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Shock and Hemorrhage
M. Alhashash MD,lecturer of general surgery,
hepatobiliary & liver transplant [email protected] 01093368234
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Defining Shock• Shock is best defined as inadequate tissue
perfusion.– Can result from a variety of disease states
and injuries.– Can affect the entire organism, or it can occur
at a tissue or cellular level.
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Defining Shock (2 of 2)
• Shock is not adequately defined by: – Pulse rate– Blood pressure– Cardiac function– Hypovolemia– Loss of systemic vascular resistance
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“Hypoperfusion can be present in the absence of significant hypotension.”
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Definitions
• Hemorrhage– Abnormal internal or external loss of blood
• Homeostasis– Tendency of the body to maintain a steady
and normal internal environment• Shock
– INADEQUATE TISSUE PERFUSION– Transition between homeostasis and death
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Definitions
• O2 Delivery - volume of gaseous O2
delivered to the tissue/min.
• O2 Consumption - volume of gaseous O2 which is actually used by the tissue/min.
• O2 Demand - volume of O2 actually needed by the tissues to function in an aerobic manner
Demand > consumption = anaerobic metabolism
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Cardiovascular System Regulation to maintain volume and oxygen
supply.
• Neural • hormonal
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Cardiovascular System Regulation
Sympathetic Nervous System• Increase
– Body activity– Heart rate– Strength of contractions– Vascular constriction
• Bowel and digestive viscera• Decreased urine production
– Bronchodilation• Increases skeletal muscle perfusion
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Baroreceptor Reflexes
• High in the neck, each carotid artery divides into external and internal carotid arteries.– At the bifurcation, the wall of the artery is thin and
contains many vine-like nerve endings.
• The small portion of the artery is the carotid sinus.– Nerve endings in this area are sensitive to stretch or
distortion.• Serve as pressure receptors or baroreceptors.
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Carotid sinus
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Baroreceptor Reflexes• Similar area found in the arch of the aorta.
– Serves as a second important baroreceptor• Large arteries, large veins, and the wall of the
myocardium also contain less important baroreceptors.
• Baroreceptor reflexes help maintain blood pressure by two negative feedback mechanisms:– By lowering blood pressure in response to increased
arterial pressure– By increasing blood pressure in response to decreased
arterial pressure
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Baroreceptor Reflexes
• Normal blood pressure partially stretches the arterial walls so that baroreceptors produce a constant, low-frequency stimulation.
• Impulses from the baroreceptors inhibit the vasoconstrictor center of the medulla and excite the vagal center when blood pressure increases.– Results in vasodilation in the peripheral circulatory
system and a decrease in the heart rate and force of contraction.
• Combined effect is a decrease in arterial pressure.
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Baroreceptor Reflexes
• Baroreceptors adapt in 1 to 3 days to whatever pressure level they are exposed. Therefore, they do not change the average blood pressure on a long-term basis. This adaptation is common in people who have chronic hypertension.
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Baroreceptor Reflexes
• When baroreceptor stimulation ceases due to a fall in arterial pressure, several cardiovascular responses are evoked:– Vagal stimulation is reduced and sympathetic response is
increased.– The increase in sympathetic impulses results in increased
peripheral resistance and an increase in heart rate and stroke volume.
• Sympathetic discharges also produce generalized arteriolar vasoconstriction, which decreases the container size.
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Chemoreceptor Reflexes
• Chemoreceptors– Monitor level of CO2 in CSF
– Monitor level of O2 in blood
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Carotid body
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Chemoreceptor Physiology• Low arterial pressure leads to hypoxemia and/or
acidosis.• Hypoxemia/acidosis stimulate peripheral
chemoreceptor cells within the carotid and aortic bodies.– These bodies have an abundant blood supply.
• When oxygen or pH decreases, these cells stimulate the vasomotor center of the medulla.– The rate and depth of ventilation are also increased to help
eliminate excess carbon dioxide and maintain acid-base balance.
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CV System and Hormone Regulation
• Catecholamines– Epinephrine– Norepinephrine
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Role of Adrenal Medulla in Regulating
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CV System and Hormone Regulation
• Antidiuretic Hormone (ADH)(water & pressure regulation)– Release
• Posterior pituitary• Drop in BP or increase in serum osmolarity
– Action• Increase in peripheral vascular resistance• Increase water retention by kidneys• Decrease urine output• Splenic vasoconstriction
– 200 mL of free blood to circulation
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BPRenin-Angiotensin-Aldosterone Mechanism in Regulating BP
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CV System and Hormone Regulation
• Angiotensin II– Release
• Primary chemical from kidneys• Lowered BP and decreased perfusion
– Action• Converted from renin into angiotensin I
– Modified in lungs to angiotensin II» 20-minute process» Potent systemic vasoconstrictor» 1-hour duration» Causes release of ADH, aldosterone, and epinephrine
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CV System and Hormone
• Aldosterone– Release
• Adrenal cortex• Stimulated by angiotensin II
– Action• Maintain kidney ion balance• Retention of sodium and water• Reduce insensible fluid loss
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CV System and Hormone
• Glucagon– Release
• Alpha cells of pancreas• Triggered by epinephrine
– Action• Causes liver and skeletal muscles to convert glycogen
into glucose• Gluconeogenesis
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CV System and Hormone Regulation
• Insulin– Release
• Beta cells of pancreas
– Action• Facilitates transport of glucose across cell membrane
• Erythropoietin– Release
• Kidneys• Hypoperfusion or hypoxia
– Action• Increases production and maturation of RBCs in the
bone marrow
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Reabsorption of Tissue Fluids
• Arterial hypotension, arteriolar constriction, and reduced venous pressure during hypovolemia lower the blood pressure in the capillaries (hydrostatic pressure).
• The decrease promotes reabsorption of interstitial fluid into the vascular compartment.– Considerable quantities of fluid may be drawn into
the circulation during hemorrhage.
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Reabsorption of Tissue Fluids
• Approximately 0.25 mL/min/kg of body weight (1 L/hr in the adult male) can be autotransfused from the interstitial spaces after acute blood loss.
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Blood
• Blood Volume– Average adult male has a blood volume of 7% of
total body weight.– Average adult female has a blood volume of 6.5%
of body weight.– Normal adult blood volume is 4.5–5 L.
• Remains fairly constant in the healthy body.
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Blood Components
• Erythrocyte: 45%– Hemoglobin– Hematocrit
• Miscellaneous blood products: <1%– Platelets– Leukocytes
• Monocytes, basophils, esonophils, neutrophils
• Plasma: 54%
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Signs of Organ Hypoperfusion
• Mental Status Changes
• Oliguria
• Lactic Acidosis
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Categories of Shock
• HYPOVOLEMIC
• CARDIOGENIC
• DISTRIBUTIVE
• OBSTRUCTIVE
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Stages of ShockCellular Level
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Four Stages
• Stage 1: Vasoconstriction• Stage 2: Capillary and venule opening• Stage 3: Disseminated intravascular
coagulation• Stage 4: Multiple organ failure
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Capillary-Cellular Relationship in Shock
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Stage 1: Vasoconstriction (1 of 4)
• < 15 % loss of blood volume. • Vasoconstriction begins as minimal perfusion
to capillaries continues.– Oxygen and substrate delivery to the cells supplied
by these capillaries decreases.– Anaerobic metabolism replaces aerobic
metabolism.
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Stage 1: Vasoconstriction (2 of 4)
• Production of lactate and hydrogen ions increases.– The lining of the capillaries may begin to lose the
ability to retain large molecular structures within its walls.
– Protein-containing fluid leaks into the interstitial spaces (leaky capillary syndrome).
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Stage 1: Vasoconstriction (3 of 4)
• Sympathetic stimulation produces:– Pale, sweaty skin– Rapid, thready pulse– Elevated blood glucose levels
• The release of epinephrine dilates coronary, cerebral, and skeletal muscle arterioles and constricts other arterioles.– Blood is shunted to the heart, brain, skeletal muscle, and
capillary flow to the kidneys and abdominal viscera decreases.
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Stage 1: Vasoconstriction (4 of 4)
If this stage of shock is not treated by prompt restoration of circulatory
volume, shock progresses to the next stage.
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Stage 2: Capillary and Venule Opening (1 of 5)
• Stage 2 occurs with a 15% to 25% decrease in intravascular blood volume. Heart rate, respiratory rate, and capillary refill are increased, and pulse pressure is decreased at this stage. Blood pressure may still be normal.
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Stage 2: Capillary and Venule Opening (2 of 5)
• As the syndrome continues, the precapillary sphincters relax with some expansion of the vascular space.
• Postcapillary sphincters resist local effects and remain closed, causing blood to pool or stagnate in the capillary system, producing capillary engorgement.
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Stage 2: Capillary and Venule Opening (3 of 5)
• As increasing hypoxemia and acidosis lead to opening of additional venules and capillaries, the vascular space expands greatly.– Even normal blood volume may be inadequate to fill the
container.• The capillary and venule capacity may become great
enough to reduce the volume of available blood for the great veins and vena cava.– Resulting in decreased venous return and a fall in cardiac
output.
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Stage 2: Capillary and Venule Opening (4 of 5)
• Low arterial blood pressure and many open capillaries result in stagnant capillary flow.
• Sluggish blood flow and the reduced delivery of oxygen result in increased anaerobic metabolism and the production of lactic acid.– The respiratory system attempts to compensate for the
acidosis by increasing ventilation to blow off carbon dioxide.
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Stage 2: Capillary and Venule Opening (5 of 5)
• As acidosis increases and pH falls, the RBCs may cluster together (rouleaux formation).– Halts perfusion – Affects nutritional flow and prevents removal of cellular metabolites
• Clotting mechanisms are also affected, leading to hypercoagulability.
• This stage of shock often progresses to the third stage if fluid resuscitation is inadequate or delayed, or if the shock state is complicated by trauma or sepsis.
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Stage 3: Disseminated Intravascular Coagulation (DIC) (1 of 4)
• Time of onset will depend on degree of shock, patient age, and pre-existing medical conditions.
• Stage 3 occurs with 25% to 35% decrease in intravascular blood volume. At this stage, hypotension occurs. This stage of shock usually requires blood replacement.
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Stage 3: Disseminated Intravascular Coagulation (DIC) (2 of 4)
• Stage 3 is resistant to treatment (refractory shock), but is still reversible.
• Blood begins to coagulate in the microcirculation, clogging capillaries.– Capillaries become occluded by clumps of RBCs.
• Decreases capillary perfusion and prevents removal of metabolites
– Distal tissue cells use anaerobic metabolism, and lactic acid production increases.
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Stage 3: Disseminated Intravascular Coagulation (DIC) (3 of 4)
• Lactic acid accumulates around the cell.– Cell membranes no longer have the energy
needed to maintain homeostasis.– Water and sodium leak in, potassium leaks
out, and the cells swell and die.
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Stage 3: Disseminated Intravascular Coagulation (DIC) (4 of 4)
• Pulmonary capillaries become permeable, leading to pulmonary edema.– Decreases the absorption of oxygen and results in
possible alterations in carbon dioxide elimination– May lead to acute respiratory failure or adult
respiratory distress syndrome (ARDS)• If shock and disseminated intravascular
coagulation (DIC) continue, the patient progresses to multiple organ failure.
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Stage 4: Multiple Organ Failure (1 of 2)
• The amount of cellular necrosis required to produce organ failure varies with each organ and the underlying condition of the organ.– Usually hepatic failure occurs, followed by renal
failure, and then heart failure.– If capillary occlusion persists for more than 1 to 2
hours, the cells nourished by that capillary undergo changes that rapidly become irreversible.
• In this stage, blood pressure falls dramatically (to levels of 60 mmHg or less).– Cells can no longer use oxygen, and metabolism
stops.
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Stage 4: Multiple Organ Failure (2 of 2)
• If a critical amount of the vital organ is damaged by cellular necrosis, the organ soon fails.– Failure of the liver is common and often presents
early.– Capillary blockage may cause heart failure.– GI bleeding and sepsis may result from GI mucosal
necrosis.– Pancreatic necrosis may lead to further clotting
disorders and severe pancreatitis.• Pulmonary thrombosis may produce hemorrhage
and fluid loss into the alveoli.– Leading to death from respiratory failure.
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Goals of Shock Resuscitation
• Restore blood pressure
• Normalize systemic perfusion
• Preserve organ function
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Hypovolemic Shock
• Causes– hemorrhage– vomiting– diarrhea– dehydration– third-space loss– burns
• Signs– cardiac
output– PAOP– SVR
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Hypovolemic Shock
• Hemorrhagic Shock
Parameter I II III IV
Blood loss (ml) <750 750–1500 1500–2000 >2000
Blood loss (%) <15% 15–30% 30–40% >40%
Pulse rate (beats/min) <100 >100 >120 >140
Blood pressure Normal Decreased Decreased Decreased
Respiratory rate (bpm) 14–20 20–30 30–40 >35
Urine output (ml/hour) >30 20–30 5–15 Negligible
CNS symptoms Normal Anxious Confused Lethargic
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Cardiogenic Shock
• Results from pump failure– Decreased systolic function– Resultant decreased cardiac output
• Etiologic categories– Myopathic– Arrhythmic– Mechanical– Extracardiac (obstructive)
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Obstructive Shock
• Causes– Cardiac Tamponade– Tension Pneumothorax– Massive Pulmonary Embolus
• Signs– cardiac output– PAOP– SVR
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Distributive Shock
• Types– Sepsis– Anaphylactic– Acute adrenal insufficiency– Neurogenic
• Signs– ± cardiac output– PAOP(pulmonary artery occlusive pressure)– SVR
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Summary
Type PAOP C.O. SVR
HYPOVOLEMIC
CARDIOGENIC
DISTRIBUTIVE or N varies
OBSTRUCTIVE
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Clinical Presentation
• Clinical presentation varies with type and cause, but there are features in common
• Hypotension (SBP<90 or Delta>40)• Cool, clammy skin (exceptions – early
distributive, terminal shock)• Oliguria• Change in mental status• Metabolic acidosis
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Initial Assessment
• Airway
• Breathing
• Circulation
• Disability
• Expose body surfaces
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Treatment
• Manage the emergency• Determine the underlying cause• Definitive management or support
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Definitive Management
• Hypovolemic – Fluid resuscitate (blood or crystalloid) and control ongoing loss
• Cardiogenic - Restore blood pressure (chemical and mechanical) and prevent ongoing cardiac death
• Distributive – Fluid resuscitate, pressors for maintenance, immediate abx/surgical control for infection, steroids for adrenocortical insufficiency
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Vasopressors & Inotropic Agents
• Dopamine
• Dobutamine
• Norepinephrine
• Epinephrine
• Amrinone
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Differential Shock Assessment Findings
• Assumed to be hypovolemic until proven otherwise
• Cardiogenic shock– Differentiate from hypovolemic shock by:
• Chief complaint– Chest pain– Dyspnea– Tachycardia
• Heart rate • Signs of congestive heart failure • Dysrhythmias
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Differential Shock Assessment Findings
• Distributive shock– Differentiate from hypovolemic shock by:
• Mechanism suggesting vasodilation– Spinal cord injury– Drug overdose– Sepsis– Anaphylaxis
• Warm, flushed skin • Lack of tachycardia response (not reliable)
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Differential Shock Assessment Findings
• Obstructive shock– Differentiate from hypovolemic shock by signs and
symptoms of:• Cardiac tamponade• Tension pneumothorax• Pulmonary embolism
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Detailed Physical Examination
• Vital signs– Pulse– Blood pressure– Orthostatic vital signs
• Evaluate patient’s ECG
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Crystalloids
• Solutions with dissolved crystals in water– Less osmotic pressure than colloids– Can equilibrate more quickly between vascular
and extravascular spaces• 2/3 of crystalloid fluid leaves vascular space < 1 hr• 3 mL of crystalloid replaces 1 mL of blood
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Hypertonic and Hypotonic Solutions
• Hypertonic solutions– Higher osmotic pressure than body cells
• 7.5% saline
• Hypotonic solutions– Lower osmotic pressure than body cells
• Distilled water• 0.45% sodium chloride (0.45% NaCl)
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Isotonic Solutions
• Lactated Ringer's solution
• Normal saline
• Glucose-containing solutions (e.g., D5W)
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Colloids• Solutions that contain molecules too large to pass
through capillary membrane
• Remain within blood vessels longer
• Examples– Whole blood– Plasma– Packed red blood cells– dextran
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Cardiogenic Shock
• Improve pumping action of heart and manage dysrhythmias– Fluid replacement– Drug therapy (if needed)– Cardiogenic shock due to myocardial ischemia or
infarction requires:• Reperfusion strategies• Possible circulatory support
– Manage tension pneumothorax and cardiac tamponade
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Neurogenic Shock
• Treatment similar to hypovolemia– Avoid circulatory overload– Monitor lung sounds for pulmonary congestion
• Vasopressors may be indicated
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Anaphylactic Shock
• Subcutaneous epinephrine in acute anaphylactic reactions
• Other therapy– Oral, IV, or IM antihistamines– Bronchodilators – Steroids reduce inflammatory response– Crystalloid volume replacement– Airway management
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Septic Shock Treatment• Management of hypovolemia (if present)
• Correction of metabolic acid-base imbalance
• Antibiotics in one hour.
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Hemorrhage
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ETIOLOGY OF HAEMORRHAGECAUSES OF HAEMORRHAGE
• INJURY /TRAUMA [+ operations]-It commonly results in
tearing or cutting of a blood-vessel-integrity of wall breached - Trivial OR Major
• DISEASES that alter coagulation Congenital –platelet defects Coagulation factor defects Acquired scurvy Sepsis DIC
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TYPES OF HAEMORRHAGE
• AMOUNT OF LOSS --MINOR/MAJOR • ACUTE/CHRONIC• ARTERIAL/VENOUS/CAPILLARY/MIXED• LOCALIZED/DIFFUSE• EXTERNAL/ INTERNAL • OVERT/OCCULT
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TYPES OF HAEMORRHAGE
SPECIFIC TYPES
• Bruise or ecchymosis . Extravasation of blood /pouring out of
blood into the areolar tissues, which become
boggy • Haematemesis and melena • Haemoptysis . • Haematuria • Epistaxis
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TYPES OF HAEMORRHAGE (operative)
CLASSIFICATION OF SURGICAL HAEMORRHAGE
1-Primary, occurring at the time of the injury
2-Reactionary, or within twenty-four hours of the accident, during the stage of reaction
3-Secondary, occurring at a later period and caused by faulty application of a ligature or septic condition of the wound . In severe haemorrhage, as from the division of a large artery, the patient may collapse and death ensue from syncope .
4-Tertiery : infection
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Hemorrhage Classification
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External Hemorrhage• Results from soft tissue injury.• Most soft tissue trauma is accompanied by mild hemorrhage
and is not life threatening.– Can carry significant risks of patient morbidity and disfigurement
• The seriousness of the injury is dependent on:– Anatomical source of the hemorrhage (arterial, venous,
capillary)– Degree of vascular disruption– Amount of blood loss that can be tolerated by the patient
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Internal Hemorrhage (1 of 2)
• Can result from:– Blunt or penetrating trauma– Acute or chronic medical illnesses
• Internal bleeding that can cause hemodynamic instability usually occurs in one of four body cavities:– Chest– Abdomen– Pelvis– Retroperitoneum
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Internal Hemorrhage (2 of 2)
• Signs and symptoms that may suggest significant internal hemorrhage include:– Bright red blood from mouth, rectum, or other
orifice– Coffee-ground appearance of vomitus– Melena (black, tarry stools)– Dizziness or syncope on sitting or standing– Orthostatic hypotension
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Internal hemorrhage is associated with higher morbidity and
mortality than external hemorrhage.
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EFFECTS OF HAEMORRHAGEDepend upon following:• Acute loss vs Chronic loss• The amount of loss• The compensatory mechanisms• General state of health
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Physiological Response to Hemorrhage
• The body’s initial response to hemorrhage is to stop bleeding by chemical means (hemostasis).– This vascular reaction involves:
• Local vasoconstriction• Formation of a platelet plug• Coagulation• Growth of tissue into the blood clot that permanently
closes and seals the injured vessel
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Haemostasis overview:
BV Injury
PlateletAggregation
PlateletActivation
Blood Vessel Constriction
Coagulation Cascade
Stable Hemostatic Plug
Fibrin formation
Reduced
Blood flow
Contact/ Tissue Factor
Primary hemostatic plug
Neural
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MANAGEMENT OF HAEMORRHAGE
• Prevention• Precautions during surgery• Operative method of control of haemorrhage • Blood Transfusion
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Hemorrhage Control
• External Hemorrhage– Direct pressure and pressure dressing– General management
• Direct pressure• Elevation• Ice• Pressure points• Constricting band• Tourniquet
– May use a BP cuff by inflating the cuff 20–30 mmHg above the SBP
– Release may send toxins to heart» Lactic acid and electrolytes
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Tourniquets are ONLY used as a last resort!
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Specific Wound Considerations (1 of 2)
• Head Wounds– Presentation
• Severe bleeding• Skull fracture
– Management• Gentle direct
pressure• Fluid drainage
from ears and nose– DO NOT pack– Cover and
bandage loosely
• Neck Wounds– Presentation
• Large vessel can entrap air
– Management• Consider direct
digital pressure• Occlusive dressing
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Specific Wound Considerations (2 of 2)
• Gaping Wounds– Presentation
• Multiple sites• Gaping prevents
uniform pressure– Management
• Bulky dressing– Trauma dressing
• Sterile, non-adherent surface to wound
• Compression dressing
• Crush Injury– Presentation
• Difficult to locate source of bleeding
• Normal hemorrhage control mechanism nonfunctional
– Management• Consider an air-
splint and pressure dressing
• Consider tourniquet
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NB
Fit Individuals may have more effective compensatory mechanisms before experiencing cardiovascular collapse.
Elderly patients or those with chronic medical conditions may have less tolerance to blood loss, less ability to compensate, and may take medications such as betablockers that can potentially blunt the cardiovascular response
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SURGICAL HAEMOSTASIS
Surgical treatment of haemorrhage DIRECT PRESSURE In small blood-vessels pressure will be
sufficient to arrest haemorrhage permanently .
LIGATURE In large vessels with a reef-knot main artery of the limb exposed by dissection
at the most accessible point .
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SURGICAL HAEMOSTASIS
Surgical treatment of haemorrhage
• Diathermy• Sutures• Harmonic devices
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SURGICAL HAEMOSTASISINTERNAL HAEMORRHAGE
/WOUNDS
Causes• Penetrating wounds chest,abdomen,neck,limbs• Upper GI haemorrhage BleedingUlcers• Lower GI haemorrhage Diverticulosis Haemorrhoids Carcinomas
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SURGICAL HAEMOSTASISINTERNAL HAEMORRHAGE /WOUNDSPrinciples of managementTreat the primary causeAvoid irreversible shockFluid & electrolytesBlood and blood products
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TRANSFUSION MANAGEMENT
• Early recognition of significant blood loss • it is commoner to see patients who have been
under-transfused than over-transfused. • It is essential to pay attention to and act on
recordings of pulse rate and blood pressure. • In a fit patient without cardiac disease, persistent
tachycardia − even if blood pressure is maintained − is likely to indicate continuing blood loss.
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Transfusion management
• All patients require large-bore intravenous cannulas. Central venous pressure monitoring is valuable in major haemorrhage or if there is cardio-respiratory disease.
• Haemoglobin concentration − interpretation
• The haemoglobin can underestimate the extent of blood loss in cases of acute haemorrhage before haemodilution has occurred, or can overestimate it if the patient is already anaemic from chronic blood loss.
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Concluding Remarks
• Know how to distinguish different types of shock and treat accordingly
• Look for early signs of shock
• SHOCK = hypotension