shock ppt.pptx

shock

1. SHOCK- PATHOPHYSIOLOGY, TYPES & MANAGEMENT PRESENTED BY MALA. M GUIDED BY Dr. SANTOSH A NANDIMATH

2. 2 CONTENTS History Definition Classification Aetiology Incidence General pathogenesis Stages of shock Haemorrhagic shock Cardiogenic shock Septic shock Anaphylactic shock Conclusion

3. 3 Brief history As proposed by the historians, the first written definition of shock is made by Celsus (AD 20) after a penetrating heart injury as “The pulse fades away, the color is extremely pallid, cold and malodorous sweats break out the body as if the body has been wetted by dew, the extremities become cold and death quickly follows” . LeDran , a military surgeon, derived a word shock as “The bullet thrown from the gunpowder acquires such rapid force that the whole animal participates in the jarring (shock and agitation)” in his article in 1743 .

4. 4 The term “golden hour” is widely attributed to R. Adams Cowley, who in a 1975 article stated, “the first hour after injury will largely determine a critically injured person’s chances for survival”—this was in an era characterized by a lack of an organized trauma system and inadequate prehospital care. An analogous concept, the “platinum 10 minutes” places a time constraint on the prehospital care of seriously injured patients: no patient should have more than 10 min of scene-time stabilization by the prehospital team prior to transport to definitive care at a trauma center .

5. 5 SHOCK- “A PHYSIOLOGICAL STATE OF WAR” DEFINITION OF SHOCK “It is defined as a life-threatening, generalized form of acute circulatory failure associated with inadequate oxygen utilization by the cells”

6. 6 CLASSIFICATION

7. 7 Relative incidence of various types of shock According to a European multicenter trial, septic shock Is the most common (62%) hypovolemic (16%), cardiogenic (16%), Distributive other than septic (4%), and obstructive shock (2%)

8. 8 Pathophysiology of Shock In general, all forms of shock involve following 3 derangements: Reduced effective circulating blood volume. Reduced supply of oxygen to the cells and tissues with resultant anoxia. Inflammatory mediators and toxins released from shock induced cellular injury

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14. Haemorrhagic Shock 14

15. 15 Hemorrhagic shock develops as a result of intravascular volume loss due to bleeding out of the body or into the anatomical spaces inside, causing insufficient oxygen delivery to the cells. Hemorrhagic shock is a type of hypovolemic shock. If the bleeding does not stop, inadequate oxygen supply may lead to death. Hemorrhagic shock in trauma patients is a predictor of worse outcomes and contributes to early mortality

16. 16 Shock may develop due to several reasons including trauma, maternal hemorrhage, gastrointestinal hemorrhage, perioperative hemorrhage, or ruptured aneurysms . Mortality due to bleeding is substantial on a global scale. Annually, 1.9 million people in the world lose their lives due to hemorrhage and its consequences. Out of them, 1.5 million people die of physical trauma around the world each year. Unexpectedly, it is more common in young people.

17. 17 Classification of haemorrhage Based on the source of bleeding: Arterial : is bright red in colour, spurting like jet along with pulse of the patient. Venous : is dark red, steady and continuous flow. Blood loss may be severe and rapid when bleeding is from femoral vein, jugular vein, other major veins, varicose veins, portal vein, esophageal varices. Pulmonary arterial blood is dark red in colour and pulmonary venous blood is bright red in colour. Capillary : Here bleeding is rapid and bright red. It is often torrential due to continuous ooze.

18. 18 II. Based on the time of onset of bleeding in relation to any operative procedure: 1.Primary : Occurs at the time of injury or operation. 2. Reactionary : It occurs within 24 hours after surgery or after injury (commonly in 4–6 hours). 3. Secondary : It usually occurs in 14 days after surgery

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20. 20 IV. Based on the duration of haemorrhage: 1. Acute haemorrhage : It is sudden, severe haemorrhage after trauma, surgery. 2. Chronic haemorrhage : It is chronic repeated bleeding for a long period like in haemorrhoids, bleeding peptic ulcer, carcinoma caecum, etc. They present with chronic anaemia with hyperdynamic cardiac failure. in a state of chronic hypoxia. It is corrected by packed cell transfusion not by whole blood itself. Cause has to be treated accordingly. 3. Acute on chronic haemorrage : It is more dangerous as the bleeding occurs in individuals who are already hypoxic, which may get worsened faster .

21. 21 V. Based on the possible intervention : 1. Surgical haemorrhage —can be corrected by surgical intervention. 2. Nonsurgical haemorrhage —is diffuse ooze due to coagulation abnormalities and DIC.

22. 22 Classification of Hemorrhagic Shock

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24. 24 Lethal triad of hemorrhagic shock The lethal triad of acidosis, hypothermia, and coagulopathy is commonly seen in patients with severe hemorrhagic shock Each factor in triad influences the other factors, and the patients with this lethal triad show high mortality in spite of aggressive management.

25. 25 MANAGEMENT CLINICAL ASSESSMENT IDENTIFICATION OF SOURCE OF BLEEDING LABORATORY TESTS RESUSCITATION

26. 26 The source of bleeding In traumatic shock, penetrating trauma such as stab wounds or gunshot wounds usually has more obvious source of bleeding than blunt trauma and requires surgical bleeding control. In nontraumatic hemorrhagic shock, the approximate source of bleeding could be determined by the patient’s symptoms such as hematemesis, hematuria. If a source of bleeding is identified, immediate procedures for bleeding control should be considered unless initial resuscitation is successful

27. 27 Unidentified Source of Bleeding In contrast, a patient without obvious source of bleeding should undergo further investigation. In traumatic shock, early diagnostic imaging techniques such as ultrasonography or contrast enhanced computed tomography (CT) are recommended for the detection of free fluid in patients with torso trauma . Ultrasonography is a rapid, noninvasive imaging technique for detection of intra-abdominal fluid and can be performed in bedside without moving the patients. Extended focused assessment with sonography for trauma ( eFAST ) was introduced for trauma as a screening test for blood in the pericardium, abdominal cavity, or pleural space, and also for a pneumothorax. The six areas that are examined are subcostal (subxiphoid), RUQ (hepatorenal recess), LUQ ( perisplenic space), pelvis, and thorax

28. 28 The CT scan has been widely used to detect the source of bleeding in patients with hemorrhagic shock in both trauma and non-trauma, and the usefulness of the CT scan has been well known. Recently, multi-detector CT (MDCT) may require less than 30  s for scanning the whole body, and the usefulness of the CT scan has been well known. In addition, contrast enhanced CT scan could detect active bleeding more accurately than non-enhanced CT scan.

29. 29 Measurement of Blood Loss Clot size of a clenched fist is 500 ml. Weighing the swab before and after use is an important method of on-table assessment of blood loss.

30. 30 Laboratory Tests Laboratory tests are a part of diagnostic workup for patients with hemorrhagic shock. They can help assess the condition and severity of the patient and identify the patients who may require aggressive diagnostic and therapeutic interventions. Hemoglobin and hematocrit, lactate, base deficit, and tests for coagulation.

31. 31 Initial Management of Hemorrhagic Shock The goal of initial resuscitation for hemorrhagic shock is to arrest ongoing bleeding, to restore the effective circulating blood volume, and to restore tissue perfusion. Management protocol of hemorrhagic shock has developed based on the treatment of trauma patients. There was a concept of damage control surgery (DCS) as a surgical approach to the trauma, and this has been expanded to the early management of trauma patients as damage control resuscitation (DCR). Early recognition of the patients with high risk and prevention of lethal triad of coagulopathy, hypothermia, and acidosis are main purposes of the DCR. 

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33. 33 Restoration of the intravascular fluid volume Four issues should be considered when treating hemorrhagic shock: type of fluid to give, how much, how fast, and what the therapeutic end-points are. The ideal fluid for resuscitation has not been established. The three-to-one rule(that is, 3 ml of crystalloid (Ringers lactate or normal saline) for every 1 ml of blood loss replaced). has been applied to the classification of hemorrhage to establish a baseline for guiding therapy , and use of crystalloid (Ringers lactate or normal saline) is recommended by the American College of Surgeons .

34. 34 Although resuscitative end-points are similar when using Ringers lactate or normal saline, metabolic hyperchloremic acidosis has been reported when infusing large volumes of normal saline (>10 l)  Colloidal solutions, such as albumin and hetastarch (6% hydroxyethyl starch in 0.9% NaCl), can be administered to increase circulatory volume rapidly. the use of albumin solutions in the initial resuscitation stages has not proven to be more effective than crystalloid.

35. 35 Pharmacologic Agents and Blood Products Tranexamic acid Calcium Local hemostatic agents Blood products and their derivatives

36. 36 Tranexamic Acid Tranexamic acid is a synthetic lysine analogue and an antifibrinolytic agent as a competitive inhibitor of plasminogen. In a prospective cohort study, tranexamic acid reduced organ failure and mortality in traumatic shock patients . A prospective randomized study showed that early administration of tranexamic acid reduced mortality in trauma patients with shock and the rate of thrombosis was not increased with the use of tranexamic acid. The recommended dose is a loading dose of 1 g over 10  min, followed by infusion of 1  g over 8  h, and tranexamic acid is not recommended more than 3 h after injury.

37. 37 Calcium Hypocalcemia is a common complication of massive transfusion. Low ionized calcium concentration was associated with increased mortality and massive transfusion. Therefore, ionized calcium concentration should be monitored and maintained within normal range .

38. 38 Local Hemostatic Agents Various local hemostatic agents are available for the control of hemorrhage.

39. 39 BLOOD TRANSFUSION Indications Acute blood loss following trauma, >15% of total body volume in otherwise healthy individuals (liver, spleen, kidney, GIT injuries, fractures, hemothorax, perineal injuries). A hypotensive patient who fails to respond to 2 l crystalloid in the phase of probable hemorrhage should be treated with blood and blood products. During major surgeries— Following burns. In septicemia. As a prophylactic measure prior to surgery. Whole blood is given in acute blood loss. Packed cells are given in chronic anemia. Blood fractions are given in ITP, haemophilias . Note: Blood transfusion is required if Hb% is < 8 g%

40. 40 Collection of Blood Blood is collected in a sac containing 75 ml of CPD (Citrate phosphate dextrose) solution and stored in special refrigerators at 4 degree celcius . CPD blood lasts for 3 weeks. Adenosine can be added to increase the storage life of the blood up to 5 weeks; it is called as CPDA solution. In storage period, RBCs lose their ability to release oxygen in 7 days even though RBCs last for 3 weeks; so blood should be transfused within 7 days ideally. WBCs are destroyed in 2 days. Platelets and clotting factors are destroyed very early in 1–2 days

41. 41 Infusing Packed Red Blood Cells Whole blood is not available for replacement of blood loss, and erythrocyte losses are replaced with stored units of concentrated erythrocytes called packed red blood cells. Each unit of packed RBCs has a hematocrit of 55% to 60%, which imparts a high viscosity As a result, packed RBCs can flow sluggishly unless diluted with saline. When infused alone, the flow rate of packed RBCs through average sized (18-gauge or 20-gauge) peripheral catheters is 3–5 mL/min, which means that one unit of undiluted packed RBCs (which has a volume of about 350 mL) can be infused over 70–117 minutes (about 1–2 hours). This is sufficient for replacing erythrocyte losses in hemodynamically stable patients, but more rapid flow rates may be needed for patients with active bleeding .

42. 42 Dilution of packed rbcs with 100 ml of isotonic saline results in 7-fold to 8-fold increases in infusion rates, while dilution with 250 ml saline increases flow rates over 10-fold. At the highest infusion rate of 96 ml/min in the 16- gauge catheter, one unit of packed rbcs (350 ml plus 250 ml saline) can be infused in 6–7 minutes. More rapid rates require pressurized infusions, which can increase infusion rates to 120 ml/min using a 16-gauge catheter

43. 43 Blood products and their derivatives

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46. 46 Conclusion Of hemorrhagic shock Hemorrhagic shock can be rapidly fatal. The primary goal is to stop the bleeding. Resuscitation may well depend on estimated severity of hemorrhage. patients who have moderate hypotension from moderate bleeding may well benefit from a delay in massive resuscitation in order to reach a definitive care facility. On the other hand, when patients are obviously in severe hemorrhagic shock, the use of intravenous crystalloids or colloids and blood products when available can be life saving. Uncertainties remain regarding the best method for resuscitation, what type of fluid, how much, when, and how fast

47. 47 A hemoglobin level of 7–8 g/dl is an appropriate threshold for transfusion in critically ill patients with no risk factors for tissue hypoxia. Maintaining a hemoglobin level of 10 g/dl is a reasonable goal for patients who are actively bleeding, the elderly, or individuals at risk for a myocardial infarction. Moreover, hemoglobin concentration should not be the only therapeutic guide in actively bleeding patients. Instead, therapy should be aimed at restoring intravascular volume and adequate hemodynamic parameters.

48. CARDIOGENIC SHOCK 48

49. 49 Introduction Cardiogenic shock is a serious complication of acute myocardial infarction and is an important cause of hospital death. Cardiogenic shock is a condition in which, myocardium unable to pump enough blood to meet your body’s needs. The condition is most often caused by a severe heart attack. Cardiogenic shock is rare, but it’s often fatal if not treated immediately. If treated immediately, about half the people who develop the condition survive.

50. 50 Definition of Cardiogenic Shock Cardiogenic shock is a life-threatening medical condition resulting from an inadequate circulation of blood due to primary failure of the ventricles of the heart to function effectively The incidence of cardiogenic shock is about 5% in patients with acute myocardial infarction (AMI) and three times more in ST-segment elevation myocardial infarction (STEMI) than in non-STEMI

51. 51 The definition of CS consists of hemodynamic instability of various parameters

52. Causes of CS 52

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55. 55 Treatment and Management A patient in cardiogenic shock should undergo immediate comprehensive assessment. Chest X-ray, electrocardiogram (ECG), and echocardiography are required immediately in all patients with suspected cardiogenic shock.

56. 56 Chest X-ray can be a useful test for the diagnosis of cardiogenic shock. Pulmonary venous congestion, pleural effusion, interstitial or alveolar edema, and cardiomegaly are the most specific findings for cardiogenic shock ECG is rarely normal in cardiogenic shock. It is also helpful in identifying underlying cardiac disease and potential precipitant

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58. SEPTIC SHOCK 58

59. 59 The first definition of sepsis, published in 1992, was based on the presence of a suspected or proven infection with two or more criteria of the systemic inflammatory response syndrome (SIRS) . Sepsis was defined, as the presence of two or more positive SIRS criteria with a confirmed or suspected infection as the underlying cause. If signs of organ dysfunction were seen, the diagnosis was changed to severe sepsis. Septic shock was defined by the presence of acute circulatory failure and arterial hypotension along with features of sepsis .

60. 60 SIRS CRITERIA SIRS was based on an inflammatory response to an infectious inoculation. Many thought the definition was not helpful largely because the definition place a large emphasis on inflammation, causing many patients without bacterial or viral infections to receive empiric antibiotic therapy and over-resuscitation . The SIRS criteria were also thought to be remarkably sensitive, not taking into account any outside factors, multi-drug resistance and the ability to attain source control. Based on the old definition of sepsis using the SIRS criteria, patients have been incorrectly identified as being septic.

61. 61 Due to these inaccuracies in the SIRS criteria, the new Sepsis-3 definitions recommend using the SOFA score; The SOFA score is an aggregate score, from 0 to 4, for each organ system, including respiratory, coagulation, liver, cardiovascular, renal and central nervous systems. An acute increase in the total score of 2 or more reflects an overall mortality risk in patients suspected of infection. Calculating the SOFA score at the bedside or in a noncritical care unit and in patients who do not have full laboratory testing, is challenging Since the SOFA score is based on biochemical criteria, clinical qSOFA screening tool which is based on respiratory rate, systolic blood pressure and altered mental state was developed . If 2 of the 3 clinical variables are positive, the predictive validity is similar to the entire SOFA score when used outside the ICU setting

62. 62 In 2016, the Third International Consensus Definition for Sepsis and Septic Shock Defined sepsis as a life-threatening organ dysfunction resulting from dysregulated host responses to infection, and defined septic shock as a subset of sepsis in which underlying circulatory, cellular, and metabolic abnormalities are profound enough to substantially increase the risk of mortality.

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64. 64 Septic shock may be due to gram-positive organisms, gram negative organisms, fungi, viruses or protozoal origin.

65. 65 Septic shock is typically a vasodilatory shock wherein there is peripheral vasodilatation causing hypotension which is resistant to vasopressors. This is due to toxin induced release of isoform of nitric oxide synthetase from the vessel wall which causes sustained prolonged release of high levels of nitric oxide. Magnitude of infection is quantified as: Sepsis which shows fever, tachycardia, leucocytosis. Severe sepsis which shows low tissue perfusion with organ dysfunction (lactic acidosis, dysfunction of liver, kidney, lungs). Septic shock with systemic hypotension (BP < 90 mmHg in spite adequate fluid therapy), severe organ dysfunction (acute lung, kidney, liver injury), maldistribution of blood flow, shunting in microcirculation.

66. 66 Stages of septic shock Hyperdynamic (warm) shock : This stage is reversible stage. Patient is still having inflammatory response and so presents with fever, tachycardia, and tachypnoea. Pyrogenic response is still intact. Patient should be treated properly at this stage. Based on blood culture, urine culture (depending on the focus of infection), higher antibiotics like third generation cephalosporins, aminoglycosides, metronidazole are started. The underlying cause is treated like draining the pus. Ventilatory support with ICU monitoring may prevent the patient going for the next cold stage of sepsis .

67. 67 b. Hypodynamic hypovolaemic septic shock (cold septic shock): Here pyrogenic response is lost. Patient is in decompensated shock. It is an irreversible stage along with MODS (Multi-organ dysfunction syndrome) with anuria, respiratory failure (cyanosis), jaundice (liver failure), cardiac depression, pulmonary oedema, hypoxia, drowsiness, eventually coma and death occurs (Irreversible stage)

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70. ANAPHYLACTIC SHOCK 70

71. 71 Anaphylaxis is a life threatening hypersensitivity reaction that can cause shock. Epidemiology studies show anaphylaxis and anaphylactic shock is relatively rare, but its incidence is increasing. Defined according to the World Allergy Organization (WAO) definition ‘a severe, life-threatening generalized or systemic hypersensitivity reaction’ Anaphylactic shock is an end manifestation of anaphylaxis, occurs when there is inadequate tissue perfusion causing end organ damage.

72. 72 ETIOLOGY

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75. 75 Physiologic effects of mediators

76. 76 Signs and Symptoms Anaphylaxis causes a generalized systemic reaction affecting multiple organ systems, symptoms involving the skin occur in 80–90% of cases, respiratory tract in 70%, GI in 45%, CV in 45%, and CNS involvement in 15%. The cardiovascular and respiratory systems are the principal shock organs in fatal anaphylaxis. Death occurs in most often due to shock or acute respiratory distress. Anaphylaxis develops rapidly with symptoms developing in minutes. Biphasic reactions, where symptoms resolve and then reappear later occurs around 20% of the time. A systematic review of biphasic reactions found the medium time between resolution of initial symptoms and onset of delayed symptoms to be 11 h, with a range of 0.2–72 h

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79. 79 Management Epinephrine is the first line treatment of anaphylaxis, and delayed administration increases the likelihood of poor outcomes In most situations intramuscular administration is preferred. IM epinephrine should be given in 0.2–0.5 mg doses (1:1000 dilution), and repeated every 5 min depending on the resolution of symptoms

80. 80 Mechanism of action Epinephrine exerts its effects via alpha and beta adrenergic receptors in a dose dependent response where beta receptors effects are dominant at low doses, but alpha receptors effects are seen at higher doses. The α1 receptors cause vasoconstriction increasing peripheral vascular resistance and blood pressure and improving coronary and cerebral perfusion. The β1 receptors exert positive chronotropic and inotropic effects which improves cardiac output and increases blood pressure. In the respiratory system, β2 receptors stimulation results in bronchodilation, and relief and respiratory symptoms. β receptors also inhibit release of mediators from mast cells and basophils, via increased cAMP production

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83. 83 Additional consideration Beta blockers may complicate the treatment of anaphylaxis, as some of the beneficial effects of epinephrine will be diminished . In patients on betablockers who do not respond to epinephrine , other vasopressors should be considered. Glucagon has been reported to be a successful treatment in several case reports of patients on beta blockers who experienced anaphylactic shock. Vasopressin or phenylephrine can be used to increase systemic vascular resistance without further increasing heart rate. Methylene blue has been reported to be an effective treatment in cases of severe anaphylaxis not responding to epinephrine, as well as cases of anaphylaxis without hypotension.

84. 84 Summary

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