Uploaded bySiddhartha Sinha
Shock
The document outlines the aetiopathogenesis, clinical features, and management principles of shock in orthopaedics, defining it as a systemic state of low tissue perfusion. It discusses different types of shock, including hypovolemic, cardiogenic, obstructive, and distributive shocks, along with their causes, consequences, and stages. Finally, it details management strategies such as fluid resuscitation, controlling blood loss, and the use of vasopressors and inotropes based on the patient's response.
More Related Content
More from Siddhartha Sinha
Shock
- 1. Shock Dr Siddhartha Sinha (Dept.of Orthopaedics)
- 2. Competency • Describe anddiscuss the aetiopathogenesis, clinical features, investigations and principles of management of shock
- 3. SLOs • By theend of the lecture students should be able to 1. Define shock 2. Describe and discuss the aetiopathogenesis of shock in orthopaedics 3. Discuss and classify different types of shock. 4. Identify and differentiate the clinical features of different types of shock. 5. Describe in detail the principles involved in management of shock
- 4. Definition • Shock isa systemic state of low tissue perfusion which is inadequate for normal cellular respiration.
- 5. Pathophysiology 1. Low tissueperfusion 2. Insufficient delivery of oxygen and glucose 3. Switch from aerobic to anaerobic metabolism
- 6. Shock Hypotension Decreased perfusion to tissues Cellular hypoxia Reversiblecellular injury initially Cause persists Irreversible cellular injury and cellular death Cause resolved Possibility of recovery Systemic Hypoperfusion
- 7. Persistence of ischemia –Activation of the immune and coagulation systems. – Complement and prime neutrophils activation – Generation of oxygen free radicals and cytokine – Injury to capillary endothelial cells- tissue edema & hypoxia – Further activation of immune and coagulation systems (vicious cycle)
- 9. Systemic effects ofshock Cardiovascular Increased sympathetic activity Catecholamine release: Vasoconstriction (except in septic shock) & tachycardia Respiratory Increased respiratory rate Increased minute ventilation (respiratory alkylosis-compensate for metabolic acidosis) Renal Decreased GFR Decreased U.O. RAAS activation- vasoconstriction and Na & water absorption Endocrine RAAS ADH (hypothalamus) Cortisol (also help sensitize cells to effect of cathecolamine)
- 11. Types of Shockand Characteristics Type of Shock CW and PCWP Cardiac Output Systemic Vascular Resistance Venous 02 Saturation Base Deficit Hypovolemic ↓ ↓ ↑ ↓ ↑ Cardiogenic ↑ ↓ ↑ ↓ ↑ Obstructive ↑ ↓ ↑ ↓ ↑ Distributive ↓ ↑ ↓ ↑ ↑
- 12. Hypovolemic Shock • Mostcommon • Reduced circulating volume. – Hemorrhagic – Non Hemorrhagic: • Poor intake • Excessive loss (vomiting, diarrhea, urinary loss, Diabetes Mellitus/Incipidus) • Burns
- 14. Cardiogenic shock • Primaryfailure of the heart to pump blood to the tissues • Causes: – Myocardial infarction, – Cardiac dysrhythmias, – Valvular heart disease, – Blunt myocardial injury – Cardiomyopathy. – Endogenous factors (e.g. bacterial and humoral agents released in sepsis) – Exogenous factors, such as pharmaceutical agents or drug abuse.
- 15. Obstructive shock • Reducedfilling of the left and/or right sides of the heart – Mechanical obstruction • Decreased preload • Fall in cardiac output. • Causes: – Cardiac tamponade – Tension pneumothorax – Massive pulmonary embolus or air embolus
- 16. Distributive shock • Inadequateorgan perfusion is accompanied by vascular dilatation with hypotension, • Low systemic vascular resistance, inadequate after-load and • Abnormally high cardiac output. • Causes: – Septic shock (bacterial endotoxin) – Anaphylaxis (histamine release) – Spinal cord injury. (failure of sympathetic outflow and adequate vascular tone)
- 17. Endocrine • Combination ofhypovolemic, cardiogenic or distributive shock • Causes – Hypo- and hyperthyroidism – Adrenal insufficiency.
- 18. Staging and Gradingof Shock
- 19. Stages of shock 1.Pre shock: (warm shock/ compensated shock), all insults being successfully compensated by body 2. Shock: no compensations and appearance of clinical features 3. End organ dysfunction: irreversible organ damage and loss of function
- 20. Compensated Mild ModerateSevere Blood loss 0-15% 15-30% 30-40% >40% Level of consciousness Normal Mild anxiety Drowsy, mild confusion Comatose Pulse Mild increase, Cool peripheries, CFT increased Increased, Cool peripheries, increased CFT Increased Increased, cold peripheries Respiratory rate Normal Increased Increased Labored BP Normal Normal Mild hypotension Severe hypotension Pulse pressure Decreased Decreased Decreased Narrowed pulse pressure (or immeasurable diastolic pressure) Urine output Normal Normal Reduced (<.0.5mL/kg/hr Anuric Lactic Acidosis + ++ ++ +++
- 21. Compensated shock • Decreasedflow to non essential organs. • Aims to preserve preload and flow to essential organs – Lungs – Brain – Kidney • Tachycardia and cool extremities • Clinically occult – leads to multiple organ failure and death if prolonged due to the ischaemia–reperfusion effect
- 22. Ischaemia–reperfusion syndrome • Cellularinjury occurs once normal circulation is restored to hypoperfused tissues. • Acid and potassium load – direct myocardial depression – vascular dilatation • Cellular and humoral elements activated by the hypoxia (complement, neutrophils, microvascular thrombi) are flushed back into the circulation where they cause further endothelial injury (sp kidney and lungs) • Prevent by reducing the extend and duration of tissue hypoperfusion. hypotension
- 23. Decompensation • BP fallsusually when 30-40% of circulating volume has been lost • Upto 15% loss can be compensated well.
- 24. Consequences of shock Unresuscitatableshock • Ability of the body to compensate is lost. • myocardial depression and loss of responsiveness to fluid or inotropic therapy • loss of the ability to maintain systemic vascular resistance • Death is the inevitable result. Multiple organ failure • Multiple organ failure is defined as two or more failed organ systems • Lung: Acute respiratory distress syndrome • Kidney: Acute liver insufficiency • Clotting: Coagulopathy • Cardiac: Cardiovascular failure • NO SPECIFIC TREATMENT, ONLY SUPPORTIVE OR PREVENTIVE • 60% mortality
- 25. Management • 3 goalsfor treatment of the patient with hypovolemic shock: 1. Maximize oxygen delivery - completed by ensuring adequacy of ventilation, increasing oxygen saturation of the blood, and restoring blood flow 2. Control further blood loss 3. Fluid resuscitation
- 26. Maximize Oxygen delivery •Assessed immediately upon arrival and stabilized if necessary – Airway, Breathing: • Depth and rate of respirations, breath sounds – Address immediate causes • pneumothorax, hemothorax, flail chest, cardiac tamponade etc. – High-flow supplemental oxygen – Ventilatory support
- 27. Circulation • Two large-boreIV lines: – IV access • Antecubital veins • Venous cutdown • Central line – Intraosseous access for hypotensive children younger than 6 years. – Arterial line for patients with severe hemorrhage.
- 28. Initial fluid resuscitation –Isotonic crystalloid • Normal saline • Ringer lactate solution • Initial bolus of 1-2 L is given in an adult • 20 mL/kg in a pediatric patient • In total, 250–500 mL of fluid is rapidly given (over 5–10 minutes)
- 29. Maintainance fluid (if resuscitation succeeds) • (4-2-1 rule) – 4 mL/kg for 1st 10 kg (0-10kg) – 2 mL/kg for 2nd 10 kg (11-20kg) – 1 mL/kg for >20kg
- 30. Monitoring patients inshock • Required parameters – ECG – Pulse oximetry – Blood Pressure – Urine output • Additional monitoring – Central Venous Pressure – Invasive Blood Pressure – Cardiac Output – Base Deficit – Serum Lactate
- 31. Dynamic fluid response •Responders: – improvement in their cardiovascular status which is sustained. – Not actively loosing blood • Transient responders – improvement which then reverts to the previous state over the next 10–20 minutes. – Moderate ongoing fluid losses. • Non-responders – severely volume depleted ,likely to have major ongoing loss of intravascular volume, persistent uncontrolled haemorrhage
- 32. • Initial resuscitationrequires rapid re- expansion of the circulating intravascular blood volume along with interventions to control on going losses. • Starling’s law: stroke volume and cardiac output rise with the increase in preload. • If in doubt about cause assume to be hypovolemic and treat.
- 33. Controlling further bloodloss • Identify source of bleeding and manage. – Assess if surgical intervention is required
- 34. • In traumacases – Resuscitation and surgery should be simultaneous e.g (tractions for long bone #) • In surgical cases fluid resuscitate and then operate.(if not inflammatory response is exacerbated)
- 35. • PRBCs shouldbe transfused if the patient remains unstable after 2000 mL of crystalloid resuscitation. • Administer 2 U rapidly, and assess response. • Acute situations, O-negative non-crossmatched blood can be considered. • FFP used when the patient shows signs of coagulopathy.
- 36. Resuscitation • Crystalloids arethe first fluid of choice for resuscitation. – Initial therapy with 2 L of isotonic sodium chloride solution or lactated Ringer’s solution • Each liter of fluid expands the blood volume by 20-30%; (1:3 Crystalloid) – E.g: 3 L of fluid need to be administered to raise the intravascular volume by 1 L.
- 37. • Colloids restorevolume in a 1:1 ratio. – Human albumin – hydroxy-ethyl starch products (mixed in either 0.9% isotonic sodium chloride solution or lactated Ringer’s solution) – Hypertonic saline-dextran combinations. • Maintenance of the pulmonary hydrostatic pressure at less than 15 mm for preventing pulmonary edema.
- 38. • Current recommendationsare for aggressive fluid resuscitation with lactated Ringer solution or normal saline in all patients with signs and symptoms of shock, regardless of underlying cause
- 39. Vasopressor and inotropicsupport • Not indicated as first line. • in the absence of adequate preload rapidly leads to decreased coronary perfusion and depletion of myocardial oxygen reserves. • Cardiogenic Shock- dobutamine • Distributive shock: – phenylephrine,noradrenaline – Vasopressin for resistant catecholamines
- 40. • In uncontrolledhemorrhagic shock (UCHS), in which the bleeding has temporarily stopped because of hypotension, vasoconstriction, and clot formation, fluid treatment is aimed at: – Restoration of radial pulse – Restoration of sensorium – Obtaining a blood pressure of 80 mm Hg by aliquots of 250 mL of lactated Ringer's solution (hypotensive resuscitation).
- 41. References • Baileys andLove’s Short Practice of Surgery 26th Edition. • Apleys System of Orthopaedics 9th edition. • Harrisons Principles of Internal Medicine 19th edition. • www.google.com • www.medscape.com