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SHOCK AND HAEMORRHAGE...............pptx
- 1. SHOCK & HAEMORRHAGE Presented by - Dr. Vipul Gupta (MDS 1st year) (Department of Orthodontics & Dentofacial Orthopaedics)
- 2. CONTENTS • DEFINITION • CLASSIFICATION • PATHOPHYSIOLOGY OF HAEMORRHAGE • CAUSES • CLINICAL FEATURES OF ACUTE BLOOD LOSS • HAEMATOLOGICAL INVESTIGATIONS • HAEMORRHAGE IN ORAL SURGERY • FLUID RESUSCITATION IN HAEMORRHAGE • HAEMOSTASIS - DEFINITION - MECHANISM - METHODS OF ACHIEVING HAEMOSTASIS
- 3. DEFINITION Haemorrhage is defined as the escape of the blood from the cardiovascular system to the surface of the body or into the body tissues or the cavities. The amount of the blood lost due to haemorrhage can range from minimal to significant quantities.
- 4. CLASSIFICATION OF HAEMORRHAGE • Petechial • Ecchymosis • Haematoma • External • Internal • Primary • Secondary • Reactionary • Arterial • Venous • Capillary BASED ON SOURCE OF BLOOD LOSS BASED ON TIME OF OCCURENCE BASED ON CLINICAL SIGNS OF HEMORRHAGE BASED ON VISUALISATION OF HEMORRHAGE
- 5. PATHOPHYSIOLOGY OF HAEMORRHAGE • Bleeding • Hypovolaemia • Low cardiac output • Tachycardia & shutting of blood from splanchic vessels • Hypoxia • Activation of cardiac depressants
- 6. • Anaerobic metabolism & altered cell membrane function • Hyponatremia, Hyperkalemia, Hypocalcaemia, Metabolic acidosis • Lysis of cell lysosomes • Sick cell syndrome • Activation of platelets & coaggulants • Progressive haemodilution
- 7. CAUSES OF HAEMORRHAGE • Trauma • Infections • Local irritants • Congenital malformations • Surgical • Abnormalities in clotting factors • Abnormalities in platelets • Systemic disease
- 8. CLINICAL FEATURES OF ACUTE BLOOD LOSS • Increasing pallor of skin • Increasing pulse rate • Restlessness • Air hunger • Cold clammy skin • Tinnitus • Blindness • Blood pressure – Normal / Slightly raised • Reduced urinary output • Haemoglobin level – may fall after some hours
- 9. HOW TO MEASURE BLOOD LOSS • 1) Indirect method • 2) Direct method- RISA- radioactive isotope serum albumin CVP – measurement of central venous pressure
- 10. 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 • Platelet aggregation tests (viscoelastometry)
- 11. HAEMORRHAGE IN ORAL SURGERY HAEMORRHAGE LOCAL CAUSES SOFT TISSUE BLEEDING BONY (OSSEOUS) BLEEDING SYSTEMIC CAUSES HAEMOPHILIA, THROMBOCYTOPENIA, UNCONTROLLED HYPERTENSION, ORAL ANTICOAGGULANTS
- 12. COMPLICATIONS • Pneumothorax • Haemothorax • Artery rupture • Air embolism • Infection/ impaction
- 13. FLUID RESUSCITATION IN HAEMORRHAGE • Crystalloids • Colloids • Blood transfusion Blood- whole blood, fresh whole blood Blood products- a) cellular components- red cells, platelets, granulocyte concentrate b) plasma components- fresh frozen plasma, cryoprecipitate, stored plasma c) plasma derivatives- albumin, immunoglobulin, coagulation factors
- 14. HAEMOSTASIS VASOCONSTRICTION PRIMARY HAEMOSTASIS SECONDARY HAEMOSTASIS TERTIARY HAEMOSTASIS MECHANISM
- 17. METHODS OF ACHIEVING HAEMOSTASIS 1) Mechanical methods- Pressure Haemostat Suture ligation 2) Chemical methods 3) Thermal methods- Electrocautery / Surgical diathermy Cryosurgery Lasers
- 18. SHOCK
- 19. CONTENTS • Introduction • Definition • Classification • Pathophysiology • Stages of shock • Types of shock • General features & effects of shock • Dental considerations in shock • Management of shock in dental office • Conclusion • References
- 20. DEFINITION SHOCK • A life threatening situation due to poor tissue perfusion with impaired cellular metabolism, manifested in turn by serious pathophysiological abnormalities. – (Bailey & 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)
- 21. 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
- 22. CLASSIFICATION Hinshaw & COX (1972) - Hypovolemic shock Cardiogenic shock Extra-cardiac obstructive shock Distributive shock (Septic shock; Anaphylactic shock; Neurogenic shock)
- 23. PATHOPHYSIOLOGY Any cause of shock Low cardiac output Vasoconstriction Tachycardia Dynamic circulation increases Tachypnoea Constriction of peripheral veins Decreased renal blood flow Activation of renin angiotensin mechanism Salt & water retention ADH release Further concentration of urine occurs
- 24. 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
- 25. STAGES OF SHOCK 1) Anticipation stage 2) Pre-shock stage 3) Non- progressive ( initial; compensated reversible) shock 4) Progresssive decompensated shock 5) Decompensated (irreversible) shock
- 26. GENERAL CLINICAL FEATURES OF SHOCK • Hypotension ( systolic BP < 100 mm/Hg) • Tachycardia (>100/min) • Cold , clammy skin • Rapid, shallow respiration • Drowsiness, confusion, irritability • Oliguria (urine output<30ml/hr) • Elevated or reduced central venous pressure • Multi-organ failure
- 27. EFFECTS OF SHOCK ON- • Heart • Lungs • Cells • Brain • Kidneys • Blood
- 28. GENERAL PRINCIPLES OF SHOCK MANAGEMENT PCWP – pulmonary capillary wedge pressure (Swan Ganz catheter) CVP Initial assessment – ABCDE Airway Breathing Circulation Deficit/ Disability Exposure Fluids & electrolytes in shock IV fluid therapy; Crystalloids; Colloids
- 29. TREATMENT OF SHOCK 1) Hypovolaemic shock- replacement of fluids & electrolytes 2) Cardiogenic shock – fluids restricted ionotropic drugs 3) Septicemic shock – pus, if any is drained first culture & sensitivity test to acertain the causative bacteria antibiotics 4) Neurogenic shock – Trendlenberg position
- 30. DENTAL CONSIDERATIONS 1) Through diagnosis & treatment plan allergies systemic review of patient 2) LA used during treatment 3) Pain & Anxiety 4) Shock or Syncope due to larger duration of treatment 5) Anxiety by vision & perception of bigger & larger instruments
- 31. MANAGEMENT OF SHOCK IN DENTAL OFFICE Management of delayed onset, allergic skin Terminate dental procedure Position of patient BLS as indicated Definitive management (a) observe (b) administer oral histamines > medical consultation (c) administer I.M + Oral antihistamines every 4-6 hrs
- 32. • No signs & symptoms of allergy • Terminate dental procedure • Position of patient with legs elevated • BLS • Medical assistance • Administer oxygen • Vital signs • Definitive management
- 33. • Management of generalised anaphylaxis • Terminate dental procedure • Supine position of patient with legs elevated • BLS • Medical assistance • Administer epinephrine • Administer oxygen • Monitor vital signs • Additional drugs, antihistamines, corticosteroids
- 34. REFERENCES • 1) Schwartz’s principle of surgery – 8th ed. • 2) Essential pathology – Harsh Mohan – 3rd ed. • 3) Davidson’s principles & practice of medicine – 22nd ed. • 4.) Short practice of Surgery – Bailey And Love’s – 24th ed.
Editor's Notes
- ARTERIAL- bright red, pulsating, spurting, inc. flow VENOUS- dark red, non pulsating, steady flow, dsnt spurt CAPILLARY- intermediate red, even flo/ oozing type, 1 haem – occurs at time of surgery, due to injury to blood vessel, fracture of any bone 2 haemorrhage- occurs within 7-14 days after surgery, causes are infection ( necrosis of bv) , commonly seen in pt with retained root tips or foreign materials in extn socket; dangerous n difficult to control Reactionary haemorrhage- occurs within 24 hrs of injury due to seepage of suture or ligature leading to clot dislodgement Exteranal h- revealed; bleeding onto exterior through orifice Internal h.- concealed h ; occurs in injury to abdominal viscera; rupture of spleen is most common; other eg- fracture of any long bones n bleeding frm malignancy
- TACHYCARDIA- ----- vessels by vasoconstriction to maintain perfusion of vital organs like brain, heart, lungs n kidney
- ANAEROBIC- ---- function causing influx of more sodium n calcium inside d cell n potassium comes out of cell LYSIS OF ---releasing powerful enzymes lethal to cell ACTIVATION----- leading to formation of small clots n further bleeding PROGRESS--- leading to total circulatory failure
- ABNO IN CLOTTING FACTRS- 1) clotting factr deficiency- hereditary, liver diseases, anticoagulant therapy 2) dysfnctn of clotting ABNRM IN PLATELETS- deficiencies, excess , dysfunction Systemic diseases like – scleroderma, cirrhosis, retinal haemorrhage
- INDIRECT M- any blood clot size of fist is around 500 ml in closed fracture; swelling in lower leg indicates blood losss of 1L ; swelling in thigh- 1.5L blood loss RISA- it cn b done only in specialised centres where radioactive isotopes r available; it can be tagged with RBCs n dilution can b measured on isotope counter; it helps in measuring total amount of blood loss CVP- measured by passing a canula of length 20-25 cm through int. jugular vein into superior vena cava; this canula is attached to pressure manometer which is measured at lvl of sternal angle( norm. at sternal angle it is 0) if cvp is low, it means venous reservoir has low pressure n intra venous infusion is required; if cvp is high, iv infusion is contraindictory as it may cause pulmonary oedema– in cardiogenic shock
- Haemorrhage following oral surgical procedures can occur due to local or systemic causes. In healthy pt, the post operative bleeding is mainly due to local causes--- ST BLEED- arterial, venous , capillary in nature. Arteries in ST at risk during os procedures r those that lies in post portion of hard palate, GP artery n Buccal artery ( lies lateral to retromolar pad) OSSEOUS – troublesome bone bleeding originates either frm- nutrient canals in alveolar region; centrl vessels lyk inf. Alveolar artery; central vascular lesions ( haemangiomas or vascular malformation) Systemic- some pt with hereditary conditions lyk hemophilia, vW disease pt with thrombocytopenia (dec platelet count) leukemia etc pt with uncontrolled hypertension pt with history of prosthetic heart valve replacement, stroke, taking oral anticoagulants like aspirin or warfarin to prevent occurrence of a thromboembolic episode
- Crystalloids- for every 1 ml of shed blood, 3ml of crystalloid is used. It is the 1st line of fluid in haemorrhagic shock; ringers lactate – hypertonic saline r examples Colloids- gelatins, albumin n various hydroxy ethyl starches are examples… these r more effective than crystalloids for expanding plasma vol bcz they cntain large, poorly diffusible solute molecules that create an osmotic pressure to keep water in vascular space with less extravasation of fluid into lungs Blood– resuscitation with whole blood , component therapy n plasma in that order contribute to haemostasis in varying degrees while increasing the intra vascular volume fresh warm whole blood is more efficient than component therapy or stored whole blood in correcting coagulopathy as it has fresher RBC n better functioning n conc of platelets n plasma blood transfusion is d transfer of blood n its products frm 1 person to other person. Depending on d type of donor it can be autologous ( pre op , intra op, post op ) and frm blood bank. Depending on blood components used…. Blood products RBC transfusion is most commonly used n its indications r anaemia, trauma, any major surgeries indication for platelet n clotting factor transfusion is bleeding disorder Indication for plasma cell transfusion is liver isease n burns
- Vasoconstriction- controlled by local n systemic factors. Local involves thromboxane a2 , serotonin, fibrinopeptide b . Systemic includes- epinephrine from adrenal glands which stimulates general vasoconstriction
- In primary haemostasis, there is platelet plug formation. Firstlt there is platelet adhesion in which damage to blood vessel exposes collagen fibers which causes platelets to adhere to endothelial cells leading to release of integrins n vWF resulting in formation of 1 cell thick layer Then platelets r activated n releases adenosine diphosphate n thromboxane which causes more platelets to aggregate.
- Vasoconstriction--- occurs as a compensation to perfuse vital organs like brain, heart, kidney , liver, muscles Tachypnoea- to increase oxygen saturation Constriction--- veins that will diverge blood frm splanchnic system towards essential vital organs Dec re---- flow– reduces gfr n thus reduce urine output RAAS- further vasoconstriction n aldosterone releases
- CVP DECRESES AS VOLUME DECREASES IN HYPOVOLEMIC SHOCK, WHIKE IN CARDIOGENIC SHOCK IT REMAINS NORMAL