shock is one of the main cause of death very common encountered in day to day practice,in this presentation we look at how it happen,what are the causes and how we diagnose it in brief and its forensic importance

2.  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.

3.  Shock is classified according to the
causes to four classes:
 Hypovolemic shock
 Distributive shock
 Cardiogenic shock
 Neurogenic shock

4.  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

5.  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.

6.  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.

7.  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

8. PATHOGENESIS:-
HYPOVOLAEMIC SHOCK Effective circulating
blood volume
Haemorrhage
Trauma Venous return
Surgery to heart
Burns
Dehydration
SEPTIC (TOXAEMIC) SHOCK
Gram-ve septicaemia
Gram+ve septicaemia

9. CARDIOGENIC SHOCK Cardiac output
Deficiency of emptying
Deficiency of filling Blood flow
Outflow obstruction
Supply of oxygen
OTHER TYPES
Traumatic shock Anoxia
Neurogenic shock
Hypoadrenal shock Inflammatory mediators
SHOCK

10. 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.

11. 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.

12.  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

13.  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

14.  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

15.  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.

17.  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

19.  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

24.  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.

25.  (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.

26.  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

27.  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.

28.  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.