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01 Haemorrhage and shock
1. Haemorrhage and shock
By
Dr. Abdel-Motaleb Effat M.D.
Lecturer of Pediatric Surgery.
Tanta University.
2. Haemorrhage
Haemorrhage means escape of
blood outside its containing vessel.
Acute haemorrhage causes loss of
both circulating blood volume and
oxygen carrying capacity.
4. Timing in relation to trauma:
Primary.
Reactionary.
Secondary.
Aetiology:
Traumatic (accidental, surgical
and intervetional procedures).
Pathological (atherosclerotic,
inflammatory and neoplastic).
Bleeding diathesis.
5. Physiological response to haemorrhage:
The Physiological response to
haemorrhage has two aims:
1. Stopping the bleeding
2. Maintaining effective circulatory
volume and perfusion of critical
tissues which is achieved by
neural and endocrinal factors.
6. Neural factors.
A sympathoadrenal response
which will cause: (constriction of the
veins, constriction of arterioles raising
the peripheral resistance and
increased rate and contractility of the
heart).
Endocrine factors.
Transcapillary refill.
7. Clinical picture:
The manifestations depend upon:
Amount of haemorrhage.
Rate of haemorrhage.
Cardiovascular reserve.
Symptoms:
Weakness and fainting especially
when standing.
The patient feels cold and thirst.
8. Signs:
*Pulse : small and rapid. Later on it
becomes imperceptiple.
*B.P. : low, later on it is seriously lowered.
*Respiration : rapid and shallow.(over 35/
minute is serious)
*Lethegic mind till the end.
*Pallor and light cyanosis.
*Cold skin and clammy sweat.
*Urine flow : oliguria (normal 30-60ml./h).
*collapsed veins indicate severe oliguria.
9. Estimating blood loss:
Normal blood volume is estimated as
70 ml/kg in adults and 80ml/kg in
children.
Clinical data.
Four classes of haemorrhage are
recognized based on clinical changes
in haemodynamic parameters and
indices of tissue perfusion.
Type of injury.
Blood loss at operation.
10. Management
Stop of haemorrhage:
First aid treatment by packing,
pressure, position, and
tourniquets.
Restore blood volume:
by lactated ringer solution, and
blood transfusion to correct
deficit according to the class of
haemorrhage.
11. Management(Cont.):
Optimize oxygen delivery:
by oxygen and inotropes.
Monitoring:
pulse, blood pressure,
temperature, urine output,
conscious level, C.V.P., blood
gases and blood lactate.
12. SHOCK
Definition:
Shock is a state of peripheral
circulatory failure characterized by
hypotension, inadequate tissue
perfusion and disordered cellular
metabolism.
14. Primary (neurogenic) shock
Vasovagal syncope resulting from painful
stimuli or emotional disturbance.
Clinical picture:
*Patient collapses and fall to the ground.
Feeble pulse.
*Slow and shallow respiration.
*Low BP.
*Subnormal temperature.
*Normal CVP (5 cm water).
*Warm skin.
15. Treatment:
Transient condition responding to:
Rest and warmth.
Remove the pain or distressing factor.
Stimulants as coffee.
Adrenaline IM.
If delayed recovery, suspect
associated secondary shock.
16. Secondary (oligaemic or
hypovolaemic) shock.
Hypovolaemia due to:
Blood loss (haemorrrhage).
Plasma loss (burn).
Water loss (vomiting and
diarrhea).
17. Pathophysiology:
I.Cardiovascular responses:
Hypotension stimulates V.C.C. and
stimulation of C.N.S.with catecholamines
release causing :
1.Increased peripheral resistance due to
arteriolar vasoconstriction.
2.Increased heart rate and contractility and
cardiac output.
3.Increased vasomotor tone squeezing
blood to the central circulation.
19. Pathophysiology(Cont.):
III. Blood viscosity is increased due to
haemoconcentration resulting in
sludging and Rouleaux formation.
IV. Microcirculatory changes.
V. Cellular derangement.
VI. Acid-base impalance.
VII. Individual organs (heart, GIT, liver,
kidneys and lungs).
20. If these mechanisms succeed in
maintaining a good tissue perfusion
this is known as compensated shock.
Irreversible shock ; occurs when shock
persists leading to:
1. Vasodilatation of capillaries with
pooling of blood and severe
hypotension.
2. Progressive tissue anoxia affecting
the heart, kidneys, liver and brain
leading to death in few hours.
21. Clinical picture:
1. The cause of shock may be evident.
2. Signs:
Pulse : small and rapid. Later on it
becomes imperceptiple.
B.P. : low, later on it is seriously
lowered.
Respiration : rapid and shallow.
(over 35/minute is serious)
22. Clinical picture(Cont.):
Lethegic mind till the end.
Pallor and light cyanosis.
Cold skin clammy sweat.
Urine flow : oliguria (normal 30-60
ml./hour). collapsed veins indicate
severe oliguria.
C.V.P. markedly reduced.
25. Traumatic shock:
by Proper first aid measures.
1. Control external bleeding.
2. Ensure adequate pulmonary perfusion.
3. Deal with the injured part by dressing,
splintage, firm bandage and elevation.
4. Raise the foot end of the bed.
5. Morphia I.V.(not given I.M. nor S.C.).
6. Start I.V. therapy by Ringer solution till
blood is available.
7. Conserve body heat by blankets.
8. Transport the patient to hospital.
26. Operative shock:
1. Preoperative measures: avoid purgation
and starvation and give proper sedation.
2. Operative precautions: avoid cold and
exposure of the viscera, fine bloodless
technique, ensure adequate anaesthesia
without anoxia or hypercapnoea and
maintain the blood pressure by transfusion
and suitable infusions.
3. Postoperative measures: put in recovery
room for 24-48 hours.
27. Treatment:
The aim should be to restore normal
tissue perfusion by correcting the two
major components in shock which are:
1. The hypotension which stimulates the
sympatho-adrenal response and
2. The disturbance in the microcirculation
which leads to tissue hypoxia.
These measures should be adopted as
soon as possible to abort the onset of
irreversible or septic shock.
28. Treatment(Cont.):
1. Control external bleeding.
2. Ensure adequate pulmonary perfusion.
3. Deal with the injured part by dressing,
splintage, firm bandage and elevation.
4. Raise the foot end of the bed.
5. Morphia I.V. (not to be given I.M. nor
S.C.).
6. Start I.V. therapy by Ringer solution till
blood is available.
7. Conserve body heat by blankets.
8. Hydrocortisone I.V. injection.
30. Pathophysiology:
*Mediators cascade.
*Microcirculation.
*Cellular derangement.
*Acid-base impalance.
*Individual systems and organs
(heart, lungs, brain, kidneys, liver
and GIT).
31. Clinical features:
Occurs in two stages
1. Hyperdynamic (warm) septic shock.
The patient has:
*Restlessness and confusion.
*Fever above 38 and chills.
*Mild reduction in BP.
*Tachypnoea.
*Tachycardia.
*Flushed with warm and dry extremities.
*Oliguria.
*The cardiac output is elevated.
32. Clinical features(Cont.):
2.Hypodynamic (cold) septic shock.
If the previous stage is not
treated efficiently, the patient will
develop a picture similar to
hypovolaemic shock with reduced
cardiac output. Multiple organ
failure starts at this stage.
33. Diagnosis:
Is helped by:
*Polymorphonuclear leucocytosis.
*High lactate level.
*Looking for source of sepsis.
*Repeated blood culture at the
peak of fever or from any septic focus.
34. Treatment:
*Support different systems
(cardiovascular, respiratory and
renal support).
*Fighting infection.
*Control of blood sugar.
*Prophylaxis against DVT and stress
ulceration.
*Monitoring as in hypovolaemic shock.
