classification,recognition and management of shock

types of shock & management presentation

1. Classification, Recognition And Management Of Shock Dr. Shahnawaz Alam Dept. of General Surgery JNMCH, AMU

2. Shock : Definition Acute circulatory failure resulting in inadequate organ perfusion and cellular hypoxia.

3. Introduction Diagnosis is based on clinical, hemodynamic & biochemical signs which can be classified in three components : 1.Systemic arterial hypotension 2.Clinical signs of tissue hypoperfusion - apparent through three “windows” of body- a. cutaneous signs b. renal –urine output c. neurological signs 3.Hyperlactemia ( >1.5 mmol /L )

4. In Normal Conditions: Aerobic Metabolism 6 O 2 GLUCOSE METABOLISM 6 CO 2 6 H 2 O 36 ATP HEAT (417 kcal)

5. In Poor Perfusion States: Anaerobic Metabolism GLUCOSE METABOLISM 2 LACTIC ACID 2 ATP HEAT (32 kcal)

6. Consequences of anaerobic metabolism 6 Inadequate Cellular Oxygenation Anaerobic Metabolism Metabolic Failure Metabolic Acidosis Inadequate Energy Production Lactic Acid Production Cell Death!

7. Classification 1.Hypovolemic Shock 2.Cardiogenic Shock 3.Distributive Shock a. Septic Shock b. Anaphylactic Shock c. Neurogenic Shock 4.Obstructive Shock

8. HYPOVOLEMIC SHOCK Hemorrhagic : External hemorrhage: Trauma Hematoma Internal hemorrhage: GIT Bleeding Hemothorax/Hemoperitoneum Non-hemorrhagic External: Vomiting, Diarrhea Polyuria Dehydration Burns Internal (third spacing): Pancreatitis Bowel obstruction Ascites

9. HAEMORRHAGIC SHOCK : History suggestive of hemorrhage with Systolic blood pressure<90 mm of Hg Mean arterial pressure≤60 mm of Hg Serum lactate>2 mmol /l Hemorrhagic shock Leading preventable cause of death in trauma 9

10. ASSESSMENT Physical Examination Laboratory tests 10

11. Physical Examination First step is to recognize its presence A search for the source of bleeding This involves a careful head to toe examination Pelvic examination in obstetric patient Repeated careful physical examination and monitoring of vital signs 11

12. Clinical Assessment of hemorrhagic shock: S/S vary depending on severity of blood loss : **ninth edition, Sept 2012, American College of Surgeons Committee on Trauma,ATLS

13. Laboratory Investigation Arterial blood gas : most useful laboratory test. Metabolic acidosis- an elevated lactate level indicate inadequate tissue perfusion. Hemoglobin and hematocrit : not useful in the diagnosis of shock. may remain normal in early acute blood loss before resuscitation. serial estimate of Hb is helpful in identifying significant blood loss and potential need for blood transfusion and surgical intervention . Coagulation studies and Electrolytes 13

14. Diagnostic Options: Site of Bleeding Diagnostic Modalities Chest Bedside Chest radiography Thoracostomy tube output Abdomen Physical examination Ultrasound examination (FAST) Peritoneal lavage Long bones Physical examination Plain radiography Outside the body Physical examination 14

15. Initial management ABCs Initial measures to stop bleeding Initial fluids Crystalloid Warming – effects of hypothermia on mortality 15

16. Trauma patients are approached systematically, using the principles of the primary and secondary survey ATLS emphasizes the ABCDE mnemonic: airway, breathing, circulation, disability and exposure ATLS is based on simultaneous efforts to identify and treat life- and limb-threatening injuries, beginning with the most immediate 16

17. After the primary survey when the patient is stabilized, a more deliberate secondary examination is undertaken Any remaining injuries are diagnosed at this time and treatment plans established 17

18. Initial measures to stop bleeding Pressure to the bleeding part Elevation of the bleeding limb Tourniquet application (not usually recommended) Immediate placement of a chest tube helps expand the lung Splinting for fractured extremities Bimanual uterine compression, administration of oxytocin and uterine evacuation. 18

19. Initial fluids Warmed isotonic Crystalloid solutions are used for initial resuscitation . The usual initial dose is 1-2 liters for an adult and 20mL/kg for a pediatric patient. Advantages : availability, safety, and low cost. Interstitial losses are replaced. Disadvantage : rapid movement from the intravascular to the extravascular space, leading to three or more times requirement for replacement, and resulting in tissue edema. 19

20. More effective in rapidly restoring intravascular volume, requiring less fluid to correct hypovolemia Include albumin, hydroxyethyl starch, dextrans , and gelatins. Limitation: -Carries the risk of reaction. . -Are far more expensive Nonetheless, the interstitial fluid deficit associated with hypovolemic shock may be better treated with a crystalloid solution or a combination of colloids and crystalloids. 20 Colloid solutions

21. Replacement fluids Ringer’s lactate Adv: over NS to avoid hyperchloremic acidosis Disadv :- -slightly hypotonic , in large amounts can aggravate cerebral edema . Hypertonic salt solutions (3% and 7.5% saline) : Adv:- less cerebral edema than RL or NS in TBI -small volumes rapidly expands plasma volume Disadv: progressive hypernatremia. Dextrose containing solutions : should be avoided: exacerbate ischemic brain damage Given only when documented hypoglycemia. 21

22. Adjuvant therapies Supplemental oxygen/mechanical ventilation. Prevention of hypothermia Treatment of any electrolyte abnormality, specially hypocalcemia, hypo/ hyperkalemia, hypomagnesaemia Correction of acid base abnormality, severe metabolic acidosis Early treatment of hyperglycemia Corticosteroids. In case of adrenal failure 22

23. 23 Goals for Resuscitation Maintain systolic blood pressure at 80 -100 mm Hg Maintain hematocrit at 25% to 30%     Maintain core temperature higher than 35°C    Maintain SPO 2    Restore normal urine output Prevent an increase in serum lactate    Prevent acidosis from worsening  

24. Risks associated with aggressive volume replacement during early resuscitation Increased blood pressure Decreased blood viscosity    Decreased hematocrit    Decreased clotting factor concentration       Disruption of electrolyte balance    Direct immune suppression   Increased risk for hypothermia 24

25. Reassessment: Response to initial fluids 25

26. Blood transfusion and other products With hemorrhagic shock , blood products can be life saving. Decision to transfuse Blood Products Autotransfusion 26

27. Decision to transfuse If hemodynamic instability persists after approx. 2 L of crystalloid infusion. In resource-constrained settings the administration of precious units of blood should be delayed until hemorrhage is controlled. Use blood as part of pre-operative resuscitation, when possible. 27

28. INDICATIONS FOR BLOOD COMPONENT THERAPY Component Indication Packed RBCs Replacement of O2 carrying capacity Platelets Thrombocytopenia with bleeding Fresh frozen plasma Documented coagulopathy Cryoprecipitate Coagulopathy with low fibrinogen 28

29. Whole Blood vs Component Advantage of whole blood is no special equipment is needed for processing supplies plasma volume, red cells, platelets and coagulation factors, thereby potentially avoiding the coagulopathy often seen in hemorrhagic shock 29

30. Massive transfusion protocol Definition : replacement of > 1.5 blood volume in 24 hrs or replacement of pt. total blood volume by stored homologous bank blood in 24 hrs Indication : unresponding unstable pt. who has already transfused 2 units of PRBC with initial resuscitation It minimize dilutional coagulopathy 1:1:1 ( FFP:Platelates:PRBC ) initiated early in 1 st 2 units of transfused PRBC

31. VASOPRESSORS If despite adequate resuscitation with fluids and blood products: the CVP <= 8 cm of H2O MAP < 60 mm of Hg, Vasopressors should be considered . 31

32. Damage control resuscitation Definition: A systematic approach to severe trauma incorporating several strategy to decrease mortality & morbidity. Components: 1.Permissive hypotension 2.Hemostatic resuscitation 3.Damage control surgery Acute life-threatening bleeding within the abdominal or thoracic cavity is an indication for operation.

33. MONITORING Noninvasive monitor: ECG BP cuff Pulse oximeter ETCO2 Temperature probe Foley’s catheter- urine output Invasive monitor: Arterial line. For blood sampling & BP monitoring Central venous catheter For determining patient’s volume status. Pulmonary artery catheter. If the pt. shows signs of heart failure . 33

34. CARDIOGENIC SHOCK 34

35. Definition Cardiac output falls due to the pathology in the heart itself and is defined as cardiac index less than 2.2 L/ minute/m2. (Cardiac index is cardiac out put per meter of body surface area) 35

36. Hemodynamic criteria Sustained hypotension (systolic blood pressure < 90 mm Hg for at least 30 minutes) Reduced cardiac index (< 2.2 L/min per m 2 ) in the presence of elevated pulmonary capillary occlusion pressure (>15 mm Hg) 36

37. Pathophysiology of Cardiogenic shock 37

38. Etiology of Cardiogenic Shock Functional Myocardial infarction (most common) Blunt Cardiac Injury (trauma) Myocarditis Cardiomyopathy Septic myocardial depression Mechanical (Structural) • Valvular failure (stenotic or regurgitant) • Hypertrophic cardiomyopathy • Ventricular septal defect Arrhythmic • Bradycardia • Tachycardia Hollenberg Ann Int Med 1999; 131:47-99 38

39. Diagnosis A focused history and physical examination Blood tests Echocardiography ECG Chest X-Ray 39

40. Chest pain Dyspnea Pallor Anxiety Sweating Confusion Agitation Altered mentation Tachycardia with feeble pulse ( 90–110 beats/m ) Severe bradycardia due to high-grade heart block may be present Systolic blood pressure (BP) is reduced (<90 mmHg) with a narrow pulse pressure (<30 mmHg) Tachypnea and jugular venous distention. Characteristic murmurs of MS and MR may be audible Rales are audible with LVF Oliguria (urine output < 30 mL/h) is common 40 HISTORY AND PHYSICAL EXAMINATION

41. LABORATORY TESTS TLC - ↑ Hepatic transaminases - ↑ BUN & S.Cr - ↑ ↑ anion gap acidosis ↑ lactic acid level Arterial blood gases: hypoxemia and metabolic acidosis with compensatory respiratory alkalosis Cardiac markers CPKMB ↑ ↑ TROPONIN - I & T ↑ 41

42. Chest X-Ray Shows pulmonary vascular congestion and often pulmonary edema Echocardiography Excellent tool for confirming the diagnosis of cardiogenic shock and ruling out other causes of shock ECG >2-mm ST elevation in multiple leads or LBBB are usually present. 55% of all infarcts associated with shock are anterior in location.

43. THERAPEUTIC OPTIONS General measures Vasopressors Intra-aortic balloon pumping (IABP) Reperfusion-revascularization : percutaneous transluminal coronary angioplasty (PTCA) 43

44. GENERAL MEASURES Central venous and arterial access, bladder catheterization, and pulse oximetry are instituted Hypoxemia and acidosis must be corrected Most patients require ventilatory support to correct these abnormalities and reduce the work of breathing Electrolyte abnormalities should be corrected Hyperglycemia should be corrected with continuous infusion of insulin 44

45. Relief of pain and anxiety with Morphine sulfate (or fentanyl) Bradyarrhythmias and tachyarrhythmias may require immediate treatment with antiarrhythmic drugs, cardioversion, or pacing Hemodynamic goals: Systolic BP of ~90 mmHg or Mean BP > 60 mmHg and PCWP of ~15 mmHg 45

46. OBSTRUCTIVE SHOCK Impaired diastolic filling (decreased ventricular preload) - Tension pneumothorax - Constrictive pericarditis - Cardiac tamponade - intrathoracic obstructive tumors A form of cardiogenic shock that results from mechanical impediment to circulation leading to depressed CO rather than primary cardiac failure

47. Impaired systolic contraction (increased ventricular afterload) - Pulmonary embolus (massive) - Acute pulmonary hypertension - Aortic dissection THERAPEUTIC OPTIONS : General measures ICTD insersion Thoracotomy Pericardiocentesis embolectomy

48. Distributive Shock Inadequate perfusion of tissues through maldistribution of blood flow Intravascular volume is maldistributed because of alterations in blood vessels Cardiac pump & blood volume are normal but blood is not reaching the tissues 48

49. Distributive Shock : Septic (bacterial, fungal, viral)-most common Anaphylactic shock Neurogenic (spinal shock) Endocrinological causes- • Adrenal crisis • Thyroid storm

50. Septic shock: Syndrome of profound hypotension due to release of endotoxins / TNF / vasoactive peptides following bacterial destruction Usually associated with normal blood volume, high CO and low SVR Re-distribution of blood to splanchnic vessels with resultant poor skin perfusion

51. New definition of sepsis The terms SIRS and severe sepsis were eliminated Sepsis is now defined as life threatening organ dysfunction caused by a dysregulated host response to infection Organ dysfunction is newly defined in terms of a change in baseline SOFA (sequential organ failure assessment) score Septic shock is defined as the subset of sepsis in which underlying circulatory and cellular or metabolic abnormalities are profound enough to increase mortality substantially. **Feb 2016 Society of Critical Care Medicine and the European Society of Intensive Care Medicine.

52. Quick SOFA scoring A new clinical sepsis screening tool Components : 1.Respiratory rate >22 2.Glasgow coma score <15 3.Systolic blood pressure <100 mm hg ≥2 positive screening.

53. Clinical Manifestations of septic shock 1.Early phase: Massive vasodilation – Pink, warm, flushed skin Increased Heart Rate - Full bounding pulse Tachypnea Crackles 2.Late phase: Vasoconstriction – Skin is pale & cool Significant tachycardia Decreased BP Decreased Urine output Metabolic & respiratory acidosis with hypoxemia

54. Management of septic shock

55. SURVIVING SEPSIS CAMPAIGN BUNDLES: To be completed within 3 hours: Measure lactate level 2) Obtain blood cultures prior to administration of antibiotics 3) Administer broad spectrum antibiotics 4) Administer 30 ml/kg crystalloid for hypotension or lactate ≥4mmol/l

56. SURVIVING SEPSIS CAMPAIGN BUNDLES contn : To be completed within 6 hours: 5) Apply vasopressors for persistent hypotension- to maintain A MAP 65 mm hg 6) In the event of persistent arterial hypotension despite volume resuscitation (septic shock) or initial lactate ≥ 4 mmol /l (36 mg/dl): - Measure CVP and scvo2 7) Remeasure lactate if initial lactate was elevated *Targets for quantitative resuscitation included in the guidelines are cvp of 8 mm hg, scvo2 of 70%, and normalization of lactate

57. Commonly used Vasopressor and Inotropic Drugs

58. Drugs Calculation rule Nor epinephrine 0.3× body wt in kg is the number of mg to add to make a final volume of 50 ml Adrenaline     Then, 1ml/ hr delivers 0.1µg/kg/min Dopamine Dobutamine 3× body wt in kg is the number of mg to add to make a final volume of 50 ml Then, 1ml/hr delivers 1µg/kg/min Arenaline nor epinephrine .03× body wt in kg is the number of mg to add to make a final volume of 50 ml       Then, 1ml/ hr delivers .01 µg/kg/min The formula Rule of 3 had been stated in The Harriet Lane Handbook is as follows: “3 × weight (kg) equals the amount of drug in mg that should be added to 50 ml of solution. The infusion volume in milliliters per hour (ml/hour) will then equal the mcg/kg/minute dose ordered.”    

59. Neurogenic Shock 59

60. Neurogenic Shock Results from the loss or suppression of sympathetic tone Causes massive vasodilatation in the venous vasculature, venous return to heart, cardiac output Most common etiology: Spinal cord injury above T6 It is rarest form of shock 60

61. PATHOPHYSIOLOGY 61 Imbalance between Sympathetic and Parasympathetic stimulation Massive vasodilation Vascular tone SVR Inadequate C.O Tissue perfusion Impaired cellular metabolism SHOCK

62. DIAGNOSIS Loss of sympathetic nervous system function -Relative bradycardia and hypotension -Warm, flushed skin -Loss of bladder control 62

63. Treatment strategies Airway control should be ensured with spinal immobilization and protection . Crystalloid IV fluids should be infused Inotropic agents may be added in titrated doses if needed Severe bradycardia should be treated with Atropine 0.5 to 1.0 mg IV (every 5 min for a total dose of 3.0 mg) or with a Pacemaker In the presence of Neurologic Deficits, high-dose Methylprednisolone therapy should be instituted within 8 h of injury A 30 mg/kg bolus should be administered over 15 min followed by a continuous infusion of 5.4 mg/kg per h for the next 23 h 63

64. Anaphylactic shock 64

65. Anaphylactic shock: Immediate hypersensitivity reaction (Type I) mediated by the interaction of IgE on mast cells and basophils with the appropriate antigen Primary mediators include Histamine, Serotonin, Eosinophil, Chemotactic Factor, and Proteolytic Enzymes Secondary mediators include PAF, bradykinin, prostaglandins, and leukotrienes 65

66. CLINICAL FEATURES Early • Sensations of warmth, itching especially in axillae and groins • Feelings of anxiety or panic Progressive • Erythematous or urticarial rash • Oedema of face, neck, soft tissues Severe • Hypotension (shock) • Bronchospasm(wheezing) • Laryngeal edema(dyspnea, stridor, aphonia, drooling) • Arrhythmias, cardiac arrest. 66

67. MANAGEMENT The ABCD’s of resuscitation should be followed Administer oxygen by face mask at 6–8 L/minute 3. ADRENALINE ADULTS : Inject adrenaline 1:1000 intramuscularly: average adults (50–100 kg) give 0.50 mL large adults (>100 kg) give 0.75 mL Establish one or preferably two wide bore intravenous lines (16 gauge or larger) 5. If there is severe laryngospasm, bronchospasm, circulatory shock or coma, intubate and commence IPPV 67

68. Additional measures : • Beta2 agonists for bronchospasm • Antihistaminics • Corticosteroids • Nebulised adrenaline However, do not delay intubation if upper airways obstruction is progressive. 68

69. 71 Conclusion Survival and outcomes improve with early perfusion, adequate oxygenation and identification with appropriate treatment of the cause of shock Identification depends on signs and symptoms, basic investigations, point of care studies: RUSH protocol, TEG Target the lethal triad in trauma: hypothermia, acidosis and coagulopathy

70. Conclusion contn : DCR used during the initial phases of damage control has further been associated with improved mortality rates and reduced incidence of complications in major trauma patients Following surviving sepsis guidelines improve patient outcome in septic shock. Choice of vasopressors should be kept in mind for different types of shock .

71. Thank you