SHOCK

Guided By: Dr. Ramdas Balakrishna

Presenter: Dr. Joseph John P.G student The Dept Of Oral & Maxillofacial Surgery

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 Distributive Shock:-

Traumatic shock
Cardiogenic Shock Extracardiac obstructive Shock

Septic shock
Anaphylactic shock

Neurogenic Shock:vasovagal or vasogenic shock

psychogenic shock.

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.

Etiology
DISTRIBUTIVE (VASODILATORY) SHOCK SIRS (Systemic Inflammatory Response Syndrome) Sepsis Pancreatitis Extensive burns Multiple traumatic injuries Anaphylaxis Toxic ingestions Insect bites Transfusion reactions Heavy metal poisoning Narcotics Barbituates Anesthetics Neurogenic shock Spinal cord injury Cerebral damage

HYPOVOLEMIC SHOCK
External blood loss Trauma GIT bleeding Massive hemoptysis Internal blood loss Ruptured aortic aneurysm Hemothorax Hemoperitoneum Loss 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 SHOCK Myopathic (reduced contractility) Cardiomyopathy Advanced septic shock Myocarditis Severe acidosis Arrhythmogenic Tachyarrhythmias Bradyarrythmias Intracardiac mechanical abnormalities Papillary muscle rupture resulting in acute severe mitral regurgitation Acute aortic insufficiency from an aortic dissection Critical aortic stenosis Septal rupture Inadequate diastolic filling Massive pulmonary embolus Tension pneumothorax Severe pulmonary hypertension Severe constrictive pericarditis Positive pressure ventilation Intracardiac tumors

Stages Of Shock
An initial non progressive phase Compensatory stage progressive stage irreversible stage / Refactory Stage

AN INITIAL NON PROGRESSIVE PHASE Cells Deprived of O2 Reduced Production Of ATP Activation Of Alternate Mechanism, ANAEROBIC METABOLISM Damage to Cell Membrane

Production Of Lactic acid, Pyruvic acid

Development of SYSTEMIC MEABOLIC ACIDOSIS

COMPENSATORY STAGE Body tries to intervene

Hyperventilation Occurs

Activation of Baroreceptors

Release of Adrenaline & Nor adrenaline

Blood re routing Vasoconstruction Oligourea Increase in B.P & heart rate

PROGRESSIVE STAGE When Compensatory Mechanism Fails, This Stage Activates

Blood trap in these capillaries

Increase in H.P

Decreased perfusion
Histamine release Anaerobic metabolism Continues Leakage of fluid to extra cellular space Blood Conc. And viscosity increases Increase in metabolic acidosis Arteriolar and pre capillary sphincters construct

Slugging of micro circulation

Further compensate the perfusion to vital organs

General Symptoms/Signs
1. 2. 3. 4. 5. 6. 7. 8. Cardiovascular System Nervous System Pulmonary System Skin Kidneys GI System Hematologic System Diffuse cellular injury

General Symptoms/Signs
1. 2. 3. 4. 5. 6. 7. 8. Cardiovascular System Nervous System Pulmonary System Skin Kidneys GI System Hematologic System Diffuse cellular injury

General Symptoms/Signs
1. 2. 3. 4. 5. 6. 7. 8. Cardiovascular System Nervous System Pulmonary System Skin Kidneys GI System Hematologic System Diffuse cellular injury

General Symptoms/Signs
1. 2. 3. 4. 5. 6. 7. 8. Cardiovascular System Nervous System Pulmonary System Skin Kidneys GI System Hematologic System Diffuse cellular injury

General Symptoms/Signs
1. 2. 3. 4. 5. 6. 7. 8. Cardiovascular System Nervous System Pulmonary System Skin Kidneys GI System Hematologic System Diffuse cellular injury

General Symptoms/Signs
1. 2. 3. 4. 5. 6. 7. 8. Cardiovascular System Nervous System Pulmonary System Skin Kidneys GI System Hematologic System Diffuse cellular injury

General Symptoms/Signs
1. 2. 3. 4. 5. 6. 7. 8. Cardiovascular System Nervous System Pulmonary System Skin Kidneys GI System Hematologic System Diffuse cellular injury

General Symptoms/Signs
1. 2. 3. 4. 5. 6. 7. 8. Cardiovascular System Nervous System Pulmonary System Skin Kidneys GI System Hematologic System Diffuse cellular injury

General Symptoms/Signs
1. 2. 3. 4. 5. 6. 7. 8. Cardiovascular System Nervous System Pulmonary System Skin Kidneys GI System Hematologic System Diffuse cellular injury

Do not wait !
Start the management measures immediately

The Pulmonary Artery Catheter (SwanGanz 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
Hypovolemic Distributive Cardiogenic

CVP
/

CO

SVR

SvO2

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

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

Parameter

Class I

Class II

Class III

Class IV

% loss of blood volume

< 15%

15-30%

30-40%

> 40%

Heart rate

< 100

> 100
Mildly decreased

> 120
Severely decreased Confused

> 140

Urine output

Anuric

Mental Status

Anxious

Agitated

Lethargic

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. 2. 3. 4. 5. 6. Calculate total blood volume Determine the % of blood loss Multiple total blood volume by the % loss Replacement by: Colloid fluids, 1.5 times the result in step 3. Crystalloid fluids, 4 times the result in step 3.

 Blood: 500 ml whole blood increases Hct 2-3%, 250ml Packed RBCs 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 Shock
Results 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
SIRS Requires 2 of the following: a. Temp >38.3 or <36.0 C b. Tachypnea (RR>20 ) c. Tachycardia (HR>90, in the absence of intrinsic heart disease) d. WBC > 10,000/mm3 Severe SIRS Must meet criteria for SIRS, plus 1 of the following: a. Altered mental status b. SBP<90mmHg or fall of >40mmHg from baseline c. Impaired gas exchange d. Lactic acidosis (pH<7.30 & lactate > 1.5 x upper limit of normal) e. Oliguria or renal failure (<0.5mL/kg/hr) f. Hyperbilirubinemia g. Coagulopathy (platelets < 80,000100,000/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

Formation of micro thrombi

D.I.C
Infarction of organs and bleeding Worsening of shock Multi organ failure Death

Hypoxic injury to endothelium

Coagulation cascade

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, Tetracycline 2. Analgesics Acetyl salicylic acid, NSAIDS, Morphine 3. Antianxiety drugs Barbiturates 4. 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: 1020mg 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 untreated E.g. : untreated diabetes Results due to an extreme loss of bodily fluid E.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 Loves 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. Petersons 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.