SHOCK DR. AMITHA DEPT OF ORAL & MAXILLOFACIAL PATHOLOGY

WHAT IS SHOCK TYPES OF SHOCK ETIOLOGY AND PATHOGENESIS OF SHOCK STAGES OF SHOCK PATHOPHYSIOLOGIC CHANGES CLASSIFICATION OF SHOCK HYPOVOLEMIC SHOCK SEPTIC SHOCK TRAUMATIC SHOCK NEUROGENIC SHOCK DISTRIBUTIVE SHOCK ANAPHYLATIC SHOCK BURN SHOCK TREATMENT OF SHOCK.

CONTENTS

Shock or Cardiovascular collapse Shock may be defined as a condition in

which circulation fails to meet the nutritional needs of the cells and at the same time fails to remove the metabolic waste products.

A final common pathway for many potentially lethal clinical events (hemorrhage,trauma, burns, large MI, massive pulmonary embolism microbial sepsis)

Shock is also defined as a clinical state of cardiovascular collapse characterised by:

An acute reduction of effective circulating blood volumeAn adequate perfusion of cells and tissues.

The end result is hypotension and cellular hypoxia and if uncompensated may lead to impaired cellular metabolism and death.

1)Primary or Initial shock Is a transient and usually benign vasovagal attack resulting from sudden reduction of venous return to the heart caused by neurogenic vasodilatation and consequent peripheral pooling of the blood.

It can occur immediately followingTraumaSevere painEmotional overreaction due to a) Fearb) Sorrow and surprisec) Sight of blood

Clinically Patient develops,signs and symptoms similar to that of syncope

Unconsciousness Weakness Sinking Sensation Pale and Clammy limbs Weak and rapid pulse and Low Blood Pressure

……Primary shock can be labelled as a severe form of syncope….Lasting few seconds to minutes.

2) Secondary (or) True shock

……occurs due to haemodynomic derangements with hypoperfusion of the cells, this type of shock is the ‘true shock’.

Systemic hypoperfusion

Initially

Hypotension Impaired tissue perfusion

Cellular hypoxia

Persistence causes

reduction in -cardiac output or -effective circulating blood volume

Reversible cellular injury

Irreversible tissue injury Death

Shock

ETIOLOGY AND PATHOGENESIS OF SHOCK

Stages of shockDeteriotion of the circulation in shock is a progressive phenomenon and can be devided arbitarily into 3 stages:1. Non – progressive (initial. Compensated

reversible)shock2. Progressive decompensated shock3. Decompensated (irreversible) shock.

Widespread vasoconstriction: In resaponse to reduced blood flow(hypotension) and tissue anoxia, the neural and hormonal factors(e.g. Baroreceptors,chemoreceptors, catecholamines, renin VEM or Vasoexitor material from hypoxic kidney). Are activated. All these bring about vasoconstriction , partiularly in the vessels of the skin and abdominal viscera. It is a protective mechanism as it causes increased peripheral reasistance, increased heart rate(tacchycadia). And incresesd blood pressure.

IRREVERSIBLE STAGE

It is the progression of shock to a stage where therapy does not help.

The Brain fails to function due to cerebral ischemia Even infusion of blood fails to restore blood pressure Multiple organ failure occurs. Depression of cellular high energy phosphates Finally, cardiac failure occurs due to decreased myocardial

activity and decreased arterial tone.

If Low Perfusion States persists:

IRREVERSIBLE DEATH IMMINENT!!

In the early stage of shock, an attempt to maintain adequate cerebral and coronary blood supply by redistribution of blood so that the vital organs(brain and heart) are adequately perfused and oxygeneted. This is achieved by activation of various neurohormonal mechanism causing WIDESPREAD VASOCONSTRICTION and by FLUID CONSERVATION BY THE KIDNEY.

Non – progressive (initial. Compensated reversible)shock

Hypotension Oliguria Tachypnea, due to pulmonary hypoperfusion Acute Respiratory Distress Syndrome (ARDS) …….. due to

pulmonary hypoperfusion. Acidosis due to anoxia of liver causing reduced clearance of

lactate.

Clinically in progressive shock…….

Fluid conservation by the kidney: the following factors may assist in restoring the blood volume and improve vennous return to the heart : release of aldosterone from hypoxic kidney.Release of ADH due to to decreased effective circulayting blood volume.Reduced glomerular filtration tateShifting of tissue fluid into plasma due to lawered capillary hydrostatic pressure.

PROGRESSIVE DECOMPENSATED SHOCK: This is a stage when the patients suffer from some other

stress or risk factors besides persistance of of the shock so that there is progressive deterioration.

DECOMPENSATED (IRREVERIBLE) SH0CK At this stage patient has features like coma, worsened heart function and progressive renal failure and it is characterised by irrreversibility of shock with tissue anoxia occupying central role an dthese are under

1.PERSISTANCE OF WIDESPREAD VASOCONSTRICTION

2.VASODILATION AND INCREASED VASCULAR PERMEABILITY

3.MYOCARDIAL ISCHAEMIA 4.CEREBRAL ISCHAEMIA 5.VASODEPPRESOR MATERIAL(VDM) 6.TUMOR NECROSIS FACTORS(TNF) 7.INTESTINAL FACTORS 8.BACTERIAL FACTORS 9.HYPERCOAGULABILITY OF BLOOD

PATHOPHYSIOLOGIC CHANGES When cardiac output fall…..Cardiogenic, Hypovolaemic

or obstructive shock….BP remain stable as long as a compensatory increase in the peripheral vascular resistance occurs.

Low B.P.

Baroreceptors

Hypothalmous impulse

Adrenal Medulla

Catcholamines

Increased peripheral vascular resistance

Chronotropic and inotropic effect

Incresaed blood flow to heart & brain

Decreased blood flow to the extremities

ULTIMATE EFFECTS OF ANAEROBIC METABOLISM

InadequateEnergyProduction

MetabolicFailure

LacticAcidProduction

MetabolicAcidosisCELL

DEATH

InadequateCellularOxygenDelivery

AnaerobicMetabolism

CLASSIFICATION of shock

Hematogenic / hypovolemic shock Septic shock Cardiogenic shock Traumatic shock Neurogenic shock Miscellaneous shock (anaphylactic shock,

insulin shock etc)

Hypovolaemic shock

Results from loss of blood or plasma volume.

This may be caused by hemorrhage, fluid loss from severe burns, or trauma.

Hemorrhage usually occurs from the small veins and systemic venules.

Clinical features

Mild shock Moderate shock

Severe shock

<20% loss of blood volume

20-40% loss of blood volume

>40% loss of blood volume

Collapse of subcutaneous veins of extremities, feet – pale & cool

Features of mild shock + oliguria

Pallor, low urinary output

Sweat – forehead, palms, feet

Pulse rate increased (but <100). BP remains normal initially, may fall in later stages

Rapid pulse, low BP

Urinary output, pulse rate, BP normal

Treatment Resuscitation Control of bleeding Extracellular fluid replacement If there is blood loss, it is best replaced

by blood. Blood substitutes cannot replace blood

Septic shock

Septic shock is caused by systemic response to a severe infection.

Occurs most frequently in elderly or immunocompromised patients or those who have undergone invasive procedure in which bacterial contamination has occurred.

Septic shock is the most common cause of mortality in the intensive care unit. It is the 13th leading cause of death overall mortality ranges from 15% in patients with sepsis to 40-60% in patients with septic shock. There is a continuum of clinical manifestations from SIRS ----sepsis ----severe sepsis ---septic shock to Multiple Organ Dysfunction Syndrome (MODS).

Overview of septic shock

In these instances, widespread vasodilation causes a sudden increase in the vascular bed capacitance, which is not adequately filled by the normal circulating blood volume

hypotension, tissue hypoperfusion, and cellular anoxia result

Patients go into shock and even die within the hour The risk of anaphylaxis must be borne in mind

when certain therapeutic agents are administered. Although patients at risk can generally be identified by a previous history of some form of allergy, the absence of such a history does not preclude the possibility of an anaphylactic reaction.

Etiology

Most commonly, this occurs in the setting of gram-negative and gram positive infections, though any agent that is capable of producing infection (viruses, fungi, parasites).

The most common organisms which cause septic shock are E.coli, Klebsiella, Proteus, Pseudomonas, Bacteroids in decreasing frequency.

Pathophysiology

Sepsis is triggered by bacteria or fungi that ordinarily do not cause systemic disease in immunocompetent hosts.

Microbes exploit deficiency in the host defenses to survive in the body.

Pathogens in turn overcome the defenses by elaborating toxins or other virulence factors.

Body fails to kill the invaders and mount a severe sepsis.

Animals have exquisite mechanisms for recognizing and responding to conserved microbial molecules.

The endotoxins of a gram negative bacterial cell wall is the best example.

The lipopolysaccharides (LPS) present on the cell wall account for their endotoxic activity.

LPS consists of 3 regions Region I – polysaccharide portion

Region II – core polysaccharide.

Region III – glycolipid (lipid A) = responsible for endotoxic activity.

Engagement of TLR on endothelial cells can lead directly to down-regulation of natural anticoagulation mechanisms.

Profound mononuclear cell activation

Presumably, this series of responses helps to isolate organisms and to trigger elements of the immune system to efficiently eradicate invading microbes.

Unfortunately, depending on the dosage and numbers of macrophages that are activated, the secondary effects of LPS release can also cause severe pathologic changes, including fatal shock.

At low doses, LPS predominantly serves to activate monocytes and macrophages, with effects intended to enhance their ability to eliminate invading bacteria

With moderately severe infections, and therefore with higher levels of LPS, cytokine-induced secondary effectors become significant. Systemic effects of the cytokines such as TNF and IL-1 may begin to be seen - fever and increased synthesis of acute phase reactants

At still higher levels of LPS, the syndrome of septic shock supervenes the same cytokines and secondary mediators, now at high levels, result in:

Systemic vasodilation (hypotension)

Diminished myocardial contractility

Widespread endothelial injury and activation, causing systemic leukocyte adhesion and pulmonary alveolar capillary damage

Activation of the coagulation system, culminating in DIC

Skin remains warm, pink well perfused Cutaneous veins remains full Pulse rate is high Intermittent spikes of fever with bouts of

chills.

Treatment Treatment of infection by early surgical

debridement or drainage , appropriate antibiotics

Treatment of shock- fluid replacement, steroids

Traumatic shock

Caused by major fractures, crush injuries, burns, extensive soft tissue injuries.

Hypovolemia due to bleeding externally and internally and due to toxic factors resulting fragments of tissue entering blood stream.

The traumatized tissue activate coagulation cascade and release microthrombi into circulation.

They occlude pulmonary vasculature. Microthrombi induce a generalized

increase in capillary permeability.

Loss of plasma into interstitial tissue throughout the body.

Depletes the vascular volume to great extent

Clinical features

Similar to those of hypovolemic shock. 2 differentiating features- Presence of peripheral and pulmonary

edema in traumatic shock.- Infusion of large volumes of fluid may be

adequate for pure hypovolemic shock, is usually inadequate for traumatic shock.

Treatment Resuscitation Local treatment of trauma and control of

bleeding. Fluid replacement Full body anticoagulation (1 IV dose of

10,000 U of heparin)

Cardiogenic shock Caused by injury to heart, MI, cardiac arrythmias

Compressive cardiac shock When the heart is compressed enough from outside to

decrease cardiac output due to pneumothorax, pericardial tamponade etc

Due to right ventricle dysfunction

Due to left ventricle dysfunction

Right heart is unable to pump blood into lungs in adequate amounts.Filling of left heart decreases.Left ventricular output decreases

Unable to maintain adequate stroke volumeEngorgement of pulmonary vasculature due to normal right ventricular output, but failure of left heart.

Clinical features Initially skin is pale and cool Urine output is low Pulse becomes rapid, arterial BP is low

Right ventricular dysfunction – neck veins distended, liver enlarged

Left ventricular dysfunction – bronchial rales heard. Gradually heart is enlarged, later neck veins are also distended.

Treatment Airway is cleared with adequate

oxygenation Large doses of heparin IV (if shock is

due to massive pulmonary embolism) For pain – morphine

Neurogenic shock Caused by paraplegia, quadriplegia,

trauma to spinal cord or spinal anesthesia.

Loss of arterial and venous tone with pooling of blood in dilated peripheral venous system.

heart does not fill normally = CO falls

Clinical features

Skin is warm ,pink & well perfused Urine output may be normal Heart rate is rapid, BP is low

Treatment Elevation of legs Fluids Vasoconstrictor drugs

DISTRIBUTIVE SHOCK

This occurs when the blood volume is normal but the capacity of the circulation is increased by marked vasodilatation

Also called as “Warm shock as the skin is not cold and clammy, as it is in Hypovolemia shock

Eg: Anaphylactic shock and neurogenic shock

ANAPHYLACTIC SHOCK

It is an allergic condition in which the cardiac output and arterial pressure often fall dramatically.

A rapidly developing, severe allergic relation that sometimes occur when an individual who has previously been sensitized to an antigen is exposed to it.

CLINICAL FEATURES

Signs of profound vasodilatation a) Warm peripheries b) Low blood pressureErythema, Urticaria Angioedema, Pallor, CyanosisBronchospasm, RhinitisOdema of the Face, Pharynx and LarynxPulmonary odemaHypovolaemia due to capillary leakNausea, vomiting, abdominal cramps.

Anaphylactic shock In humans, systemic anaphylaxis may occur after

administration of foreign proteins (e.g., antisera), hormones, enzymes, polysaccharides, and drugs (such as the antibiotic penicillin).

Initiated by a generalized IgE-mediated hypersensitivity response

Said to be due to increased histamine release by combination of antigen with IgE on mast cell and basophils

The severity of the disorder varies with the level of sensitization.

Extremely small doses of antigen may trigger anaphylaxis,

Within minutes after exposure, itching, hives, and skin erythema appear, followed shortly thereafter by a striking contraction of respiratory bronchioles and respiratory distress

Laryngeal edema results in hoarseness. Vomiting, abdominal cramps, diarrhea, and laryngeal

obstruction follow, systemic vasodilation and increased vascular permeability

BURN SHOCK

The most apparent abnormality in this is loss of plasma as exudates from burned surface

• So there is increased – Hematocrit and Hemoconcentration found.

• Complex metabolic changes seen in such patients.

Biochemical Changes Seen In Such Patients

Electrolyte imbalance:.

Hypoproteinaemia:

Hyperglycemia

Increased blood urea creatinene levels due to kidney damage in extensive burns.

CHANGES IN BLOOD Hemoconcentration due to outpouring of serum

Increased number of RBC due to outpouring of serumSludging of blood – intravascular agglutination

An abrupt fall in eosinophil count during the first 12 hour which slowly begun to increase

Increased blood viscosity.

HYPOADRENAL SHOCK

The normal host response to the stress of illness, operation, or trauma requires that the adrenals glands hyper secrete cortisol in excess of that normally required.

Hypoadrenal shock occurs in settings in which the unrecognized adrenal insufficiency complicates the host response to the stress induced by acute illness or major surgery.

Treatment for shock

BLOOD TRANSFUSION PLASMA TRANSFUSION ADMINISTATION OF PLASMA

SUBSTITUTES ADMINISTRATION OF YMPATHOMIMITIC

DRUGS LIKE EPINEPHRINE AND NOREPINEPHRINE.

ADMINISTATION OF GLUCOCORTICOIDS OXYGEN THERAPHY BY CHANGING THE POSTURE

Thank you