Shock is a life-threatening condition defined as inadequate tissue perfusion and cellular respiration. The document discusses the pathophysiology, classification, signs, and management of shock. Shock can be caused by hemorrhage, sepsis, anaphylaxis, or trauma. Early recognition and treatment is critical to prevent multiple organ failure and death. Fluid resuscitation is initially used but controlling any hemorrhage is paramount to recovery. Monitoring for signs of persistent or worsening shock is also important.

1. PRINCIPLES OF SURGERY: SHOCK
Dept. of Surgery
Viswabharathi Medical
College, Kurnool
21 May 2021

2. INTRODUCTION
Shock is one of the most common causes of death in surgical patients.
Therefore, it is one of the most dreaded conditions to be managed in a
perioperative case.
A profound state of shock may rapidly result into death, unless otherwise
delayed by organic ischemia or reperfusion injury.
Therefore, it is imperative to understand the tenets and management of
such a condition.

3. SHOCK
Definition:
Shock is a systemic state of low perfusion which is inadequate for normal
cellular respiration.
Metabolism shifts from aerobic to anaerobic due to the lack of delivery of
oxygen and glucose, due to which, death may follow if not managed within
time.

4. PATHOPHYSIOLOGY OF SHOCK
The pathophysiology of shock is discussed at several levels:
Cellular :
1. As perfusion to the tissues is reduced, cellular metabolism shifts from
aerobic to anaerobic. Eventually, metabolic acidosis sets in as a
consequence of accumulation of lactic acid.
2. Failure of Na-K pumps in the cell membrane and organelles. As a
result, intracellular lysosomes release autodigestive enzymes leading
to cell lysis. Free potassium is then release into the bloodstream.

5. Microvascular:
1. Activation of immune and coagulation system as a result of prolonged
ischemia
2. Activation of complement, prime neutrophils due to hypoxia and acidosis
leads to injury of the capillary endothelial cells.
3. This results in the activation of coagulation systems, leading to leaky
endothelial lining.

6. Systemic:
1. Cardiovascular: Decrease of both preload and afterload result in
increased sympathetic activity and release of catecholamines in the
circulation, resulting in tachycardia and general vasoconstriction.
2. Respiratory: Metabolic acidosis results in increased RR and increased
excretion of carbon dioxide.
3. Renal: Decreased perfusion leads to reduced filtration at glomerulus and
decreased urine output.
4. Endocrine: Activation of Renin-angiotensin system, ADH is released as
a response to decreased preload resulting in resorption of water in the
collecting system.

7. Ischaemia-reperfusion syndrome:
1. Reperfusion leads to injury in the
tissues already suffering from
hypoxia.
2. Lactic acid and K+ overload leads to
● Myocardial depression
● Vascular dilatation
● Hypertension
1. These leads to acute lung injury,
acute renal injury and in some cases,
death.

8. CLASSIFICATION OF SHOCK

9. SEVERITY OF SHOCK
Features Compensated Mild Moderate Severe
Lactic Acidosis + ++ ++ +++
Urine Output Normal Normal Reduced Anuric
Conscious
Level
Normal Mild Anxiety Drowsy Comatose
Respiratory
Rate
Mild Increase Increased Increased Laboured
Pulse Rate Mild increase Increased Increased Increased
Blood Pressure Normal Normal Mild
Hypotension
Severe
Hypotension

10. CONSEQUENCES
Unresuscitable Shock:
Patients who are in shock for a
prolonged period fall in this
category.
Cell death follows cellular
ischemia. Peripheral loss of ability
to maintain vascular resistance
result in severe hypotension.
Condition inevitably leads to death.
Multiple Organ Failure:
Result of prolonged ischemia and
reperfusion injury result in end-organ
damage and multiple organ failure.
Effect:
● Lung: ARDS
● Clotting: Coagulopathy
● Cardiovascular Failure
● Renal Failure
● Acute Liver insufficiency

11. RESUSCITATION
Immediate resuscitation maneuvers from patients presenting in shock are to
ensure airway and breathing. Once that is ensured, focus now shifts towards
resuscitation the cardiovascular system.

12. CONDUCT OF RESUSCITATION
● Resuscitation should not be delayed for the patient.
● The timing and nature of resuscitation depends on the type of shock and
severity of the insult.
● Rapid clinical examination to find the source of bleeding, or to
differentiate between bleeding or sepsis.
● High volume fluid therapy without controlling haemorrhage is
counterproductive. In such a case, resuscitation should be carried out
parallelly.
● Conversely, a patient with hypovolemia must be resuscitated first, before
undergoing surgery.

13. FLUID THERAPY
● Before any fluid resuscitation is performed, hypovolemia must be
addressed first. Otherwise, inotropic and chronotropic agents result in
rapid emptying of the heart permanently depleting it from oxygen stores,
pushing the patient into unresuscitable shock.
● As the first line management, fluids should be introduced via a short,
wide bore catheter to allow rapid infusion.
● Long central venous catheter have too high resistance and therefore,
avoided.

14. TYPES OF FLUIDS

15. DYNAMIC FLUID RESPONSE
Type Comment
Responders Improved CVS status. Patients require filling to normovolemic status
Transient responders Improvement followed by reversal every 10-20 min. Moderate fluid loss
Non-responders Severe volume depletion due to major loss of intravascular volume.
● The status of the shock is usually determined by the cardiovascular
response to the rapid fluid infusion. Depending on pulse rate, blood
pressure and central venous pressure, the patients are classified as
follows:

16. PHARMACOLOGICAL SUPPORT
1. Vasopressors:
Phenylephrine, Noradrenaline,
Vasopressin:
Indicated in septic and neurogenic shock
where hypotension persists despite high
CO.
1. Inotropes:
Dobutamine, Milrinone:
Indicated in severe shock due to severe
sepsis and low CO.

17. MONITORING OF PATIENTS IN SHOCK
Though most of the patients need an aggressive invasive monitoring, the
minimum standard for monitoring of the patient in shock is: continuous heart
rate, O2 saturation monitoring, hourly urine output measures, frequently non-
invasive blood pressure monitoring.

18. PARAMETER CLINICAL INVESTIGATIONAL
1. SYSTEMIC
PERFUSION
BASE DEFICIT
LACTATE
MIXED ORGAN VENOUS SATURATION
2. ORGAN PERFUSION
● MUSCLE NEAR-INFRARED SPECTROSCOPY
TISSUE O2 ELECTRODE
SUBLINGUAL CAPNOMETRY
● GUT GUT MUCOSAL pH
LASER DOPPLER FLOWMETRY
● KIDNEY URINE OUTPUT
● BRAIN CONSCIOUSNESS
LEVEL (GSS)
TISSUE O2 ELECTRODE
NEAR-INFRARED SPECTROSCOPY

19. CONCLUSION: RESUSCITATION
● It is more important to determine when to stop resuscitation than when to
start it.
● One should always look for signs of occult hypoperfusion, because such
a case has 2-3 times greater mortality if left undiagnosed for t > 12 hrs.
The only sign of such a condition is lactic acidosis, and therefore, the
surgeon must be highly vigilant for developing signs of hypoperfusion.
● Despite aggressive treatment regimens, resuscitation from shock still
remains a great challenge.
● Further research and development in the field is expected to improve the
outcome of the condition.

20. HAEMORRHAGE
● Haemorrhage must be recognised timely
and aggressively managed to reduce the
severity and duration of shock.
● It has to be treated by arresting the
bleeding and not be fluid resuscitation or
blood transfusion.
● Attempting to resuscitate patient
undergoing a continuous hemorrhage
may even lead to physical exhaustion
and death.

21. HAEMORRHAGE: PATHOPHYSIOLOGY

22. SOME DEFINITIONS OF HAEMORRHAGE
REVEALED HAEMORRHAGE:
Obvious external haemorrhage like
exsanguination from an open arterial
wound or from massive hematemesis
from duodenal ulcer.
CONCEALED HAEMORRHAGE:
Haemorrhage contained within the
body cavity, something which has to
be actively investigated and
controlled. Common sites are chest,
abdomen, pelvis, retroperitoneum or
limb compartments.
Some examples include ruptured
Aortic aneurysm or occult GI
bleeding.

23. Primary
Haemorrhage
Reactionary
Haemorrhage
Secondary
Haemorrhage
● Haemorrhage
occurring immediately
due to an injury (may
or may not involve
surgery).
● Delayed Haemorrhage
occurring within 24
hours of insult is
termed as reactionary
haemorrhage.
● Usually due to clot
dislodgement, either
by resuscitation or
vasodilation.
● May also occur due to
technical failure.
● Haemorrhage
occurring within 7 o
14 days of insult.
● Most commonly due
to sloughing of wall.
● Precipitating factors:
1. Infection
2. Pressure necrosis
3. Malignancy

24. Surgical Haemorrhage:
● Due to direct injury and
therefore, is manageable by
surgery or by modern
methods like
angioembolization.
Non-Surgical Haemorrhage:
● Due to general oozing from
raw surfaces due to
coagulopathy and cannot be
stopped by surgical packing.
● Treatment includes correction
of the underlying condition.

25. CLASSIFICATION OF HEMORRHAGIC
SHOCK

26. MANAGEMENT OF HAEMORRHAGE
Steps Management
● Identify
Haemorrhage
Identify the site of haemorrhage, whether an external one or a similar internal
haemorrhage leading to hypovolemia.
● Immediate
Resuscitative
manoeuvre
Direct pressure should be placed over the site. Airway and breathing should be assessed
and controlled. Large bore IV cannula inserted and blood drawn for cross-matching.
● Identify Site of
Haemorrhage
Haemorrhage in coelomic cavities must be ruled out by rapid abdominal/pelvis x-ray,
abdominal USG or diagnostic peritoneal aspiration. Patients who are not bleeding can be
sent for more extensive work up.
● Haemorrhage
control
Patient should be taken immediately to area of haemorrhage control, placed under
surgical and anaesthetic support.
No unnecessary investigations to be done.
Damage control surgery is performed, following which aggressive resuscitation is done
to correct coagulopathy and so on.

28. THANK YOU
1. PRESENTATION:
● B. KRISHNA SANDEEP (18)
● D. VIGHNESH (34)
● G.DHIRAJ (46)
1. CREATED BY: D. VIGHNESH (34)
SOURCES:
● BAILEY AND LOVE’S SHORT PRACTICE OF SURGERY
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the_Management_of_Hemorrhagic_Shock