General Veterinary Pathology

SHOCK

• A common grave medical emergency characterized by a reduction in effective circulating blood volume and in the blood pressure.

Definition

• Shock (cardiovascular collapse) is a circulatory dishomeostasis associated with loss of circulating blood volume and reduced output and or inappropriate peripheral vascular resistance.
• Although causes of shock can be diverse the underlying cause of shock are relatively stereotyped i.e. hypoperfusion.

Causes of shock

• Trauma / burns
• Profuse haemorrhage
• Bacterial septicaemia
• Myocardial infarction (man)
• Pulmonary embolism (man)
• Psychic stimuli (man)
• Crushing injuries (automobile accidents) in dogs
• Cold, exhaustion, depression animals
• General anaesthesia

Classification of shock

• Primary shock
• Secondary shock

Primary shock (Syncope, fainting)

• Appears immediately after extensive injury
• Nervous stimuli in which widespread paralysis of capillaries occurs
• Animals
  • Rough handling of animals
  • Undue manipulation of intestine in abdominal surgery
• Humans
  • In psychic state like fear, excitement and apprehension, neurogenic impulses causes vasodilation and blood pressure decreases which leads to cerebral ischaemia and results in loss of consciousness (Pallid face, slow breathing, feeble pulse)
  • Transient / Patient recovers with rest.

Secondary shock

It is fatal

Causes of shock

1. Reduction in blood volume

• Loss of blood from injuries (Haemorrhages)
• Loss of fluid into injured tissues
  • Severe burns
  • Crushing injuries Oedema
  • Vomition
  • Diarrhoea Dehydration
  • Na deficiency
  • Addison’s disease Dehydration
  • Diabetic coma
  • Poisons (Phosgene, mustard gas, ANTU)

2. Capillary bed dilation

• Decreased cardiac output → decreased blood volume
  • Neurogenic Stimuli
    • Anxiety, fear, pain, bleeding wounds
  • Bacterial toxins
  • Burns, crushing injuries
  • Anoxia

3. Acute circulatory failure

• Infarction, cardiac tamponade
• Pulmonary embolism → No circulation → Shock

Classification based on fundamental underlying problem

• Cardiogenic shock
• Hypovolumic shock
• Blood maldistribution shock
  • Septic shock
  • Anaphylactic shock
  • Neurogenic shock

Cardiogenic shock results from failure of heart to adequately pump blood.

• This occurs due to
  • Myocardial infarction
  • Ventricular tachycardia
  • Fibrillation or other arrhythmia
  • Dilating and cardiac myopathy
  • Obstruction of blood flow from the heart
    • e.g. Pulmonary embolism and pulmonary or aortic stenosis
  • Other cardiac dysfunction
• Unsuccessful compensation leads to stagnation of blood and progressive tissue hypoperfusion.

Hypovolumic shock arises from reduced circulatory blood volume due to blood loss caused by haemorrhage of fluid loss secondary to vomiting, diarrhoea or burns. This leads to decreased vascular permeability and tissue hypoperfusion.

• Immediate compensatory mechanisms to increase vascular pressure
  • Vasoconstriction and fluid movement into plasma.
• Loss of about 10% blood volume can occurs without consequence, but when blood loss approaches 35-45% blood pressue and cardiac output can fall dramatically.

Blood maldistribution shock is characterised by decrease peripheral vascular resistance and pooling of blood in peripheral tissue.

The systemic vascular dilatation results may dramtically increase microvascular area and although the blood volume is normal. The effective circulating blood volume is decreased.

• Anaphylactic shock is generalised type I hypersensitivity.
  • Causes
    • Exposure to insect or plant allergen.
    • Drugs
    • Vaccine

Interaction of an inciting substance with Ig E and mast cell results in mast cell degranulation, release of histamine and systemic vascular dilatation, increased vascular permeability and tissue hypoperfusion.

• Neurogenic shock
  • Causes
    • Trauma (particularly nervous system)
    • Electrocution (Lightening stroke)
    • Fear
    • Emotional stress

Here autonomic discharge that results in peripheral dilatation followed by venous pooling of blood and tissue hypoperfusion. When compared to anaphylactic and endotoxic shock wherein cytotoxic plays a major role in intial peripheral vascular dilatation.

• Septic shock
  • Common type of shock associated with blood maldistribution.
  • Here components of bacteria or fungi (endotoxin, a lipopolysaccharide within the cell wall of gram negative bacteria) which are released from degenerating bacteria is potent stimulus and causes for septic shock.

Pathogenesis of shock

• Ischaemic shock

Septic shock

Vasoactive principles

Symptoms of shock

• Lethargy; recumbent; weak pulse rate
• Cold extremities
• Anxiousness
• Shallow breathing

Microscopical appearance

• Venules and capillaries engorged with blood
• Fat embolism in lungs – traumatic shock
• Fatty degeneration and necrosis in liver / heart
• Renal tubular necrosis – casts in tubules
• Adrenal cortex is foamy, due to depletion of cholesterol

Significance and results

• Recovery – on blood transfusion / supportive treatment
• Death – irreversible shock
• Renal insufficiency
  • Oliguria, anuria, uraemia
  • Pigment casts in tubules
  • Inflammatory oedema compresses renal parenchyma
  • Ischaemia – due to vascular collapse
  • Tubular degeneration and necrosis
• Cardiac failure
• Cerebral ischaemia - decreased BP → Anoxia → Neuronal degeneration

↓

Encephalomalacia

↓

Death         

  

• Pulmonary infection – Pulmonary oedema → Bacterial growth

Morphology of shock

• Hypoxic cell injury
• Brain – Neurons – reversible cell injury
  • Irreversible cell injury (ischaemic encephalopathy)
• Heart – Subpericardial / Subendocardial haemorrhages and necrosis
• Kidneys - Acute tubular necrosis
• Lungs
  • Resistant to hypoxic cell injury
  • Not affected in hypo volumic shock
  • But changes seen in endotoxic or neurogenic shock
• GIT – patchy mucosal haemorrhages “Haemorrhagic enteropathy”
• Liver – Fatty changes / central necrosis

Macroscopical appearance

• Haemorrhages – Pale tissues
• Increased vascular permaeability – Oedematous tissues
• Passive congestion of liver, kidneys, lungs, intestines
• Petechiae on serous surfaces
• Fatty changes ← necrosis in liver, kidney, heart
• Pulmonary oedema and congestion
• Kidneys enlarged, pale cortex, red – blue pyramids
• Adrenal cortex – brilliant yellow – early stage reduced size / Pale – Later stage