SHOCK

 

Definition: Shock is a clinical condition characterised by decreased blood flow to vital organs due to imbalance between size of vascular bed and effective circulating blood volume and the inability of the body tissues to metabolise nutrients normally.

Decreased blood flow to vital organs like kidneys and liver by venous return will result in incomplete oxygen supply and interfered metabolism.

George W.Crile in 1899 noted important features of hypovolemic shock as failure of venous return and low central venous pressure and improvement of venous return and increased cardiac output by saline infusions.

In 1918 Cannon noted accumulation of lactic acid in tissues and improvement by giving soda bicarb.

Earlier shock used to be explained by two famous theories as

1.Vasomotor exhaustion causing low venous return and pooling of blood in larger veins.

2.Vasoconstriction causing failure of blood flow to vital organs.

 

Etiology of Shock:

1.      Severe Haemorrhage: One 13^th         to 15^th  of body weight is blood, out of which if 20% of blood is lost, it will result in severe shock by hypovolemia called by haemorrhagic/wound/surgical shock.

2.      Trauma: Severe external violence with extreme tissue damage without haemorrahage called as traumatic shock like shock in crush injuries.

3.      Burns: Shock by plasma effusion into blisters.

4.      Toxemia due to bacteria or toxins released by them in septic shock.

5.      Anaphylactic shock : By certain drugs(Insulin shock by overdosage), antigens and foreign proteins.

6.      Rough handling of visera during surgery.

 

 

 

 

 

Clinical Symptoms:

1.      General appearance: The patient is in collapsed state, unable to raise head, sunken eyes, pupils dialated, dry, anaemic and pale  mucous membranes, vomiting, partly unconscious, superficial veins in collapsed state due to lack of blood suggests peripheral circulatory impairment, cold extremities, cold sweating. In horses and camels yawing indicates anoxia.

2.      Pulse: Rapid and imperceptible with low BP.

3.      Respiration: Shallow and rapid respiration, by nervous irritation sobbing type respiration in horse and dogs called Cheyne-stokes respiration which starts slow then shallow almost imperceptible then gradually exaggerated.

4.      Urine quantity: Reduced urine (oliguria) with high concentrates and abnormal constituents.

 

 

Classification of Shock:

1.      Based on timing:

a)      Primary	b)      Secondary
Mild form	Severe form
Immediately after injury	An hour or more after
Transient	Persistent
Nervous origin	Vascular
Symptoms are Cold sweating, Decreased BP, Slow pulse rate	More severe symptoms

 

2.      Based on organ involved:

a)	Cardiogenic
b)	Vasogenic
c)	Haematogenic
d)	Neurogenic

 

3.      Based on etiology or origin and approach to treatment (Given by MacLean)

 

1.      Hypovolemic shock  is most common type produced by

a)	Blood Loss	Severe haemorrhage internal or external
b)	Plasma Loss	Burns/ parasites/protein loss
c)	Water Loss	Enteritis/Burns

 

 

 

2.      Cardiogenic shock by

 

a)	Myocardial infarction
b)	Arrythmia
c)	Cardiomyopathy(Damaged cardiac muscle)
d)	Congestive heart failure
e)	Cardiac value problems

 

3.      Distributive shock by decreased intravascular volume of blood, dialated blood vessels and decreased systemic vascular resistance.

 

Septic Shock	Anaphylactic Shock	Neurogenic Shock
Increased infection by bacteria and fungi releases endotoxin, with adverse biochemical,immunological effects like vasodialation	By histamine released from allergens,Antigens,drugs and foreign protein, increased vasodialation and capillary permeability and resulting hypotension.	Rare form by trauma to spinal cord, with sudden loss of autonomic and motor reflexes below injury level.

 

4.      Obstructive shock:

The flow of the blood is obstructed

1.	Tension Pneumothorax	Air trapped in pleural space
2.	Cardiac Temponade	Blood in pericardial space prevents venous return and contraction of heart
3.	Pulmonary Embolism	Hypercoaguble blood, venous injury and venostasis
4.	Aortic Stenosis	Resistance to systolic ejection cause decreased cardiac function

 

5.      Shock characterised by peripheral pooling of blood due to

a)      Loss of tone in resistance vessels(arterioles supplied by sympathetic nervous system) in spinal anaesthesia.

b)      Trapping of blood in capacitance vessels(liver and splanchnic vessels) in endotoxin shock.

 

 

 

 

 

 

 

 

 

Pathophysiology of Shock:

To maintain blood pressure and proper tissue perfusion 1. Adequate blood volume, 2. Effective circulatory pump and 3. Effective vasculature are required, but when one fails others compensate. But when there is no compensation body tissue perfusion is less which results in shock leading to organ dysfunction, organ failure and ultimately death.

 

		Cause of Shock
		↓
		↓ Circulating Blood Volume
		↓
↑    ↑       ↑	↑   ↑ ↑ ↑ ↑	↓Cardiac Output
↑		↓
↑		↓ Tissue perfusion and                hypotension
↑		↓
↑		Baroreceptors stimulated
↑		↓
↑		↑ Sympathetic stimulation and cardiovascular system	↑   ↑
↑		↓	↓
↑	↑Heart rate & Contractility	Arterial constriction	Venous Constriction
↑	↓	↓	↓
↓       ↓	↑Cardiac Output	↑  Blood pressure	↑ Venous Return

 

 

 

Four stages of shock

1.Initial:

Body responds by negative feed back mechanism as a defensive act of survival. Hypoperfusion leads to hypoxia, decrease of oxygen supply,decreased ATP from mitochondria, damage to lysosomal membranes, increase in anaerobic respiration in cells, increased production of lactic and pyruvic acid leading to systemic metabolic acidosis and removal of them from also requires oxygen.

2.Compensatory:

Body uses biochemical, neural and hormonal mechanisms to reverse this condition. Hyperventilation to remove CO2 from acidotic blood increasing the PH.

By decreased BP within 30 minutes sympathetic system stimulated ,baroreceptors in aortic arch and carotid sinus will stimulate glosso pharyngeal  and vagal cranial nerves(9^th and 10^th) to vasomotor center in medulla leading to sympathetic nervous stimulation causing release of norepinephrine from post ganglionic sympathetic fibres and epinephrine from adrenal medulla which causes generalised constriction of pre capillary arterioles and post capillary venous supply leading to  increased peripheral resistance to circulation by alpha receptor stimulation  and increased heart rate and force with which heart beats by beta receptors, mean while when  arteries detect hypotension, they will send the message to anterior pituitary to release ACTH to release corticosteroids from adrenal cortex to conserve sodium , and thirst centre stimulated to drink more water from 1-48 hrs during  shock.

Because of lactic acid acid accumulation in tissues, loss of tone of precapillary arterial supply and more supply of blood to tissues and because of less effective circulating volume, catecholamines cause more intense vasoconstriction of post capillary venous supply, opening of pathological arterio-venous shunts and blood bypass to certain organs and death of organs.when shunts open there is hyperdynamic shock with elevated cardiac output but really extreme cellular damage.In shock characteristic feature is failure of microcirculation than deteriorating haemodynamics. In cattle death by respiratory failure and in dogs intestines are main target.

 Arginine and vasopressin(ADH) released from posterior pituitary to conserve the body fluids by kidneys. These harmones along with adrenocorticosteroids from adrenal cortex cause vasoconstriction to conserve the fluids and sodium from kidneys, GI tract and other organs to divert blood to heart, lungs and brain.

 Renin angiotensin system is activated, which takes place lately, in which because of less blood supply to kidneys, rennin is released which will convert angio-tensinogen to angiotensin to constrict the blood vessels to send more blood to kidneys but if overall blood is less, this proves more harmful restricting more supply of blood to kidneys.

3.Progressive:

If shock is not treated at this point, it will progress where compensatory systems fail by positive feed back mechanism, by cardiovascular deterioration, depression of cardiac output by decreased blood flow to heart muscle

Decreased perfusion of cells, Sodium increases in cells and potassium leaks out.

Anaerobic metabolism leading to increased acidosis, arteriolar and pre capillary sphincters constrict so that blood remains in capillaries, increase in hydrostatic pressure and increase histamine release from damaged tissues will cause vasodialatation, sludging of microcirculation, fluid and protein  leaks outside into surrounding tissues because of increased capillary permeability.

Release of toxins like histamine,serotonin by ischemia in tissues and absorption of endotoxins from gram negative bacteria in intestines, severe vascular dilatation, generalized cellular deterioration and tissue necrosis.

BP is maintained by VEM(vasoexitatory material) causing vasoconstriction like renin, from kidneys and VDM(vasodialatory material ) like apoferritin from liver,but they will be overpowered by hypoxia and metabolic derangement.

Glucose concentration in blood will increase because of inhibition of insulin and supply of glucose to all the tissue in need of energy like brain,heart and kidneys.

 

4.Refractory stage:

Failure of recovery after treatment, no improvement in BP/Pulse,longer duration of shock,greater irreversibility.

Organ systems fail, any amount of fluid given will be released into interstitial spaces, no shock reversal,brain damage and death.

Treatment of shock:

1.ABC `s of shock.(Restoration of airway, breathing and circulation and control of infection)

2. Animal kept  in warm and well ventilated area without direct sunlight.

2.Cause of shock to be removed like stop bleeding and draining large abscesses.

3.Restore effective circulating volume, in hypovolemic shock prompt replacement of blood volume is must, whole blood if PCV below 20, plasma in burns cases, ringers lactate and soda bicarb for acidity and colloidal plasma extenders for effective restoration of volume and making up of volume by normal saline and electrolytes. Administration of electrolytes 4-8ml per kg body weight and blood 5ml/kg, slowly up till animal urinates showing adequate perfusion. Increase of peripheral resistance to blood flow is not the cause but result of shock, it is decreased by replacement of blood volume.

4.Cardiovascular drugs:

Adrenaline or epinephrine is used to stimulate the respiratory centre in brain but it also increases heart rate and raises BP and also constriction of blood vessels by alpha 2 stimulation.

5.Corticosteroids  are used like Dexamethasone(10mg/kg) and prednisolone(30mg/kg) to inhibit post ganglionic sympathetic activity to cause vasodialatation, lysosomal cell membrane stabilization and improved mitochondrial respiration and myocardial contractability.

6.CVP is monitored continuously to avoid overloading and causing pulmonary edema.

Dehydration:

It is abnormal decrease in water content of tissues and intracellular fluid. Excess loss of water can be caused indirectly by loss of electrolytes. Dehydration can be hypertonic, hypotonic or isotonic.

Water is present intracellularly and extracellularly in plasma, cell membranes will control osmotic pressure on either side.

Loss of fluids can happen by haemorrhage, burns, excess sweat, excess loss from kidneys and lungs ,by which intracellular fluid comes to extracellular and tissue dehydration occurs.

Intracellular fluid contains more Potassium and Phosphate and extracellular fluid contains sodium and chloride. Sodium and chloride lost by kidneys and skin, by vomiting and enteritis. Decreased osmotic pressure of blood by loss of fluids, inhibiting osmsoregulation in brain, decreased production of ADH leading to more water loss from kidneys.

Acidosis /Alkalosis:

Normal blood plasma is at 7.35-7.45 PH and CO2 pressure is 40 mm of Hg at 37 degree C.

Exchange of CO2 in lungs and addition of alkaline substances alter PH. Increase of CO2 causes acidity and decrease alkalinity.

In case of  vomiting , chlorides are lost, so acids are lost leading to increase in alkalosis, but in diarrhoea, sodium is lost then increase in acidity.

In inadequate kidney function, decrease of urine output leading to acidosis by uric acid retention. Acidosis by defective lungs and kidneys, abnormal metabolism leads to metabolic acidosis.

 

 

Normal compensatory mechanisms:

1.Respiratory Acidosis: Decrease of CO2 elimination leads to acidosis, The cause is depression of respiratory centre by drugs like morphine, injury to CNS and diseases like pneumonia, emphysema. The kidneys try to compensate by retaining bicarbonate, excreating acids and increased ammonia formation.

2.Respiratory Alkalosis: Increase loss of CO2 from lungs. Renal compensation by excreating more bicarbonates, retaining acid salts, decrease ammonia formation.

3.Metabolic Acidosis: Retention of fixed acids/ loss of bicarbonates due to diarrhoea, starvation/lactic acid accumulation. Lungs and kidneys compensate.

4.Metabolic Alkalosis: Loss of fixed acids/accumulation of bicarbonates/Potassium depletion by vomiting, excess intake of bicarbonate/administration of diuretics. Lungs and kidneys compensate.

Treatment:

1.Ventilation rectified by corrective respiratory difficulties.

2. Metabolic acidosis corrected by Soda bicarb, THAM(Tri hydroxyl methyl amino methane),weak alkalizing agent used in respiratory and metabolic acidosis.

3.Saline solution advised in both acidosis/alkalosis to replace electrolyte losses.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Haemorrhage or (Bleeding )

It can be arterial,venous or capillary

Cause: Trauma, or congenital diseases like haemophilia or diseases of blood vessels.

Classification:

External Haemorrhage	Internal Haemorrhage
-From open wounds	-Blood into natural or newly formed cavity
-From Natural orifices	Blood in newly formed cavity is haematoma
-Epitaxis(Nose)- -Bright red	Haemopleura-Bleeding in pleural cavity
-Haemoptysis(Lungs)-- -Bright red	Haemoperitonium-Peritoneal cavity
Haematemesis(Vomiting blood)-Dark Brown	Haematocele-Into tunica vaginalis
Melena(Faecal blood)-Blackish	Haemarthosis-Into a joint
Haematuria-Blood in urine	Haematosalphinx-Into fallopian tube
	Haematometra-Into uterus
	Haematocolpu-Into extradural portion of spinal cord.
	Haematomyelia-into spinal cord
	Apoplexy-into brain substance
	Petechiae-pin pointed haemorrahages on skin/subcutis
	Echymosis-Haemorrhagic spots on skin and subcutis.

 

 

Classification of Haemorrhage:

Primary	Secondary	Reactionary
Immediately after injury	After 14 days due to septic disintegration of clot/sloughing of portion of vessel by septic/gangrenous lesion.	(Intermediate and recurrent haemorrhage) Haemorrhage within 24 hrs after primary bleeding is stopped, by mechanical disturbance of clot in vessel/slip of ligature.

 

General methods of control of haemorrhage:

1.      By tourniquet: A cord is tied around extremities like limb, tail, penis. Always applied proximal to bleeding point. Not too tight, not kept continuously for more than 15 minutes.

2.      By esmarchs bandage: When doing operation on limb or tail, a tight bandage is applied starting from extremity upto point above the site of operation then tourniquet is applied, to drive up the blood.

3.      Thermocautery: For small blood vessels which are difficult to hold by forceps, by electrocautery apparatus.

4.      Crushing: For vessels, in which endothelial and muscular coats are ruptured  and retracted slightly into lumen and blood clots. By artery forceps, large vessels by ecraseur.

5.      Apply artery forceps: BY haemostats to small blood vessels.

6.      Torsion or twisting of a blood vessel: Twisting on long axis preventing bleeding, castration by torsion forceps.

7.      Ligature: It is the best method.

8.      Tamponing: It is packing of cavity with sterilized gauze pieces called tampon.

9.      Adrenaline: For small bleeding vessels, it will constrict the vessel.

10.  Application of Liq. Ferri per chlor, Tin. Benzoin, Colloidion, ice , cold water arrests bleeding from small vessels.

11.  Gel-foam(patented product of fibrin) applied directly to bleeding point.Gelatin sponges have same effect.

12.  Inj. of coagulen-ciba-Physiological haemostat derived from unclotted bovine blood, containing prothrombin and thrombokinase.

13.  Inj. Vitamin K-Kapilin cattle-10-20ml,dog-1ml.

14.  Calcium administration- Calcium helps in clot formation, cattle-300ml, dog-10ml.

15.  Congo-red: 10% solution for blood coagulation.

16.  Sodium Citrate 20 % solution, Sodium Iodide 10%,Formalin 10 % and gelatine 5% given I/V ,have been proved as haemostatic.