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HAEMORRHAGE
BY DR L RAMU
OUTLINE
Classification
Pathophysiology
Clinical features
Management
CLASSIFICATION
1. Based on source:
Arterial---bright red in colour, spurting like jet along with
pulse of the patient.
Venous --- dark red, steady and continuous flow.
Capillary: Here bleeding is rapid and bright red. It is often
torrential due to continuous ooze.
2. BASED ON THE TIME OF ONSET OF BLEEDING IN RELATION
TO ANY OPERATIVE PROCEDURE
Primary haemorrhage is haemorrhage occurring immediately due
to an injury (or surgery).
Reactionary haemorrhage is delayed 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.
3. BASED ON THE TYPE OF HAEMORRHAGE:
Revealed haemorrhage is obvious external haemorrhage
Concealed haemorrhage is contained within the body cavity and
must be suspected, actively investigated and controlled.
IV. BASED ON THE DURATION OF HAEMORRHAGE:
1. Acute haemorrhage: It is sudden, severe haemorrhage after trauma,
surgery.
2. Chronic haemorrhage: It is chronic repeated bleeding for a long period
like in haemorrhoids, bleeding peptic ulcer, carcinoma caecum, etc.
3. Acute on chronic haemorrage: It is more dangerous as the bleeding
occurs in individuals who are already hypoxic, which may get worsened
faster.
V. BASED ON THE POSSIBLE INTERVENTION:
1. Surgical haemorrhage —Surgical haemorrhage is due to a
direct injury and is amenabl to surgical control (or other
techniques such as angioembolisation).
2. Non-surgical haemorrhage is the general ooze from all raw
surfaces due to coagulation abnormalities and DIC.and cannot
be stopped by surgical means (except packing). Treatment
requires correction of the coagulation abnormalities.
PATHOPHYSIOLOGY
Bleeding Hypovolaemia Low cardiac output
Hypoxia Tachycardia and shunting of blood from splanchnic vessels
by venoconstriction so as to maintain perfusion of vital
organs like brain, heart, lungs, kidney
Activation of cardiac depressants
SICK CELL SYNDROME Hyponatraemic, hyperkalaemic,
hypocalcaemic metabolic acidosis
Lysosomes of cell get lysed ---lethal to cell
Platelets and coagulants are activated leading to
formation of small clots DIC and further bleeding.
Progressive haemodilution leading to total circulatory failure.
COAGULOPATHY
ACIDOSIS
HYPOTHERMIA
LETHAL TRIAD
ATLS– ADVANCED TRAUMA LIFE SUPPORT
CLASSIFICATION OF HAEMORRHAGIC SHOCK
Class Blood loss Features
I Up to 15% (< 750 ml) Normal
II Blood loss 15-30% (750-1500 ml) Palor, thirsty, tachycardia
III Blood loss 30-40% (1500-2000 ml) Hypotension, tachycardia,
oliguria, confusion
IV Blood loss > 40% (> 2000 ml) Rapid pulse, low BP, anuria,
unconsciousness, MODS
CLINICAL FEATURES OF HAEMORRHAGE
• Pallor, thirsty, cyanosis.
• Tachycardia, tachypnoea.
• Air hunger.
• Cold clammy skin due to vasoconstriction.
• Dry face, dry mouth and goose skin appearance (due to
contraction of arrector pilorum).
• Rapid thready pulse, hypotension.
• Oliguria
SIGNS OF SIGNIFICANT BLOOD LOSS
• ™™Pulse > 100/minute
• ™™Systolic BP< 100 mmHg
• ™™Diastolic BP drop on sitting or standing > 10 mmHg
• ™™Pallor/ sweating
• ™™Shock index (ratio of heart rate to systolic blood pressure) > 1
Shock index is an indicator of haemodynamic stability
It is a better marker than pulse and b.p alone
Modified shock index = heart rate / mean arterial pressure
MEASUREMENT OF BLOOD LOSS
• Clot size of a clenched fist is 500 ml.
• Blood loss in a closed tibial fracture is 500-1500 ml; in a fracture femur is
500-2000 ml.
• Weighing the swab before and after use is an important method of on-table
assessment of blood loss.
• Substracting empty suction bottle weight from filled one. Note the volume of
irrigated fluid and substract to get final blood loss.
Rains Factor
Total difference in swab weight × 1.5
Total amount = or
of blood loss Total difference in swab weight × 2
(For larger wounds and larger operations)
Actual blood loss {ABL} =
BLOOD VOLUME { Hct (i) – Hct (f) } / Hct (m)
blood volume = body weight (in kgs) x 70 ml/kg
In neonates it is 85-90 ml/kg
Children it is 80 ml/kg
Adults it is 70 ml/kg
Hct are haematocrits initial, final, mean.
The haemoglobin level is a poor indicator of the degree of
haemorrhage as it represents a concentration and not an absolute
amount.
Treatment should therefore be based upon the degree of
hypovolaemic shock
according to vital signs, preload assessment, base deficit most
importantly, the dynamic response to fluid therapy.
Patients who are ‘non-responders’ or ‘transient responders’
are still bleeding and must have the site of haemorrhage
identified and controlled
EFFECTS OF HAEMORRHAGE
• ™™Acute renal shut down
• ™™Liver cell dysfunction
• ™™Cardiac depression
• ™™Hypoxic effect
• ™™Metabolic acidosis
• ™™GIT mucosal ischaemia
• ™™Interstitial oedema, AV shunting in lung—ARDS
• ™™Hypovolaemic shock—MODS
MANAGEMENT
INVESTIGATIONS:
• B.P , pulse
• Hb% and PCV estimation.
• ABG analysis ,serum elecrolytes, pulseoxymetry
• Blood volume estimation using radioiodine technique or micro-haematocrit
method.
• Measurement of CVP
• Investigations specific for cause:
• U/S abdomen and chest , Doppler
• angiogram in vascular injury,
• chest X-ray in haemothorax,
• CT scan in major injuries,
• CT scan head inhead injuries
Haemorrhage must be recognised and managed
aggressively to reduce the severity and duration of shock
and avoid death and/ or multiple organ failure.
Haemorrhage is treated by arresting the bleeding
– not by fluid resuscitation or blood
transfusion.
Although necessary as supportive measures to maintain
organ perfusion,
attempting to resuscitate patients who have ongoing
haemorrhage will lead to physiological exhaustion
(coagulopathy, acidosis and hypothermia) and
subsequently death.
PRINCIPLES OF MANAGEMENT
1. Identify haemorrhage
2. Immediate resuscitative manoeuvres
3. Identify the site of haemorrhage
4. Haemorrhage control
5. Damage control resuscitation
IDENTIFY HAEMORRHAGE
• External haemorrhage may be obvious, but the diagnosis
of concealed haemorrhage may be more difficult.
• Any shock should be assumed to be hypovolaemic until
proved otherwise,
similarly,
• hypovolaemia should be assumed to be due to
haemorrhage until this has been excluded
IMMEDIATE RESUSCITATIVE MANOEUVRES
ABC
• 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
• blood drawn for cross-matching
• Emergency blood should be requested if the degree of
shock and ongoing haemorrhage warrants this.
IDENTIFY THE SITE OF HAEMORRHAGE
1. identify the exact location,
2. define the next step in haemorrhage control (operation,
angioembolisation, endoscopic control).
• Clues may be in the history (previous episodes, known aneurysm,
non-steroidal therapy for gastrointestinal (GI) bleeding) or
examination (nature of blood – fresh, melaena; abdominal
tenderness, etc.).
• For shocked trauma patients, the external signs of injury may
suggest internal haemorrhage, but haemorrhage into a body cavity
(thorax, abdomen) must be excluded with rapid investigations (chest
and pelvis x-ray, abdominal ultrasound or diagnostic peritoneal
aspiration).
Investigations for blood loss must be appropriate
to the patient’s physiological condition.
Rapid bedside tests are more appropriate for profound
shock and exsanguinating haemorrhage than
investigations such as computed tomography (CT) which
take time.
Patients who are not actively bleeding can have more
methodical, definitive work-up.
HAEMORRHAGE CONTROL
• Haemorrhage control must be achieved rapidly so as to prevent
the patient entering the triad of coagulopathy–acidosis–
hypothermia and physiological exhaustion
• There should be no unnecessary investigations or procedures
prior to haemorrhage control to minimize the duration and
severity of shock
• includes prolonged attempts to volume resuscitate the patient
prior to surgery, which will result in further hypothermia and
clotting factor dilution
• Attention is paid to correction of coagulopathy with blood
component therapy to aid surgical haemorrhage control
Surgical intervention may need to be limited to the minimum
necessary to stop bleeding and control sepsis.
More definitive repairs can be delayed until the patient is
haemodynamically stable and physiologically capable of
sustaining the procedure.
This concept of tailoring the operation to match the patient’s
physiology and staged procedures to prevent
physiological exhaustion is called ‘damage control
surgery’
DAMAGE CONTROL SURGERY
1. Arrest haemorrhage
2. Control sepsis
3. Protect from further injury
4. Nothing else
Once haemorrhage is controlled, patients should
be aggressively resuscitated, warmed and
coagulopathy corrected.
DAMAGE CONTROL RESUSCITATION
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.
TREATMENT
• Restoration of blood loss: fluids, ionotropes,
blood
One unit of blood should raise 1 gm% of
haemoglobin.
• Catheterisation, foot end elevation, monitoring.
• Oxygen support/intubation/ventilator and critical
care. ABC
• Pressure, packing and head down
(Trendelenburg) position to restore BP and
blood supply of brain.
• Wound exploration and proceeding, i.e. ligation
of the small vessel, suturing the wound part,
vessel suturing (anastomosis), excision of the
tissues.
• Absolute rest, analgesics, morphine 10-20 mg
IM/IV to relieve pain, sedation.
• ICT placing for haemothorax.
• Laparotomy for liver or spleen or mesentery or
bowel injuries, suturing, splenectomy.
• Topical applications for local ooze—Oxycel,
gauze soaked with adrenaline, bone wax for
oozing from bone and other
• local haemostatic agents (collagen, thrombin).
• In venous haemorrhage, elevation, ligation of
vein or in caseof large vein suturing of venous
wall, pressure bandaging, packing will be helpful.
• Tourniquet are often used in operation theatre for
control of haemorrhage in limbs. But it is not
advisable as a first aid measure.
• TPN, CVP monitoring, electrolyte management
are all equally important.
• Steroid injection, antibiotics, ventilator support
are often required.
LOCAL HAEMOSTATIC AGENTS
™™Gelatin sponge (Gel foam)
™™Oxidised cellulose (Surgicel)
™™Collagen sponge (Helistat)
™™Microfibrillar collagen powder (Avitene)
™™Topical thrombin
™™Bone wax (derived from bees wax + almond oil)
• Gelfoam is made from denatured animal skin gelatin. Gelfoam has no
intrinsic hemostatic action,
• but it can be used in combination with topical thrombin, for which it
serves as an absorbable carrier.
• Its main hemostatic activity is related to the contact between blood and
the large surface area of the sponge transmitting pressure.
CONCLUSION
• Confirm shock, hypovolaemia and haemorrhage
by clinical assessment
• ™™Immediate resuscitation by blood, oxygen, fluid
• ™™Identify site of haemorrhage—ultrasound,
endoscopy, CT scan, diagnostic peritoneal
lavage (DPL), blood tools
• ™™Control of haemorrhage—surgery, endoscopic
control, therapeutic embolisation
• ™™Definitive treatment if any
• ™™Sepsis control
• ™™Prevention of coagulopathy by FFP, platelet
concentrate, fresh blood
• ™™Critical care management
• ™™End point resuscitation, fluid and electrolyte
management,

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Haemorrhage

  • 3. CLASSIFICATION 1. Based on source: Arterial---bright red in colour, spurting like jet along with pulse of the patient. Venous --- dark red, steady and continuous flow. Capillary: Here bleeding is rapid and bright red. It is often torrential due to continuous ooze.
  • 4. 2. BASED ON THE TIME OF ONSET OF BLEEDING IN RELATION TO ANY OPERATIVE PROCEDURE Primary haemorrhage is haemorrhage occurring immediately due to an injury (or surgery). Reactionary haemorrhage is delayed 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.
  • 5. 3. BASED ON THE TYPE OF HAEMORRHAGE: Revealed haemorrhage is obvious external haemorrhage Concealed haemorrhage is contained within the body cavity and must be suspected, actively investigated and controlled.
  • 6. IV. BASED ON THE DURATION OF HAEMORRHAGE: 1. Acute haemorrhage: It is sudden, severe haemorrhage after trauma, surgery. 2. Chronic haemorrhage: It is chronic repeated bleeding for a long period like in haemorrhoids, bleeding peptic ulcer, carcinoma caecum, etc. 3. Acute on chronic haemorrage: It is more dangerous as the bleeding occurs in individuals who are already hypoxic, which may get worsened faster.
  • 7. V. BASED ON THE POSSIBLE INTERVENTION: 1. Surgical haemorrhage —Surgical haemorrhage is due to a direct injury and is amenabl to surgical control (or other techniques such as angioembolisation). 2. Non-surgical haemorrhage is the general ooze from all raw surfaces due to coagulation abnormalities and DIC.and cannot be stopped by surgical means (except packing). Treatment requires correction of the coagulation abnormalities.
  • 8. PATHOPHYSIOLOGY Bleeding Hypovolaemia Low cardiac output Hypoxia Tachycardia and shunting of blood from splanchnic vessels by venoconstriction so as to maintain perfusion of vital organs like brain, heart, lungs, kidney Activation of cardiac depressants SICK CELL SYNDROME Hyponatraemic, hyperkalaemic, hypocalcaemic metabolic acidosis Lysosomes of cell get lysed ---lethal to cell Platelets and coagulants are activated leading to formation of small clots DIC and further bleeding. Progressive haemodilution leading to total circulatory failure.
  • 10. ATLS– ADVANCED TRAUMA LIFE SUPPORT CLASSIFICATION OF HAEMORRHAGIC SHOCK Class Blood loss Features I Up to 15% (< 750 ml) Normal II Blood loss 15-30% (750-1500 ml) Palor, thirsty, tachycardia III Blood loss 30-40% (1500-2000 ml) Hypotension, tachycardia, oliguria, confusion IV Blood loss > 40% (> 2000 ml) Rapid pulse, low BP, anuria, unconsciousness, MODS
  • 11. CLINICAL FEATURES OF HAEMORRHAGE • Pallor, thirsty, cyanosis. • Tachycardia, tachypnoea. • Air hunger. • Cold clammy skin due to vasoconstriction. • Dry face, dry mouth and goose skin appearance (due to contraction of arrector pilorum). • Rapid thready pulse, hypotension. • Oliguria
  • 12. SIGNS OF SIGNIFICANT BLOOD LOSS • ™™Pulse > 100/minute • ™™Systolic BP< 100 mmHg • ™™Diastolic BP drop on sitting or standing > 10 mmHg • ™™Pallor/ sweating • ™™Shock index (ratio of heart rate to systolic blood pressure) > 1 Shock index is an indicator of haemodynamic stability It is a better marker than pulse and b.p alone Modified shock index = heart rate / mean arterial pressure
  • 13. MEASUREMENT OF BLOOD LOSS • Clot size of a clenched fist is 500 ml. • Blood loss in a closed tibial fracture is 500-1500 ml; in a fracture femur is 500-2000 ml. • Weighing the swab before and after use is an important method of on-table assessment of blood loss. • Substracting empty suction bottle weight from filled one. Note the volume of irrigated fluid and substract to get final blood loss. Rains Factor Total difference in swab weight × 1.5 Total amount = or of blood loss Total difference in swab weight × 2 (For larger wounds and larger operations)
  • 14. Actual blood loss {ABL} = BLOOD VOLUME { Hct (i) – Hct (f) } / Hct (m) blood volume = body weight (in kgs) x 70 ml/kg In neonates it is 85-90 ml/kg Children it is 80 ml/kg Adults it is 70 ml/kg Hct are haematocrits initial, final, mean.
  • 15. The haemoglobin level is a poor indicator of the degree of haemorrhage as it represents a concentration and not an absolute amount. Treatment should therefore be based upon the degree of hypovolaemic shock according to vital signs, preload assessment, base deficit most importantly, the dynamic response to fluid therapy. Patients who are ‘non-responders’ or ‘transient responders’ are still bleeding and must have the site of haemorrhage identified and controlled
  • 16. EFFECTS OF HAEMORRHAGE • ™™Acute renal shut down • ™™Liver cell dysfunction • ™™Cardiac depression • ™™Hypoxic effect • ™™Metabolic acidosis • ™™GIT mucosal ischaemia • ™™Interstitial oedema, AV shunting in lung—ARDS • ™™Hypovolaemic shock—MODS
  • 17. MANAGEMENT INVESTIGATIONS: • B.P , pulse • Hb% and PCV estimation. • ABG analysis ,serum elecrolytes, pulseoxymetry • Blood volume estimation using radioiodine technique or micro-haematocrit method. • Measurement of CVP • Investigations specific for cause: • U/S abdomen and chest , Doppler • angiogram in vascular injury, • chest X-ray in haemothorax, • CT scan in major injuries, • CT scan head inhead injuries
  • 18. Haemorrhage must be recognised and managed aggressively to reduce the severity and duration of shock and avoid death and/ or multiple organ failure. Haemorrhage is treated by arresting the bleeding – not by fluid resuscitation or blood transfusion. Although necessary as supportive measures to maintain organ perfusion, attempting to resuscitate patients who have ongoing haemorrhage will lead to physiological exhaustion (coagulopathy, acidosis and hypothermia) and subsequently death.
  • 19. PRINCIPLES OF MANAGEMENT 1. Identify haemorrhage 2. Immediate resuscitative manoeuvres 3. Identify the site of haemorrhage 4. Haemorrhage control 5. Damage control resuscitation
  • 20. IDENTIFY HAEMORRHAGE • External haemorrhage may be obvious, but the diagnosis of concealed haemorrhage may be more difficult. • Any shock should be assumed to be hypovolaemic until proved otherwise, similarly, • hypovolaemia should be assumed to be due to haemorrhage until this has been excluded
  • 21. IMMEDIATE RESUSCITATIVE MANOEUVRES ABC • 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 • blood drawn for cross-matching • Emergency blood should be requested if the degree of shock and ongoing haemorrhage warrants this.
  • 22. IDENTIFY THE SITE OF HAEMORRHAGE 1. identify the exact location, 2. define the next step in haemorrhage control (operation, angioembolisation, endoscopic control). • Clues may be in the history (previous episodes, known aneurysm, non-steroidal therapy for gastrointestinal (GI) bleeding) or examination (nature of blood – fresh, melaena; abdominal tenderness, etc.). • For shocked trauma patients, the external signs of injury may suggest internal haemorrhage, but haemorrhage into a body cavity (thorax, abdomen) must be excluded with rapid investigations (chest and pelvis x-ray, abdominal ultrasound or diagnostic peritoneal aspiration).
  • 23. Investigations for blood loss must be appropriate to the patient’s physiological condition. Rapid bedside tests are more appropriate for profound shock and exsanguinating haemorrhage than investigations such as computed tomography (CT) which take time. Patients who are not actively bleeding can have more methodical, definitive work-up.
  • 24. HAEMORRHAGE CONTROL • Haemorrhage control must be achieved rapidly so as to prevent the patient entering the triad of coagulopathy–acidosis– hypothermia and physiological exhaustion • There should be no unnecessary investigations or procedures prior to haemorrhage control to minimize the duration and severity of shock • includes prolonged attempts to volume resuscitate the patient prior to surgery, which will result in further hypothermia and clotting factor dilution • Attention is paid to correction of coagulopathy with blood component therapy to aid surgical haemorrhage control
  • 25. Surgical intervention may need to be limited to the minimum necessary to stop bleeding and control sepsis. More definitive repairs can be delayed until the patient is haemodynamically stable and physiologically capable of sustaining the procedure. This concept of tailoring the operation to match the patient’s physiology and staged procedures to prevent physiological exhaustion is called ‘damage control surgery’
  • 26. DAMAGE CONTROL SURGERY 1. Arrest haemorrhage 2. Control sepsis 3. Protect from further injury 4. Nothing else Once haemorrhage is controlled, patients should be aggressively resuscitated, warmed and coagulopathy corrected.
  • 27. DAMAGE CONTROL RESUSCITATION 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.
  • 28. TREATMENT • Restoration of blood loss: fluids, ionotropes, blood One unit of blood should raise 1 gm% of haemoglobin. • Catheterisation, foot end elevation, monitoring. • Oxygen support/intubation/ventilator and critical care. ABC • Pressure, packing and head down (Trendelenburg) position to restore BP and blood supply of brain. • Wound exploration and proceeding, i.e. ligation of the small vessel, suturing the wound part, vessel suturing (anastomosis), excision of the tissues. • Absolute rest, analgesics, morphine 10-20 mg IM/IV to relieve pain, sedation.
  • 29. • ICT placing for haemothorax. • Laparotomy for liver or spleen or mesentery or bowel injuries, suturing, splenectomy. • Topical applications for local ooze—Oxycel, gauze soaked with adrenaline, bone wax for oozing from bone and other • local haemostatic agents (collagen, thrombin). • In venous haemorrhage, elevation, ligation of vein or in caseof large vein suturing of venous wall, pressure bandaging, packing will be helpful. • Tourniquet are often used in operation theatre for control of haemorrhage in limbs. But it is not advisable as a first aid measure. • TPN, CVP monitoring, electrolyte management are all equally important. • Steroid injection, antibiotics, ventilator support are often required.
  • 30. LOCAL HAEMOSTATIC AGENTS ™™Gelatin sponge (Gel foam) ™™Oxidised cellulose (Surgicel) ™™Collagen sponge (Helistat) ™™Microfibrillar collagen powder (Avitene) ™™Topical thrombin ™™Bone wax (derived from bees wax + almond oil) • Gelfoam is made from denatured animal skin gelatin. Gelfoam has no intrinsic hemostatic action, • but it can be used in combination with topical thrombin, for which it serves as an absorbable carrier. • Its main hemostatic activity is related to the contact between blood and the large surface area of the sponge transmitting pressure.
  • 31. CONCLUSION • Confirm shock, hypovolaemia and haemorrhage by clinical assessment • ™™Immediate resuscitation by blood, oxygen, fluid • ™™Identify site of haemorrhage—ultrasound, endoscopy, CT scan, diagnostic peritoneal lavage (DPL), blood tools • ™™Control of haemorrhage—surgery, endoscopic control, therapeutic embolisation • ™™Definitive treatment if any • ™™Sepsis control • ™™Prevention of coagulopathy by FFP, platelet concentrate, fresh blood • ™™Critical care management • ™™End point resuscitation, fluid and electrolyte management,