1. Consultant Hepatobiliary Surgeon
Shock
HAMAD ALQAHTANI
Professor of Surgery
Consultant Hepatobiliary Surgeon
College of Medicine
King Saud University

2. Definition
Shock exists when circulating blood has failed to deliver the required oxygen to meet the cell’s metabolic requirements.

3. Introduction
Shock is the commonest cause of death in surgical patients.
Early and rapidly: Severe profound shock state.
Late: Ischemia, reperfusion, and organs failure.
It is important to understand the following points in shock
Etiology
Pathophysiology
Diagnosis
Management priorities of shock.
Early recognition and treatment of shock is needed to prevent irreversible tissue damage and organs failure.

4. Shock state does not mean hypotension.
Hypotension is one of the latest signs of shock.
Young healthy patients are able to maintain blood pressure until late stages of shock by increasing:
Stroke volume
Peripheral vasoconstriction.

5. Old patient decompensate earlier than the young patient.
Beta-blockers and pacemaker can prevent the tachycardic response and the diagnosis of shock can be challenging in this situation.

6. consequences of delayed or untreated shock
1. Reduced oxygen consumption 2. Anaerobic cell metabolism 3. Tissue acidosis 4. Cellular dysfunction 5. Multiple organ dysfunction 6. Death

7. Types of shock (1) Hypovolemic shock
It is the commonest type and the most treatable cause of shock in surgical practice.
It is due to reduced intravascular fluid volume secondary to:
Hemorrhagic causes
Trauma
Surgery
Gastrointestinal
Others

8. Non-hemorrhagic causes
Poor fluid intake
Excessive fluid loss due to vomiting, diarrhea, fistula, urinary loss (diabetes ketoacidosis).
Evaporation during prolonged surgery
Third spacing where the fluid is lost into the interstitial compartment (e.g. acute pancreatitis or burn).

9. Severity of hypovolemic shock
The severity of hemorrhagic shock is classified according to the percentage of estimated blood volume loss.

10. Classification of Hypovolaemic Shock
Class I
Class II
Class III
Class IV
CNS Symptoms
Normal
Anxious
Confused
Lethargic
Blood Loss (ml)
< 750
750–1500
1500–2000
> 2000
Blood Loss
(% EBV)
< 15 %
15–30%
30–40%
> 40%
Pulse
< 100
> 100
> 120
> 140
Blood Pressure
Decreased
Respiratory Rate
14–20
20–30
30–35
> 35
Urine Output
(ml/h)
> 30
5–15
Negligible

11. (2) Septic shock
It can be defined as sepsis-induced hypotension that persist despite adequate intravascular fluid resuscitation.
It causes disturbances in oxygen delivery and consumption.

12. Sepsis usually arises from a localized bacterial focus of infection in the lungs, abdomen, pelvis, urinary tract, and skin.
It is most commonly due to Gram-positive, followed by endotoxin-producing Gram-negative bacteria.

13. Infection in septic shock triggers a cytokine-mediated proinflammatory response which results in:
1. Peripheral vasodilation
2. Redistribution of blood flow
3. Endothelial cell activation
4. Increased vascular permeability
5. Formation of microthrombi within the microcirculation

14. Typically cardiac output increases in septic shock in compensation for the peripheral vasodilation.
Microcirculatory dysfunction in septic shock impairs the delivery of oxygen to the cells, despite hyperdynamic circulation with a global increase in oxygen delivery.

15. The late stage of septic shock characterized by hypotension due to:
1. Vasodilatation
2. Loss of intravascular fluid to the interstitial compartment (third spacing resulting in edema)
3. Myocardial depression

16. (3) Cardiogenic Shock
This occurs due to heart failure (pump failure) to maintain the cardiac output that meets the metabolic requirements of the body.
Causes of cardiogenic shock:
1. Arrhythmias
2. Cardiomyopathy
3. Myocardial infarction
4. Valvular heart disease
5. Blunt myocardial injury

17. 6. Myocardial depression (e.g. humoral agents during sepsis or drugs)
7. Cardiac tamponade
8. Massive pulmonary embolism
9. Tension pneumothorax

18. (4) Anaphylactic Shock
This is a severe systemic hypersensitivity reaction following exposure to an allergen which triggers the release of vasoactive mediators (prostaglandins, histamine, and kinins) from basophils and mast cells.
This systemic reaction cause shock by the following cardiovascular changes:
1. Vasodilation
2. Intravascular volume redistribution
3. Capillary leak
4. Reduction in cardiac output

19. Common causes of anaphylaxis in surgical practice:
Drugs (e.g. β-lactam antibiotics)
2. Colloid solutions (e.g. dextrans)
3. Radiological contrast media (intravenous injection of contrast)
4. Latex (e.g. latex medical gloves)

20. (5) Neurogenic Shock
This is due to loss of sympathetic tone in the vascular smooth muscle. This occurs most commonly due to injury to the cervical or thoracic spinal cord and results in:
1. Profound vasodilation
2. Fall in systemic vascular resistance
3. Warm, flushed skin due to vasodilation
4. Bradycardia
5. Hypotension
6. Respiratory arrest (injury above the 3rd cervical vertebra)

21. The terminology used in the Classification of Shock
Obstructive Shock
This term is used to indicates the reduction in the preload and cardiac filling.
Massive pulmonary embolism
Air embolism
Tension pneumothorax
Cardiac tamponade

22. Distributive Shock
This response is characterized by inadequate tissue perfusion, vasodilatation, hypotension, low systemic vascular resistance, and low afterload. All results in the high cardiac output.
Neurogenic
Septic
Anaphylactic shock

23. Pathophysiology of shock
Cells
Deprivation of cells from oxygen
Switch of the cell’s metabolism from aerobic to anaerobic
Lactic acidosis

24. 4. Failure of sodium/potassium pump in the cell membrane and intracellular organelle failed which results in two major events:
Intracellular release of autodigestive enzymes from lysosomes resulting in cell lysis and death.
The release of intracellular contents, including the potassium into the systemic circulation.

25. Microcirculation
Progression of hypoxia, ischemia, and acidosis will activate the immune system (neutrophils and complements) and coagulation system.
Release of oxygen free radicles and cytokines
Injury to the endothelial cells
Further activate the immune and complement systems
Loss of the integrity of endothelial cells and becomes “leaky”.
Fluid loss through the spaces between the endothelial cells will cause tissue edema and exacerbation of cellular hypoxia.

26. Systems/Organs
Adequate perfusion and oxygen delivery to vital organs (brain, heart, skeletal muscle) will be compromised when compensatory mechanisms have failed.
In severe, prolonged or uncorrected shock (‘decompensated’ shock), the clinical manifestations of organ hypoperfusion become apparent due to prolonged severe hypoxia and acidosis which may result in organ dysfunction and failure.

27. Nervous System
1. Restlessness 2. Confusion 3. Stupor 4. Coma 5. Encephalopathy and/or delirium are common in sepsis or septic shock

28. Cardiovascular System
Reduced preload and afterload compensatory baroreceptor responses (increased sympathetic response and release of catecholamines) tachycardia and systemic vasoconstriction (except in septic shock).
2. Decrease diastolic pressure reduced coronary blood flow.

29. 3. Decrease myocardial oxygen delivery may result in:
Myocardial ischemia
Decreased myocardial contractility
Decreased cardiac output.
4. Acidosis, electrolyte disturbances and hypoxia arrhythmias
5. Widespread endothelial cell activation microcirculatory dysfunction.

30. Respiratory System
1. The increased sympathetic response and metabolic acidosis result in:
Tachypnea
Increased minute ventilation to increase carbon dioxide elimination (compensatory respiratory alkalosis).
2. Increased ventilation/perfusion mismatch and shunting, which will result in hypoxia

31. 3. Pulmonary edema (common in cardiogenic shock) with hypoxia 4
3. Pulmonary edema (common in cardiogenic shock) with hypoxia 4. Acute lung injury and acute respiratory distress syndrome with hypoxia

32. Gastrointestinal Tract
Splanchnic hypoperfusion will lead to the breakdown of the gut mucosal barrier
Translocation of bacteria/bacterial wall contents into the bloodstream will lead to the systemic inflammatory response syndrome and sepsis

33. 3. Acute ischaemic hepatitis (in the severe case may result in prolonged prothrombin time, hypoglycemia and very high transaminases –ALT and AST)
4. Stress ulceration and gastroduodenal bleeding
5. Decreased motility and impaired absorption

34. Renal System Activation of the renin-angiotensin system:
Vasoconstriction
Sodium and water reabsorption in the kidney.
2. Oliguria (< 0.5 ml/kg/h urine)
3. Anuria
4. Acute renal failure (Acute tubular necrosis) with high urea and creatinine, hyperkalemia and metabolic acidosis.

35. Endocrine System Adrenal activation with release of catecholamines
Renin-angiotensin-aldosterone system activation, which increase reabsorption of sodium followed by water in the distal renal tubules and collecting ducts of the kidneys.

36. Release of vasopressin (antidiuretic hormone-ADH) from the hypothalamus
Vasoconstriction
Water resorption in the renal collecting tubules.
Cortisol release from adrenal glands
Sodium and water resorption
Sensitization of the cells to catecholamines.

37. Ischemia-Reperfusion Effect of Shock
Hypoperfusion and hypoxia
Damage to the cells and organs
Restoration of normal organ perfusion cause further damage
Acidosis and hyperkalemia
Myocardial depression
Vasodilatation with further aggravation of hypotension.
Neutrophils, complements and microthrombi will be flushed back into circulation after reperfusion
Endothelial injury in the lung, kidneys and other organs.
Acute renal, and lung injury, other organ failure, and death.
This ischemia-reperfusion effects can only be attenuated by reducing the extent and duration of hypoperfusion.

38. Clinical features of shock
Initially, the endocrine and cardiovascular compensatory responses reduce the blood flow to non-essential organs (skin, muscles, gastrointestinal tract) to maintain the blood flow to the kidneys, lungs, and brain.
During this stage, there is metabolic acidosis and activation of humoral and cellular elements in the non-perfused organs.

39. If the shock is inadequately treated, the compensation stage will result in decompensation with:
Profound hypotension
Tachycardia
Hypoperfusion of organs,
This result in:
Impaired level of consciousness
Oliguria
Anuria
Increased in lactic acid
Ultimately organ failure and death.
Tachycardia may not be a manifestation of shock in some patients, such as the patient on beta-blocker or implanted cardiac pacemaker. These patients are unable during shock to mount a tachycardia.

40. Mild Shock Tachycardia Tachypnea Mild drop in the urine output
Mild anxiety
Blood pressure is maintained despite
Decreased pulse pressure
Peripheries are cool
Sweaty with prolonged capillary filling time
Patients with septic shock will have flushed, warm peripheries, with briskly capillary refilling despite profound shock.

41. Moderate Shock Tachycardia Drop in the blood pressure Mildly confused
Drowsy.
Urine output below 0.5 ml / kg/hour.

42. Severe Shock Profound tachycardia Profound hypotension Unconsciousness
Labored respiration
Urine output drop to zero (anuria)

43. Hypovolemic Shock Management of shock
Airway, breathing, and circulation (ABC)
Oxygenation
Fluid resuscitation (crystalloid or colloid).
Urinary catheterization is required to monitor the urine output.
Blood transfusion.

44. Control of hemorrhage
Analgesia
Inotropes
Admission
Massive transfusion can cause:
Hypothermia
Hypocalcemia
Hyper-or hypokalaemia
Coagulopathy

45. Septic Shock
The most important aspect of septic shock is early recognition, which requires a high index of suspicion, with a detailed history and physical examination to identify potential sources of infection and signs of organ dysfunction.

46. Septic shock is associated with relative and absolute hypovolemia as a result of: 1. Profound vasodilation 2. Fluid extravasation from the intravascular space to the interstitial space (third spacing).
The two main principles guiding the management of septic shock are:
The identification and treatment of underlying infection
Early optimization of tissue oxygen delivery.

47. 1. Airway, breathing, and circulation (ABC) 2
1. Airway, breathing, and circulation (ABC) 2. Fluid (crystalloid or colloid) resuscitation 3. Oxygenation. 4. Vasopressor 5. Intravenous hydrocortisone

48. 6. Treatment of infection
Intravenous antibiotics must be administered as soon as possible.
It should cover all likely pathogens (bacterial and/or fungal).
It usually involves the use of empirical broad-spectrum antibiotics to be changed according to the microbiological investigations (gram stain & culture and sensitivity).
Peripheral blood culture should be taken prior to the antibiotics administration.

49. Targeted imaging, including chest x-ray, ultrasound, computed tomography may be required to localize the site of the focus of infection.
Adequate source control which includes removal of infected devices abscess drainage and debridement of infected tissue
Interventions to prevent ongoing microbial contamination such as biliary drainage or repair of a perforated viscus.
It should be performed immediately after initial resuscitation and should be achieved with the minimum physiological disturbance.
Percutaneous or endoscopic interventions are preferable to open surgery where possible.

50. Cardiogenic Shock
Acute anterior myocardial infarction is the commonest cause of cardiogenic shock. The major disturbances in cardiogenic shock are a reduced cardiac output with a compensatory increase in systemic vascular resistance.

51. Correction of electrolytes abnormalities
Airway, breathing, and circulation (ABC)
Administration of oxygen
Intravenous opiates
Correction of hypovolemia
Correction of electrolytes abnormalities
Investigations (underling cause)
Glyceryl trinitrate
Adrenaline (α- and β-agonist)
Dobutamine (β1-agonist)
Intra-aortic balloon pump
Interventional treatment

52. Anaphylactic Shock 1. ABC 2. Lie patient flat with the feet elevated
3. Maintain airway and give oxygen (100%)
4. Intravascular volume expansion with crystalloid or colloid
5. Stop administration of causative agents (drug/fluid)
6. Call for help
7. Adrenaline (epinephrine)
8. Second-line therapy
Antihistamine: Chlorphenamine
Corticosteroid: Hydrocortisone

53. The indication of Intubation of Patient with Shock
Severe hypoxemia
Cardiovascular instability
Depressed conscious level or exhaustion

54. Monitoring of Patients with Shock
Conscious level: Restlessness, anxiety, stupor, and coma are common features and suggest cerebral hypoperfusion
Peripheral perfusion: Cold peripheries suggest vasoconstriction; warm peripheries suggest vasodilatation.
Pulse: Low volume, thready pulse consistent with the low-output state; high volume, bounding pulse with the high-output state
Blood pressure: Changes in diastolic may precede a fall in systolic blood pressure, with a drop in diastolic in sepsis and increase in hypovolaemic and cardiogenic shock
Pulse oximetry: Hypoxemia a common feature of all forms of shock.
ECG monitoring: Myocardial ischemia is the commonest cause of cardiogenic shock, but common in all forms of shock
Urine output: Renal hypoperfusion may cause oliguria (urine output < 0.5 ml/kg/h) or anuria.
CVP measurement: Low CVP with collapsing central veins consistent with hypovolemia
Arterial blood gas: Metabolic acidosis and high lactate consistent with tissue hypoperfusion

55. THE END
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