2. shock.pptx and this is a power point on shock

this is a power point on shock

1. SHOCK Abdudin Heru MD

2. Outline Introduction Pathophysiology Classification Approach to patient Management Reference

3. O bjectives By the end of this session you should know about T he definition and classification of shock Approach and management of patient in shock

4. Introduction Shock is the failure to meet the metabolic needs of the cell and the consequences that ensue . S hock is the most common and therefore the most important cause of death among surgical patients The initial cellular injury that occurs is reversible; however, the injury will become irreversible if tissue perfusion is prolonged or severe enough such that, at the cellular level, compensation is no longer possible With insufficient delivery of oxygen and glucose, cells switch from aerobic to anaerobic metabolism that's why lactate level will be high

5. A central component of shock is decreased tissue perfusion. This may be a direct consequence of the etiology of shock, such as in hypovolemic/hemorrhagic, cardiogenic, or neurogenic etiologies, or It may be secondary to elaborated or released molecules or cellular products that result in endothelial/ cellular activation, such as in septic shock or traumatic shock . Hemodynamic parameters such as blood pressure and heart rate are relatively insensitive measures of shock, and additional considerations must be used to help aid in early diagnosis and treatment of patients in shock

6. Pathophysiology

7. cont.… Regardless of etiology, the initial physiologic responses in shock are driven by tissue hypoperfusion and the developing cellular energy deficit. Many of the organ-specific responses are aimed at maintaining perfusion in the cerebral and coronary circulation. Our body tries to preserve the most vital organ and this process is called diving reflex

8. These are regulated at multiple levels including S tretch receptors and baroreceptors in the heart and vasculature (carotid sinus and aortic arch) chemoreceptor cerebral ischemia responses release of endogenous vasoconstrictors shifting of fluid into the intravascular space and RAAS Posterior pituitary –ADH/Vasopressin Adrenal cortex-cortisol

9. The goal of the neuroendocrine response to hemorrhage is to maintain perfusion to the heart and the brain, even at the expense of other organ system The magnitude of the neuroendocrine response is based on both the volume of blood lost and the rate at which it is lost Afferent impulses transmitted from the periphery are processed within the central nervous system (CNS) and activate the reflexive effector responses or efferent impulses . These effector responses are designed to expand plasma volume, maintain peripheral perfusion and tissue O2 delivery, and restore homeostasis

10. Ischemia-reperfusion syndrome The acid and potassium load that has built up during shock can lead to direct myocardial depression , vascular dilatation and further hypotension. The cellular and humoral activated by the hypoxia (complement, neutrophils, microvascular thrombi) are flushed back into the circulation where they cause further endothelial injury to organs such as the lungs and kidneys. This leads to acute lung injury , acute renal injury, multiple organ failure and death . Reperfusion injury can currently only be attenuated by reducing the extent and duration of tissue hypoperfusion.

11. Stages of shock Compensated shock Vital organ function maintained BP remains normal Uncompensated shock Microvascular perfusion becomes marginal Organ and cellular function deteriorates Hypotension developed Irreversible shock Multi-organ system dysfunction with end organ injury.

12. Classification of shock Hypovolemic Haemorrhage Severe burns Severe dehydration secondary to GI losses Cardiogenic Myocardial infarction Congestive heart failure Valve problems Cardiomyopathy Distributive Sepsis Anaphylaxis Neurogenic shock Acute adrenal insufficiency Obstructive Cardiac tamponade Tension pneumothorax Massive pulmonary embolism

13. 1. HYPOVOLEMIC The most common cause of shock in the surgical or trauma patient is loss of circulating volume from hemorrhage Acute blood loss results in reflexive decreased baroreceptor stimulation from stretch receptors in the large arteries, resulting in decreased inhibition of vasoconstrictor centers in the brain stem, increased chemoreceptor stimulation of vasomotor centers, and diminished output from atrial stretch receptors . Peripheral vasoconstriction is prominent, while lack of sympathetic effects on cerebral and coronary vessels and local auto regulation promote maintenance of cardiac and CNS blood flow

14. Shock in a trauma patient or postoperative patient should be presumed to be due to hemorrhage until proven otherwise. substantial volumes of blood may be lost before the classic clinical manifestations of shock are evident at least 25% to 30%

15. Serum lactate and base deficit are measurements that are helpful to both estimate and monitor the extent of bleeding and shock It must be noted that lack of a depression in the initial hematocrit does not rule out substantial blood loss or ongoing bleeding Blood loss sufficient to cause shock is generally of a large volume, and there are a limited number of sites that can harbor sufficient extravascular blood volume to induce hypotension (e.g., external, intrathoracic, intra-abdominal, retroperitoneal, and long bone fractures) Intraperitoneal hemorrhage is probably the most common source of blood loss that induces shock . I ntraperitoneal blood may be rapidly identified by diagnostic ultrasound or diagnostic peritoneal lavage

16. Cont.… Causes Loss of fluid from all body compartments reduced fluid intake 3 rd spacing of fluid eg . burns large GI losses eg . pyloric stenosis, high ouput ileostomy large renal losses eg . diabetes insipidus Acute loss of blood volume e.g. trauma (haemorrhagic shock)

17. ↓i ntravascular volume Cont.… ↓ cardiac filling pressure Mechanisms Initially; BP maintained Brain and heart initially protected through autoregulation Eventually if untreated; compensatory mechanisms will fail ↓ SV baroreceptor stimulated reflex tachycardia (initially maintaining CO) release of endogenous catecholamines ↑ PVR and myocardial contractility

18. 2. TRAUMATIC The hypoperfusion deficit in traumatic shock is magnified by the proinflammatory activation that occurs following the induction of shock At the cellular level, this may be attributable to the release of cellular products termed damage associated molecular patterns ( DAMPs ) that activate the same set of cell surface receptors as bacterial products, initiating similar cell signaling These receptors are termed pattern recognition receptors ( PRRs) and include the TLR family of proteins. Examples of traumatic shock include small volume hemorrhage accompanied by soft tissue injury (femur fracture, crush injury)

19. 3.SEPTIC (VASODILATORY ) Vasodilatory shock is the result of dysfunction of the endothelium and vasculature secondary to circulating inflammatory mediators and cells or as a response to prolonged and severe hypoperfusion Vasodilatory shock is characterized by peripheral vasodilation with resultant hypotension and resistance to treatment with vasopressors In septic shock, the vasodilatory effects are due, in part , to the upregulation of the inducible isoform of nitric oxide synthase ( iNOS or NOS 2) in the vessel wall. iNOS produces large quantities of nitric oxide for sustained periods of time. This potent vasodilator suppresses vascular tone and renders the vasculature resistant to the effects of vasoconstricting agents.

20. BASIC TERMS Systemic inflammatory response syndrome (SIRS) - Any 2 of: T o >38 C or <36 C; RR>24 BPM; PR>90 BPM; WBC>12,000/  l or < 4000 /  l or > 10% bands Sepsis: SIRS with suspected or proven microbial etiology Severe Sepsis or sepsis syndrome: Sepsis with organ dysfunction including hypotension, Hypoperfusion, or organ dysfunction Septic shock : Sepsis with hypotension for > 1hr despite adequate fluid resuscitation or requiring vasopressors to keep SBP > 90 mmHg /MAP> 70 mmHg Refractory Septic Shock : Septic shock lasting for > 1 hour and doesn’t respond to fluid and vasopressors

21. 3.CARDIOGENIC Cardiogenic shock is defined clinically as circulatory pump failure leading to diminished forward flow and subsequent tissue hypoxia, in the setting of adequate intravascular volume . Hemodynamic criteria include sustained hypotension (i.e., SBP <90 mmHg for at least 30 minutes), reduced cardiac index (< 2.2 L/min per square meter), and elevated pulmonary artery wedge pressure (>15 mmHg ). Mortality rates for cardiogenic shock are 50% to 80%. Acute , extensive MI is the most common cause of cardiogenic shock

22. 4. OBSTRUCTIVE Although obstructive shock can be caused by a number of different etiologies that result in mechanical obstruction of venous return in trauma patients this is most commonly due to the presence of tension pneumothorax and cardiac tamponade. With either cardiac tamponade or tension pneumothorax, reduced filling of the right side of the heart from either increased intrapleural pressure secondary to air accumulation (tension pneumothorax) or increased intrapericardial pressure precluding atrial filling secondary to blood accumulation (cardiac tamponade) results in decreased cardiac output associated with increased central venous pressure. Beck’s triad consists of hypotension, muffled heart tones, and neck vein distention. Unfortunately, absence of these clinical findings may not be sufficient to exclude cardiac injury and cardiac tamponade

23. 5.Neurogenic Neurogenic shock refers to diminished tissue perfusion as a result of loss of vasomotor tone to peripheral arterial beds. N eurogenic shock is usually secondary to spinal cord injuries from vertebral body fractures of the cervical or high thoracic region that disrupt sympathetic regulation of peripheral vascular tone The classic description of neurogenic shock consists of decreased blood pressure associated with bradycardia (absence of reflexive tachycardia due to disrupted sympathetic discharge), warm extremities (loss of peripheral vasoconstriction), motor and sensory deficits indicative of a spinal cord injury, and radiographic evidence of a vertebral column fracture. In a subset of patients with spinal cord injuries from penetrating wounds, most of the patients with hypotension had blood loss as the etiology (74%) rather than neurogenic causes, and few (7%) had the classic findings of neurogenic shock.

24. Overview of different types of shock Comparison table different types of shock Hypo-volaemic Cardiogenic Distributive Sepsis Distributive Neurogenic Obstructive Peripheries cold cold warm warm cold Heart rate increased increased increased may be bradycardic increased Pulse pressure reduced may be reduced may be increased normal may be reduced (pulsus paradoxus) CVP reduced increased reduced reduced increased Temperature may be reduced normal may be increased normal normal

25. How to approach patient with shock For trauma patient follow the ATLS principle because maintaining circulation with out adequate oxygenation is not important at all So manage the airway first then breathing , making sure both are not affected check the circulation To effectively manage patient with shock focus mainly on the cause so take targeted history and try to find common signs of sock

26. Management Treatment of shock is initially empiric . A secure airway must be confirmed or established in obtunded patients The priority is the initiation of volume infusion while the search for the cause of the hypotension is pursued Shock in a trauma patient or postoperative patient should be presumed to be due to hemorrhage until proven otherwise In management of trauma patients, understanding the patterns of injury of the patient in shock will help direct the evaluation and management.

27. Hypovolemic The appropriate priorities in these patients are as follows: (a) control the source of blood loss, (b) perform IV volume resuscitation with blood products in the hypotensive patient, and (c) secure the airway In trauma, identifying the body cavity harboring active hemorrhage will help focus operative efforts; however, because time is of the essence, rapid treatment is essential Initial resuscitation is limited to keep SBP around 80 to 90 mmHg. This prevents renewed bleeding from recently clotted vessels Resuscitation and intravascular volume resuscitation is accomplished with blood products and limited crystalloids like NS and RL

28. Cont.… The infusion of 2–3 L of salt solution over 20–30 min should restore normal hemodynamic parameters Continued hemodynamic instability implies that shock has not been reversed and/or that there are significant ongoing blood or volume losses Too little volume allowing persistent severe hypotension and hypoperfusion is dangerous, yet too vigorous of a volume resuscitation may be just as deleterious Fluid resuscitation is a major adjunct to physically controlling hemorrhage in patients with shock

29. In patients with severe hemorrhage, restoration of intravascular volume should be achieved with blood products ( PRBC is preferred ) In the presence of severe and/or prolonged hypovolemia , inotropic support with dopamine, vasopressin, or dobutamine may be required to maintain adequate ventricular performance after blood volume has been restored Once hemorrhage is controlled and the patient has stabilized, blood transfusions should not be continued unless the hemoglobin is <7g/ dL .

30. Generally based the response to initial fluid--can be divided into 3 a. rapid response, b. transient response, and c. minimal or no response. A. RAPID RESPONSE rapidly to the initial fluid bolus and remain hemodynamically normal after the initial fluid bolus usually have lost minimal (less than 20%) blood volume No further fluid bolus or immediate blood administration Typed and crosshatched blood should be kept available. Surgical consultation and evaluation are necessary during initial assessment and treatment, as operative intervention may still be necessary

31. B. TRANSIENT RESPONSE respond to the initial fluid bolus. However , they begin to show deterioration of perfusion indices as the initial fluids are slowed to maintenance levels, indicating either an ongoing blood loss or inadequate resuscitation. Most of these patients initially have lost an estimated 20% to 40% of their blood volume Transfusion of blood and blood products is indicated, but more important is the recognition that this patient requires operative or angiographic control of hemorrhage. patients who are still bleeding and require rapid surgical intervention.

32. C. MINIMAL OR NO RESPONSE Failure to respond to crystalloid and blood in the ER dictates the need for immediate , definitive intervention (e.g., operation or Angioembolization ) to control exsanguinating hemorrhage . So the possible DDX are blunt cardiac injury cardiac tamponade tension pneumothorax Non hemorrhagic shock Cardiogenic Septic Central venous pressure monitoring and cardiac ultrasonography help to differentiate between the various causes of shock

33. TRAUMATIC Follow the ATLS guideline initially Treatment of traumatic shock is focused on correction of the individual elements to diminish the cascade of proinflammatory activation, and includes prompt control of hemorrhage, adequate volume resuscitation to correct O2 debt, debridement of nonviable tissue, stabilization of bony injuries, and appropriate treatment of soft tissue injuries Supplementation of depleted endogenous antioxidants also reduces subsequent organ failure and mortality

34. SEPTIC Because vasodilation and decrease in total peripheral resistance may produce hypotension, fluid resuscitation and restoration of circulatory volume with balanced salt solutions is essential. Fluid resuscitation should begin within the first hour and should be at least 30 mL/kg for hypotensive patients Empiric antibiotics must be chosen carefully based on the most likely pathogens ( gram-negative rods , gram-positive cocci , and anaerobes) because the portal of entry of the offending organism and its identity may not be evident until culture data return or imaging studies are completed. After first-line therapy of the septic patient with antibiotics, IV fluids, and intubation if necessary, vasopressors may be necessary to treat patients with septic shock

35. Catecholamine's are the vasopressors used most often, with norepinephrine being the first-line agent followed by epinephrine Occasionally, patients with septic shock will develop arterial resistance to catecholamines . Arginine vasopressin, a potent vasoconstrictor, is often efficacious in this setting and is often added to norepinephrine A single IV dose of 50 mg of hydrocortisone improved mean arterial blood pressure response relationships to norepinephrine in patients with septic shock and was most notable in patients with relative adrenal insufficiency

36. Cardiogenic J udicious fluid administration to avoid fluid overload and development of cardiogenic pulmonary edema Electrolyte abnormalities , commonly hypokalemia and hypomagnesemia , should be corrected Dobutamine primarily stimulates cardiac β1- receptors to increase cardiac output but may also vasodilate peripheral vascular beds, lower total peripheral resistance, and lower systemic blood pressure through effects on β2- receptors . Ensuring adequate preload and intravascular volume is therefore essential prior to instituting therapy with dobutamine Dopamine may be preferable to dobutamine in treatment of cardiac dysfunction in hypotensive patients.

37. Patients whose cardiac dysfunction is refractory to cardiotonics may require mechanical circulatory support with an intra-aortic balloon pump . NEUROGENIC Most patients with neurogenic shock will respond to restoration of intravascular volume alone, with satisfactory improvement in perfusion and resolution of hypotension Vasoconstrictor should only be considered once hypovolemia is excluded as the cause of the hypotension and the diagnosis of neurogenic shock is established D opamine may be used first. A pure α-agonist, such as phenylephrine, may be used primarily or in patients unresponsive to dopamine

38. End point in resuscitation it is much easier to know when to start resuscitation than when to stop Even with normalization of blood pressure , heart rate, and urine output, 80% to 85% of trauma patients have inadequate tissue perfusion, as evidenced by increased lactate or decreased mixed venous O2 saturation. Resuscitation algorithms directed at correcting global perfusion endpoints (base deficit, lactate, mixed venous oxygen saturation) rather than traditional endpoints like PR &BP Resuscitation is complete when O2 debt is repaid , tissue acidosis is corrected, and aerobic metabolism restored.

39. ADJUNCT THERAPY The sympathomimetic amines dobutamine , dopamine, and norepinephrine are widely used in the treatment of all forms of shock Arginine-vasopressin (antidiuretic hormone) is also being used increasingly and may better protect vital organ blood flow and prevent pathologic vasodilation. Positioning of the patient may be a valuable adjunct in the initial treatment of hypovolemic shock. The NASG and the military antishock trousers (MAST) Rewarming or avoidance of hypothermia

40. NASG

41. Reference Schwartz principle of surgery 11 ed Sabiston textbook of surgery Baily and love short practice of surgery Up-to-date 21.6 Slide share (Google)

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