haemorrhageshock-1804141638.pptx hemorrhage

haemorrhage

1. DR. SWATI SAHU MDS FELLOW DEPT. OF ORAL & MAXILLOFACIAL SURGERY

2. HAEMORRHAGE

3. CONTENTS Defination Classification a. Based on source of blood loss b. Based on time of occurrence c. Based on visualisation of haemorrhage d. Based on clinical signs of haemorrhage 3. Pathophysiology of haemorrhage 4. Causes 5. Clinical features of acute blood loss 6. Haematological Investigations 7. Haemorrhage in oral surgery 8. Fluid Resuscitation in Haemorrhage 9. Haemostasis a. Definition b. Mechanism - vasoconstriction - Primary haemostasis - Secondary haemostasis - Tertiary haemostasis c. Methods of achieving haemostasis - Mechanical methods - Chemical methods - Thermal agents

4. DEFINITION Haemorrhage is the escape of blood from the cardiovascular system to the surface of the body or into the body tissues or cavities. The amount of blood lost as a result of hemorrhage can range from minimal to significant quantities.

5. CLASSIFICATION BASED ON SOURCE OF BLOOD LOSS BASED ON TIME OF OCCURENCE BASED ON VISUALISATION OF HAEMORRHAGE BASED ON CLINICAL SIGNS OF HAEMORRHAGE ARTERIAL VENOUS CAPILLARY 1. PRIMARY 2. SECONDARY 3. REACTIONARY 1. EXTERNAL 2. INTERNAL PETECHIAL ECCHYMOSIS HAEMATOMA

6. BASED ON SOURCE OF BLOOD LOSS ARTERIAL HAEMORRHAGE – a. Bright red b. pulsating c. vigour of flow – increased d. spurt – spurt with each heartbeat from the cut end of the artery

7. VENOUS HAEMORRHAGE a. Dark red b. Not pulsating c. Vigour of flow – less rapid d. Spurt – does not spurt

8. 3. CAPILLARY HAEMORRHAGE a. Intermediate red b. May be quite aggressive (due to strong pulse on one side of capillaries) c. Vigour of flow – oozing type d. Spurt – ooze from raw surface

9. BASED ON TIME OF OCCURENCE PRIMARY HAEMORRHAGE occurs at the time of surgery

10. 2. SECONDARY HAEMORRHAGE a. Occurs weeks after injury or even later than that b . Cause – infection c. Reopening of bleeder vessels d. Commonly seen – patients with retained root tips or foreign materials in extraction socket

11. REACTIONARY HAEMORRHAGE a. Recurrence of bleeding within 24 hours of injury or surgery b. Cause – dislodgement of clot due to - rise in blood pressure after injury - restlessness in postoperative period - coughing / vomiting - after vasoconstrictive effects of LA wears off

12. BASED ON VISUALISATION OF HAEMORRHAGE EXTERNAL HAEMORRHAGE a. Revealed haemorrhage b. bleeding onto exterior / through orifice

13. 2. INTERNAL HAEMORRHAGE a. Concealed haemorrhage b. Occurs in injury to abdominal viscera c. Rupture of spleen – common

14. BASED ON CLINICAL SIGNS OF HAEMORRHAGE PETECHIAE ECCHYMOSIS HAEMATOMA

15. PATHOPHYSIOLOGY OF HAEMORRHAGE BLEEDING HYPOVOLEMIA LOW CARDIAC OUTPUT TACHYCARDIA & SHUNTING OF BLOOD FROM SPLANCHIC VESSELS BY VENOCONSTRICTION TO MAINTAIN PERFUSION OF VITAL ORGANS LIKE BRAIN , HEART, LUNGS, KIDNEY HYPOXIA ACTIVATION OF CARDIAC DEPRESSANTS

16. ANAEROBIC METABOLISM & ALTERED CELL MEMBRANE FUNCTION CAUSING INFLUX OF MORE SODIUM & CALCIUM INSIDE THE CELL & POTASSIUM COMES OUT OF THE CELL HYPONATRAEMIC , HYPERKALEMIC, HYPOCALCAEMIC METABOLIC ACIDOSIS LYSOSOMES OF CELL GET LYSED RELEASING POWERFUL ENZYMES LETHAL TO CELL SICK CELL SYNDROME PLATELETS & COAGULANTS ARE ACTIVATED LEADING TO FORMATION OF SMALL CLOTS DIC & FURTHER BLEEDING PROGRESSIVE HAEMODILUTION LEADING TO TOTAL CIRCULATORY FAILURE

17. CAUSES OF HAEMORRHAGE Trauma Infections Local irritants Congenital malformations Surgical Due to abnormalities in clotting factors a. clotting factor deficiencies - Hereditary - Anticoagulant therapy - Liver disease b. Dysfunction of clotting Due to abnormalities in Platelets a. Deficiencies b. Excess c. Dysfunction 8. Due to systemic disease

18. CLINICAL FEATURES OF ACUTE BLOOD LOSS Increasing pallor Increasing pulse rate Restlessness Air hunger Cold clammy skin Thrist Tinnitus Blindness Blood pressure – normal / slightly raised Urinary output – reduced Haemoglobin level – may fall after some hours

19. HAEMATOLOGICAL INVESTIGATIONS Complete blood count Activated partial thromboplastin time (APTT) Prothrombin time & International normalised ratio (INR) Thrombin time (TT) Platelet count Serum for blood grouping & cross matching Factor VII clotting activity vWF antigen Ristocetin cofactor activity vWF multimers Platelet aggregation tests

20. HAEMORRHAGE IN ORAL SURGERY

21. The overwhelming majority of patients who undergo oral surgical procedures are those who have normal haemostatic mechanism. Therefore, significant or major hemorrhages are not that common in oral surgery except in patients who have a bleeding / clotting disorder or those who are on anticoagulants.

22. However, uncontrolled and persistent bleeding can occur in some healthy patients after dental extraction. Therefore , it is still important to achieve proper hemostasis in all patients during oral surgical procedures, so as to prevent excessive post-operative blood loss.

23. Hemorrhage following Oral Surgical procedures can occur due to local or systemic causes. In healthy patients the postoperative bleeding is mainly due to local causes.

24. LOCAL CAUSES BONY (OSSEOUS) BLEEDING SOFT TISSUE BLEEDING

25. SOFT TISSUE BLEEDING Soft tissue bleeding is either arterial, venous, or capillary in nature. Arterial bleeding is bright red and spurting in nature. Arteries in the soft tissues at risk during oral surgical procedures are those lies posterior portion of hard palate, greater palatine artery and the buccal artery (lies lateral to the retromolar pad)

26. Venous blood is dark red in color and flows steadily and heavily especially if the vein is large . Capillary bleeding is bright red in color and is more of a minimal ooze.

27. BONY (OSSEOUS) BLEEDING Troublesome bone bleeding originates either from nutrient canals in the alveolar region central vessels, such as the inferior alveolar artery central vascular lesions ( Hemangioma or Vascular malformation)

28. SYSTEMIC CAUSES Some patients with heriditary conditions such as hemophilia, Von Willebrand’s disease Patients with thrombocytopenia (decreased platelet count) , Leukemia, etc. Patients with uncontrolled hypertension . Patients with H/O prosthetic heart valve replacement, Stroke (Cerebrovascular accident) e.t.c ., take oral anticoagulants like Aspirin or Warfarin to prevent the occurrence of a thromboembolic episode.

29. FLUIDS RESUSCITATION IN HAEMORRHAGE CRYSTALLOIDS Crystalloids in a ratio of 3:1 (3 ml of crystalloid for every ml of shed blood) - first line of fluid in haemorrhagic shock If the only available fluid is crystalloid then, ringer lactate is preferred over NS because it does not produce the hyperchloremic acidosis and the concern of lactate in RL causing acidosis is some what unfounded RL is more acidic, slightly hypotonic and contains calcium which may cause blood to coagulate if used with packed red blood cells (PRBC) or whole blood. Hypertonic saline dextran (HSD) and hypertonic saline (HS) improve hemodynamic and metabolic responses, modulate immune function and reduce brain oedema

30. COLLOIDS Colloids [ Gelatins , various Hydroxy ethyl starches (HES) and albumin] are more effective than crystalloids for expanding the plasma volume because they contain large, poorly diffusible solute molecules that create an osmotic pressure to keep water in the vascular space with less extravasation of fluid into the lung than RL with a resulting improvement in oxygenation

31. BLOOD & BLOOD PRODUCTS Resuscitation with whole blood, component therapy and plasma in that order best fulfil the criteria of DCR as they contribute to haemostasis in varying degrees while increasing the intravascular volume. Fresh warm whole blood (FWWB) to more efficient than component therapy or stored whole blood in correcting coagulopathy as it has fresher RBC and better functioning and concentration of platelets and plasma . The amount of fresh warm whole blood transfused is independently associated with improved 48-h and 30-day survival and the amount of stored red blood cells transfused is independently associated with decreased 48-h and 30-day survival for patients with traumatic injuries that require massive transfusion 

32. HAEMOSTASIS VASOCONSTRICTION PRIMARY HAEMOSTASIS SECONDARY HAEMOSTASIS TERTIARY HAEMOSTASIS MECHANISM

33. VASOCONSTRICTION Damaged blood vessels – limit blood loss by slowing down flow Narrowing of lumen Controlled by – LOCAL CONTROL FACTORS Thromboxane A2 Serotonin Fibrinopeptide B SYSTEMIC CONTROL FACTORS Epinephrine from adrenal glands – stimulates general vasoconstriction

34. PRIMARY HAEMOSTASIS PLATELET PLUG FORMATION PLATELET ADHESION – D amage to blood vessels exposure of collagen fibres Integrins adherence of platelets to endothelial cells vWF forms one cell thick carpet

35. 2. PLATELET ACTIVATION – On activation, platelet releases local factors – - adenosine diphosphate (ADP) - thromboxane Causes more platelets to aggregate

36. 3. PLATELET AGGREGATION – Platelet plug is formed by self association of platelets Platelet aggregation can be inhibited naturally by – - absence of calcium - presence of prostacyclins - drugs like ASPIRIN Platelet plug – still weak ; bleed should not be wiped but DAPPED using the capillary action of dry towel

37. SECONDARY HAEMOSTASIS EXTRINSIC PATHWAY

38. INTRINSIC PATHWAY

39. TERTIARY HAEMOSTASIS Maturation of clot Cross – linking of fibrin monomers within the clot Controlled activation of fibrinolytic system CLOT RETRACTION

40. METHODS OF ACHIEVING HAEMOSTASIS MECHANICAL METHODS CHEMICAL METHODS THERMAL METHODS Pressure Haemostat Suture Ligation Adrenaline Thrombin Surgicel Surgical fibrillar Oxycel Gelfoam Microfibrillar collagen Fibrous glue Styptics Alginic acid Bone wax Fibrin sponge Ostene Electrocautery / surgical diathermy - Monopolar - Diathermy Cryosurgery Lasers

41. MECHANICAL METHODS PRESSURE Most commonly used method Simplest Firm pressure over the bleeding site for atleast 5 minutes Using fingers / gauge

42. HAEMOSTAT Causes direct occlusion of bleeding vessels

43. SUTURES & LIGATION Sutures & ties – used as ligatures to tie off blood vessels Chances of tissue reaction , injury & allergic reactions For staples, stapling devices required Ligating clips – quick & easy to apply

44. CHEMICAL METHODS ADRENALINE Causes direct vasoconstriction Applied topically 1:10000 concentration for haemostasis over oozing site

45. THROMBIN Helps in converting fibrinogen into Fibrous clot Acts as haemostat

46. SURGICEL Oxidised cellulose polymer Composed of irregular solid fibres Acts by forming acid products from partial dissolution that coagulates plasma proteins to form black / brown sticky gelatinous clot Resorbs from site – 4 to 8 weeks

47. SURGICEL FIBRILLAR Modified surgical Oxidised regenerated cellulose Adapted to irregular surfaces / inaccessible areas Complete resorption - 2 weeks

48. OXYCEL Oxidised cellulose polymer product Cellulosic acid – affinity for Haemoglobin ; leads to formation of artificial clot Applied on dry surface Bacteriostatic Available in gauge form / pellet form Composed of hollow ‘twisted tubule’ fibres

49. GELATINE SPONGE / GELFOAM / SURGIFOAM Non-antigenic Absorbable Capacity to absorb 45 times its weight in blood Resorbs completely in 4 – 6 weeks

50. AVITENE Derived from purified bovine dermal collagen Effective – capillary, venous & small arterial bleeding Attracts platelets Promote platelet plug formation Adverse effects – allergic reactions , adhesion formation, abscess formation

51. FIBRIN GLUE Biological adhesive Contains thrombin, fibrinogen , factor VII , aprotinin

52. STYPTICS & ASTRINGENTS Precipitates protein Arrests bleeding Monsel’s solution – commonly used

53. ALGINIC ACID Available in powder form Placed over bleeding site protective film forms compresses capillaries stabilizes blood clot

54. NATURAL COLLAGEN SPONGE White sponge material Non-antigenic Fully absorbable Stimulates platelet aggregation; enhances haemostasis Activates coagulation factor XI & XIII

55. FIBRIN SPONGE Non-antigenic Obtained from bovine material Applied in the bleeding site Stimulates collagen ; forms normal clot Acts as temporary plug Fully absorbed by tissues within 4-6 weeks

56. BONE WAX Consists of – - wax (white bees wax, paraffin wax & isopropyl ester of palmitic acid) - 7 parts by weight - olive oil – 2 parts by weight - phenol – 1 parts by weight Indication - bleeding from bone or chipped edges of bone Mechanism – mechanical obstruction of the osseous cavity containing bleeding vessels Disadvantage – Frequent use may lead to formation of Wax granuloma ( foreign body)

57. OSTENE New water soluble bone haemostatic agent No incidence of adverse response in cortical defect, medullary cavity or surrounding tissue

58. ELECTROCAUTERY / SURGICAL DIATHERMY THERMAL AGENTS Surgical technique that depends on thermal effects of electric current High frequency electric current is applied to specific area of the body for the purpose of removal of unwanted tissue, coagulation & to create surgical incision Frequency – 1 to 3 MHz Cleaner, safer, efficient

59. CRYOSURGERY Process of rapidly freezing tissue by exposing it to intensely low temperatures Liquid nitrogen is used GENERAL CLINICAL USES – - Solar keratosis - Seborrhoeic keratosis - Viral warts - Skin tags - Xanthelasmas - Lentigenous macules - Actinic chelitis - Erosive lichen planus DISADVANTAGES – - Delayed bleeding - Paraesthesia - Neuropathy - Nitrogen gas insulfation - Alopecia - Cartilage necrosis

60. LASERS Helps in coagulating small vessels

61. THANK YOU

62. SHOCK

63. Introduction Definition Classification Pathophysiology Stages of shock General features and effects of shock Types of shock Dental considerations in shock Management of shock in dental office Conclusion References CONTENTS

64. INTRODUCTION Shock is a physiologic event with many different causes; but if untreated it has a single clinical outcome. Mortality rate - 20%.

65. DEFINATION Shock is a life threatening situation due to poor tissue perfusion with impaired cellular metabolism, manifested in turn by serious pathophysiological abnormalities . (Bailey and love ) Shock is a term used to describe the clinical syndrome that develops when there is critical impairment of tissue perfusion due to some form of acute circulatory failure. ( Davidson’s) Shock may be defined as inadequate delivery of oxygen and nutrients to maintain normal tissue and cellular function .( Schwartz’s) The state in which profound and widespread reduction of effective tissue perfusion leads first to reversible , and then if prolonged, to irreversible cellular injury. (Kumar and Parrillo ,1995 )

66. A life-threatening clinical syndrome of cardiovascular collapse characterized by : -An acute reduction of effective circulating blood volume (hypovolemia) -An inadequate perfusion of cells and tissues ( hypoperfusion ) If uncompensated, may lead to impaired cellular metabolism and death . The clinical manifestations of shock are the result of stimulation of the sympathetic and neuroendocrine stress responses, inadequate oxygen delivery, end-organ dysfunction.

67. CAUSES OF SHOCK Severe or sudden blood loss Large drop in body fluids Myocardial infarction Major infections High spinal injuries Anaphylaxis Extreme heat or cold

68. CLASSIFICATION ACCORDING TO ETIOLOGY HYPOVOLEMIC SHOCK CARDIOGENIC SHOCK SEPTIC SHOCK OTHER TYPES : TRAUMATIC NEUROGENIC HYPOADRENAL (Harsh Mohan 4 th ed )

69. Vasovagal Psychogenic Neurogenic Hypovolemic Traumatic Burns Cardiogenic Septic (endotoxin) Anaphylactic (Bailey & Love’s short practice of surgery)

70. Hypovolemic shock Cardiogenic shock Extra cardiac obstructive shock Distributive shock Septic shock Anaphylactic shock Neurogenic shock Proposed by HINSHAW and COX (1972)

71. PATHOPHYSIOLOGY ANY CAUSE OF SHOCK LOW CARDIAC OUTPUT VASOCONSTRICTION OCCURS AS A COMPENSATION TO PERFUSE VITAL ORGANS (BRAIN, HEART, KIDNEY, LIVER, MUSCLES) BECAUSE OF VASOCONSTRICTION & TACHYCARDIA DYNAMIC CIRCULATION INCREASES TACHYPNOEA OCCURS TO INCREASE OXYGEN SATURATION PERIPHERAL VEINS CONSTRICT DIVERTING BLOOD FROM SPLANCHNIC SYSTEM TOWARDS ESSENTIAL VITAL ORGANS 1

72. SALT & WATER RETENTION ADH RELEASED RENIN ANGIOTENSIN MECHANISM GETS ACTIVATED CAUSING FURTHER VASOCONSTRICTION & ALDOSTERON RELEASE FURTHER CONCENTRATION OF URINE OCCURS DECREASED RENAL BLOOD FLOW REDUCES GFR & THEREBY URINE OUTPUT

73. WHEN SHOCK PERSISTS CARDIAC OUTPUT FALLS FURTHER HYPOTENSION & TACHYCARDIA OCCURS LEADING TO POOR PERFUSION OF CORONARIES HYPOXIA – METABOLIC ACIDOSIS RELEASE OF CARDIAC DEPRESSANTS CARDIAC (PUMP) FAILURE 2

74. 3 HYPOXIA CELL WALL DAMAGE HYPERKALEMIA, HYPONATREMIA & HYPOCALCEMIA ANAEROBIC METABOLISM LACTIC ACIDOSIS SODIUM & CALCIUM ENTERS THE CELL POTASSIUM LEAKS OUT OF THE CELL

75. FURTHER BLEEDING DISSEMINATED INTRAVASCULAR COAGULATION (DIC) PLATELETS ARE ACTIVATED FORMING SMALL CLOTS SICK CELL SYNDROME INTRACELLULAR LYSOSOMES BREAKDOWN RELEASING POWERFUL ENZYMES WHICH DESTROY OWN CELL

76. STAGES OF SHOCK 1. ANTICIPATION STAGE 2. PRE-SHOCK STAGE 3. NON-PROGRESSIVE (INITIAL, COMPENSATED REVERSIBLE) SHOCK 4. PROGRESSIVE DECOMPENSATED SHOCK 5. DECOMPENSATED (IRREVERSIBLE) SHOCK

77. 1. ANTICIPATION STAGE

78. 2. PRE-SHOCK STAGE

79. 3. NON- PROGRESSIVE (COMPENSATED) SHOCK

80. 4 . PROGRESSIVE / DECOMPENSATED SHOCK

81. 5 . DECOMPENSATED (IRREVERSIBLE) SHOCK

82. GENERAL CLINICAL FEATURES OF SHOCK Hypotension (Systolic BP<100mmHg) Tachycardia (> 100/min) Cold , Clammy Skin Rapid, Shallow Respiration Drowsiness, Confusion, Irritability Oliguria (Urine Output<30ml/hour) Elevated or Reduced central venous pressure Multi-Organ Failure

83. HOW TO MEASURE AMOUNT OF BLOOD LOSS ??????

84. SWAN GANZ CATHETER

85. GENERAL PRINCIPLES OF MANAGEMENT OF SHOCK Patients should be treated in ICUs preferably Continuous electrocardiographic monitoring Pulse oximetry A reduction of elevated serum lactate levels is one good indicator of successful resuscitation and is often used as a therapeutic goal

86. Airway: Does patient have mental status to protect airway? GCS less than “eight” means “intubate ” (E4 V5 M6) Airway is compromised in anaphylaxis Breathing: If patient is conversing, A & B are fine Place patient on oxygen Circulation: Vitals (HR, BP) IV, start fluids, put on continuous monitor INITIAL ASSESSMENT - ABC

87. In a trauma, perform ABCDE, not just ABC Deficit or Disability - Assess for obvious neurologic deficit - Movement of all four extremities? Pupils? - Glasgow Coma Scale (V5, M6, E4 ) Exposure - Loosening of clothing on trauma patients.

88. FLUIDS & ELECTROLYTES IN SHOCK

89. It is an effective, and efficient method of supplying fluid directly into intravenous fluid compartment producing rapid effect ,with availability of injecting large volume of fluid more than any other method of administration . IV THERAPY

90. BODY FLUIDS COMPARTMENT

91. Insensible fluid input – 300 ml oxidation Insensible fluid loss – skin+lung+stool =1000ml Normal daily insensible fluid loss = 700 ml Daily fluid requirement = UO + insensible losses INSENSIBLE FLUID LOSS

92. 1. Mole : 1 mole is atomic wt or mol wt of that substance in gms 2. Equivalent : atomic wt (mole) * valence 3. Osmolality : number of moles of a chemical compound that contributes to the solution's osmotic pressure and is expressed as mOsm /kg of water 4. Osmolarity : number of osmoles of solute particles per unit volume of solution ( mosm /L) 5. Osmotic pressure : pressure exerted by osmotically active particles in the fluid. depends on number of particles / unit vol DEFINATIONS

93. 6. Plasma osmolality : determined largely by sodium salts Normal plasma osmolality = 275-295 mosm /kg Plasma osmolality = 2*Na + glucose/18 + BUN/2.8 7. Effective plasma osmolality : determined by those solutes in plasma which do not permeate cell wall freely and act to hold water within ECF Effective osmolality = 2*Na + glucose/18

94. Electrolyte Composition of fluid Compartments

95. Intravenous fluid therapy Indications 1. Coma, anaesthesia, Severe vomiting and diarrhoea, D ehydration and shock 2. Hypoglycemia 3. Vehicle for – antibiotics, chemotherapy agents 4. TPN 5. Critical problems – anaphylaxis, status asthmaticus or epilepticus , cardiac arrest , forced diuresis in drug overdose, poisoning

96. Advantages - Accurate , controlled and predictable way of administration - Immediate response due to direct infusion - Prompt correction of serous fluid and electrolyte disturbances

97. Disadvantages - More expensive, need asepsis, and under skilled supervision - Improper selection of type, volume , rate and technique can lead to serious problems Contra indications - Avoided if patient can take oral fluids - CHF, pulmonary edema

98. Complications 1. L ocal : hematoma , infusion phlebitis 2. systemic : - Large volume can lead to circulatory overload - Rigors, air embolism - Septicemia - others – fluid contamination, mixing of incompatible drugs

99. TYPES OF IV FLUIDS:

100. CRYSTALLOIDS: Isotonic, Hypotonic and Hypertonic

101. ISOTONIC SOLUTIONS INDICATIONS : Isotonic solutions contain electrolytes such as Nacl,KCL,Cacl and sodium lactate. Indicated in the treatment of vascular dehydration, replaces sodium and chloride. 5%D/W is isotonic when infused but becomes hypotonic when dextrose has been metabolized. Use cautiously in patients who are fluid-overloaded or who would be compromised if vasscular volume would increase such as renal and cardiac patients.

102. ISOTONIC FLUIDS AND THEIR USES 0.9% Nacl Lactated Ringers’ D5W

103. HYPOTONIC SOLUTIONS INDICATIONS ( <250mOsm/L) 0.45% Nacl ½ normal saline

104. HYPERTONIC SOLUTIONS INDICATIONS 5%Dextrose in 0.9% Nacl ( D5NS) 5%Dextrose in Lactated Ringers’ ( D5LR) 5% Dextrose in 0.45% Nacl (D51/2NS)

105. These contain large insoluble particles such as “gelatin”. Used if crystalloids do not improve blood volume. BLOOD can be categorized as a colloid. Act like HYPERTONIC solutions causing shifting of fluid out of the cell increasing ECF. Long lasting effect than crystalloid hence should be infused slowly and watch out for circulatory overload. USES: Emergency treatment of shock,circulatory collapse ,hypotonic dehydration. ACTIONS OF COLLOIDS: (Plasma Expanders)

106. Classification of iv fluids 1. Maintenance fluids : replaces insensible fluid losses 5 % dextrose, dextrose with 0.45 % NS 2. Replacement fluids : correct body fluid deficit gastric drainage, vomiting,diarrhoea , infection , trauma, burns 3. Special fluids : Hypoglycemia – 25 % dextrose Hypokalemia – inj Kcl Metabolic acidosis – inj soda bicarbonate

107. 5 % dextrose Composition : Glucose 50 gms Pharmacological basis : Corrects dehydration and supplies energy( 170Kcal/L) Indications : - Prevention and treatment of dehydration - Pre and post op fluid replacement - IV administration of various drugs - Prevention of ketosis in starvation, vomiting, diarrhea - Adequate glucose infusion protects liver against toxic substances - Correction of hypernatremia

108. Contra indications C erebral edema , neuro surgical procedures A cute ischaemic stroke H ypovolemic shock H yponatremia , water intoxication Same iv line blood transfusion – hemolysis , clumping occurs U ncontrolled DM , severe hyperglycemia Rate of adminstration 0.5 gm / kgBW / hr or 666ml/ hr 5 % D or 333ml/ hr 10 %D

109. Isotonic saline(0.9 % NS) Composition : Na 154 mEq , Cl 154 meq Pharmacological basis : - Provide major EC electrolytes. - Corrects both water and electrolyte deficit. - Increase the iv volume substantially Contra indications - Avoid in pre eclamptic patients, CHF, renal disease and cirrhosis - Dehydration with severe hypokalemia – deficit of IC potassium - Large volume may lead to hyperchloremic acidosis.

110. - Water and salt depletion – diarrhoea, vomiting, - Excessive diuresis - Hypovolemic shock - Alkalosis with dehydration - Severe salt depletion and hyponatremia - Initial fluid therapy in DKA - Hypercalcemia - Fluid challenge in prerenal ARF - Irrigation – washing of body fluids Vehicle for certain drugs I ndications

111. DNS Composition : Na Cl – 154 mEq , glucose 50 gm Pharmacological basis : Supply major EC electrolytes, energy and fluid to correct dehydration Indications : Conditions with salt depletion ,hypovolemia Correction of vomiting or NGT aspiration induced alkalosis and hypochloremia Contra indications : Anasarca – cardiac, hepatic or renal Severe hypovolemic shock

112. Ringer’s lactate Composition – Na, k , cl, lactate , ca each 100 ml – sodium lactate 320 mg, Nacl -600mg, kcl-40mg, calcium chloride 27 mg Pharmacological basis : Most physiological fluid , rapidly expand s iv volume.. Lactate metabolised in liver to bicarbonate providing buffering capacity Acetate instead of lactate advantageous in severe shock.

113. Indications Correction in severe hypovolemia Replacing fluid in post op patients, burns Diarrhoea induced hypokalemic metabolic acidosis Fluid of choice in diarrhoea induced dehydration in paediatrics DKA , provides water, correct metabolic acidosis and supplies potassium Maintaining normal ECF fluid and electrolyte balance

114. Contraindications Liver disease, severe hypoxia and shock Severe CHF , lactic acidosis takes place Addison’s disease Vomiting or NGT induced alkalosis Simultaneous infusion of RL and blood Certain drugs – amphotericin, thiopental, ampicillin, doxycycline

115. Isolyte fluids

116. Isolyte G : Vomiting or NGT induced hypochloremic , hypokalemic metabolic alkalosis NH4 gets converted to H+ and urea in liver Treatment of metabolic alkalosis Contraindications : Hepatic failure, renal failure, metabolic acidosis Isolyte M Richest source of potassium (35 mEq ) Ideal fluid for maintenance Correction of hypokalemia Contraindications : Renal failure, burns, adrenocortical insufficiency

117. Isolyte P Maintenance fluid for children – as they require less electrolytes and more water Excessive water loss or inability to concentrate urine Contraindications : hyponatremia , renal failure Isolyte E Extracellular replacement solution, additional K and acetate (47mEq) Only iv fluid to correct Mg deficiency Treatment of diarrhoea, metabolic acidosis Contraindications – metabolic alkalosis

118. Effects of large volume crystalloid infusion - Extravascular accumulation in skin, connective tissue , lungs and kidney - Inhibition of GI motility - Delayed healing of anastomosis - Large volume ,rapid infusion crystalloids causes hypercoagulability. Due to reduction in AT 3 Ruttmann TG, James MF. Effects on coagulation due to intravenous crystalloid or colloid in patients undergoing vascular surgery. Br J Anesth 2002 ; 89 : 999 - 1003

119. Albumin Maintain plasma oncotic pressure – 80 % Heat treated preparation of albumin – 5%, 20% and 25% commercially available Pharmacalogical basis : 5% albumin – COP of 20 mmHg 25 % albumin – COP of 70mmHg ,expands plasma volume to 4-5 times the volume infused Rate of infusion : Adults – initial infusion of 25 gm 1 to 2 ml/min – 5% albumin 1 ml/min - 25% albumin

120. Indications : Plasma volume expansion in acute hypovolemic shock, burns, severe hypoalbuminemia Hypoproteinemia – liver disease, Diuretic resistant nephrotic syndrome In therapeutic plasmapheresis , as an exchange fluid Contraindications : Severe anaemia, cardiac failure Hypersensitive reaction

121. Dextran Dextran are glucose polymers produced by bacteria( leuconostoc mesenteroides ) 2 forms : dextran 70(MW 70,000) and dextran 40(40,000 ) Pharmacological basis : Effectively expand iv volume Dextran 40 as 10% sol greater expansion , short duration( 6hrs) – rapid renal excretion Anti thrombotic , inhibits platelet aggregation Improves micro circulatory flow

122. Indications : Hypovolemia correction Prophylaxis of DVT and post operative thromboembolism Improves blood flow and micro circulation in threatened vascular gangrene Myocardial ischemia, cerebral ischemia, PVD and maintaining vacular graft patency Priming in ECC Adverse effects Acute renal failure Interfere with blood grouping and cross matching Hypersensitive reaction

123. Precautions/CI : Severe oligo -anuria CHF, circulatory overload Bleeding disorders like thrombocytopenia. Severe dehydration Anticoagulant effect of heparin enhanced Hypersensitive to dextran Administration : Adult patient in shock – rapid 500 ml iv infusion First 24 hrs – dose should not exceed 20ml/kg Next 5 days – 10 ml/kg/ day

124. Crystalloids or colloids…??? Crystalloids – recommended as the initial fluid of choice in resuscitating patients from hemorrhagic shock Svensen C, Ponzer S… Volume kinetics of Ringer solution after surgery for hip fracture. Canadian journal of anesthesia 1999 ; 46 : 133 – 141 COCHRANE Collaboration in critically ill patients – “ No evidence from RCT that resuscitation with colloids reduces the risk of death, compared with crystalloids in patients with trauma or burns after surgery ” Roberts I, Alderson P, Bunn F et al : Colloids versus crystalloids for fluid resuscitation in critically ill patients.. Cochrane Database Syst Rev(4) : CD 000567, 2004

125. EFFECTS OF SHOCK HEART Low perfusion Low venous return Decreased cardiac output Hypotension Tachycardia Persistent shock Hypoxia Release of Myocardial Depressants Further cardiac damage

126. LUNGS Interstitial Oedema Decreased gaseous exchange Pulmonary arteriovenous shunting Tachypnoea Acute respiratory distress syndrome (ARDS) & Pulmonary Oedema

127. CELLULAR CHANGES Occurs in persistent shock Due to release of Lysosomal enzymes Alters the Cell membrane permeability Cell Death Sick Cell Syndrome

128. BRAIN Decrease in Brain perfusion Patient becomes Drowsy BRAIN IS THE LAST ORGAN TO GET UNDERPERFUSED IN SHOCK

129. KIDNEYS GFR decreases Tubular reabsorbtion of salt & water increases for Compensatory response In severe cases, tubular necrosis sets in leading to irreversible damage

130. BLOOD Alteration in cellular components including platelets Leads to DIC ( Disseminated Intravascular Coagulation) Bleeding from all organs

131. HYPOVOLEMIC SHOCK Occurs from inadequate circulating blood volume Major effects are due to decreased cardiac output and low intra cardiac pressure Severity of clinical features depends on degree of blood volume lost

132. HEMORRHAGIC : TRAUMA GASTROINTESTINAL BLEEDING NON-HEMORRHAGIC : EXTERNAL FLUID LOSS DIARRHOEA VOMITING POLYUREA FLUID REDISTRIBUTION BURNS ANAPHYLAXIS CLASSIFICATION

133. CLASSIFICATION OF ACUTE BLOOD LOSS

134. Anxiety , restlessness, altered mental state Hypotension A rapid, weak, thready pulse Cool , clammy skin Rapid and shallow respirations Hypothermia Thirst and dry mouth Distracted look in the eyes SIGNS & SYMPTOMS

135. COMPENSATORY MECHANISM

136. Blood pressure Respiration Urine output Central venous pressure ECG Swan- Ganz catheter * cardiac output * mixed venous oxygen level * vascular pressure Pulmonary artery wedge pressure CLINICAL MONITERING

137. OBJECTIVES a. Increase Cardiac Output b. Increase Tissue Perfusion The plan of action should be based on a. Primary problem b. Adequate fluid replacement c. Improving myocardial contractility d. Correcting acid-base disturbances MANAGEMENT

138. Resuscitation Immediate control of bleeding : Rest, Pressure Packing, Operative Methods Extracellular fluid replacement: a. Infusion of fluid is the fundamental treatment b. Crystalloids , for initial resuscitation for most forms of hypovolemic shock. c. After the initial resuscitation, with up to several liters of crystalloid fluid, use of colloids. Drugs 1. Sedatives 2. Chronotropic agents 3. Inotropic agents

139. As in hypovolemic shock, there is an insufficient intravascular volume of blood This form of "relative" hypovolemia is the result of dilation of blood vessels which diminishes systemic vascular resistance Examples of this form of shock : Septic shock Anaphylactic shock Neurogenic shock DISTRIBUTIVE SHOCK

140. TRAUMATIC SHOCK Primarily due to h ypovolemia from : Bleeding externally eg : open wounds , fractures Bleeding internally eg : ruptured liver , spleen Clinical features : Presence of peripheral & pulmonary edema. Infusion of large amount of fluid which is adequate in hypovolemic shock is inadequate here.

141. Traumatic tissue activates the coagulation system ↓ Release of micro-thrombi into circulation ↓ Obstruction parts of pulmonary micro vasculature ↓ Increased pulmonary vascular resistance ↓ Increased right ventricular diastolic & right atrial pressure ↓ Humoral products of thrombi induce increase in capillary permeability ↓ Loss of plasma into interstitial tissue ↓ Depletion of Vascular volume PATHOPHYSIOLOGY

142. 1. Resuscitation 2. Local treatment of trauma & control of bleeding , surgical debridement of ischemic & dead tissue & immobilization of fracture . 3. Fluid replacement - Ringers lactate, Ringers acetate, Normal saline. 4. Anticoagulants - one intravenous dose of 10,000 units of heparin MANAGEMENT

143. Primary dysfunction of one ventricle or the other Dysfunction may be due to - Myocardial infarction - Chronic congestive heart failure - Cardiac arrhythmias - Pulmonary embolism - Systemic arterial hypertension CARDIOGENIC SHOCK

144. Dysfunction of right ventricle - R ight heart unable to pump blood in adequate amount into lungs , filling of left heart decreases , so left ventricular output decreases . Dysfunction of left ventricle - L eft ventricle unable to maintain adequate stroke volume , left ventricular output & systemic arterial blood pressure decreases ,there is engorgement of the pulmonary vasculature due to normal right ventricular output , but failure of left heart

145. Cardiogenic compressive shock: Arises when heart is compressed from outside to decrease cardiac output , the cause may be * Tension pneumothorax * Pericardial t amponade * Diaphragmatic rupture with herniation of the bowel into the chest.

146. Skin is pale U rine out put is low Pulse becomes rapid & systemic blood pressure is low Right ventricular dysfunction, neck veins are distended & liver is enlarged Left ventricular dysfunction , there are bronchial rales & third heart sound heard Gradually, the heart also becomes enlarged CLINICAL FEATURES

147. Airway must be cleaned Initial measures - supplemental oxygen and, when systolic blood pressure permits, administration of i.v. nitroglycerin . Insertion of an intra-aortic balloon pump decreases ventricular after load, improving myocardial performance Revascularization - angioplasty or bypass surgery have suggested improved survival Vasodilators Beta-Blockers MANAGEMENT

148. In case of pulmonary embolus - Treated with large doses of heparin, IV Pain - Sedatives like morphine Fulminant pulmonary edema - Diuretics Drugs - Inotrophic agents

149. Flow of blood is obstructed, which impedes circulation and can result in circulatory arrest Several conditions result in this form of shock Cardiac tamponade Constrictive pericarditis Tension pneumothorax Massive pulmonary embolism OBSTRUCTIVE SHOCK

150. Pericardial drainage via surgery – Treatment of choice Pulmonary embolism usually treated with systemic anticoagulation ; massive pulmonary embolism causes right ventricular failure and shock, thrombolytic therapy should be strongly considered TREATMENT

151. NEUROGENIC SHOCK Primarily due to blockade of sympathetic nervous system  loss of arterial & venous tone with pooling of blood in the dilated peripheral venous system The heart does not fill  the cardiac output falls Neurogenic shock caused by: Paraplegia Quadriplegia Trauma to Spinal cord Spinal anesthesia

152. Dilatation of the systemic vasculature ↓ Decreased systemic arterial pressure ↓ Pooling of blood in systemic venules & small veins ↓ The right heart filling & stroke volume decreases ↓ Decreased pulmonary blood volume & left heart filling ↓ Discharge of angiotensin & vasopressin though they fail to restore the cardiac output to normal PATHOPHYSIOLOGY

153. CLINICAL FEATURES – Warm skin, pink & well perfused Heart rate is rapid Blood pressure is low Urine output may be normal

154. Assuming Trendelenburg position - displaces blood from systemic venules into right heart & increases cardiac output 2. Administration of fluids 3. Vasoconstrictor drugs - Phenylephrine & Metaraminol Only type of shock safely treated with vasoconstrictor . Its prompt action saves patient from immediate damage to important organs like brain , heart & kidney . MANAGEMENT

155. Part of neurogenic shock Pathophysiology : pooling of blood due to dilatation of peripheral vascular system particularly in the limb muscle & in splanchnic bed . This causes - reduced venous return to the heart leading to low cardiac output & bradycardia - blood flow to brain is reduced causing cerebral hypoxia & unconsciousness. Management: Trendelenberg position - increases cerebral flow - consciousness is restored VASOVAGAL / VASOGENIC SHOCK

156. Part of Neurogenic shock. Occurs following sudden fright from unexpected bad news or at the sight of horrible accident. Effect may vary in intensity from temporary unconsciousness to even sudden death. PSYCHOGENIC SHOCK

157. Most often due to gram-negative & gram-positive septicemia It occurs in cases of - - Severe septicemia - Cholangitis - Peritonitis - Meningitis etc . Organisms – - E.coli - klebsiella - aerobactor - proteus - pseudomonas - bacteroides , etc SEPTIC SHOCK

158. C aused by dissemination of a potent exotoxin liberated from gram positive bacteria without evidence of bacteremia S een in Clostridium Tetany or Clostridium Perfringes infection D ue to massive fluid losses Arterial resistance - falls N o fall in cardiac output Urine output - normal . GRAM POSITIVE SEPSIS & SHOCK

159. GRAM NEGATIVE SEPSIS & SHOCK M ost common cause - genito -urinary infection Persons who have had operations of the genito -urinary tract P atients who have undergone tracheostomy Gastrointestinal system infections The severity may vary from mild hypotension to fulminating septic shock which has a poor prognosis The prognosis is more favorable when the infection is accessible to surgical drainage .

160. PATHOPHYSIOLOGY OF SEPTIC SHOCK Toxins / endotoxins from organisms like E-coli, Klebsiella , Pseudomonas & Proteus Inflammation, Cellular activation of Macrophages, Neutrophiles & Monocytes Release of Cytotoxins , Free radicals Chemotaxis of cells, endothelial injury, altered coagulation cascade - SIRS Reversible hyperdynamic warm stage of septic shock with fever, tachycardia, tachypnoea Severe circulatory failure with MODS ( lungs, liver, kidney, heart) with DIC Hypodynamic , irreversible cold stage of septic shock

161. STAGES OF SEPTIC SHOCK

162. MANAGEMENT OF SEPTIC SHOCK Correction of fluid & electrolyte – Crystalloids , Blood transfusion Appropriate Antibiotics Treat the cause / focus – drainage of abscess , wound excision etc. Investigations – Pus, Urine , Discharge, Blood Culture & Sensitivity Critical Care - Oxygen, ventilatory support, Dobutamine / Dopamine/ Noradrenaline to maintain Blood pressure & Urine Output Activated C protein – prevents release of inflammatory mediators Monitoring – Pulse oximetry , Cardiac status, Urine output, Arterial blood gas analysis

163. Etiology : The most common cause of anaphylaxis is the administration of penicillin The other causes include anesthesia, dextrans , serum injections, stings, consumption of shell fish Pathophysiology: The antigen combines with Ig E on the mast cell & basophils releasing large amounts of histamine and slow releasing substances of anaphylaxis ANAPHYLACTIC SHOCK

164. Clinical features - Bronchospasm L aryngeal edema R espiratory distress Hypoxia M assive vasodilatation H ypotension and shock.

165. Immediate & aggressive management is imperative if the patient is to survive. Step 1: Position the patient Place the patient in a supine position with the legs slightly elevated Step 2 : A-B-C Open the airway by tilting the head. Breathing & circulation should be established carrying BLS as needed Step 3 : Definitive care As soon as a systemic allergy is suspected emergency medical help is sought. MANAGEMENT

166. PHARMACOTHERAPY 1. ADRENALINE Adrenaline (epinephrine) intramuscularly (IM) in the anterolateral aspect of the middle third of the thigh (safe, easy, and effective) Adult IM dose 0.5 mg IM (=500 μ g = 0.5 mL of 1:1000) adrenaline >12 years: 500 μg IM (0.5 mL) that is, the same as the adult dose 6-12 years: 300 μg IM (0.3 mL ) <6 years: 150 μg IM (0.15 mL ) 2. BETA – AGONIST Isoproterenol (pure beta-agonist): In patients taking beta-blockers adrenaline would be less effective Give epinephrine first If the patient is not responding to epinephrine, use isoproterenol (1 mg in 500 mL ) Continuing respiratory deterioration requires further treatment with the bronchodilators, such as salbutamol (inhaled or IV), ipratropium (inhaled ), aminophylline (0.25-0.5 g IV )

167. Chlorphenamine : (after initial resuscitation ) Dose depends on age: 12 years and adults: 10 mg IM or IV slowly 6-12 years: 5 mg IM or IV slowly 6 months to 6 years: 2.5 mg IM or IV slowly <6 months: 250 μg /kg IM or IV slowly Diphenhydramine: 50 mg or 1 mg/kg IV slowly repeated if necessary Ranitidine: 50 mg IV 8 hourly 3. ANTIHISTAMINES - 4. GLUCAGON - Atropine or glucagon IV if the patient is on beta-blocker failing to respond. 5. α – AGONISTS - Dopamine: If hypotension persists 5 μg /kg/min . Increased to 10-20 μg /kg/min.

168. 6. CORTICOSTEROIDS – Hydrocortisone : (after initial resuscitation). Dose depends on age: >12 years and adults: 200 mg IM or IV slowly. >6-12 years: 100 mg IM or IV slowly. >6 months to 6 years: 50 mg IM or IV slowly. <6 months: 25 mg IM or IV slowly.

169. 1. Through diagnosis and treatment plan Allergies Systemic review of the patient 2. Local anesthesia used during dental treatment 3. Pain and anxiety 4. Anxiety by the vision and perception of bigger and larger instrument in periodontology, oral surgery etc. 5. Shock (or) Syncope due to longer duration of treatment . DENTAL CONSIDERATIONS IN SHOCK

170. MANAGEMENT OF DELAYED ONSET, ALLERGIC SKIN TERMINATE DENTAL PROCEDURE POSITION THE PATIENT BASIC LIFE SUPPORT AS INDICATED DEFINITIVE MANAGEMENT OBSERVE PATIENT ADMINISTER ORAL ANTIHISTAMINES ADMINISTER I.M .+ORAL ANTIHISTAMINE EVERY 4-6 HOURS MEDICAL CONSULTATION MANAGEMENT OF SHOCK IN DENTAL OFFICE

171. NO SIGNS AND SYMPTOMS OF ALLERGY TERMINATE DENTAL PROCEDURE POSITION THE PATIENT(SUPINE WITH LEGS ELEVATED ) BASIC LIFE SUPPORT AS INDICATED SUMMON MEDICAL ASSISTANCE ADMINISTER OXYGEN MONITOR VITAL SIGNS DEFINITIVE MANAGEMENT

172. MANAGEMENT OF GENERALISED ANAPHYLAXIS (SIGNS AND SYMPTOMS OF ALLERGY ) TERMINATE DENTAL PROCEDURE POSITION THE PATIENT (SUPINE WITH LEGS ELEVATED ) BASIC LIFE SUPPORT AS INDICATED SUMMON MEDICAL ASSISTANCE ADMINISTER EPINEPHRINE (SC, IM, IV ) ADMINISTER OXYGEN MONITOR VITAL SIGNS ADDITIONAL DRUGS; ANTI HISTAMINES, CORTICOSTEROIDS

173. Schwartz’s Principles Of Surgery – 8 th ed. Davidson’s Principles And Practice Of Medicine – 22 nd ed. Essential Pathology- Harsh Mohan – 3 rd ed. Septic Shock: Vasopressin, Norepinephrine, and Urgency - Joseph E. Parrillo , M.D. - The New England Journal of Medicine. Understanding Hypovolemic, Cardiogenic and Septic Shock. Nursing Standard . 50,21,46-55. Sepsis, Severe Sepsis and Septic Shock in adults and anesthesia – Dr. H.M.Radford . South African Journal Of Anesthesia and Analgesia, May 2002. REFERENCES