HAEMORRHAGE

A Hemorrhage (or hemorrhage) is defined as an escape of blood from a vessel, or simply, bleeding. It
can be arterial, venous or capillary. It can either be minor involving superficial blood vessels causing
petechiae and ecchymosis, or severe leading to fluctuating vital signs and even altered mental status.
Hemorrhaging can be acute (sudden, with larger quantities of blood) or chronic (with small amounts
of blood over a period of time).

External hemorrhage occurs from wounds and body orifices and Internal hemorrhage is an internal
bleeding, may be within the body cavities (Hemothorax/ hemoperitoneum/ hemopericardium, etc.)
or simply into the viscera. Internal hemorrhaging is a leading cause of preventable deaths especially
in case of acute trauma. It requires physical and lab tests, imaging and monitoring of vital signs to
assess the risk.

LEARNING OUTCOMES
1.Hemorrhage-Introduction
2. Etiology of Hemorrhage
3. Clinical Presentation and Complications
4. Shock
5.Pathogenesis in Shock
6.Stages of Shock

WORDS TO UNDERSTAND
1. Hematoma- Pooling of blood out of the vessels into the surrounding
tissues causes swelling.
2. Ecchymosis- Hemorrhaging into the skin and mucus membrane causes
a discoloration on the skin of about 1 to 2 centimeters in size.
3. Purpura- A Small area of haemorrhage with discolored skin of about 3
to 5 centimeters in size.
4. Petechiae- Pinhead sized haemorrhages/ red dots on the skin.
5. Diapedesis- Microscopic hemorrhaging of erythrocytes into loose
tissues around them, mostly after a congestion.

ETIOLOGY OF HEMORRHAGE
The presentation of hemorrhage varies by anatomic location. After acute trauma, hemorrhage can
subdivided into several anatomic areas: external wounds, bleeding within the skull, chest cavity,
abdominal cavity, retroperitoneum, and from long bone fractures. Taking a thorough history and
also perform a clear physical examination to locate the source and the etiology of a hemorrhage.
 Trauma to the vessel wall
Spontaneous hemorrhage
Inflammatory lesions of
the vessel wall
Neoplastic invasion
Vascular diseases
Elevated pressure in the
vessels
A penetrating wound in heart or big blood vessels or during labor,
etc.
Septicemia, Ruptured aneurysm (ballooning of a weak part in an
artery wall), Scurvy, Acute Anemia/ Leukemias, or bleeding diathesis
(e.g., Purpura).
Bleeding in chronic peptic ulcer, thyroid ulcers, vessels crossing a
tuberculous cavity in lung, Syphilitic aorta, and polyarteritis nodosa.
Vascular involvement in case of the cancer of tongue.
Atherosclerosis.
Systemic Hypertension with cerebral and retinal bleeding, varicose
vein hemorrhage due to elevated pressure in the legs or esophagus.

Many other causes that trigger hemorrhage is the long-term alcohol/ drug abuse (intracranial
bleeding), many carcinomas, complications of a medical procedure, post-partum, hereditary
disorders such as hereditary hemorrhagic telangiectasia, hemophilia and other bleeding/ clotting
disorders, viral hemorrhagic fever, epistaxis (nose bleeds), subarachnoid hemorrhage (a stroke
caused by head trauma), etc.

CLINICAL PRESENTATION AND COMPLICATIONS

Blood loss may make a person feel-

1.Cold to touch.

2.Dizzy.

3.Tired.

4.Nauseous.

5.Short of breath.

6.Weakness.

Complications-
1.Chest pain.

2.Confusion.

3.Faster breathing or heart rate.

4.Organ failure.

5.Seizures.

6.Shock.

7. Coma or death.

How far the symptoms and damage can go in a hemorrhage depends on

a. The amount of blood lost,

b. The speed in which it is lost, and

c. The anatomical location of the bleeding.

A 20% loss in the volume of blood gives mild clinical effects due to compensatory mechanisms, a
sudden blood loss of about 33% of the volume may be fatal, and 50% of chronic blood loss over a
period of 24 hours need not cause death. However, chronic hemorrhage leads to iron deficiency
anemia, whereas an acute bleeding leads to Hypovolemic shock (discussed later in the document).

SHOCK
A life-threatening clinical state of cardiovascular collapse characterized by deficient blood supply,
causes oxygen deprivation in the tissues, toxin build up and eventual organ failure, and Death. Shock
requires immediate treatment and can get worse very rapidly. As many as 1 in 5 people in shock will
die from it.

It results from a change in one or a combination of the following:

a.Hypotension- An acute reduction of effectively circulating blood volume and

b.Hypoperfusion- Insufficient perfusion of the cells and tissues.

c.If left unchecked, the above two mechanisms may cause poor metabolism at the cellular level and
death.

TYPES OF SHOCK
Primarily shocks are divided into:

Primary/ Initial Transient/ benign vasovagal attack from a sudden reduction of venous return
shock to the head, which leads to neurogenic vasodilatation and a resultant
peripheral pooling of the blood. (After trauma, severe pain or emotional
overreaction due to fear, sorrow or surprise). A brief period of
unconsciousness, weakness, sinking feeling, pale, cold, clammy limbs,
palpitations and low blood pressure might be noticed here.
Secondary True shock where the circulatory imbalance between oxygen supply and
shock demand occurs at a cellular level. Hence called as Circulatory shock.
Anaphylactic This is not a from of shock with circulatory origin but from a type 1
shock immunologic reaction.

TYPES OF SHOCK
Apart from those mentioned above, shock can be classified based on the etiology into 3 major and a
few other types of shocks.

1.Hypovolemic shock, where the circulatory blood volume is severely reduced either due to a loss of
plasma volume with or without loss of red cell mass. Causes are given below:

i) Acute Hemorrhage

ii)Dehydration from vomitings, diarrhea etc

iii)Burns

iv)Excessive use of Diuretics

v)Acute pancreatitis
2.Cardiogenic shock, due to acute circulatory failure without a decrease in blood volume is typically
caused by the acute heart diseases, leading to a fall in cardiac output such as

In case of Myocardial infraction, Cardiomyopathies, Rupture of the heart, ventricle, papillary muscle,
pulmonary embolism, tension pneumothorax etc

3.Septic shock or Toxemic shock, due to severe bacterial infections or septicemia. This can be
Endotoxic (gram negative bacteria) or Exotoxic (gram positive bacteria), some of them are

i) Gram negative septicaemia (endotoxic shock)- Due to infection with different bacterial species
such as the, E.coli, Klebsiella, Pseudomonas

ii)Gram positive septicaemia-Due to infection with Streptococci, pneumococci etc

4.Other types of shocks and their etiology are as follows:

PATHOGENESIS
No matter what’s the type of shock, derangements occur in 3 ways.

1. Reduced Effective Circulating Blood Volume:

6. This happens either by actual blood loss like in case of hypovolemic shock, or
by decrease in cardiac output with normal volume, like in case of cardiogenic
or septic shock.
2. Impaired Tissue Oxygenation: Due to the decreased effective circulating blood
volume, there is a decrease in venous return to the heart, which leads to tissue
hypoxia/ anoxia (absence of oxygen) ending in cell injury.
3. Release of inflammatory mediators: Cell injury triggers the body ‘s defense,
releasing the inflammatory mediators, however, this later causes further
damage. Pro-inflammatory mediators (like in cases where the endotoxins in a
bacterial wall in septic shock stimulate massive release of cytokines) are released
from monocytes-macrophages, leucocytes, tumor necrosis factor (TNF)-α, and
interleukin (IL)- 1 cytokines.

Now, we shall study in detail the features pertaining to each type of shock.
PATHOGENESIS IN HYPOVOLEMIC SHOCK-
By now we know that the effects of shock here are due to inadequate circulation of blood, followed
by a fall in the cardiac output and low intracardiac pressure. There are 4 types of hemorrhagic
shocks:

1. Compensated (About 1000 ml or less).

2. Mild (1000-1500 ml).
3. Moderate (1500-2000 ml).
4. Severe (2000 ml or more).
7. Tachycardia (increased heart rate), Hypotension (fall in blood pressure),
oliguria/ anuria (fall in urine output), altered mental state (agitation-
confusion- lethargy) are the clinical features.

PATHOGENESIS IN CARDIOGENIC SHOCK-

A severe left ventricular dysfunction from various cases can trigger this type of shock which
eventually ends in decreased cardiac output and tissue perfusion and the movement of fluid from
pulmonary vascular bed into the pulmonary interstitial space (initial pulmonary oedema), and even
the alveolar spaces (alveolar pulmonary oedema).

PATHOGENESIS IN SEPTIC SHOCK-

Endotoxic shock due to bacterial infections in Gut, genitourinary tract, respiratory tract, or skin are
often seen than the Exotoxic shock. Septic shock involves immune system activation and severe
systemic inflammatory response as follows.

a) Activated macrophage-monocytes: Endotoxins from lysed bacteria are released into the blood
forming a lipopolysaccharide binding protein (LBP), which binds to CD14 molecule on the surface of
a monocyte/ macrophage releasing cytokines (TNF-α and IL-1).

b) Activation of other inflammatory responses: Activation of complement pathway, mast cells,

coagulation system and kinin system occur.

The above mechanisms result in vasodilatation and increased vascular permeability, leading to
hyperdynamic circulation in septic shock, in contrast to hypovolemic and cardiogenic types. Raised
permeability leads to oedema. DIC (Disseminated intravascular coagulation) might occur due to
endothelial cell injury by toxins. Low blood flow leads to hypotension results in inadequate perfusion
followed by organ dysfunction.
STAGES OF SHOCK-

Three stages of shock are Compensated (non-progressive, initial, reversible) shock, progressive
decompensated shock, and Irreversible decompensated shock, are discussed here in detail:

COMPENSATED SHOCK (Reversible/ non-progressive/ initial shock)-

Initially the compensatory redistribution of blood to the vital organs such as the brain and heart
occurs so that they are adequately perfused and oxygenated. The mechanisms involved here are

-Widespread vasoconstriction occurs especially in the skin and abdominal viscera to increase
resistance, heart rate and blood pressure.

-Fluid conservation by the kidney to compensate the lost volume of blood and improve venous
return to the heart.

-Stimulation of adrenal medulla due to low cardiac output which releases epinephrine and non-
epinephrine to increase heart rate, and in turn trying to increase cardiac output.

PROGRESSIVE DECOMPENSATED SHOCK

Stress or risk factors such as the pre-existing cardiovascular or lung disease persists besides the
shock, causing progressive deterioration. Pulmonary hypoperfusion and tissue ischemia occur where
clinically the patient develops confusion and poor renal function.

IRREVERSIBLE DECOMPENSATED SHOCK

Severe shock is where the compensatory mechanisms and therapy won’t work. Here, progressive
vasodilatation (due to damaged vessel walls which do not respond to vasoconstrictors) occurs
resulting in pooling of blood and further reduce in blood circulation. Increased vascular permeability
allows fluid into the interstitial tissues, Myocardial depressant factor (MDF) is released decreasing
the cardiac output even more.

-Worsening pulmonary hypoperfusion causes respiratory distress because of pulmonary oedema,

tachypnoea and ARDS (Adult respiratory distress syndrome).

-Anoxic damage to heart, kidney, and brain happens, leading to metabolic acidosis.
-Hypercoagulability of blood happens due to the activation of coagulation cascade after the tissue
damage. Increased coagulability of blood with consequent microthrombi impair the blood flow and
causes tissue necrosis. Clinically at this point the patient has features of coma, worsened heart
function, and progressive renal failure due to acute tubular necrosis.

CLINICAL FEATURES AND COMPLICATIONS OF A DECOMPENSATED SHOCK

1. Depression of 4 vital processes- Blood pressure is very low, temperature is
subnormal, pulse is irregular and feeble, and shallow sighing respiration.
2. Patients in shock have sunken eyes, weakness, pale face, cold and clammy skin.

Hypoxic cell injury results in immune-inflammatory complications including

1. ARDS (Adult Respiratory Distress Syndrome)

2. DIC (Disseminated Intravascular Coagulation)
3. ARF (Acute Renal Failure)
4. MODS (Multiple Organ Dysfunction Syndrome)
8. If unchecked, it furthers leads to Stupor, Coma, And Death.