SHOCK

SHOCK

Presenter:Dr. Joseph John

P.G studentThe Dept Of Oral & Maxillofacial Surgery

Guided By:Dr. Ramdas Balakrishna

Introduction

• Shock is an acute state in which tissue perfusion is inadequate to maintain the supply of oxygen and nutrients necessary for normal cell function which results in widespread hypoxia.

• “As an acute, generalized , inadequate perfusion of the vital organs that, if continued, will produce serious pathophysiologic consequences.”

Classification

Hypovolemic Shock

Traumatic shock

Cardiogenic Shock

Extracardiac obstructive

Shock

Distributive Shock:-

Septic shock

Anaphylactic shock

Neurogenic Shock:-

vasovagal or vasogenic shock

psychogenic shock.

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Shock?

• Its Progressive• Positive Feedback.• Cell membrane ion pump dysfunction• Intracellular edema• Leakage of intracellular contents into the

extracellular space• Inadequate regulation of intracellular pH.

Why Shock?

• Low SVR.• low contractility.• low preload.

EtiologyDISTRIBUTIVE (VASODILATORY) SHOCK SIRS (Systemic Inflammatory Response Syndrome) Sepsis

PancreatitisExtensive burnsMultiple traumatic injuries

AnaphylaxisToxic ingestions

Insect bitesTransfusion reactionsHeavy metal poisoningNarcoticsBarbituatesAnesthetics

Neurogenic shockSpinal cord injuryCerebral damage

HYPOVOLEMIC SHOCK External blood loss

Trauma GIT bleeding Massive hemoptysis

Internal blood loss Ruptured aortic aneurysm

Hemothorax HemoperitoneumLoss of plasma volume

GI losses Diarrhea/Vomiting

Renal losses Diabetes insipitus Overzealous use of diuretics

Transcutaneous losses Extensive burns

Inadequate repletion of insensible loses

CARDIOGENIC SHOCKMyopathic (reduced contractility)

CardiomyopathyAdvanced septic shockMyocarditisSevere acidosis

ArrhythmogenicTachyarrhythmiasBradyarrythmias

Intracardiac mechanical abnormalitiesPapillary muscle rupture resulting in acute severe mitral regurgitationAcute aortic insufficiency from an aortic dissectionCritical aortic stenosisSeptal rupture

Inadequate diastolic fillingMassive pulmonary embolusTension pneumothoraxSevere pulmonary hypertensionSevere constrictive pericarditisPositive pressure ventilationIntracardiac tumors

Stages Of Shock An initial non progressive phase

Compensatory stage

progressive stage

irreversible stage / Refactory Stage

Cells Deprived of O2

Reduced Production Of ATP

Damage to Cell Membrane

Activation Of Alternate Mechanism, ANAEROBIC

METABOLISM

Production Of Lactic acid, Pyruvic acid

Development of SYSTEMIC MEABOLIC ACIDOSIS

AN INITIAL NON PROGRESSIVE PHASE

Body tries to intervene

Hyperventilation Occurs

Activation of Baroreceptors

Release of Adrenaline & Nor adrenaline

Vasoconstruction

Increase in B.P & heart rate

Blood re routing

Oligourea

COMPENSATORY STAGE

When Compensatory

Mechanism Fails, This Stage Activates

Decreased perfusion

Anaerobic metabolism Continues

Increase in metabolic acidosis

Arteriolar and pre capillary sphincters

construct

Blood trap in these capillaries

Increase in H.P

Histamine release

Leakage of fluid to extra cellular space

Blood Conc. And viscosity increases

Slugging of micro circulation

Further compensate the perfusion to vital organs

PROGRESSIVE STAGE

General Symptoms/Signs

1. Cardiovascular System2. Nervous System3. Pulmonary System4. Skin5. Kidneys6. GI System7. Hematologic System8. Diffuse cellular injury

















Do not wait !

Start the management measures immediately

The Pulmonary Artery Catheter (Swan-Ganz catheter)

1. Central venous, pulmonary artery, and pulmonary capillary pressures.

2. Cardiac output and vascular resistance.

3. Sampling of mixed venous blood.

Categories of Shock

CVP CO SVR SvO2

Hypovolemic ↓ ↓ ↑ ↓

Distributive ↓ / ↔ ↑ ↓ ↑

Cardiogenic ↑ ↓ ↑ ↓

HYPOVOLAEMIC OR HAEMATOSHOCK

• Results from blood loss.• Decreased blood volume causes a decrease in

blood pressure.• Insufficient amounts of O2 is being transported

to body tissues and organs .

HEMORRHAGIC :

• a. Trauma (RTA, interpersonal violence, Sport and athletic . injuries, Industrial accidents)

b. Gastrointestinal bleeding

NON HEMORRHAGIC :

External fluid loss Diarrhoea Vomiting Polyurea Fluid redistribution Burns

Parameter Class I Class II Class III Class IV

% loss of blood volume

< 15% 15-30% 30-40% > 40%

Heart rate < 100 > 100 > 120 > 140

Urine outputMildly

decreasedSeverely

decreasedAnuric

Mental Status Anxious Agitated Confused Lethargic

Classification Of Hemorrhagic Shock By American College Of Surgeons Committee On Trauma

PATHOPHYSIOLOGY

Loss of blood

decreased filling of the right heart( dec. in venous return)

decrease of filling of the pulmonary vasculature

decreases filling of the left atrium and ventricle

left ventricular stroke volume decreases

Drop in arterial pressure which leads to reduced perfusion to vital organs leading to multiple organ failure and finally death if

untreated

Compensatory mechanisms

• Increase in Heart Rate & Vascular Resistance.

• Increase water and Na retention.

Clinical features • Skin: cool, moist, pale skin

• Resp. rate: rate and depth are increased

• Heart rate: pulse is weak and thready, MAP is decreased, pulse pressure is narrow

• Blood pressure: increases then decreases

• Urine output: decreased

• Mentation: Loss of consciousness, restlessness, agitation, mild confusion

Management : A,B,C,D IMMEDIATE MANAGEMENT RESUSCITATION : maintenance of patent airway(A), and

breathing(B) IMMEDIATE CONTROL OF BLEEDING QUICK ASSESSMENT EXTRACELLULAR FLUID REPLACEMENT :-maintenance of

circulation and B.P DRUGS : (D)

SEDATIVES CHRONOTROPIC AGENTS INOTROPIC AGENTS VASODILATORS VASOCONSTRICTORS BETA-BLOCKERS DIURETICS

PHYSICAL EXAMINATION AND MONITORING

Immediate Management : POSITION

Immediate control of bleeding Compression

bandages/pressure packs

Local hemostatic agents

ElectroCautery Ligature of vessels

Quick examination

• The patients clothing is cut away & the whole body is visualized, palpated & examined for other injuries or bleeding sites.

• Assessment of blood loss :

• Blood loss with fractures considered as :- 1,000 to 2,000 mL for pelvic fractures, 500 to 1,000 mL for femur fractures,

250 to 500 mL for tibia or humerus fractures,

125 to 250 mL for fractures of smaller bones.

• A hematoma the size of an apple usually contains at least 500 mL of blood.

Neurological examination :

– Glasgow coma scale

Fluid replacement• Crystalloids : Fluid replacement should be started with a crystalloid

• 3 ltrs. Over a time of 45 min is sufficient or depends on the vital signs(pulse, b.p, CVP,urine output)

• In the mean time blood should be sent for cross matching

• Colloids: (ex: albumin) – Will increase osmotic pressure, watch for pulmonary

oedema – Remains in vascular space longer (several hrs)

How much Fluid?

1. Calculate total blood volume2. Determine the % of blood loss3. Multiple total blood volume by the % loss4. Replacement by:5. Colloid fluids, 1.5 times the result in step 3.6. Crystalloid fluids, 4 times the result in step 3.

• Blood: – 500 ml whole blood increases Hct 2-3%, 250ml

Packed RBC’s increases Hct 3-4%

Drugs (common in all types)

• Sedatives : to reduce pain– Morphine : 10 mg i.m– Pethidine : 100 mg i.m

• Chronotropic agents : increases H.R– Adrenaline : 1-8 mcg/min

• Ionotropic agents : inc. cardiac contractility– Dopamine : 3-10 mcg/min

• Vasoconstrictors– Phenylephrine : 20 mcg/min

Central Venous Pressure Normal value : 10-15 mm of Hg In hypovolemic shock, the blood volume is decreased, so is

the CVP is also decreased. In cardiogenic shock there is no depletion of blood volume

and the CVP remains normal.

Urine

Urine output is a good indication of severity of shock. Urine output is affected quite early even in moderate shock. It is also a good index of adequacy of replacement therapy.

Normal output : 60-70 ml/hr. In shock : <30 ml/hr

Septic ShockResults due to a severe infections Usually a bacterial

infection(gram-negative bacteria)

Definitions:• SIRS (Systemic inflammatory response syndrome• Severe SIRS• Sepsis• Severe Sepsis• Septic Shock

Venn diagram displaying the various terminology surrounding sepsis and SIRS:

(Adapted from: Marini JJ, et al. Critical Care Medicine, 2nd ed. 1997.)

Diagnostic Criteria

SIRSRequires 2 of the following:

Severe SIRSMust meet criteria for SIRS, plus 1 of the

following:a. Temp >38.3° or <36.0° Cb. Tachypnea (RR>20 )c. Tachycardia (HR>90, in the

absence of intrinsic heart disease)

d. WBC > 10,000/mm3

a. Altered mental statusb. SBP<90mmHg or fall of >40mmHg from

baselinec. Impaired gas exchanged. Lactic acidosis (pH<7.30 & lactate > 1.5 x

upper limit of normal)e. Oliguria or renal failure (<0.5mL/kg/hr)f. Hyperbilirubinemiag. Coagulopathy (platelets < 80,000-100,000/mm3, INR >2.0, PTT >1.5 x control, or elevated fibrin degredation products)

Etiology

The most frequent causative organisms are gram-negative bacteria, though any agent capable of producing infection (including viruses, parasites and fungi) may cause septic shock.

This type of shock is usually caused by dissemination of a potent endotoxin liberated from gram-negative bacteria without evidence of bacteraemia

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Pathopysiology Infections Release of toxins

Vasodialatation

Decreased B.P,C.O

Shock

Hypoxic injury to endothelium

Coagulation cascade

Formation of micro thrombi

D.I.C

Infarction of organs and bleeding

Worsening of shock

Multi organ failure

Death

Treatments

• Fluid resuscitation• Vasopressors• Antibiotics initially : empirical antibiotics later : specific antibiotics(based on appropriate culture

and sensitivity test) Empirical therapy Cephalothin (6 to 8 Gm/day I.V. in 4 to 6 divided doses), Gentamicin ( 5 mg/Kg./,day ), Clindamycin (particularly when infecting organism is

Bacteroids)

• Respiratory Support• Transfusions• Recombinant Activated Protein C• Corticosteroids• Glycemic Control

• Respiratory Support• Transfusions• Recombinant Activated Protein C• Corticosteroids• Glycemic Control

Anaphylactic Shock

Pathopysiology

Anaphylaxis is the type I hypersensitivity reaction — (immediate, antigen induced or antibody mediated.)

The resultant antigen - antibody reaction causes degranulation of mast cells, which in turn releases vasoactive amines known as anaphylatoxins.

they cause increase in capillary permeability & widespread dilatation of arterioles & capillaries.

Etiological agents:

These include drugs, insect venom or antisera (serum containing antibodies)

Drugs:1. Antibiotics — Penicillin, Tetracycline2. Analgesics — Acetyl salicylic acid, NSAIDS, Morphine3. Antianxiety drugs — Barbiturates4. Local anesthetics (methyl paraben preservative)5. Methyl methacrylate

Management 1. Epinephrine: 0.5- 1 ml of 1:1000 epinephrine s.c or i.m & repeated every 15 minutes

until improvement. If IV, 1:10000 conc.

2. Histamine (H1) antagonists: 10—20mg chlorpheniramine may be given slowly I.V. & repeated if

required for 24 hours. It counteracts the effects of histamine . It is particularly effective in the management of angioedema, pruritis &

urticaria

3. Corticosteroids: 200 mg of hydrocortisone hemisuccinate I.V.

4. Miscellaneous: Bronchodilators: Aminophyline, salbutamol or terbutaline –

for bronchospasm. Oxygen with assisted ventilation. Emergency tracheostomy for laryngeal oedema or

respiratory obstruction

Cardiogenic Shock

Results due to the inability of the heart to pump enough blood to the body

It is usually due to primary dysfunction of one ventricle : myocardial infarction chronic congestive heart failure cardiac arrhythmia pulmonary embolism systemic arterial hypertension.

Pathophysiology

Clinical features

• Pale & Cool Skin.• Reduced cardiac output: <2.2L/min.• Fall in B.P.• Stagnation of Blood in Atrium… pulmonary oedema.• Increased CVP• Low urine output.

Treatment

Can be divide into 2: Treatment of shock : Treatment of underlying cause

In case of right sided failure . pain in cases of left sided failure : morphin should be prescribed. Fulminant pulmonary oedema : diuretics.

Obstructive shock The symptoms are those of shock plus

congestion of the lungs and viscera because the heart fails to put out all the venous blood returned to it.

• Chest wall trauma : Inability to ventilate adequately

• Tension pneumothorax : Compression of lung tissue and kinking of vena cava

• Pulmonary embolus : Obstruction of the pulmonary artery & inefficient loading of RBC at the lungs

Metabolic Shock

Results due to a severe illness that goes untreatedE.g. : untreated diabetes

Results due to an extreme loss of bodily fluidE.g. excessive urination, diarrhea, or vomiting

References • Review of medical physiology by William F. Ganong – 22nd

edition.• Text book of medical physiology by Guyton & Hall – 11th

edition• Robbins, Pathological basis of diseases – 6th edition, by

Cotran, Kumar, Collins.• Baileys and Love’s Short Practice of Surgery, 23rd edition,

edited by- R.C.G. Russell, Norman S. Williams & Christopher J.K. Bulstrode, Arnold International students edition

• Oral and Maxillofacial trauma; Fonseca Walker; volume 1.• Peterson’s principles of oral and maxillofacial surgery vol. I • J Oral Maxillofac Surg. 54:292-295, 1996.• Oral Maxillofacial Surg Clin N Am 18 (2006) 261 – 273.

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SHOCK