Shock from a surgical point of view

1. SHOCK
PATHOPHYSIOLOGY
CLINICAL FEATURES
MANAGEMENT
DR ANKIT SHARMA
DR ARUN KUMAR M
1

2. SAMUEL V GROSS, 1872
“Shock is the
manifestation of
the rude unhinging
of the machinery
of life”
2

3. HISTORICAL
PERSPECTIVE
• Ambroise Paré (1510) – Fluids to injured patients
• ‘Shock’ – 1743 – act of impact/ collision
• Guthrie (1815) – described physiological instability
• Crile (1899) – Importance of measuring BP
• Claude Bernard – Milieu intérieur
• Walter B. Cannon – Homeostasis
• WW I – Disturbance of nervous system
• Alfred Blalock (1934) – 4 categories of shock
• Carl John Wiggers (1950) – Wiggers prep
3

4. Definition
A systemic state of tissue hypo-perfusion, which is inadequate for
normal cellular respiration
 Systemic – global phenomenon
 Hypoperfusion (relative/ absolute)
 Inadequate cellular respiration
 Anaerobic, dysfunction
 Body responses thereof
4

5. Types
• Hypovolemic
• Cardiogenic
• Septic (vasogenic)
• Neurogenic
• Traumatic
• Obstructive
5

6. Hypovolemic shock
• Hemorrhagic
• Trauma
• Bleeding disorders
• GI/ GU bleed
• Non- hemorrhagic
• Dehydration
• “Inter compartmental fluid mal-adjustments”
• Third spacing
6

7. Cardiogenic Shock
• Pump failure
• Adequate but ineffective intravascular volume.
• Cardiac causes
• Pulmonary embolism
• High mortality rates
8

8. Cardiogenic shock
• Hemodynamic criteria:
1. Sustained Hypotension (i.e. SBP <90 mm Hg
for at least 30 minutes)
2. Reduced Cardiac Index (<2.2 L/min per
square meter) &
3. Elevated Pulmonary Artery Wedge Pressure
(>15 mm Hg)
9

9. SEPTIC SHOCK
• Four sepsis-related clinical syndromes = Four steps of
increasingly exaggerated systemic inflammatory responses
SIRS
Sepsis
Severe Sepsis (Sepsis Syndrome)
Septic Shock
11

10. DEFINITIONS DESCRIBING THE
CONDITION OF SEPTIC PATIENTS
Bacteremia: Bacteria in blood
Positive blood cultures
Septicemia: Microbes or their toxins in blood
12

11. DEFINITIONS DESCRIBING THE
CONDITION OF SEPTIC PATIENTS
SIRS: Two or more of the following
 (1) Temperature >38°C or <36°C
 (2) Heart Rate > 90/ min
 (3) Respi rate > 24/ min
 (4) TLC >12,000/mm3 or <4,000/mm3)
or >10% bands on PBS
◦ SIRS may have a noninfectious etiology
Sepsis: SIRS that has a proven/ suspected microbial etiology
13

12. DEFINITIONS DESCRIBING THE
CONDITION OF SEPTIC PATIENTS
Severe Sepsis (Similar to sepsis syndr): Sepsis with one or more signs of
organ dysfunction:
1. Cardiovascular
2. Renal
3. Respiratory
4. Hematologic
5. Unexplained metabolic acidosis
6. Adequate fluid resuscitation
14

13. DEFINITIONS DESCRIBING THE
CONDITION OF SEPTIC PATIENTS
Septic Shock: Sepsis + Hypotension
or
Need for vasopressors to
maintain systolic BP 90 mmHg
or MAP70 mmHg
15

14. DEFINITIONS DESCRIBING THE
CONDITION OF SEPTIC PATIENTS
Refractory septic shock: Septic shock
◦ lasting for >1 h
◦ Not responding to fluid or pressor administration
MODS: Dysfunction of more than one organ system,
requiring intervention (individual organ support) to maintain
homeostasis
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15. NEUROGENIC SHOCK
• Acute loss of sympathetic vascular tone
• Loss of vascular resistance
◦ Pooling in capacitance vessels
◦ Reduced preload
◦ Poor cardiac output
◦ Inadequate pressure in arterial system to
maintain capillary perfusion
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16. NEUROGENIC SHOCK
Etiology:
◦ High cervical spinal cord injury (vertebral body #)
◦ inadvertent cephalad migration of spinal anaesthesia
◦ epidural hematoma or devastating head injury
Failure of fluid resuscitation to improve hemodynamics, where no source of blood
loss or sepsis can be identified
Vasopressors are necessary to treat this condition
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17. TRAUMATIC SHOCK
• Hemorrhage overtly controlled, but
patients continues to lose plasma volume
into the interstitium
• Secondary microcirculatory injury
• Excessive pro-inflammatory response
• Third spacing
19

18. OBSTRUCTIVE SHOCK
• Reduction in preload due to mechanical
obstruction of cardiac filling
•Common causes: cardiac tamponade,
tension pneumothorax, massive pulmonary
embolus or air embolus
20

19. PATHOPHYSIOLOGY OF SHOCK
• Initial response driven by
• Tissue hypoperfusion
• Developing cellular energy deficit.
• Demand-supply mismatch
• Neuro-endocrine & inflammatory response (proportional
to degree & duration of shock)
• The specific responses depends on etiology of shock
21

20. 22SHOCK INDUCED VICIOUS CYCLE

21. CELLULAR PATHOPHYSIOLOGY
• Compensation/ Dysfunction/ Death
23

22. ↓ O2 concn in cells
↓
↓ oxidative phosphorylation
↓
↓ ATP synthesis
↓
shift from aerobic to anaerobic glycolysis
↓
Pyruvate converted to lactate
↓
accumulation of lactate & inorganic phosphate, thus ↓ pH
↓
intracellular metabolic acidosis  lactate & other wastes exit cells
↓
systemic metabolic acidosis
25

23. MICROVASCULAR
PATHOPHYSIOLOGY
• α1 receptors – vasoconstriction
• ẞ2 receptors - vasodilation.
• Shock  norepinephrine & epinephrine from
adrenal medulla → α1 receptors
• Other constrictors: A-II, vasopressin, endothelin 1,
and TxA2
• Vasodilators: PG I2, NO and adenosine
28

24. Hypoxia & acidosis
↓
Complement & neutrophil activation
↓
Free radical & cytokine release
↓
Injury to capillary endothelial cells
↓
Further activation of immune & coagulation systems
↓
Damage to endothelium with loss of integrity
↓
Leaky capillary endothelium
↓
Tissue edema & cellular hypoxia
29

25. CARDIOVASCULAR
PATHOPHYSIOLOGY
30
Shock
↓
↓ Preload & ↓ Afterload
↓
↑ sympathetic output
↓
catecholamine release from adrenal medulla
↓
↑ heart rate & contractility
venous and arterial vasoconstriction (Except in sepsis)

26. 31
• Arterial vasoconstriction with regional
variations
• Shunting of blood away from less essential
organ beds such as the intestine, kidney, and
skin
• Brain & heart – autoregulatory mechanisms
CARDIOVASCULAR
PATHOPHYSIOLOGY

27. PULMONARY PATHOPHYSIOLOGY
• Tachypnea
• ↑ minute ventilation & ↑ CO2 excretion
• Compensatory respiratory alkalosis
• Resuscitation induced O2 free radical injury
• ALI & ARDS
• Non cardiogenic pulmonary edema
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28. RENAL PATHOPHYSIOLOGY
• Decreased renal blood flow
• RAS activation
• ↓ GFR + ↑ aldosterone & vasopressin → Oliguria
• Further vasoconstriction → ↑ sodium & water
retention → edema
• Toxic tubular injury & Tubular obstruction
33

29. ENDOCRINE PATHOPHYSIOLOGY
• Na+ & water retention  K+ & H+ lost
• Hypovolaemia  ADH
• Adrenergic drive  Norepinephrine release
•Vasoconstriction
•↑ glycogenolysis & ↑ gluconeogenesis
•↓ Insulin release
34

30. CRH (Hypothalamus)
↓
ACTH (pituitary)
↓
Cortisol (Adrenal Cortex)
↓
Cortisol + Epinephrine + Glucagon  Catabolic state
↓
Gluconeogenesis & Insulin resistance
↓
Hyperglycemia, Muscle protein break down, lipolysis
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ENDOCRINE PATHOPHYSIOLOGY

31. METABOLIC
DERANGEMENTS
• Disruption of C-P-L metabolism
• Anaerobic metabolism  Lactate
• ↑ Hepatic gluconeogenesis
• Hepatic lipogenesis  ↑ TG
• Protein catabolism → muscle wasting
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32. INFLAMMATORY &
IMMUNE RESPONSE
Pro-inflammatory Anti-inflammatory
IL-1α/ẞ IL-4
IL-2 IL-10
IL-6 IL-13
IL-8 IL-1Ra
IFN-ϒ PGE2
TNF-α TGF-β
PAF
TNFR- I/II
37

33. INFLAMMATORY &
IMMUNE RESPONSE
• MODS
• Counter-regulatory immune response
• Delayed MOF
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34. SEPTIC SHOCK
• Culture proven etiology +/-
• Any class of micro-organism
• Gram (-) ve bacteria > Gram (+) ve bacteria >
polymicrobial infection > fungi
• Gm (-) ve bacteria = Enterobacteriaceae, pseudomonads,
Haemophilus etc.
•Gm (+) ve bacteria = S.aureus, coagulase (-) ve staph,
enterococci, S.pneumoniae etc.
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35. SEPTIC SHOCK
Myocardial depression
+ Hypovolemia
+ other factors
↓
Tissue hypoxia (hypodynamic pd)
↓
↑ blood lactate & ↓ central venous O2 saturation
41

36. SEPTIC SHOCK
After fluid administration
↓
↓ peripheral vascular resistance
(vasodilatory phase)
Hallmark of septic shock
42

37. Clinical Features & Management
45

38. Severity of shock
Compensated shock
Decompensation
•Mild shock
•Moderate shock
•Severe shock
Unresuscitable Shock
MOF
46

39. Severity of shock
Compensated shock
◦ Loss of up to 15% of circulatory volume
◦ Maintain central blood volume
◦ If prolonged (>12 hrs)  Ischaemia-Reperfusion effect
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40. Severity of shock
Decompensation
◦ Loss of > 15% of circulating volume.
◦ Progressive Renal, Respiratory & Cardiovascular decompensation.
◦ Hypotension  >30-40% volume loss.
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41. Severity of shock
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42. Hemorrhagic shock
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43. Hemorrhagic shock
Most common cause of shock in the surgical or trauma patients
Young patients vs elderly patients
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44. Hemorrhagic shock
Classification of hemorrhage
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45. Hemorrhagic shock
Approach to Hemorrhagic shock
Identify haemorrhage
Immediate resuscitative maneuvers
Identify the site of haemorrhage
Haemorrhage control
Damage control resuscitation
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46. Hemorrhagic shock
Treatment concurrently with diagnostic evaluation
Time dependent survival
Resuscitative maneuvers
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47. Hemorrhagic shock
History
Root cause of hemorrhage & its site
Any underlying Pathology
Any co-morbidities/medications
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48. Hemorrhagic shock
Symptoms & Signs:
Agitation, Cold clammy extremities
Tachycardia, Hypotension
Pallor
Weak or absent peripheral pulses
Prolonged capillary refill time
Systemic examination
Symptoms specific to site of Hemorrhage
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49. Hemorrhagic shock
Site specific Symptoms & Signs:
Penetrating wounds / Blunt trauma
Sites that can harbor sufficient extra-vascular volume:
Intrathoracic (2-3L/ pleural cavity)
Intraabdominal
Retroperitoneal
# long bones
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50. Hemorrhagic shock
Investigations
Hematological & Biochemical Investigations
Lactate levels
Blood grouping & cross matching
Radiological investigations as indicated
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51. Hemorrhagic shock
Damage control resuscitation
Permissive hypotension
Use of limited crystalloids and blood products
Anticipate and treat coagulopathy
Hypothermia
DCS
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52. Hemorrhagic shock
Fluid therapy
Crystalloid
Hypotonic solutions
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53. Hemorrhagic shock
Fluid therapy : Dynamic Fluid Response
To determine shock status
250-500ml bolus over 5-10min
HR, BP & CVP are measured
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54. Hemorrhagic shock
Responders
• Sustained improvement in CVS status after bolus
• No active bleeding, require fluids to attain normal volume status
Transient Responders
• Initial improvement followed by reverting to previous state over 10-20 min
• Moderate ongoing fluid losses
Non responders
• No improvement in CVS status following bolus
• Severely volume depleted and likely to have ongoing loss( persistent uncontrolled
Hemorrhage)
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55. Hemorrhagic shock
Transfusion of blood and blood products
Coagulation factor-based products
Blood product Aim
PRBC Hb 7-9 gm/dl
Platelets > 50,000/ml
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56. Hemorrhagic shock
Monitoring of response
◦ Clinical : Conscious level, BP, Urine output
◦ ECG
◦ Pulse oximetry
◦ CVP, Invasive BP monitoring
◦ Cardiac output
◦ Base deficit & serum lactate
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57. Hemorrhagic shock
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58. Traumatic shock
Initial resuscitation
Control of Hemorrhage
Early stabilization of the fractures, debridement or evacuation of
hematoma
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59. Septic Shock
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60. Septic shock
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61. SEPSIS SIX
The Sepsis Six is the name given to a bundle of medical therapies designed to reduce
the mortality of patients with sepsis.
The Sepsis Six consists of three diagnostic and three therapeutic steps – all to be
delivered within one hour of the initial diagnosis of sepsis.
◦ Deliver high-flow oxygen.
◦ Take blood cultures.
◦ Administer empiric intravenous antibiotics.
◦ Measure serum lactate and send full blood count.
◦ Start intravenous fluid resuscitation.
◦ Commence accurate urine output measurement.
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62. Management of severe sepsis
Initial Resuscitation and Infection Issues
Hemodynamic Support and Adjunctive Therapy
Supportive Therapy of Severe Sepsis
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63. Initial Resuscitation and Infection Issues
A. Initial Resuscitation
B. Screening for Sepsis and Performance Improvement
C. Diagnosis
D. Antimicrobial Therapy
E. Source Control
F. Infection Prevention
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64. A. Initial Resuscitation
Resuscitation of patients with sepsis- induced tissue
hypoperfusion
◦ defined as hypotension persisting after initial fluid challenge or blood
lactate concentration ≥ 4 mmol/L
EGDT (first 6 hrs of resuscitation)
◦ a) CVP 8–12 mm Hg
◦ b) MAP ≥ 65 mm Hg
◦ c) Urine output ≥ 0.5 mL/kg/hr
◦ d) Scvo2 or Svo2 70% or 65%, respectively
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65. B. Screening for Sepsis and Performance
Improvement
Routine screening of seriously ill patients for severe sepsis to
increase the early identification of sepsis
allow implementation of early sepsis therapy
Performance improvement efforts to improve patient outcomes
and decrease sepsis-related mortality.
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66. 74

67. C. Diagnosis
Cultures
Imaging studies
1,3 β-d-glucan assay ,mannan and anti-mannan antibody assays
75

68. D. Antimicrobial Therapy
Initial empiric anti-infective therapy
Broad spectrum
Anti fungals
Reassessed daily for potential de-escalation
Combination empiric therapy
Duration & De-escalation
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69. E. Source Control
Intervention for source control within the first 12 hr of diagnosis.
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70. Haemodynamic support & Adjunctive therapy
Fluid therapy
Vasopressors
Inotropic support
Corticosteroids
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71. Haemodynamic support & Adjunctive therapy
Fluid therapy
Crystalloids
Albumin
Vasopressors
Noradrenaline
Adrenaline
Vasopressin
Dopamine
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Ionotropic agents : Dobutamine
Corticosteroid

72. Supportive therapy
Blood products administration
Mechanical ventilation of sepsis
induced ARDS
Sedation, analgesia & neuromuscular
blockade
Glucose control
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Renal replacement therapy
DVT prophylaxis
Stress ulcer prophylaxis
Nutrition
Setting goals of care

73. Cardiogenic Shock
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74. Cardiogenic shock
Causes:
◦ Acute MI (most common)
◦ Arrythmia
◦ End stage cardiomyopathy
◦ Myocarditis
◦ Severe myocardial contusion
◦ LV outflow obstruction
◦ Obstruction to LV filling
◦ MR
◦ Acute aortic insufficiency
◦ Metabolic
◦ Drug reactions
82

75. Cardiogenic shock
Diagnosis
ECG & ECHO
CXR
ABG
Cardiac enzymes
Invasive monitoring
83

76. Cardiogenic shock
Treatment
Aims of treatment
Adequate oxygenation
Judicious fluid administration
Adequate Analgesia
Correcting electrolyte imbalances
84

77. Cardiogenic shock
Treatment
Ionotropic support (Dopamine/Dobutamine)
Treatment of cause
85

78. Obstructive Shock
86

79. Obstructive shock
Causes:
◦ Tension Pneumothorax
◦ Pericardial Tamponade
◦ Pulmonary embolus
◦ IVC obstruction [Gravid uterus, DVT, Neoplasm]
◦ Increased Intra-thoracic pressure [ Excess end-expiratory pressure, Neoplasm]
87

80. Obstructive shock
Diagnosis
Diagnosis is clinical
Chest X-Ray
Echocardiography
Pericardiocentesis
Treatment of the cause
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81. Neurogenic Shock
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82. Neurogenic shock
Causes
Spinal cord Trauma
Spinal cord Neoplasm
Spinal / Epidural anesthesia
90

83. Neurogenic shock
Diagnosis:
Hypotension with bradycardia
Warm extremities
Motor and sensory deficits
Radiographic evidence of vertebral fracture
91

84. Neurogenic shock
Treatment
Fluid resuscitation
Ionotropic support
Operative attempt to stabilise the vertebral fracture.
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85. THANK YOU
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