shock : types and management

الرحمنهللابسم

الرحيم

THE SHOCK

PROF. DR. NAWEL HUSSEIN

حسينناول /.د.أM.B.,B.Ch, M.S., FRCS (Ed. UK), MDPROFESSOR OF ONCOSURGERY

SHOCK

Definition: It is a state of acute circulatory

failure in which the cardiac output unable to

maintain tissue perfusion for nutrition,

oxygenation and waste disposal. Shock is common and the most important cause

of death among surgical patients.

In some cases a patient may have a combination

of more than one types of shock, as in trauma

and burn, hypovolaemic and neurogenic shock

occurs at the same time.

SHOCK

Types of shock: Neurogenic shock: this is due to peripheral

vasodilatation and peripheral pooling of the

blood.

Hypovolaemic shock: due to decrease of blood

volume.

Cardiogenic shock: due to failure of the heart.

Septic shock: when infection is sever, it releases

chemical mediators which affects the

microcirculation resulting in failure of peripheral

resistance and ending in failure of the heart.

Anaphylactic shock: due to antigen antibody

reaction that leads to failure of peripheral

resistance.

Endocrinal shock: due to hypo- and

1-NEUROGENIC SHOCK

Definition: This is due to peripheral vasodilatation and

peripheral pooling of the blood in the skeletal

muscles and inadequate venous return, this type

is also referred to as fainting , collapse or

Vasovagal attack.

Causes: Painful stimulation as catheterization or severe

trauma to the testis or to the abdomen

Reaction to fear or fight or hearing bad news .

Following spinal anesthesia or fracture spin

(spinal shock)

Clinical pictures: Increasing pallor of the face, cold extremities.

Fall of the blood pressure together with

1-NEUROGENIC SHOCK

Treatment: Put the patient in the shock position i.e. patient

lie flat in the bed with elevation of the lower

limbs to increase venous return and cardiac

output

Atropine in vasovagal shock to improve

bradycardia which occurs due to increase of the

vagal tone

Vasoconstrictors as ephedrine in spinal shock to

elevate blood pressure by increasing peripheral

resistance.

I.V fluids if the shock persists for more than 20

minutes.

2-HYPOVOLAEMIC SHOCK

Causes: Blood loss: as in haemorrhage due to trauma,

operation, GIT bleeding or blood diseases.

Plasma loss: as in burn

Water and electrolyte loss: as in vomiting,

diarrhea high output intestinal fistula.

Third spacing loss: the fluid is lost into the GIT

lumen and interstitial spaces as for example in

intestinal obstruction and pancreatitis.


Clinical pictures: Mild shock: (up to 20% blood volume loss) non

vital organs are affected as (skin, muscles and

bone) Pallor, cold skin

Mild tachycardia and may postural hypotension.

Moderate shock: (up to 40% blood volume loss)

where the kidneys, liver, intestine are also

affected, so, plus to the above manifestations,

there are: Tachycardia increased and hypotension.

Oliguria or anuria (urine output of less 0.5 cc/kg/hours

indicates marked hypovolaemia.)

Severe shock: (more than 40% blood volume loss)

brain and heart are also affected. so, plus to the

above manifestations there are :


Irreversible shock: Progressive renal, respiratory, cardiac and CNS

decompensations.

Acidosis: due to accumulation of acidic metabolites

Hypothermia

Consumption coagulopathy due to DIC

Electrolyte disturbance as hyperkalaemia

Multiple organ failure syndrome


Patho-physiology Cardiovascular and endocrine compensatory

responses: Aims to restores the intravascular volume, maintain

blood pressure and tissue perfusion and reduce flow to

non-vital organs to preserve flow to vital organs as

(brain, heart and kidney) by:

stimulation of baroreceptors in carotid sinus and

aortic arch to increase heart rate and peripheral

vasoconstriction then blood pressure elevated

Increase secretion of ADH, which leads to

vasoconstriction & oliguria, so, blood pressure

elevated

Renal ischaemia rennin secretion angiotensin I

&II - vasoconstriction and aldosterone secretion

(salt & water retention) so, blood pressure

elevated.

EARLY COMPENSATED STAGE(ADAPTIVE PHASE OR

NEUROENDOCRINE RESPONSE):

.1Neural reflexes: Stimulation of baroreceptors in wall of atria,

carotid sinus & in aortic arch → ↑ sympathetic

activity → Selective VC of blood vessels of skin, muscles, kidneys

& splanchnic organs → Shift of blood to heart & brain.

Vasoconstriction of veins (veins carry about 2/3 of

blood volume) will shift the blood to arterial side of

circulation.

↑ HR & contractility of heart.

Stimulation of chemoreceptors in aortic arch &

carotid bodies (sensitive to minor changes in PH,

O2 tension & CO2 level) ….result in splanchnic VC

(splanchnic blood flow represents 20% of blood

volume) & coronary blood vessel dilatation.


Microcirculatory changes: In compensated shock :

Under the effect of catecholamines the pre-

capillary sphincters constrict decrease of

capillary pressure refilling from the interstitial

fluids to increase the intra vascular fluids (one

liter / hour in healthy person increase blood

pressure.

In de-compensated shock: Opening of A-V shunts leads to more capillary

ischemia and more cellular distress release of

histamine and other chemical mediators

contraction of post-capillary sphincter more

slowing of the capillary flow & more ischemia.

Paralysis of pre-capillary sphincter due to


Cellular changes: Hypoxia anaerobic glycolysis lactic acid

production (metabolic acidosis) and small amount of

energy. Body tries to correct acidosis by

hyperventilation.

With more hypoxia cellular functions deteriorates,

specially Na/K pump which results in increase

intracellular Na and water and increase extracellular

potassium (hyperkalaemia)


Multiple organ failure(MOF): MOF is defined as two or more failed organ systems

Lung failure -- acute respiratory distress syndrome

(ARDS)

Kidney failure acute renal insufficiency

Liver failure - acute liver insufficiency

Clotting coagulopathy

Heart failure

There is no specific treatment for MOF, management is

by supporting organ systems with ventilation,

cardiovascular support and dialysis until there is

recovery of organ function

MOF currently carries a mortality rate of 60%, thus

prevention is vital by early aggressive identification

and treatment of shock.

Adaptive mechanisms are very poor in

children & elderly because: Pediatric patients: Have smaller total blood volumes & therefore, they

are at risk to lose a proportionately greater

percentage of blood.

Children < 2 years, their kidneys are immature →

power to concentrate solute.

Large body surface with rapid heat loss → early

hypothermia, → Coagulopathy.

Elderly people: Altered physiology

Atherosclerosis & elastin → Poor arterial

contraction & retraction.

Ability to respond to hypotension by tachycardia.

Preexisting medical conditions with medications that

may affect the compensatory response to shock.


Measurements needed in shock: Urine output: urine output of less 0.5

cc/kg/hour indicates marked hypovolaemia.

Central venous pressure (CVP): Normal 5-15 cm water

Increased in: cardiogenic shock, Rt side heart failure,

fluid overload

Decreased in hypovolaemic shock

Swan Ganz catheter: can measure COP and

pulmonary artery wedged pressure good

indicator of left ventricular function.

Arterial blood gases and blood PH.

Serum electrolytes & haematocrit value.


Treatment of hypovolaemic shock :

Immediate resuscitation for shocked patient

is to insure a patent airway and adequate

oxygenation and ventilation, then attention

is directed to cardiovascular resuscitation.

Fluid therapy: The mainstays of initial

treatment of shock are the infusion of fluids Insert two large pore cannula, blood is drawn

for typing and cross matching.

1000-2000 ml of lactated ringer's solution

over 45 minutes. Patients can be divided into

Responders in whom Bl.P and pulse improved

with good urine output as in only fluid loss

(intestinal obstruction) or in mild non active

bleeding

Transient responder improvement then return

to previous state over 20 min, these patients

either have moderate on-going fluid losses.

Non-responders are severely volume depleted

and are likely to have major on-going fluid losses

usually through uncontrolled haemorrhage.

Blood: the most effective, specially with blood

loss. In patients who are actively bleeding (major

trauma, ruptured aortic aneurysm, GIT

haemorrhage) elevation of Bl.P without

controlling site of Hge., merely increase bleeding

from these sites. Thus operative Hge. control

should not be delayed and resuscitation should

be done in parallel with surgery .

Colloid solution: in the absence of whole blood,

many substances have been proposed as human


Pulmonary support: Mask oxygen for all shocked patient at high

concentration

Evidence of respiratory failure is an indication for

endo-tracheal intubation and mechanical

ventilation.

Position: elevation of lower limb with

maintaining the trunk in supine position

Heating of the patient with blankets to avoid

sense of coolness.


Medications: in the form of: Corticosteroids: may be beneficial in these

cases.

Sedation (morphine): relives pain& anxiety and

reduces tissue requirements for oxygen. It is

contraindicated in abdominal and head injuries

and with respiratory depression. It must be give

I.V to avoid toxicity.

Antibiotics: third generation cephalosporines to

avoid septic complications.

Inotropic drugs (dopamine): are used when the

condition fails to improve despite adequate

volume replacement and oxygenation. It is used

to improve myocardial contractility and increase

renal blood flow and urine output as well.

3-SEPTIC SHOCK

This is the most lethal shock, and considered

as one of the major killers in surgical

practice. If not well treated mortality ranged

from 25%-90%.

Causes: The commonest organism is gram–ve bacteria &

its endotoxins ( part of cell wall of dead

bacteria),

The common sources are peritonitis due to

rupture viscus, cholangitis, GIT infection &

severely infected diabetic foot.

Predisposing factors includes, extremities of age,

DM, malignancy ,chemotherapy, corticosteroid

therapy &AIDS

3-SEPTIC SHOCK

Pathophysiology: Bacterial endotoxin stimulates macrophages and

Kupffer cells of the liver to release cytokines (as

: tumour necrosis factor "TNF", platelet

activation factor, prostaglandins & nitric acid) in

large amount harmful effect on

microcirculation with capillary endothelium

damage.

These cytokines lead to peripheral vasodilatation

and opening of A-V shunt, which lead to capillary

bypass and tissue hypoxia.

capillary endothelium damage under the effect

of cytokines, lead to leakage of protein-rich fluid

from the circulation to the interstitial space

causing oedema.

3-SEPTIC SHOCK

Clinical pictures:

The patient passes through two stages, the

diagnosis of the patient in the early stage

and prompt management can save the

patient. Hyperdynamic (warm) stage: diagnosis is

difficult and a high index of suspicion is required

to detect cases at this early stage. Fever (> 38oc) with warm dry skin.

Tachycardia , hypotension & tachypnoea .

Oliguria.

The cardiac out-put is normal or elevated and If not

treated, patient will pass to the next stage.

3-SEPTIC SHOCK

Clinical pictures:

Hypodynamic (cold) stage: Sever tachycardia , hypotension & tachypnoea

Cold clammy skin

Restlessness and confusion

Marked oliguria.

Complicated by:

1. Acute erosive gastritis.

2. Systemic inflammatory response

syndrome(SIRS)

3. Adult respiratory distress syndrome (ARDS)

4. Multiple organ failure (MOF)

5. DIC and death.

3-SEPTIC SHOCK

Diagnosis: is helped by CBC polymorphonuclear leucocytosis with

abundant immature forms

High lactate level in blood

Search for the source of infection

Repeated blood culture at peak of fever

3-SEPTIC SHOCK

Treatment:Treatment must be started as early as possible and

should be carried in ICU, by two arms hand by

hand, 1-control infection 2- support of body

systems with good monitoring.

1- Control of infection: Eradication of infection: drainage of peritonitis or

big abscess, resection of gangrenous bowel or

amputation of diabetic severely infected limb.

Antibiotics: aggressive multiple antibiotics as

combination of (cephalosporin, garamycin and

metronidazole), till results of culture and sensitivity is

available.

Control of predisposing conditions as DM

Corticosteroids may have a role

3-SEPTIC SHOCK

2- Support of different systems: The main priority is to maintain cardiovascular

system with reasonable blood pressure by: Fluid replacement: huge amount of ringer lactate may

be needed to replace fluid deficits till CVP reach 12-

15 mm.Hg.

Medications (inotropes and vasopressors) if the patient

remains hypotensive despite adequate fluid

replacement as shown by CVP dopamine drip is given

to raise the blood pressure. If there is still no response

careful noradrenaline administration may be used.

Oxygen administration is essential by mask in

mild hypoxia and by intubation and mechanical

ventilation in severe hypoxia.

Observing urine output, and if not improved by

fluids, dopamine will be added, if no

improvement haemodialysis may be needed in

4- CARDIOGENIC SHOCK

Causes:

The deficiency of tissue perfusion here is not

due to loose of blood volume but due to

failure of the heart to pump and low cardiac

output as in1. Massive acute myocardial infarction

(commonest cause).

2. Severe arrhythmia.

3. massive pulmonary embolism

4. Cardiac tamponade.

5. myocarditis

6. High spinal anaesthesia, can cause paralysis

of the sympathetic supply of the heart.


Clinical pictures: Pictures of the cause

Cold sweaty skin

Manifestations of acute heart failure

Dyspnea, cyanosis and pulmonary oedema.

Congested neck veins and high CVP.

Fall of the systolic and diastolic Blood pressure

and collapse.

Increasing metabolic acidosis.


Treatment: Oxygen should be administered

Treatment of the cause

Inotropic drugs as Dubotamin

Mechanical support by intra-aortic balloon

pulsation device to elevate diastolic Bl.P, hence

better filling of the coronary arteries and

reduction of myocardial work.

5- ANAPHYLACIC SHOCK

This type of shock occurs due to Antigen

antibody reaction (allergic reaction) leads to

release of large amount of histamine which

causes capillary paralysis, dilatation and

pooling. The best example is penicillin

injection in a sensitized patient.

Clinical pictures: Skin eruption,

bronchospasm, laryngeal oedema and

respiratory distress and collapse.

Treatment: Immediate stop of further

injection of the causing drug , give the

patient corticosteroid injection ,adrenaline ,

antihistaminics and O2 .

6- ENDOCRINAL SHOCK

This may occur in patients with Addisons

disease or those receiving continuous

cortisone therapy if they are subjected to

any stressful situation, as infection or

surgery.

The patient develops sever shock due to

failure of release of corticosteroids necessary

to cope with the stress from the suppressed

adrenal cortex. The result will be a state of

peripheral circulatory failure, hyponatraemia

and hyperkalaemia.

Treatment is essentially prophylactic. Any

patient liable to this problem should receive

an additional dose of hydrocortisone IV prior

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shock : types and management

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