This document provides an overview of shock, including its definition, pathophysiology, classification, signs and symptoms, initial management, and specific types such as hypovolemic, septic, cardiogenic, and obstructive shock. It defines shock as inadequate tissue perfusion and oxygen delivery, discusses the body's compensatory mechanisms and their failure in severe shock. It classifies shock into hypovolemic, cardiogenic, distributive, and obstructive types and provides details on managing each type, including damage control resuscitation for hemorrhagic shock and use of vasopressors for neurogenic shock. Key goals in shock management are outlined as well as factors like lactate and base deficit that can guide res

1. Management of shock
Presenter:Dr Khagendra Shrestha
1st year resident,
MS, General surgery.

2. Objectives:
To know about:
• Shock: sign and symptoms
• Different types of shock
• Initial management of shock
• Cause specific management of shock

3. Definition:
• Shock is a life threatening situation due to poor
tissue perfusion with impaired cellular
metabolism, manifested in turn by serious
patho-physiological abnormalities. (Bailey and
love 27th edition)
• Shock may be defined as inadequate delivery
of oxygen and nutrients to maintain normal
tissue and cellular function.(Schwartz’s 11th edition)

4. Pathophysiology
• All forms of shock involve following:
– Reduced effective circulating volume.
– Reduced supply of oxygen to the cells and tissues
with resultant anoxia.
– Inflammatory mediators and toxins released from
shock induced cellular injury.

5. Pathophysiology(contd.)

6. Pathophysiology(contd.)
Inadequate perfusion
Cell hypoxia
Energy deficit
Lactic acid accumulation and
fall in pH
Anaerobic metabolism

7. Metabolic acidosis
Cell membrane dysfunction and failure of
sodium pump.
Intracellular lysosomes release digestive
enzymes
Toxic substances enter circulation.

8. Capillary endothelium damaged
Destruction, dysfunction and cell death.

9. Classification of shock:
1. Hypovolemic
– Hemorrhage, dehydration, vomiting, diarrhoea,
urinary loss, pancreatitis.
2. Cardiogenic
– MI, Cardiac dysrhythmias, valvular heart disease,
cardiomyopathy.
3. Obstructive shock
– Cardiac tamponade, tension pneumothorax,
pulmonary embolus/air emoblus.

10. Classification of shock(contd.)
4. Distributive shock:
– Septic shock
– Anaphylactic shock
– Neurogenic shock
5. Endocrine shock
– hypo/hyperthyroidism, adrenal insufficiency.

11. Sign and symptoms
• Cold extremities, sweating and thirst
• Pallor, rapid and weak pulse detected on major
arteries
• Low blood pressure (BP), narrow pulse
pressure, BP sometimes undetectable.
• Capillary refill time (CRT) > 3 seconds.
• Cyanosis, dyspnoea, tachypnoea
• Anxiety, confusion, agitation or apathy.
• Oliguria or anuria.

12. Signs specific to shock
Anaphylactic shock
– Significant/sudden drop in BP
– Tachycardia
– Frequent cutaneous signs: rash, urticaria,
angioedema
– Respiratory signs: dyspnoea, bronchospasm

13. Septic shock
– High fever or hypothermia (< 36 °C), rigors,
confusion
– BP may be initially maintained, but rapidly,
same pattern as for hypovolaemic shock
Cardiogenic shock
– Tachypnoea, crepitations on auscultation.
– Raised jugular venous pressure, hepatojugular
reflux

14. Clinical features of shock
compensat
ed
Mild Moderate Severe
Lactic acidosis + ++ ++ +++
Urine output Normal Normal Reduced Anuric
Conscious
level
Normal Mild anxiety Drowsy Comatose
Respiratory
rate
Normal Increased Increased Laboured
Pulse rate Mild increase Increased Increased Increased
BP Normal Normal Mild
hypotension
Severe
hypotension

15. Initial management of shock
Assess the patient from an ABCDE perspective
• Maintain a patent airway
• Deliver high flow oxygen 15L/min via
reservoir mask to keep saturation over 94%
• Attach monitoring
–Pulse oximetry and non-invasive blood
pressure
–Three-lead cardiac monitoring

16. • Request 12 lead ECG and portable CXR
• Obtain large-bore intravenous (IV) access and
take bloods including blood gas to check pH
and lactate
• Fluid resuscitation IV
Insert 2 peripheral IV lines, give RL or 0.9%
NaCl(Replace = 3*Loss) and/or plasma substitute
(Replace = 1.5*Loss)

17. • Urethral catheterization and fluid balance
monitoring aiming for a urine output >0.5
ml/kg/hour
• If BP fails to respond consider referral to ICU
for
–Central line insertion with central venous
pressure (CVP) and central venous oxygen
saturation (ScvO2) monitoring
–Arterial line insertion and invasive arterial
BP monitoring
–Vasopressor and/or inotrope infusion

18. Investigation of shock
• Bloods including blood gas to check pH and
lactate
• Electrocardiogram (ECG)
• Chest radiograph (CXR)
• Echocardiography
• In trauma
–Pelvic XR
–CT chest/abdomen/pelvis as indicated
–FAST

19. Assessment of the shock patient:
Monitor vitals closely, strict I/O charting, ECG
Monitor CVP, Base deficit and s/lactate.
Monitor lab values:
ABG with lactate
CBC
Coagulation panel: PT, PTT, INR and D-dimer.
BUN, creatinine, troponin.
Glucose initially elevated then decreases after
glycogen is depleted.

20. Age related considerations:
• Paediatric
– Increases CO by increasing heart rate.
– Sustains arterial pressure despite significant
volume loss.
– Loses 25% of circulating volume before signs of
shock occur.
• Geriatric
– Shock progression is rapid
– Reduced compensatory mechanisms
– Preexisting disease states contributes to co-
morbidities

21. Hypovolemic shock

22. Hypovolemic shock
• Loss or redistribution of blood, plasma, other
body fluids, results in decreased circulatory
volume.
• Decreased preload lead to decrease CO.

23. Hemorrhagic shock:
• Trauma induced coagulopathy (TIC):
1. Ongoing bleeding with fluid and RBC
resuscitation leads to dilution of coagulation
factors.
2. Decrease function of coagulation proteases in
acidosis.
3. Hypothermia d/t underperfused muscle.

24. Hemorrhagic shock:

25. Hemorrhagic shock(contd.)
• Management:
1. Identify hemorrhage
2. Immediate resuscitative maneuvers
• Direct pressure, ABCDE.
3. Identify the site of hemorrhage
• H/O, O/E, hemorrhage in the body cavity
4. Hemorrhage control
• Damage control surgery, angiography, endoscopy.

26. Hemorrhagic shock(contd.):
• Damage control resuscitation:
1. Anticipate and treat acute traumatic
coagulopathy.
2. Permissive hypotension until hemorrhage
control.
3. Limit crystalloid and colloid infusion to avoid
dilutional coagulopathy.
4. Damage control surgery to control hemorrhage
and preserve physiology.

27. Endpoints in resuscitation:
• It is easier to know when to start resuscitation
than when to stop.
• Traditionally resuscitation stopped after
normal vitals: BP, HR, Urine output.
• 80%-85% of trauma patients have inadequate
tissue perfusion even with normal vitals.

28. Endpoints in resuscitation(contd.):
• Can be divided into;
1. Systemic/global
o Lactate
o Base deficit
o Cardiac output
o Oxygen delivery and consumption.
2. Tissue specific
o Gastric tonometry
o Tissue pH,O2,CO2
o Near infrared spectroscopy
3. Cellular: membrane potential, ATP

29. Septic shock

32. Maximum SOFA score Mortality
0 to 6 <10%
7 to 9 15-20%
10 to 12 40-50%
13 to 14 50-60%
15 >80%
15 to 24 >90%

35. Anaphylactic shock:

37. Neurogenic shock:

38. • Unlike most forms of shock, the state
of neurogenic shock is unlikely to be corrected
or improved with fluid resuscitation.
• The primary management for neurogenic
shock involves the administration of
vasopressors and inotropic agents:
1.dopamine (inotropic)
2.vasopressin,
3.norepinephrine, and
4.atropine.

39. Cardiogenic shock:

40. Diagnostic criteria

41. Obstructive shock:
• Tension pneumothorax:
Needle decompression
Tube thoracostomy
• Pericardial tamponade:
Pericardiocentesis
20ml/kg NS or RL bolus
• Pulmonary embolism:
20ml/kg NS or RL bolus
Thrombolytics , anticoagulants
• Ductal dependent(LV outflow obstruction):
Prostaglandin E1

42. Clinically significant facts:
• Shock in a trauma/post-op: Hemorrhage.
• Clinical manifestation of shock appears only after
significant blood volume loss.
• Elderly patients:
– Promote bleeding: warfarin or aspirin,
– Mask the compensatory responses to bleeding
(e.g., β-blockers).

43. • Serum lactate and base deficit: Monitor extent
& therapeutic effect of shock
• Davis and colleagues stratified the extent of
base deficit into:
1. Mild (3 to 5 mmol/L),
2. Moderate (6 to 14 mmol/L), and
3. Severe (>15 mmol/L),

44. • The mortality of trauma patients:
– 3 times higher incidence of infection in patients
with persistent rise of lactic acid > 12hr of
admission.
– If elevated base deficit/lactic acidosis: Ongoing
bleeding.
– Base deficit >15 mmol/L: 2X the volume of fluid
infusion and 6X more blood transfusion in the 1st
24 hours compared to patients with mild acidosis.

45. References
• Bailey and love 27th edition,Shock.
• Schwartz’s principle of surgery 11th edition,Chapter 5th Shock
• Oxford handbook of clinical surgery,Page 150-152,Shock
• American heart association management of shock
• Civetta, Taylor, & Kirby's: Critical Care, 4th Edition,Section
VI - Shock States,Chapter 59 - Neurogenic Shock

46. THANK YOU