization)
 lactate and base deficit
HAEMORRHAGE;
 Bleeding, (hemorrhage) is blood escaping from the circulatory system from
damaged blood vessels
 Bleeding can occur internally, or externally either through a natural opening
such as the mouth, nose, ear, urethra, vagina or anus, or through a wound in
the skin.
 Hypovolemia is a massive decrease in blood volume, and death by excessive loss
of blood is referred to as exsanguination.
 The stopping or controlling of bleeding is called hemostasis
 Hemorrhaging is broken down into four classes
 Class I Hemorrhage involves up to 15% of blood volume. There is typically no
change in vital signs and fluid resuscitation is not usually necessary.
 Class II Hemorrhage involves 15-30% of total blood volume. Volume resuscitation
with crystalloids (Saline solution or Lactated Ringer's solution) is all that is
typically required. Blood transfusion is not usually required.
 Class III Hemorrhage involves loss of 30-40% of circulating blood volume.. Fluid
resuscitation with crystalloid and blood transfusion are usually necessary.
 Class IV Hemorrhage involves loss of >40% of circulating blood volume. The limit
of the body's compensation is reached and aggressive resuscitation is required
to prevent death.
Bleeding arises due to either traumatic injury, underlying medical condition, or a
combination.

Traumatic injury
Abrasion - this is caused by transverse action of a foreign object against the skin,
and usually does not penetrate below the epidermis.
Excoriation - caused by mechanical destruction of the skin, although it usually has
an underlying medical cause.
Hematoma -Caused by damage to a blood vessel that in turn causes blood to collect
under the skin.
Laceration - Irregular wound caused by blunt impact to soft tissue overlying hard
tissue or tearing such as in childbirth. In some instances, this can also be used to
describe an incision.
Incision - A cut into a body tissue or organ, such as by a scalpel, during surgery.
Puncture Wound - Caused by an object that penetrated the skin and underlying
layers, such as a nail, needle or knife.
Contusion - Also known as a bruise, this is a blunt trauma damaging tissue under
the surface of the skin.
Crushing Injuries - Caused by a great or extreme amount of force
gunshot wounds Caused by a projectile weapon such as a firearm.
Medical condition
Blood can escape from blood vessels as a result of 3
basic patterns of injury:
Intravascular changes - changes of the blood within
vessels (e.g. ↑ blood pressure, ↓ clotting factors)
Intramural changes; changes arising within the walls
of blood vessels(e.g.
aneurysm,dissections,AVMs,vasculitis)
Extravascular changes - changes arising outside
blood vessels (e.g. H pylori infection, brain
abscess, brain tumor)
Pathophysiology;
 Haemorrhage leads to a state of hypovolaemic shock. The combination of tissue
trauma and hypovolaemic shock leads to the development of an endogenous
coagulopathy called acute traumatic coagulopathy (ATC).
 Ongoing bleeding with fluid and red blood cell resuscitation leads to a dilution
of coagulation factors which worsens the coagulopathy.
 In addition, the acidosis induced by the hypoperfused state leads to decreased
function of the coagulation proteases, resulting in coagulopathy and further
haemorrhage.
 The reduced tissue perfusion includes reduced blood supply to muscle beds.
Underperfused muscle is unable to generate heat and hypothermia ensues.
Coagulation functions poorly at low temperatures and there is further
haemorrhage,
 Intravenous blood and fluids are cold and exacerbate hypothermia.
 Further heat is lost by opening body cavities during surgery.
 Every effort must therefore be made to rapidly identify and stop
haemorrhage, and to avoid (preferably) or limit physiological exhaustion from
coagulopathy, acidosis and hypothermia.
Definitions;
Revealed and concealed haemorrhage;
Revealed haemorrhage is obvious external haemorrhage, (wound, haematemesis )
Concealed haemorrhage is contained within the body cavity chest, abdomen, pelvis,
retroperitoneum or in the limbs

Primary, reactionary and secondary haemorrhage;

Primary haemorrhage
is haemorrhage occurring immediately due to an injury (or
surgery).
Reactionary haemorrhage(within 24 hours)
and is usually due to dislodgement of clot by resuscitation,
normalisation of blood pressure and vasodilatation. Reactionary
haemorrhage may also be due to technical failure, such as
slippage of a ligature.
Secondary haemorrhage
is due to sloughing of the wall of a vessel. It usually occurs 7–
14 days after injury and is precipitated by factors such as
infection, pressure necrosis (such as from a drain) or
malignancy.
* Surgical and non-surgical haemorrhage;
Surgical haemorrhage is due to a direct injury and is amenable to
surgical control
Non-surgical haemorrhage is the general ooze from all raw surfaces due
to coagulopathy and cannot be stopped by surgical means (except
packing). Treatment requires correction of the coagulation
abnormalities

The adult human has approximately 5 litres of blood (70 mL/ kg

children and adults, 80 mL/kg neonates). . .
The haemoglobin level is a poor indicator of the degree of haemorrhage
as it represents a concentration and not amount.

In the early stages of rapid haemorrhage, the haemo globin

concentration is unchanged (as whole blood is lost).
Later, as fluid shifts from the intracellular and interstitial spaces into
the vascular compartment, the haemoglobin and haematocrit levels will
fall.
Management;
Identify haemorrhage
Immediate resuscitative manoeuvres
Direct pressure should be placed over the site of external haemorrhage.
Airway and breathing should be assessed and controlled as necessary.
Large-bore intravenous access should be instituted and blood drawn for
cross-matching .
Emergency blood should be requested if the degree of shock and ongoing
haemorrhage warrants this.

the site of haemorrhage must be rapidly identified to define the next step in
haemorrhage control (operation, angioembolisation, endoscopic control).

Clues may be in the history (previous episodes, known aneurysm, non-

steroidal therapy,
examination (nature of blood – fresh, melaena; abdominal tenderness, etc.).
investigations (chest and pelvis x-ray, abdominal ultrasound or diagnostic
peritoneal aspiration
The four central strategies of DCR are: *
1 Anticipate and treat acute traumatic
coagulopathy
2 Permissive hypotension until haemorrhage
control
3 Limit crystalloid and colloid infusion to avoid
dilutional coagulopathy
4 Damage control surgery to control haemorrhage
and preserve physiology.
Damage control resuscitation strategies have been
shown to reduce mortality and morbidity in
patients with exsanguinating trauma and may be
.applicable in other forms of acute haemorrhage