Shock - Septic and Hypovolemic and others

1. Vi k a s h B h a t t a r a i ( I n t e r n )
F o r S u r g e r y D e p a r t m e n t
C M S - T H B h a r a t p u r
SHOCK

2. Introduction
 Shock is a clinical syndrome that results from inadequate tissue
perfusion leading to imbalance between delivery and requirement
for oxygen and substrates which causes cellular ischemia and
dysfunction.
 The cellular ischemia which occurs induces the production and
release of inflammatory mediators that further compromises the
perfusion.
 It is the most common so, important cause of deaths among
surgical patients. So every surgeons must know…..

3. Pathophysiology of shock
 Cellular level:
 Micro-vascular level:
 Systemic:
 Cardiovascular
 Respiratory
 Renal
 Endocine
 Ischemia-perfusion syndrome:
perfusion to the tissues is reduced
cells are deprived of oxygen
switch from aerobic to anaerobic metabolism.
Accumulation of lactic acid in the blood
systemic metabolic acidosis.
glucose within cells is exhausted, anaerobic respiration
ceases
failure of sodium/potassium pumps
Intracellular lysosomes release autodigestive enzymes
cell lysis
Intracellular contents, including potassium are released
into the blood stream.
tissue ischaemia progresses
activation of the immune and coagulation systems
Hypoxia and acidosis activate complement and prime
neutrophils
generation of oxygen free radicals and cytokine
injury of the capillary endothelial cells
further activate the immune and coagulation systems
Damaged endothelium becomes ‘leaky’
tissue edema, exacerbating cellular hypoxia
As preload and afterload decrease
Compensatory baroreceptor response
increased sympathetic activity
release of catecholamines into the circulation
tachycardia and systemic vasoconstriction
(except in sepsis)
metabolic acidosis and
increased sympathetic response
increased respiratory rate
increased minute ventilation
excretion of carbon dioxide
compensatory respiratory alkalosis
Decreased perfusion to kidney
Reduced filtration at the glomerulus
renin–angiotensin–aldosterone axis
is stimulated
further vasoconstriction
increased sodium and water
reabsorption
decreased urine output
decreased preload
activation of the adrenal and
renin–angiotensin systems
vasopressin (antidiuretic
hormone)- hypothalamus
Cortisol – adrenal cortex
vasoconstriction and
resorption of water
decreased urine output
During systemic hypoperfusion
cellular and organ damage due to tissue hypoxia and
local activation of inflammation.
Further injury occurs once normal circulation is restored
The acid and potassium load
direct myocardial depression, vascular dilatation and further hypotension
cellular and humoral elements activated by the hypoxia (complement,
neutrophils, microvascular thrombi)
flushed back into circulation
further endothelial injury to organs such as the lungs and the kidneys
acute lung injury
acute renal injury
multiple organ failure and death.
Reperfusion injury can currently only be attenuated by reducing
the extent and duration of tissue hypoperfusion.

4. Classification of Shock

5. Clinical manifestations
• Hypotension (mean arterial BP <60 mmHg)
• Tachycardia
• Tachypnea
• Pallor
• Restlessness
• Altered sensorium
• Signs of intense peripheral vasoconstriction, weak pulses and cold
clammy extremities.
•In distributive (e.g., septic) shock, vasodilatation
predominates and extremities are warm.
Sepsis  Fever
• Oliguria (<400 mL/day) and metabolic acidosis common
• If not controlled, anuria (<100 mL/day)

6. Severity Of Shock
 Compensated
 Decompensation
 Mild
 Moderate
 Severe

7. Pitfalls
• The classic cardiovascular responses are not elicited in every patient.
• The patient in shock may not be recognized.
• Tachycardia:
Patients on beta-blockers, pacemakers, penetrating injury with
less tissue injury
• Blood pressure: one should recognise it as one of the last signs of shock
Children and young fit patients, elderly who are normally
hypertensive
• Capillary refill:
Distributive shock, patients are not cold, clammy but have brisk
capillary refill

8. Possible consequences
 Unresuscitable Shock:
profound shock for prolonged period
delayed, inadequate or inappropriate resuscitation
death is inevitable
 Multiple organ failure:
defined as 2 or more failed organ systems
prolonged ongoing systemic ischemia (Occult hypoperfusion) 
Ischemia reperfusion syndrome……..Mgt?

9. Resuscitation
 Immediate – Ensure airway and adequate oxygenation and
ventilation
 Then attention is directed to Cardiovascular resuscitation
 NEVER DELAY resuscitation for definitive Dx
 Rapid and careful clinical examination – clues to make appropriate
initial determination
 People actively bleeding  high volume therapy is
counterproductive  immediate operation for control of bleeding
with parallel resuscitation should be done

10.  While securing ABC, also don’t forget to draw blood for investigations
like:
 CBC, haematocrit (remember in Hypovolemia……..)
 Blood grouping and cross matching
 Blood culture and Culture sensitivity ( if septic shock suspected…)
 PT, INR, PTT, D - dimer
 ABG, Base deficit
 Electrolytes
 Lactate level
 LFT, RFT
 Other Inv’s:
 Urinalysis
 Gram stain and culture of sputum, urine, and other suspected sites
 Obtain ECG (myocardial ischemia or acute arrhythmia)
 Chest x-ray(heart failure, tension pneumothorax, pneumonia)
 Echocardiogram (cardiac tamponade, left/right ventricular
dysfunction, aortic dissection)

11.  In all cases of shock, FIRST LINE THERAPY SHOULD ALWAYS
BE iv FLUIDS to correct hypovolemia and inadequate pre-load
 Otherwise, EMPTY heart will rapidly and permanently deplete
myocardium of oxygen store  becomes unresponsive to
resuscitation
 For initial resuscitation  wide short bore catheters better than
long narrow line Central venous catheter, which is more
appropriate for monitoring than Fluid replacement

12. Types of fluids
 There is no ideal Res. Fluid and is matter of debate
 Studies show no overt differences b/n crystalloids and colloids
 Rather colloids are more expensive and have worse side-effect
profiles
 MOST IMPtly Both have ZERO oxygen carrying capacity, and if
blood is lost ideal replacement is blood  but they help buying
time while awaiting blood products
 Don’t use hypotonic solutions like Dextrose  Poor plasma
volume expanders (exception, if free water loss as in DI, and
sodium overload in cirrhosis.)

13. Dynamic Fluid response
 One of the methods to determine Shock status of patient
 250-500 mL fluid given over 5-10 mins and Cardiovascular
response observed (HR, BP, CVP)
 Responders: not actively losing fluid but require filling
 Transient responders: moderate ongoing fluid loss
 Non-responders: severely volume depleted

14.  After fluid challenge, There should be raise in CVP of 2-5 cmH2O
which gradually drifts back over 10-20 mins
 Those not showing change  further fluid resuscitation
 Vasopressors/Inotropic therapy may be required
 Once HR, BP, CVP, UO restored patient is kept on maintenance fluid
therapy.
 4-2-1 mL/kg/hr for 1st 10 kg, 2nd 10kg and rest respectively
or,
 100-50-20 mL/kg/day for 1st 10 kg, 2nd 10kg and rest respectively

15. Vasopressors and inotropic support

16. Monitoring
 CO, SVR and preload monitoring (real time monitoring of cardiovascular response)
 Invasive: Pulmonary Artery Catheter
 Non-invasive: Doppler Ultrasound, Pulse waveform analysis and Indicator dilution method
 Mixed Venous Oxygen saturation (N- 50-70%, Sepsis > 70%, Others - <50%)
 Level of consciousness  adequate marker of cerebral perfusion
 New methods: monitoring regional tissue perfusion
 Muscular tissue oxygen probes
 Near infrared spectroscopy
 Sub lingual capnometry
ICU setup is
appropriate

17.  Base excess: Normal range +2 to -2 mEq/L
Base deficit - when base excess is negative.
Patients with a base deficit over 6 mmol/L have a much higher morbidity and mortality than those with no
metabolic acidosis
• Lactate Level: Normal – 0.5 to 1.6 mmol/L in arterial blood
0.5 to 2.2 mmol/L in venous blood
mild to moderate hyperlactatemia  2-4 mmol/L
Lactic acidosis = >4-5 mmol/L with pH = <7.35

18. Endpoints of resuscitation
 Easy to know WHEN TO START, hard to know WHEN TO STOP
 Traditionally patients resuscitated until vitals and U.O. normalized
Which is WRONG, as some tissues may still be in OH, Later MOF
 New concept, resuscitation not stopped until sensitive parameters
like Base deficit, Lactate level and mixed venous oxygen saturation
are normalised.

19. Antimicrobial Regimens (IV Therapy)
• Immunocompetent adult
(1) piperacillin-tazobactam (3.375 g q4–6h)
(2) imipenem-cilastatin (0.5 g q6h) or meropenem (1 g q8h); or (3)
cefepime (2 g q12h).
If the pt is allergic to β- lactam agents, use ciprofloxacin(400 mg q12h)
orlevofloxacin (500–750 mg q12h)plus clindamycin (600 mg q8h).
Vancomycin(15 mg/kg q12h) should be added to each of the above
regimens.
• Neutropenia (<500 neutrophils/μL)
(1) imipenem-cilastatin (0.5 g q6h) or meropenem (1 g q8h) or cefepime
(2 g q8h)
(2) piperacillin-tazobactam (3.375 g q4h)plus tobramycin (5–7 mg/kg
q24h).
Vancomycin(15 mg/kg q12h) should be added if the pt has an indwelling
vascular catheter, has received quinolone prophylaxis, or has received
intensive chemotherapy that produces mucosal damage

20. • Splenectomy
Cefotaxime (2 g q6–8h) or ceftriaxone (2 g q12h)should be
used. If the local prevalence of cephalosporin-resistant
pneumococci is high, add vancomycin.
If the pt is allergic to β- lactam drugs, vancomycin (15 mg/kg
q12h) plus either moxifloxacin (400 mg q24h) or levofloxacin
(750 mg q24h) or aztreonam (2 g q8h) should be used.
• IV drug user
Vancomycin (15 mg/kg q12h)
• AIDS
Cefepime (2 g q8h) or piperacillin-tazobactam (3.375 g q4h)
plus tobramycin (5–7 mg/kg q24h) should be used.
If the pt is allergic to β- lactam drugs, ciprofloxacin (400 mg
q12h) or levofloxacin 750 mg q12h) plus vancomycin (15
mg/kg q12h) plus tobramycin should be used.

21. Management of Hemorrhagic shock
Every effort directed towards rapidly identifying and
stopping Haemorrhage
Identify haemorrhage
Immediate resuscitative manoeuvres
Identify the site of haemorrhage
Haemorrhage control
The bleeding, shocked patient must
be moved rapidly to a place
of haemorrhage control.

22. Summary

23. Thank You!