Definition, type and management of septic shock

1. SHOCK
Capt Htet Ko
PG 1
ORL-HNS
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2. • Shock is defined as a circulatory state in which tissue perfusion is inadequate to
meet demand and may or may not be associated with hypotension.
• Shock is characterized by decreased oxygen delivery and/or increased oxygen
consumption or inadequate oxygen utilization leading to cellular or tissue
hypoxia.
• It is life-threatening condition of circulatory failure ad often defined as by
systolic pressure <9ommHg or mean arterial pressure <65mmHg with evidence
of tissue hypoperfusion, e.g., urine output <0.5ml/kg/hr.
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3. Classification
1. Distributive shock
i. Septic shock
ii. Systemic Inflammatory Response Syndrome
iii. Anaphylactic shock
iv. Neurogenic shock
v. Endocrine Shock
2. Hypovolemic shock
i. Haemorrhagic shock
ii. Non-haemorrhagic shock
3. Cardiogenic shock
4. Obstructive shock
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4. 1. Distributive shock
• Distributive shock describes the pattern of cardiovascular response characterising
a variety of conditions, including septic shock, anaphylaxis and spinal cord injury.
• Inadequate organ perfusion is accompanied by vascular dilatation with
hypotension, low systemic vascular resistance, inadequate afterload and a resulting
abnormally high cardiac output.
• In anaphylaxis, vasodilatation is due to histamine release, while in high spinal
cord injury there is failure of sympathetic outfow and adequate vascular tone
(neurogenic shock).
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5. • The cause in sepsis is less clear but is related to the release of bacterial products
(endotoxin) and the activation of cellular and humoral components of the immune
system.
• Endocrine shock may present as a combination of hypovolaemic, cardiogenic or
distributive shock.
• Causes of endocrine shock include hypo and hyperthyroidism and adrenal
insuffciency.
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6. 2. Hypovolemic shock
• Hypovolemic shock is due to a reduced circulating volume.
• Hypovolemia may be due to haemorrhagic or nonhaemorrhagic causes.
• Nonhaemorrhagic causes include poor fuid intake (dehydration), excessive fluid
loss due to vomiting, diarrhoea, urinary loss (e.g. diabetes), evaporation or ‘third
spacing’, where fluid is lost into the gastrointestinal tract and interstitial spaces, as
for example in bowel obstruction or pancreatitis.
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7. 3. Cardiogenic shock
• Cardiogenic shock is due to primary failure of the heart to pump blood to the
tissues.
• Causes of cardiogenic shock include myocardial infarction, cardiac dysrhythmias,
valvular heart disease, blunt myocardial injury and cardiomyopathy.
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8. 4. Obstructive shock
• In obstructive shock there is a reduction in preload and mechanical obstruction of
cardiac filling.
• Common causes of obstructive shock include cardiac tamponade, tension
pneumothorax, massive pulmonary embolus or air embolus.
• In each case, there is reduced filling of the left and/or right sides of the heart,
leading to low cardiac output.
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9. Pathophysiology
Cellular
• As perfusion to the tissues is reduced, cells are lack of oxygen and must switch
from aerobic to anaerobic metabolism.
• The product of anaerobic respiration is not carbon dioxide but lactic acid.
• When enough tissue is underperfused the accumulation of lactic acid in the blood
produces a systemic metabolic acidosis.
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10. Systemic
Cardiovascular
• As preload and afterload decrease, there is a compensatory baroreceptor response,
resulting in increased sympathetic activity and release of catecholamines into the
circulation.
• This results in tachycardia and systemic vasoconstriction.
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11. Respiratory
• The metabolic acidosis and increased sympathetic response result in an increased
respiratory rate and minute ventilation to increase the excretion of carbon dioxide
(and so produce a compensatory respiratory alkalosis).
Renal
• Decreased perfusion pressure in the kidney leads to reduced fltration at the
glomerulus and a decreased urine output.
• The renin–angiotensin–aldosterone axis is stimulated, resulting in further
vasoconstriction and increased sodium and water reabsorption by the kidney.
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12. Endocrine
• As well as activation of the adrenal and renin–angiotensin systems, vasopressin
(antidiuretic hormone) is released in response to decreased preload and results in
vasoconstriction and resorption of water in the renal collecting system.
• Cortisol is also released from the adrenal cortex, contributing to the sodium and
water resorption and sensitising cells to catecholamines.
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13. Septic shock
• Sepsis is defined as life-threatening organ dysfunction resulting from dysregulated
host response to infection.
• Septic shock is a subset of sepsis with severe circulatory, cellular, and metabolic
abnormalities resulting in tissue hypoperfusion manifested as hypotension.
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14. • The pathophysiology of septic shock involves a complex interplay between the
immune system, inflammatory response, and the cardiovascular system.
• When an infection occurs, the body's immune system responds by releasing
cytokines and other inflammatory mediators such as interleukin-1 (IL-1), tumor
necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6), which activate the
endothelial cells lining the blood vessels.
• This activation leads to increased permeability of the blood vessels, allowing fluid
and proteins to leak out into the surrounding tissue, causing swelling and edema.
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15. • At the same time, the inflammatory mediators cause vasodilation and a decrease in
systemic vascular resistance, leading to a drop in blood pressure.
• In sepsis shock, these changes in vascular permeability and vasodilation become
extreme, leading to severe hypotension and impaired tissue perfusion.
• The heart compensates by increasing its pumping activity, but this can lead to
further damage to the heart muscle and worsen the circulatory dysfunction.
• Additionally, the release of inflammatory mediators and the activation of the
coagulation system can lead to the formation of microthrombi, which can further
impair blood flow to vital organs, such as the kidneys, liver, and brain.
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16. Management of septic shock
Principle of resuscitation
1. Volume replacement in order to maintain cardiac preload or central venous
pressure
2. Give O2 to maintain total O2 delivery
3. Maintain BP to ensure adequate organ perfusion
4. Investigate and treat causes of sepsis
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17. Investigation
1. Arterial blood gas (ABG), lactic acid level
2. Urea and electrolytes, creatinine and liver enzymes
3. Chest X-ray (PA)
4. Blood for C&S and appropriate sample (urine, sputum, discharge)
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18. Resuscitation
1. Volume resuscitation
IV infusion of appropriate fluid to facilitate administration of drugs and to
maintain circulatory volume. E.g., give fluid 7ml/kg colloid (albumin, gelofusine) or
20ml/kg crystalloid (NS, DW, RL) by IV line.
Refer to ICU if possible and monitoring. Aware of cardiac overload and pulmonary
oedema. If not response, give vasoactive agents. Primary goal is for adequate mean
arterial pressure (65-70mmHg)
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19. 2. Vasoactive agents
a. Dopamine - used in initial therapy in hypotension. It improves cardiac
performance and increases systemic vascular resistance and dose is 2.5-5
µg/kg/min)
b. Dobutamine – usually not indicated d/t its vasodilator effect. Both drugs can
cause unacceptable tachycardia or dysarrythemias.
c. Norepinephrine – it causes peripheral vasoconstriction and increased
inotropy. Dose 4mg in 500ml of DW.
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20. 3. Antibiotic treatment
Initial treatment with empirical broad-spectrum antibiotics to cover most
likely organisms. E.g., Co-amoxiclav 1.2G/8hr or meropenem 1g/8hr or gentamycin
+ antipseudomonal penicillin (ticarcillin, piperacillin). Then change according to
C&S result.
4. Vasopressin
Vasopressin level low in septic shock due to impaired secretion or depletion.
IV infusion of vasopressin 004u/min can give to maintain BP and vascular
resistance and urine output.
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21. 5. Activated protein C
For fibrinolysis and to pervert thrombosis and inflammation. Dose – IV
24µg/kg/hr for up to 96hr.
6. Metabolic acidosis treatment
Sever acidosis can cause poor myocardial function. 50-100ml of NaHCO3
may be given.
7. Steroid
Low dose steroid may improve BP but not improve mortality.
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22. THANK YOU
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