Shock is a common emergency in medical practice, learn how to properly evaluate and manage a patient in shock

1. PRINCIPLES OF MANAGEMENT OF
SHOCK
PRESENTED BY DR NCHWANG MARCEL
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2. OUTLINE
• INTRODUCTION
• CLASSIFICATION
• CLINICAL FEATURES
• PRINCIPLES OF MANAGEMENT
• COMPLICATIONS
• CONCLUSION
• REFERENCES
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3. INTRODUCTION
• Shock describes a clinical condition that results from cellular hypoxia
due to poor tissue perfusion that is the result of reduced effective
circulatory volume.
• Simply put, it is a syndrome, a constellation of signs that depict
cellular hypoxia
• Shock is a common clinical condition and an emergency.
• Shock occurs in stages and can often be fatal depending on the cause
and presence of intervention or not
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4. Understanding shock…
• The outlook shows it is a process that can progress initially from
deranged cellular metabolism and end in cell death, organ damage,
multi-organ failure and death
• The end result yields, anaerobic metabolism (metabolic acidosis),
failure of ATPase pumps, swelling of the mitochondria, cell death and
organ dysfunction.
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5. CLASSIFICATION
• There are basically 3 classes of shock
• Hypovolaemic shock
• Cardiogenic shock
• Distributive shock
• Septic shock
• Neurogenic shock
• Anaphylactic shock
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6. Classification…Hypovolaemic shock
• Very common
• Could be hemorrhagic or non-hemorrhagic
• Hemorrhagic. Most common; due to blood loss from trauma
• Non-hemorrhagic due to loss of plasma alone; from AGE, burns, fluid
deprivation…
• Results in depletion of intravascular volume reduced preload
reduced CO
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7. Hemorrhagic shock
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8. Hemorrhagic shock… classes
• Class 1
• Up to 15% blood loss
• Minimal CVS/RS changes
• Compensatory mechanism restore blood vol in 24 hours
• Class 2
• 15-30% (750-1500mls) blood loss
• Tachycardia and tachypnea
• UO 20-30mls/hr
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9. Hemorrhagic shock… classes
• Class 3
• 30-40% (1500-2000mls) blood loss
• UO 5-15mls/hr
• Marked tachypnea and tachycardia
• Hypotension
• Class 4
• Up to 40% blood loss (>2000mls)
• Severe hypotension SBP may fall to <80mmhg
• Tachycardia >140bpm
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10. Classification…cardiogenic shock
• Primary a cardiac pump failure
• From IHD, cardiac tamponade, CCF, CHD…
• The heart fails to produce the required CO
• Compensation is to increase TPR
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11. Classification…Distributive shock
• Septic; fever or hypothermia
• common with gram – and + bacteria, fungi, viruses
• Warm (common with gram -, increased CO, reduced TPR with warm
extremeties)
• Cold (severe sepsis,reduced CO and increased TPR and cold extremeties)
• Neurogenic due to reduction in TPR due to loss of sympathetic tone
common in spinal cord injury, spinal anaesthesia
• Anaphylactic due to exaggerated responses to drugs, toxins, allergens
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12. Clinical Features
• The features seen depend on the stage of shock
• Early stage/compensated shock
• Late stage/ decompensated shock
• The features seen are the result of
• The primary cause of the shock
• The body’s response to the shock
• The effects of cellular hypoxia, tissue injury and end organ damage
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13. Early stage/decompensated shock
• Here the patient has minimal to no symptoms as the neurohumoral
mechanisms earlier outlined ensure tissue perfusion is adequate
• The magnitude of response is based on vol and rate of fluid loss
• Blood is shunted from GIT, skin and kidneys to ensure the heart and
CNS are adequately perfused
• Baroreceptors, RAAS
• The mechanisms ensure CO is maintained with increase in
HRtachycardia, thirst
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14. Late/ decompensated stage
• Here the shock and its effect progresses, the symptoms become more
profound and in late stages the previously compensatory mechanisms
become deleterious, break down and ends in MOD and death
• CVS: rapid weak and thready pulses which may be absent or not
palpable with hypotension in late stages
• RS: due to metabolic acidosis and stimulation of the bronchioles there
is an increased respiratory rate with deep breathing and cyanosis.
• Skin: the skin is cool and clammy (warm in septic shock) due to
vasoconstriction with dry and pale mucous membranes
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15. Late/ decompensated stage
• CNS: restlessness and lethargy and even coma
• UGS: the shunting decreases GFR oliguria and anuria
• Eventually MOD sets in and death
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16. PRINCIPLES OF MANAGEMENT
• The principles
• Resuscitation: keep pt alive, medical vs surgical
• ATLS
• Fluid therapy
• Treat the Cause
• Provide Supportive care
• monitoring of patient
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17. Goals in management of shock…
• Maintain MAP 0f > 80mmhg
• O2 saturation of >94%
• UO of > 1ml/kg/hr
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18. Resuscitation…
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19. RESUSCITATION
• When a patient is suspected to have shock, diagnostic evaluation
goes alongside resuscitation
• The aim is to ensure a patent airway and adequate oxygenation and
ventilation and then circulatory support. As majority are
polytraumatised patients and presentation varies
• Resuscitation is viz-a-viz focused clinical assessment as it determines
the timing and nature of resuscitation because fluid therapy may not
always be ideal and should be targeted.
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20. Resuscitation
• Initial assessment is targeted at
• Respiration: if present? Then rate and depth
• Presence of active bleeds and wounds
• Skin: moist or dry? Warm or cool
• pulses/blood pressure: present? Rate? Volume?
• Mental status: conscious? lethargic? Restless? Coma?
• As a myriad of causes exists, when uncertain, it may be safe to
assume hypovolaemic shock and commence fluid therapy
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21. Resuscitation…fluid therapy
• In all cases of shock, hypovolaemia must be addressed before
instituting other care
• IV access with wide bore cannulae and appropriate fluids is the initial
step
• Choice of fluid remains controversial. Blood is preferred for
hypovolaemia from blood loss
• Crystalloids (NS, RL, Hartmanns) have proven superior to colloids
(albumin, hetastarch, dextran) and are used for volume expansion
• It is important to then assess and classify responders, transient and
non-responders to direct next line of management
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22. Management…Treat the cause
• This may go alongside initial resuscitation or follow initial
resuscitation
• Targets the specific type of shock and its cause
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23. Treat the cause….hypovolaemic
• Adequate fluids noting choice in non-hemorrhagic
• In hemorrhagic
• Identify hemorrhage
• Emergency resuscitation
• Identify site of hemorrhage
• Control hemorrhage
• -+ transfusion
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24. Treat the cause….cardiogenic
• Depending on the cause
• Others
• Ionotropes
• Antiarrhthmics
• cardioversion
• O2
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25. Treat the cause….septic shock
• Aim is to improve perfusion by expanding vol. and eliminating source
of infection(surgical and non-surgical)
• Generally involves
• Fluid therapy
• ionotropes
• Antibiotics
• 02
• steroids
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26. Treat the cause….anaphylactic shock
• Commonly anaphylaxis from whatever cause is feared for its
bronchoconstriction and widespread vasodilation
• Its treatment involves
• Antihistamines
• Vasopressors
• Airway management
• aminophylline?
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27. Management…supportive care
• Supportive care is clinical and laboratory
• Clinical depends on cause of shock
• Generally includes
• Oxygen
• Elevate limbs
• Nursing care
• Appropriate positioning
• Analgesia
• Corticosteroids
• Catheter
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28. Management…supportive care
• Laboratory
• Imaging: x-ray, ct, USS
• Pcv GXM
• FBC, ESR
• Clottology
• Electrolytes
• Sepsis screening
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29. Management…monitoring
• These patients need aggressive monitoring as MODS and progression
to death or irreversible shock can be rapid
• At the barest minimum,
• Heart rate
• Pulse
• Bloop pressure
• Temperature
• Oxygen saturation
• Urine output
• Mental status
• Skin colour/feel
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30. Management…monitoring
• Other monitoring (some may be invasive) includes
• CO and TPR
• CVP
• Sr Lactate
• ECG
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31. Complications
• Shock commonly results in organ dysfunction or even death
• From resuscitation
• Fluid overload: PE
• HF
• Oxygen toxicity
• Blood transfusion reactions
• Iatrogenic infections
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32. complications
• From shock
• UGS: AKI, adrenal insufficiency, waterhouse FS
• RS: RDS
• GIT: stress ulcers, liver failure
• CNS: ischaemic encephalopathy
• MODS
• DIC
• Death
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33. References
• Baja’s principles and practice of surgery in the tropics. 5th edition
• Bailey and Love’s short practice of surgery. 27th edition
• Robbins and cotran pathologic basis of disease. 9th edition
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34. Thank you
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