Haemorrhage and shock

By

Dr. Abdel-Motaleb Effat M.D.Lecturer of Pediatric Surgery.

Tanta University.

Haemorrhage

Haemorrhage means escape of blood outside its containing vessel.Acute haemorrhage causes loss of both circulating blood volume and

oxygen carrying capacity.

Classification:According to:Site:

External (revealed).Internal(concealed).

Type of disrupted blood vessel:Arterial.Venous.Capillary.

Timing in relation to trauma:Primary.Reactionary.Secondary.

Aetiology:Traumatic (accidental, surgical

and intervetional procedures).Pathological (atherosclerotic,

inflammatory and neoplastic).Bleeding diathesis.

Physiological response to haemorrhage:

The Physiological response to haemorrhage has two aims:

1. Stopping the bleeding2. Maintaining effective circulatory volume and perfusion of critical tissues which is achieved by neural and endocrinal factors.

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.

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.

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.

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.

ManagementStop 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.

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.

SHOCKDefinition:

Shock is a state of peripheral circulatory failure characterized by hypotension, inadequate tissue perfusion and disordered cellular metabolism.

Types:1.Primary (neurogenic) shock.2. Secondary (oligaemic or hypovolaemic) shock.3. Cardiogenic shock.4. Septic shock.5. Anaphylactic shock.6. Endocrinal shock.7. Obstructive Shock.

Primary (neurogenic) shockVasovagal 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.

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.

Secondary (oligaemic or hypovolaemic) shock.

Hypovolaemia due to:

Blood loss (haemorrrhage).Plasma loss (burn).Water loss (vomiting and diarrhea).

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.

Pathophysiology(Cont.):

II.Endocrine response:*A.D.H. is released by baroreceptors

stimulation *Increased aldosterone.*Stimulation of rennin angiotensin mechanism.

All of these cause salt and water retention.

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).

Pathophysiology: 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.

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)

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.

Measurements:

*Urine output.*C.V.P.*Arterial blood gases.*Haematocrit.*Arterial blood lactate.*Cardiac output.

Prophylaxis:

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.

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.

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 and2. 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.

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.

Septic shock

Aetiology:*Causative organisms.*Common sources of infection.*Predisposing factors.

Pathophysiology:*Mediators cascade.*Microcirculation.*Cellular derangement.*Acid-base impalance.*Individual systems and organs

(heart, lungs, brain, kidneys, liver and GIT).

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.

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.

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.

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.

Prognosis:

Mortality ranges from 25 to 90%.

Thank you