SHOCK

DR : KESHENI LEMI
 OUTLINE

• Definition
• Types
• Pathophysiology
• Clinical Presentation
• Investigations
• Management
• A physiological state characterized by systemic
reduction in tissue perfusion leading to inadequate
delivery of 02 & glucose to cells
• This leading to
– Cellular dysfunction and damage
– Organ dysfunction and damage
 Circulatory System

Pump
Pressure
Gauge Pipe

Fluid
 Maintaining perfusion requires:
• Pump
• Vessels
• Volume
• Failure of one or more of these causes shock
 Types
• Hypovolaemic
• Cardiogenic
• Obstructive
• Distributive
• Traumatic
 Classification of Shock
TYPE CAUSE CATERGORIES EXAMPLES

Hypovolaemic Haemorrhagic Trauma

↓ circulating volume (From bleeding) GI Bleeding, ectopic preg
Acute reduction in effective GU bleeding
intravascular volume
Non haemorrhagic •GI losses (eg, diarrhea,
(From body fluid loss) vomiting);
•Skin losses-burns,
•Third space losses (eg, I.O
pancreatitis, peritonitis)

Cardiogenic Pump failure Cardiomyopathic •MI,

•DCM
•Myocarditis

Arrhythmogenic •Tachyarrhythmia
•Bradyarrhythmia
Mechanical Dysfunction Valvular insufficiency/ rupture,
Severe ventricular septal wall
defect
 Classification of Shock
TYPE CAUSE CATERGORIES EXAMPLES

Distributive Loss of vessel tone Septic Septic burns

(vasogenic) (↓ resistance in
capacitance vessels) anaphylatic Drug and transfusion reactions
Neurogenic C –spine injuries-acute loss of sympathetic
vascular tone
Obstructive ↓ in preload because of mechanical obstruction of cardiac cardiac tamponade
refilling tension pneumothorax
mechanical obstruction of venous return massive pulmonary embolus
air embolus

Traumatic Soft tissue and bone damage activates inflammatory small volume hemorrhage accompanied by soft
cascade – release of inflammatory & vaso actives tissue injury (femur fracture, crush injury),
substances
Combined with haemorrhage any combination of hypovolemic, neurogenic,
cardiogenic, and obstructive shock that precipitate
rapidly progressive proinflammatory activation
 Traumatic Shock
• Soft tissue and bony injury
• Lead to the activation of inflammatory cells and the release of
circulating factors, such as cytokines and intracellular molecules
that modulate the immune response.
• The inflammatory mediators released in response to tissue injury
activate similar signaling pathways as do bacterial products
elaborated in sepsis
• These effects of tissue injury are combined with the effects of
hemorrhage, creating a more complex and amplified deviation from
homeostasis.
 Obstructive Shock
• Cardiac tamponade occurs when sufficient fluid has accumulated in the
pericardial sac to obstruct blood flow to the ventricles.
• Acutely, the pericardium does not distend; thus small volumes of blood may
produce cardiac tamponade.
• Cardiac tamponade results from the accumulation of blood within the pericardial
sac, usually from penetrating trauma or chronic medical conditions such as heart
failure or uremia
• With either cardiac tamponade or tension pneumothorax, reduced filling of the
right side of the heart from either increased intrapleural pressure secondary to
air accumulation (tension pneumothorax) or increased intrapericardial pressure
precluding atrial filling secondary to blood accumulation (cardiac tamponade)
results in decreased cardiac output associated with increased central venous
pressure
 Neurogenic Shock
• Neurogenic shock refers to diminished • Causes of neurogenic shock
tissue perfusion as a result of loss of
vasomotor tone to peripheral arterial beds. • Spinal cord trauma
• Loss of vasoconstrictor impulses results in • Spinal cord neoplasm
increased vascular capacitance, decreased • Spinal/epidural anaesthesia
venous return, and decreased cardiac
output.
• Usually secondary to spinal cord injuries
from vertebral body fractures of the
cervical or high thoracic region that
disrupt sympathetic regulation of
peripheral vascular tone
PATHOPHYSIOLOGY
Inadequate
Cellular
Oxygen
Delivery

Lactic
Inadequate
Energy Aerobic → Anaerobic Acid
Production Metabolism Production

Glucose inadequacy Metabolic

Metabolic CELL Acidosis
Failure DEATH
 Inadequate perfusion

Cell hypoxia
Energy deficit

I. Depression of cell metabolism leads to anaerobic metabolism and lactic

acidosis.

• Metabolic Acidosis
• Accumulation of lactic acid and fall in PH
II. Cell membrane dysfunction and failure of Na ⁺ - K ⁺ pump

leading to efflux of K+ and influx of Na + and water

III. Damage to intracellular mitochondria and lysosomal

membranes with release of potassium, digestive enzymes and
toxic substances into circulation
IV. Trauma and sepsis activate coagulation and inflammation
with damage to vascular endothelium with extravasation of
protein, water, sodium and chloride

• In massive oedema,
• Interference of microcirculatory perfusion and cell metabolism
eventually leading to multiple organ failure(MOF) and death
Effects on organs
 Shock
• Progressive syndrome
• Three phases
– Compensated
– Decompensated
– Irreversible
 Stages of Shock

Insult

Preshock
(Compensation) Timeline and progression will depend on:
- Cause
Shock -Patient Characteristics
(Compensation
-Intervention
Overwhelmed)

End organ
Damage

Death
Signs and symptoms
 Signs and symptoms In babies
• Poor tone,
• Unfocused gaze,
• Weak cry, Lethargy/Coma,
• (Sunken or bulging fontanelle)
 Management - Generally
• ABCD
– Airway
– Breathing
– Circulation
– Disability
– Exposure
• Treat underlying cause
Treatment: Airway and Breathing
• Give oxygen
• Consider Intubation
– Is the cause quickly reversible?
• Generally no need for intubation

– reasons to intubate in the setting of shock

• Inability to oxygenate
• Inability to maintain airway
 Treatment: Circulation
• Treat the early signs of shock (Cold, clammy? Decreased
capillary refill? Tachycardic? Agitated?)

• DO NOT WAIT for hypotension

• Fluids - 20 ml/kg bolus x 3 - WARM
– Normal saline/Ringer’s lactate
• Start IV +/- Central line (or Intraosseous), Saphenous Cutdown
• Do Blood Work +/- Blood Cultures
 Investigations
Laboratory Others
• CBC • ECG
• Electrolytes • Urinalysis
• RFT’s • CXR
• +/- Lactate • +/- Echo
• RBS
• +/- Cardiac Enzymes
• Blood Cultures - from two different
sites
• Beta HCG
• +/- blood group & Cross Match
 Monitoring Shock Patients
• Continuous BP monitor
• Pulse Oximetry measures Spo2 + PR
• EKG/ECG
• Temperature
• Fluid in put & urine output
• Monitor mental state too
• Keep the patient warm

• The goal of treatment is restoration of oxygen delivery to the cell

• Remember the Pump, pipes & fluids to sort out unusual causes of hypotension

• s
 Core principles in management - Hypovolaemic

• Control of active haemorrhage must occur promptly

• Volume resuscitation with blood products with limited volume
of crystalloid must occur while operative control of bleeding is
achieved;
• Unrecognized or inadequately corrected hypo perfusion
increases morbidity and mortality (i.e., inadequate resuscitation
results in avoidable early deaths from shock)
• Excessive fluid resuscitation may exacerbate bleeding (i.e.,
uncontrolled resuscitation is harmful).
Classification of Hemorrhagic Shock
 Hemorrhagic (Hypovolemic Shock)
– cABC’s
• Monitors
• O2
• IV lines x 2, Fluid boluses, Call for Blood - O type
• Blood work including cross match
– Treat Underlying Cause
• Give Blood
• Call the surgeon ASAP
• Plan to take to the Operating Room
 Core principles in management- Septic
• septic shock is an emergency, and treatment/resuscitation should begin as early as
possible – q –SOFA, Score of ≥ 2 ; High risk of poor outcome in a patient with
suspected infection
• Identification of source of infection and dealing with it ASAP specific
• Initiation of broad spectrum antibiotics within 1 hour of diagnosis;
• In the resuscitation from sepsis-induced hypoperfusion, at least 30 ml/kg of
intravenous crystalloid fluid be given within the first 3 hours, and additional fluids be
guided by frequent reassessment of hemodynamic status;
• vasopressors (norepinephrine) should be added to achieve a mean arterial pressure of
65 mmHg if fluid resuscitation is inadequate. 1 st line norepinephrine then epinephrine
• Then dobutamine
• Insulin administration in hyperglycaemia
• Controversial steroid use
SEPTIC SHOCK
• Monitor and ABCs -
• O₂ if SPO2 < 94%.
• IV Access and send samples for FBC,
UEC, VBG, Serum lactate, Blood
culture
• Hypotension or Lactate ≥ 2 mmol/L -
Administer 30ml/kg NS or RL
• Administer broad-spectrum antibiotics
• Vasopressors if MAP < 65 during or
after rapid intravascular fluid
administration -noraepinephrine
• ID source of infection deal with it
• Give Dobutamine infusion up to 20
μg/kg/min
• Hydrocortisone 200mg IV bolus
• Monitor urine output hourly
• Admit HDU/ICU
 Traumatic Shock
• Treatment of traumatic shock is focused on correction of the
individual elements to diminish the cascade of proinflammatory
activation, and includes
• prompt control of hemorrhage,
• adequate volume resuscitation
• correct O₂ debt,
• debridement of nonviable tissue,
• stabilization of bony injuries,
• appropriate treatment of soft tissue injuries.
 ANAPHYLATIC SHOCK
• IV Fluids
General measures • Oxygen
• IM Adrenaline (epinephrine)
• Remove cause • Repeat every 5-10 minutes according
• Secure the airways to BP, PR,RR
• In severely affected patients -
• Restore BP: lay the Hydrocortisone 200 mg IM or slow IV
stat
patient flat and raise feet • If urticaria/itching - Antihistamine
• Keep patient warm • Repeat adrenaline and hydrocortisone
every 2-6 hours PRN depending on the
patient’s progress
• +/- Nebulization with salbutamol
 Cardiogenic Shock
• Known cardiac patient (SBP < 90; altered mentation, cold
extremities)
• ABC Admin oxygen
• Emergency Scan FOR IVC DIAMETER ≥2.1cm & OR JVP
≥5cm
• YES- IV Dobutamine at 10mcg/kg/min(preferred) or IV
Dopamine at 10mcg/kg/min(alternative
• Establish cause and treat
• Admit to HDU and Consult a Physician
• Electrolyte abnormalities, commonly hypokalemia and
hypomagnesemia,should be corrected.
• Pain is treated with IV morphine sulfate or fentanyl.
• Significant dysrhythmias and heart block must be treated with
antiarrhythmic drugs, pacing, or cardioversion, if necessary.
• Early consultation with cardiology is essential in current
management of cardiogenic shock, particularly in the setting of
acute MI
 Obstructive Shock
Tension pneumothorax • ABC
• respiratory distress (in an awake • Oxygen
patient), • CXR - deviation of mediastinal
• hypotension, structures, depression of the
• diminished breath sounds over one hemidiaphragm, and hypo-
hemithorax, opacification with absent lung
• Hyperresonance to percussion markings.
• jugular venous distention, • Decompress pleural space with a
• Shift of mediastinal structures to the large caliber needle.
unaffected side with tracheal • Chest tube with under water seal
deviation. drain
 Obstructive Shock
• Cardiac Tamponade
• total circulatory collapse • emergency pericardial
• cardiac arrest decompression, usually through a
• Beck’s triad -hypotension, left thoracotomy
muffled heart tones, and neck
vein distention
• Others - dyspnea,
orthopnea,cough, peripheral
edema, chest pain, tachycardia,
muffled heart tones, jugular
venous distention, and elevated
central venous pressure.
 Management of acute spinal cord
injury
• Attention to BP control, oxygenation, and hemodynamics,.
• Patients with hypotension from spinal cord injury are best
monitored in an ICU and carefully followed for evidence of
cardiac or respiratory dysfunction.
 Clinical Presentation
• Decreased BP associated with bradycardia (absence of reflexive
tachycardia due to disrupted sympathetic discharge),
• Warm extremities (loss of peripheral vasoconstriction),
• motor and sensory deficits indicative of a spinal cord injury, e.g
loss of anal sphincter tone, loss of bladder function, loss of LL
function
• Radiographic evidence of a vertebral column fracture
 Mx- neurogenic shock
• airway is secured and ventilation is adequate,
• fluid resuscitation and restoration of intravascular volume
• once hypovolemia is excluded as the cause of the hypotension and the diagnosis of
neurogenic shock is established
• Patient not eurovolaemic
• Admin vasoconstrictors to improve peripheral vascular tone, decrease vascular
capacitance, and increase venous return
• dopamine may be used first.
• A pure α-agonist, such as phenylephrine, may be used primarily or in patients
unresponsive to dopamine.
• Specific treatment for the hypotension is often of brief duration, as the need to
administer vasoconstrictors typically lasts 24 to 48 hours
• Spinal decompression to stabilize fracture
 REFERENCES
1. ATLS®Advanced Trauma Life Support, Student Course Manual, 10 TH Edition
2. Bailey and Love’s Short Practice of Surgery 25th Edition
3. Uganda Clinical Guidelines 2020, MOH Uganda
4. Schwatz Principles of Surgery, 17th Edition
5. Schmidt, G., & Mandel, J. (2020). Evaluation and management of suspected
sepsis and septic shock in adults. Retrieved
from: https://www.uptodate.com/contents/evaluation-and-management-of-
suspected-sepsis-and-septic-shock-in-adults
6. Muraro, A., et al (2014). Anaphylaxis: Guidelines from the European Academy
of Allergy and Clinical Immunology. Allergy: European Journal of Allergy and
Clinical Immunology, 69(8), 1026–1045. https://doi.org/10.1111/all.12437
Questions??
SHOCK ADDITION
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