Uploaded byDr. Roopam Jain
SHOCK
This document defines and classifies shock, discussing its pathogenesis and clinical features. It describes shock as a life-threatening condition characterized by reduced circulating blood volume and tissue perfusion. The document classifies shock into four main types - hypovolemic, cardiogenic, septic, and anaphylactic - and discusses their specific causes and pathophysiology. It also outlines the potential morbidities of shock including acute lung injury, kidney failure, liver dysfunction, and multi-organ failure.
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SHOCK
- 1. SHOCK DR. ROOPAM JAIN PROFESSOR& HEAD, DEPT. OF PATHOLOGY
- 2. SHOCK Definition • Shock isa life-threatening clinical syndrome of cardiovascular collapse characterised by: an acute reduction of effective circulating blood volume (hypotension) ” an inadequate perfusion of cells and tissues (hypoperfusion) • If uncompensated, these mechanisms may lead to impaired cellular metabolism and death.
- 3. • ” “true (orsecondary) shock” is a circulatory imbalance between oxygen supply and oxygen requirements at the cellular level (circulatory shock) • “initial (or primary) shock” is used for transient and usually a benign vasovagal attack resulting from sudden reduction of venous return to the heart caused by neurogenic vasodilatation and consequent peripheral pooling of blood e.g. immediately following trauma, severe pain or emotional overreaction such as due to fear, sorrow or surprise. • Clinically, patients of primary shock suffer from the attack lasting for a few seconds or minutes and develop brief unconsciousness, weakness, sinking sensation, pale and clammy limbs, weak and rapid pulse, and low blood pressure. • Another type of shock which is not due to circulatory derangement is anaphylactic shock from type 1 immunologic (amaphylactic) reaction.
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- 5. Classification and Etiology •3 major types and a few other variants: 1. Hypovolaemic shock Results from inadequate circulatory blood volume by various etiologic factors that may be either from the loss of red cell mass and plasma due to haemorrhage, or from the loss of plasma volume alone. 2. Cardiogenic shock Acute circulatory failure with sudden fall in cardiac output from acute diseases of the heart withoutactual reduction of blood volume (normovolaemia) results in cardiogenic shock.
- 6. 3. Septic (Toxaemic)shock Severe bacterial infections or septicaemia induce septic shock. It may be the result of Gram-negative septicaemia (endotoxic shock) which is more common, or less often from Gram-positive septicaemia (exotoxic shock). 4. Other types : i) Traumatic shock resulting from trauma is initially due to hypovolaemia ii) Neurogenic shock results from causes of interruption of sympathetic vasomotor supply. iii) Hypoadrenal shock occurs from unknown adrenal insufficiency in which the patient fails to respond normally to the stress of trauma, surgery or illness
- 7. Classification & etiologyof shock
- 8. Classification & etiologyof shock
- 9. Classification & etiologyof shock
- 10. Classification and etiologyof shock
- 11. Pathogenesis • In general,3 derangements: i) Reduced effective circulating blood volume. ii) Reduced supply of oxygen to the cells and tissues with resultant anoxia. iii) Inflammatory mediators and toxins released from shock induced cellular injury.
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- 13. Response of inflammatorymediators in shock
- 14. PATHOGENESIS OF HYPOVOLAEMICSHOCK • Hypovolaemic shock occurs from inadequate circulating blood volume due to various causes, most often from loss of red cell mass due to haemorrhage and, therefore, also called as haemorrhagic shock. • The severity of clinical features depends upon degree of blood volume lost; accordingly haemorrhagic shock is divided into 4 types: i) < 1000 ml: Compensated ii) 1000-1500 ml: Mild iii) 1500-2000 ml: Moderate iv) >2000 ml: Severe • Major clinical features are increased heart rate (tachycardia), low blood pressure (hypotension), low urinary output (oliguria to anuria) and alteration in mental state (agitated to confused to lethargic).
- 15. PATHOGENESIS OF CARDIOGENICSHOCK • Cardiogenic shock results from a severe left ventricular dysfunction from various causes such as acute myocardial infarction. • The resultant decreased cardiac output has its effects in the form of decreased tissue perfusion and movement of fluid from pulmonary vascular bed into pulmonary interstitial space initially (interstitial pulmonary oedema) and later into alveolar spaces (alveolar pulmonary oedema).
- 16. PATHOGENESIS OF SEPTICSHOCK • Gram-negative bacteria entering the body from genitourinary tract, alimentary tract, respiratory tract or skin, and less often from Gram-positive bacteria. • The net result of above mechanisms is vasodilatation and increased vascular permeability in septic shock. • Profound peripheral vasodilatation and pooling of blood causes hyperdynamic circulation in septic shock, in contrast to hypovolaemic and cardiogenic shock
- 17. Major pathogenic pathwaysin septic shock Microbial products (PAMPs, or pathogen-associated molecular patterns) activate endothelial cells and cellular and humoral elements of the innate immune system, initiating a cascade of events that lead to end-stage multiorgan failure
- 18. Pathophysiology (Stages ofShock) • Deterioration of the circulation in shock is a progressive and continuous phenomenon and compensatory mechanisms become progressively less effective • 3 stages: 1. Compensated (non-progressive, initial, reversible) shock 2. Progressive decompensated shock 3. Irreversible decompensated shock
- 19. Mechanisms & effectsof 3 stages of shock
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- 21. 1. HYPOXIC ENCEPHALOPATHY •Cerebral ischaemia - state of consciousness. • Grossly, • severe ischaemic necrosis • Microscopically, • the changes are noticeable if ischaemia is prolonged for 12 to 24 hours. • Neurons, particularly Purkinje cells, are more prone to develop the effects of ischaemia. • The cytoplasm of the affected neurons is intensely eosinophilic and the nucleus is small pyknotic. • Dead and dying nerve cells are replaced by gliosis.
- 22. 2. HEART INSHOCK • The heart is more vulnerable • i) Haemorrhages and necrosis There may be small or large ischaemic areas or infarcts, particularly located in the subepicardial and subendocardial region. • ii) Zonal lesions These are opaque transverse contraction bands in the myocytes near the intercalated disc.
- 23. 3. SHOCK LUNG •morphologic changes in lungs are quite prominent termed ‘shock lung’. • Grossly, the lungs are heavy and wet. • Microscopically • changes include congestion, • interstitial and alveolar oedema, • interstitial lymphocytic infiltrate, • alveolar hyaline membranes, • thickening and fibrosis of alveolar septa, and fibrin and platelet thrombi in the pulmonary microvasculature.
- 24. 4. SHOCK KIDNEY •One of the important complications of shock is irreversible renal injury, first noted in persons who sustained crush injuries in building collapses in air raids in World War II. • Grossly, the kidneys are soft and swollen. • Sectioned surface shows blurred architectural markings. • Microscopically, tubular lesions are seen at all levels of nephron and are referred to as acute tubular necrosis (ATN).
- 25. 5. ADRENALS INSHOCK • The adrenals show stress response in shock. • In severe shock, acute adrenal haemorrhagic necrosis may occur.
- 26. 6. HAEMORRHAGIC GASTROENTEROPATHY •mucosal and mural infarction called haemorrhagic gastroenteropathy . • In shock due to burns, acute stress ulcers of the stomach or duodenum may occur and are known as Curling’s ulcers. • Grossly, the lesions are multifocal and widely distributed throughout the bowel. • The lesions are superficial ulcers, reddish purple in colour. • Microscopically, the involved surface of the bowel shows dilated and congested vessels and haemorrhagic necrosis of the mucosa and sometimes submucosa.
- 27. 7. LIVER INSHOCK • Grossly • faint nutmeg appearance is seen. • Microscopically, • depending upon the time gap between injury and cell death, ischaemic shrinkage, hydropic change, focal necrosis, or fatty change may be seen.
- 28. 8. OTHER ORGANS •Other organs such as lymph nodes, spleen and pancreas may also show foci of necrosis in shock.
- 29. Clinical Features • Theclassical features of decompensated shock are characterised by depression of 4 vital processes: i) Very low blood pressure ii) Subnormal temperature iii) Feeble and irregular pulse iv) Shallow and sighing respiration • In addition, the patients in shock have pale face, sunken eyes, weakness, cold and clammy skin.
- 30. Complications • Life-threatening complicationsin shock are due to hypoxic cell injury resulting in immuno-inflammatory responses and activation of various cascades (clotting, complement, kinin). These include the following*: 1. Acute respiratory distress syndrome (ARDS) 2. Disseminated intravascular coagulation (DIC) 3. Acute renal failure (ARF) 4. Multiple organ dysfunction syndrome (MODS) • With progression of the condition, the patient may develop stupor, coma and death.