Pathogenesis and Medico legal Aspect of Shock

Moderator : Prof H. Nabachandra presenter :Dr Soreingam

Ragui

What is Shock ?

Shock is any condition in which the circulatory system is unable to provide adequate circulation to the vital body organs such as the brain, heart and lungs. As a result of a decrease in the blood pressure.

Shock is usually accompanied by renal failure, as a normal compensatory mechanism, because the blood flow to the kidney is decreased to keep enough blood for the vital organs.

Classification of Shock

Shock is classified according to the causes to four classes:

Hypovolemic shock Distributive shock Cardiogenic shock Neurogenic shock

Causes of Shock 1.Hypovolemic shock is caused by low blood

volume. Normal blood volume is 5 L and by losing 1-2

L it can lead to shock. The Decrease in blood volume is caused by: External blood loss: ex. Hemorrhage Internal blood loss: ex. Ruptured spleen

caused by blunt trauma. Severe dehydration as a result of: Vomiting Diarrhea This is a typical condition in cholera. Burns

2. Distributive shock is caused by excess vasodilatation (ex. Anaphylactic shock and septicaemia)

Vasodilatation Arteriole resistance increase blood exchange from the vessels to the peripheral tissues decrease blood return to the heart BP shock.

Anaphylaxis, drug, toxin reactions Trauma: crush injuries, major fractures, major

burns. Infection/sepsis: G(-/+ ) septicemia,

pneumonia, peritonitis, meningitis, cholangitis, pyelonephritis, necrotic tissue, pancreatitis, wet gangrene, toxic shock syndrome, etc.

3.Cardiogenic shock ( heart does not pump enough blood) is caused by:

A) Myocardial infarction leads to weak cardiac

As a result Muscle contraction Ischemia of B) Arrhythmia ( such as ventricular

fibrillation, which will stop the heart pump and that will decrease BP)

Note: Supraventricular (Atria) fibrillation will not cause shock because 75% of the blood transfer from the atrium to the ventricles by passive transport.

C) Valve problems, ex. Valvular stenosis which is narrowing of the valves, or leakage of blood through the valves ( Regurgitation).

D) Problems in the A-V shunt. 4.Neurogenic shock Mechanism: Loss of autonomic

innervation of the cardiovascular system (arterioles, venules, small veins, including the heart)

Causes: Spinal cord injury Regional anesthesia Drugs Neurological disorders

PATHOGENESIS:-

HYPOVOLAEMIC SHOCK Effective circulating blood volumeHaemorrhageTrauma Venous returnSurgery to heart Burns Dehydration

SEPTIC (TOXAEMIC) SHOCK

Gram-ve septicaemiaGram+ve septicaemia

CARDIOGENIC SHOCK Cardiac outputDeficiency of emptyingDeficiency of filling Blood flowOutflow obstruction

Supply of oxygenOTHER TYPESTraumatic shock AnoxiaNeurogenic shockHypoadrenal shock Inflammatory mediators

SHOCK

Pathophysiology of Shock

Common mediators of septic shock include TNF-α, IL-1, NO, and Ceramide.All of these cytokines released during sepsis cause extreme diffuse vasodilation and vascular leakage, leading to distributive shock. Reduced SVR is a hallmark of septic shock.

Hypoxic Cell injury

Activation of innate immunity

Stimulation of macrophages

Release of inflammatory mediators

TNF-α IL-1 Others

Synthesis of Vasodilatation Other cytokines Nitric oxide (IL-6, 12, 8, PAF)

Generation of Hypotension Free radicals Free radicals C3a, C5a

Figure: Response of inflammatory mediators in shock.

Kidneys Shock causes “pre-renal” acute renal failure.

Ischemia of tubule epithelium leads to vasoconstriction, reduced GFR, oliguria, and azotemia

Ischemia leads to Acute Tubular Necrosis (ATN)

Brain Altered mental status occurs early in shock,

due both to hypoxemia and metabolic problems

GI tract The GI tract is at very high risk of infarction.

Shock causes infarction of the GI epithelium

Liver Centrilobular necrosis is common. There is

diminished reticuloendothelial clearance Blood -- DIC WBC count may go up or down. Platelets go way down as they are all used

up in DIC. Diffuse fibrin thrombosis consumes

feedback inhibitors, leading to more and more clotting

Pathology of Shock

Shock leads to multi-organ dysfunction syndrome (MODS).

The lungs are usually the first organ to fail, followed by kidneys, liver, GI tract, and then brain.

Heart Grossly, subendocardial hemorrhages

are common. Microscopically, contraction bands are

seen in myocardial cells. Fatty change – 18 to 24 hrs well

marked in 3 to 4 days

Lung Shock causes release of inflammatory

mediators such as TNF-α. This injures endothelial cells.

Endothelial injury allows leakage of proteinaceous fluid and neutrophils into the interstitium.

interstitial edema and inflammation common in shock.

Edema is well discernible after 2 to 3 days Since it’s interstitial, not alveolar, the septae

between alveoli are greatly widened. Lungs become heavy, stiff, and hemorrhagic.

The alveolar septa are prominent, due to marked congestion of the capillaries. The alveolar lumens contain pale-staining edema fluid.

Brain Watershed infarcts are a common consequence

of shock. These are long, wedge-shaped infarcts at the very distal tips of a major arterial supply.

Laminar necrosis is another common consequence of shock.

GI tract Shock often causes mucosal hemorrhage and

necrosis Grossly, the GI tract may appear swollen and

bloody. Adrenal The may be evidence of focal lipid depletion in

the cortical area within 1 to2 days

Compare the thinned and discolored cerebral cortex on the left side to the relatively preserved cortex on the right side. Neurons in different areas of the brain have different susceptibilities to global ischemic damage, such as may occur in shock. Most patients with shock who are diagnosed and treated early suffer no or only mild ischemic damage to the brain, which may result only in a confusional state. However, more severe, prolonged, and irreversible shock can lead to laminar cortical necrosis.

Liver Fatty change become evident within 18

to 24 hrs Shock generally causes centrilobular necrosis,

because the hepatocytes closest to the central vein are the furthest from the blood supply.

Kidneys The most susceptible kidney cells are those in

the proximal tubules and thick ascending Loop of Henle.

Microscopically, you will see acute tubular necrosis (ATN). There will be dilation of proximal tubules due to flattening of the epithelium. Brownish casts may be seen

A photomicrograph of renal biopsy shows renal medulla, which is composed mainly of renal tubules. Patchy or diffuse denudation of the renal tubular cells is observed, suggesting acute tubular necrosis (ATN) as the cause of acute kidney injury (AKI).

Acute tubular necrosis (ATN). Flattening of the renal tubule cells due to tubular dilation.

Acute tubular necrosis. Intratubular cast formation.

Sloughing of cells, which is responsible for the formation of granular casts, a feature of acute tubular necrosis (ATN

Medicolegal importance In a person with haemorrhagic diathesis or

haemophilia, minor injury produce death from hge. A trivial bruise causes loss of 20-30ml of blood

loss. So an extensive bruise without any other injury might also cause dead .

Examination of crime scene is important to calculate the amount of blood loss.

Men withstand hge better than women. Sudden rise of BP in neurogenic shock can

precipitate serious complications like – (a) Intracerebral hge from rupture of

arteriosclerotic cerebral vessels or of berry aneurysm.

(b) Rupture of a dissecting aneurysm of aorta.

Under such conditions even when the deceased received minor trauma before death, the essential cause of death will be underlying disease process.

Minor stimuli or injury over receptic spots may cause sudden death from neurogenic shock.

In persons of neurotic or emotional temperament, in deeply intoxicated, severely ill or feeble old and young children, death from primary shock occurs readily.

CONCLUSION

Shock is a complex, dynamic disorder of tissue and cellular hypoperfusion, produced by multiple interacting mechanisms that may lead to MODS & death. Successful treatment of patients with shock requires prompt recognition of the shock state and a thorough understanding of the pathophysiology of various types of shock

In case of any sudden death meticulous history taken to rule out any precipitating factor of shock is a must.

There may not be any evidence of injury in some cases of death from violence.

E.g sudden death due to vagal inhibition In such case after full and meticulously

done autopsy, even absence of violence or morbid cause to account for sudden death of the subject who was ordinarily healthy previous to infliction of violence there might not to be any hesitation to ascribe the death to be due to functional effect of the injuries.

Autopsy finding in case of death due to neurogenic shock are mainly inferential and the diagnosis is arrived at from history of sudden death following blow or injury over the area and negative finding. E.g absence of fatal injuries, poisoning or natural disease etc

So careful history taking is a must besides other investigations in establishing the cause of death.

Thank you