DEFINITION
SHOCK IS A CIRCULATORY SYSTEM
ABNORMALITY THAT RESULTS IN
INADEQUATE OXYGEN PERFUSION AND
TISSUE OXYGENATION
PHYSIOLOGICAL EXHAUSTION-THE
TRIAD OF DEATH
HYPOTHERMIA
ACIDOSISCOAGULOPATHY
 HYPOPERFUSION STATE RESULTS IN CELLULAR
ANAEROBIC METABOLISM AND LACTIC
ACIDOSIS.ACIDOSIS LEADS TO DECREASED
FUNCTION OF COAGULATION PROTEASES-LEADS
TO COAGULOPATHY AND FURTHER
HAEMORRHAGE.
UNDERPERFUSED MUSCLE IS UNABLE TO
GENERATE HEAT AND HYPOTHERMIA
OCCURS.COAGULATION FUNCTIONS POORLY AT
LOW TEMPERATURE AND THERE IS FURHER
HAEMORRHAGE,HYPOPERFUSION AND
HYPOTHERMIA.THESE 3 FACTORS RESULT IN A
DOWNWARD SPIRAL LEADIING TO
PHYSIOLOGICAL EXHAUSTION AND DEATH
1.HYPOVOLEMIC-HAEMORRHAGIC
NON-HAEMORRHAGIC
2.CARDIOGENIC SHOCK
3.OBSTRUCTIVE
3.DISTRIBUTIVE SHOCK-ANAPHYLACTIC
SEPTIC
4.ENDOCRINE SHOCK
STAGES OF SHOCK
 COMPENSATED-- HR, Vasoconstriction, CO,
normal BP
 DECOMPENSATED--, HR, hypothermia, blood
pressure, prolonged capillary refill time, poor
peripheral pulses, and eventually urine output.
 IRREVERSIBLE SHOCK
BLEEDING-TRAUMA,GI BLEED,RUPTURED
ANEURYSM
PROTRACTED VOMITING OR DIARRHEA
ADRENAL INSUFFICIENCY
THIRD SPACING-INTESTINAL
OBSTRUCTION,PANCREATITIS
 HAEMORRHAGIC SHOCK-COMMONEST CAUSE
OF SHOCK IN TRAUMA PATIENTS
 NON-HAEMORRHAGIC CAUSES
 CARDIAC PUMP PROBLEMS-CARDIAC
TAMPONADE,TENSION
PNEUMOTHORAX,MYOCARDIAL CONTUSION
 NEUROGENIC SHOCK
 SEPTIC SHOCK
HAEMORRHAGIC SHOCK
 HAEMORRHAGE MAY BE REVEALED OR
CONCEALED.
 HAEMORRHAGE –EXSANGUINATION FROM
OPEN ARTERIAL WOUND OR FROM
HAEMETEMESIS FROM A DUODENAL ULCER
 CONCEALED HAEMORRHAGE IS CONTAINED
WITHIN THE BODY CAVITY.EG-WITHIN
CHEST,ABDOMEN,PELVIS WITH CONTAINED
VASCULAR INJURY
PRIMARY,SECONDARY AND
REACTIONARY HAEMORRHAGE
 PRIMARY HAEMORRHAGE IS HAEMORRHAGE
OCCURING IMMEDIATELY AS A RESULT OF INJURY
 REACTIONARY HAEMORRHAGE (WITHIN 24 HOURS)
CAUSED BY DISLOGEMENT OF
CLOT BY RESUSCITATION,NORMALISATION OF BP AND
VASODILATATION
 SECONDARY HAEMORRHAGE IS CAUSED BY
SLOUGHING OF VESSEL WALL .IT USUALLY OCCURS
AFTER 7-14 DAYS AFTER INJURY BY FACTORS SUCH
AS INFECTION,PRESSURE NECROSIS(DRAIN)OR
MALIGNANCY
•BLOOD LOSS IN SITE
FRACTURE TIBIA/HUMERUS-750 ML BLOOD
FRACTURE FEMUR-1500 ML BLOOD
FRACTURE PELVIS-2 TO 3 LITRES
•OBLIGATORY EDEMA IN SOFT TISSUES
SBP<110mm Hg
Tachycardia>90/mt
Tachypnea
Oliguria
Metabolic acidemia
Hypoxemia
Cutaneous vasoconstriction
Mental changes-anxiety,agitation,lethargy
APPROPRIATE HISTORY AND CLINICAL
EXAMINATION
•ADJUNCTS FOR CONFIRMATION
CVP
CHEST/PELVIC XRAY
ULTRASOUND
MINIMUM REQUIREMENTS
MONITOR SBP,URINE OUTPUT,BP,HR,MENTAL
STATE
ADDITIONAL MODALITIES
CVP
INVASIVE BP MONITORING
CARDIAC OUTPUT
BASE DEFICIT
SERUM LACTATE
CLASSIFICATION OF DEGREE OF
HAEMORRHAGE
INITIAL MANAGEMENT OF
HAEMORRHAGIC SHOCK
 DIAGNOSIS AND TREATMENT IS DONE
SIMULTANEOUSLY
 2 BASIC PRINCIPLES ARE
• STOP BLEEDING
• REPLACE THE VOLUME
• ANY SHOCK SHOULD BE ASSUMED HYPOVOLEMIC
UNTIL PROVED OTHERWISE AND HYPOVOLEMIA
SHOULD BE ASSUMED TO BE DUE TO HAEMORRHAGE
UNTIL THIS HAS BEEN EXCLUDED
INITIAL MANAGEMENT OF
HAEMORRHAGIC SHOCK
 ASSESS ABCDE
 BASELINE RECORDINGS-BP,PR,URINE OUTPUT,LEVEL OF
CONSCIOUSNESS
 CONTROL OBVIOUS HAEMORRHAGE.DIRECT PRESSURE
SHOULD BE PLACED OVER SITE OF EXTERNAL
HAEMORRHAGE
 ADEQUATE IV ACCESS-2 LARGE BORE IV CANNULA(MINIMUM
16 GUAGE)
 IF PERIPHERAL LINE NOT POSSIBLE-CENTRAL LINE,VENOUS
CUT DOWN.BLOOD DRAWN FOR CROSS MATCHING
 ASSESS TISSUE PERFUSION
INITIAL FLUID THERAPY
 RINGER LACTATE IS THE FIRST CHOICE,2ND IS
NORMAL SALINE
 AN INTIAL BOLUS IS GIVEN AS RAPIDLY AS
POSSIBLE.DOSE OF 1 -2 LITRES FOR ADULTS
 20 ML/KG FOR CHILDREN.
DYNAMIC FLUID RESPONSE
 PATIENTS CAN BE DIVIDED INTO RAPID
RESPONDERS,TRANSIENT RESPONDERS AND
NON RESPONDERS BASED ON RESPONSE TO
FLUID THERAPY
RESPONSES TO INITIAL FLUID
RESUSCITATIONRAPID
RESPONS
E
TRANSIENT
RESPONSE
NO RESPONSE
VITAL SIGNS RETURN
TO
NORMAL
TRANSIENT
IMPROVEM
ENT
ABNORMAL
ESTIMATED
BLOOD LOSS
MINIMAL
(10 – 20 %)
MODERATE
AND
ONGOING
(20 – 40 %)
SEVERE
(>40%)
NEED FOR
MORE
CRYSTALLOID
LOW MODERATE IMMEDIATE
NEED FOR POSSIBLY LIKELY HIGHLY LIKELY
 EXCESSIVE BLOOD LOSS FROM FRACTURED BONE
MAY BE PREVENTED BY AVOIDING MOVING THE
PATIENT FROM ONE COUCH TO ANOTHER.
.FOR FRACTURES OF PELVIS,TEMPORARY
STABILISATION WITH AN EXTERNAL FIXATOR
HAS BEEN FOUND TO BE USEFUL IN REDUCING
HAEMORRHAGE
I.V. Solutions
 Crystalloid
 Colloid
 Whole Blood or Blood Products
 Water and Glucose
Crystalloids (Isotonic)
 Solutions of ions with an osmolarity similar to that
of plasma.
 Effective, short term, volume replacement
 Do NOT have O2 carrying capacity
 Do NOT contain protein
Crystalloids (Isotonic)
 Most common crystalloids
 Normal saline
 Fluid of choice in combat
 Ringers lactate
 Most physiologically adaptable
solution available
 Hartmann,s solution
Crystalloids (Isotonic)
 Precautions
 Always consider fluid volume overload
 Excessive infusion of electrolytes may cause
electrolyte imbalances
 DO NOT use in patient’s with
 Cardiac failure
 Liver disease
 0.9% NaCl is C/I in metabolic axidosis as it is an
acidifying solution, which may slow down the
resolution of the metabolic acidosis, so in that case
use RL
C OLLOIDS
 are large molecules that cannot freely diffuse through the
capillary membrane
 NO oxygen carrying capacity
 ALBUMIN
 HETASTARCH – SYNTHETIC
 The advantage of colloids is that since they do not rapidly
diffuse across the capillary membrane, they act to hold
water in the
intravascular space and maintain intravascular volume
expansion for longer periods of time than crystalloids
Water and Glucose
 These solutions are Hypotonic
 Most common concentrations:
 D5W – Fluid replacement and caloric
supplementation
 D50W – treats hypoglycemic (low blood sugar) in
adults
Water and Glucose
 Contraindications:
 DO NOT use in HEAD INJURIES
 Will cause cellular swelling
 Precautions:
 Volume overload
 Electrolyte imbalance
Whole Blood
 Ideal replacement fluid if blood is being lost
 Indications
 Acute massive blood loss
 Will resolve symptoms of hypovolemic shock and
anemia
VASSOPRESSOR AND IONOTROPICS
 NOT AS FIRST LINE THERAPY
 Administration of this agents in absence of
adequqte preload lead to decrease coronary
perfusion and depletion of myocardial oxygen
reserve
 Noradrenaline – distributive shock
 Ionotrops in - cardiogenic shock
SEPTIC SHOCK
 Severe sepsis with cardiovascular organ dysfunction,
i.e. hypotension (systolic blood pressure [SBP] < 5th
centile
 non-specific systemic inflammatory response to
infection,trauma, burns, surgery etc.
 Characterized by abnormalities in 2 or more of the
following • body temperature• heart rate• respiratory
function
• peripheral leucocyte count
SEPTIC SHOCK --management
 RESUSCITATION– ABC
 FLUID THERAPY-- aggressive fluid resuscitation with
crystalloids or colloids at 20 mls/kg as rapid IVpush
over 5-10 mins. Can be repeated up to 60 mls/kg or
more.
 - correct hypoglycaemia and hypocalcaemia
 IONOTROPES -- IV Dopamine 5 - 15 μg/kg min
 IV Dobutamine 5 - 15 μg/kg/min
 - for fluid refractory and dopamine/dobutamine
refractory shock Adrenaline is given
 ANTIMICROBIAL-- IV antibiotics should be
administered immediately after appropriate cultures
are taken.
 Start empirical, broad spectrum to cover all likely
pathogens
 antibiotic regime to be modified accordingly once C&S
results
 RESPIRATORY SUPPORT- use PEEP and FIO2 to keep
SaO2 > 90%, PaO2 > 80 mmHg
 SUPPORTIVE THERAPY-
 packed cells transfusion if Hb <10g%
 - platelet concentrate transfusion if platelet count < 20
000
 - if overt clinical bleeding, correct coagulopathy or
DIVC
 - bicarbonate therapy: give bicarbonate only in
refractory metabolic acidosis,
 - maintain normal electrolytes and blood sugar
THANK YOU

Shock

  • 2.
    DEFINITION SHOCK IS ACIRCULATORY SYSTEM ABNORMALITY THAT RESULTS IN INADEQUATE OXYGEN PERFUSION AND TISSUE OXYGENATION
  • 3.
    PHYSIOLOGICAL EXHAUSTION-THE TRIAD OFDEATH HYPOTHERMIA ACIDOSISCOAGULOPATHY
  • 5.
     HYPOPERFUSION STATERESULTS IN CELLULAR ANAEROBIC METABOLISM AND LACTIC ACIDOSIS.ACIDOSIS LEADS TO DECREASED FUNCTION OF COAGULATION PROTEASES-LEADS TO COAGULOPATHY AND FURTHER HAEMORRHAGE.
  • 6.
    UNDERPERFUSED MUSCLE ISUNABLE TO GENERATE HEAT AND HYPOTHERMIA OCCURS.COAGULATION FUNCTIONS POORLY AT LOW TEMPERATURE AND THERE IS FURHER HAEMORRHAGE,HYPOPERFUSION AND HYPOTHERMIA.THESE 3 FACTORS RESULT IN A DOWNWARD SPIRAL LEADIING TO PHYSIOLOGICAL EXHAUSTION AND DEATH
  • 7.
  • 8.
    STAGES OF SHOCK COMPENSATED-- HR, Vasoconstriction, CO, normal BP  DECOMPENSATED--, HR, hypothermia, blood pressure, prolonged capillary refill time, poor peripheral pulses, and eventually urine output.  IRREVERSIBLE SHOCK
  • 9.
    BLEEDING-TRAUMA,GI BLEED,RUPTURED ANEURYSM PROTRACTED VOMITINGOR DIARRHEA ADRENAL INSUFFICIENCY THIRD SPACING-INTESTINAL OBSTRUCTION,PANCREATITIS
  • 10.
     HAEMORRHAGIC SHOCK-COMMONESTCAUSE OF SHOCK IN TRAUMA PATIENTS  NON-HAEMORRHAGIC CAUSES  CARDIAC PUMP PROBLEMS-CARDIAC TAMPONADE,TENSION PNEUMOTHORAX,MYOCARDIAL CONTUSION  NEUROGENIC SHOCK  SEPTIC SHOCK
  • 11.
    HAEMORRHAGIC SHOCK  HAEMORRHAGEMAY BE REVEALED OR CONCEALED.  HAEMORRHAGE –EXSANGUINATION FROM OPEN ARTERIAL WOUND OR FROM HAEMETEMESIS FROM A DUODENAL ULCER  CONCEALED HAEMORRHAGE IS CONTAINED WITHIN THE BODY CAVITY.EG-WITHIN CHEST,ABDOMEN,PELVIS WITH CONTAINED VASCULAR INJURY
  • 12.
    PRIMARY,SECONDARY AND REACTIONARY HAEMORRHAGE PRIMARY HAEMORRHAGE IS HAEMORRHAGE OCCURING IMMEDIATELY AS A RESULT OF INJURY  REACTIONARY HAEMORRHAGE (WITHIN 24 HOURS) CAUSED BY DISLOGEMENT OF CLOT BY RESUSCITATION,NORMALISATION OF BP AND VASODILATATION  SECONDARY HAEMORRHAGE IS CAUSED BY SLOUGHING OF VESSEL WALL .IT USUALLY OCCURS AFTER 7-14 DAYS AFTER INJURY BY FACTORS SUCH AS INFECTION,PRESSURE NECROSIS(DRAIN)OR MALIGNANCY
  • 13.
    •BLOOD LOSS INSITE FRACTURE TIBIA/HUMERUS-750 ML BLOOD FRACTURE FEMUR-1500 ML BLOOD FRACTURE PELVIS-2 TO 3 LITRES •OBLIGATORY EDEMA IN SOFT TISSUES
  • 14.
    SBP<110mm Hg Tachycardia>90/mt Tachypnea Oliguria Metabolic acidemia Hypoxemia Cutaneousvasoconstriction Mental changes-anxiety,agitation,lethargy
  • 15.
    APPROPRIATE HISTORY ANDCLINICAL EXAMINATION •ADJUNCTS FOR CONFIRMATION CVP CHEST/PELVIC XRAY ULTRASOUND
  • 16.
    MINIMUM REQUIREMENTS MONITOR SBP,URINEOUTPUT,BP,HR,MENTAL STATE ADDITIONAL MODALITIES CVP INVASIVE BP MONITORING CARDIAC OUTPUT BASE DEFICIT SERUM LACTATE
  • 17.
  • 18.
    INITIAL MANAGEMENT OF HAEMORRHAGICSHOCK  DIAGNOSIS AND TREATMENT IS DONE SIMULTANEOUSLY  2 BASIC PRINCIPLES ARE • STOP BLEEDING • REPLACE THE VOLUME • ANY SHOCK SHOULD BE ASSUMED HYPOVOLEMIC UNTIL PROVED OTHERWISE AND HYPOVOLEMIA SHOULD BE ASSUMED TO BE DUE TO HAEMORRHAGE UNTIL THIS HAS BEEN EXCLUDED
  • 19.
    INITIAL MANAGEMENT OF HAEMORRHAGICSHOCK  ASSESS ABCDE  BASELINE RECORDINGS-BP,PR,URINE OUTPUT,LEVEL OF CONSCIOUSNESS  CONTROL OBVIOUS HAEMORRHAGE.DIRECT PRESSURE SHOULD BE PLACED OVER SITE OF EXTERNAL HAEMORRHAGE  ADEQUATE IV ACCESS-2 LARGE BORE IV CANNULA(MINIMUM 16 GUAGE)  IF PERIPHERAL LINE NOT POSSIBLE-CENTRAL LINE,VENOUS CUT DOWN.BLOOD DRAWN FOR CROSS MATCHING  ASSESS TISSUE PERFUSION
  • 20.
    INITIAL FLUID THERAPY RINGER LACTATE IS THE FIRST CHOICE,2ND IS NORMAL SALINE  AN INTIAL BOLUS IS GIVEN AS RAPIDLY AS POSSIBLE.DOSE OF 1 -2 LITRES FOR ADULTS  20 ML/KG FOR CHILDREN.
  • 21.
    DYNAMIC FLUID RESPONSE PATIENTS CAN BE DIVIDED INTO RAPID RESPONDERS,TRANSIENT RESPONDERS AND NON RESPONDERS BASED ON RESPONSE TO FLUID THERAPY
  • 22.
    RESPONSES TO INITIALFLUID RESUSCITATIONRAPID RESPONS E TRANSIENT RESPONSE NO RESPONSE VITAL SIGNS RETURN TO NORMAL TRANSIENT IMPROVEM ENT ABNORMAL ESTIMATED BLOOD LOSS MINIMAL (10 – 20 %) MODERATE AND ONGOING (20 – 40 %) SEVERE (>40%) NEED FOR MORE CRYSTALLOID LOW MODERATE IMMEDIATE NEED FOR POSSIBLY LIKELY HIGHLY LIKELY
  • 23.
     EXCESSIVE BLOODLOSS FROM FRACTURED BONE MAY BE PREVENTED BY AVOIDING MOVING THE PATIENT FROM ONE COUCH TO ANOTHER. .FOR FRACTURES OF PELVIS,TEMPORARY STABILISATION WITH AN EXTERNAL FIXATOR HAS BEEN FOUND TO BE USEFUL IN REDUCING HAEMORRHAGE
  • 24.
    I.V. Solutions  Crystalloid Colloid  Whole Blood or Blood Products  Water and Glucose
  • 25.
    Crystalloids (Isotonic)  Solutionsof ions with an osmolarity similar to that of plasma.  Effective, short term, volume replacement  Do NOT have O2 carrying capacity  Do NOT contain protein
  • 26.
    Crystalloids (Isotonic)  Mostcommon crystalloids  Normal saline  Fluid of choice in combat  Ringers lactate  Most physiologically adaptable solution available  Hartmann,s solution
  • 27.
    Crystalloids (Isotonic)  Precautions Always consider fluid volume overload  Excessive infusion of electrolytes may cause electrolyte imbalances  DO NOT use in patient’s with  Cardiac failure  Liver disease  0.9% NaCl is C/I in metabolic axidosis as it is an acidifying solution, which may slow down the resolution of the metabolic acidosis, so in that case use RL
  • 28.
    C OLLOIDS  arelarge molecules that cannot freely diffuse through the capillary membrane  NO oxygen carrying capacity  ALBUMIN  HETASTARCH – SYNTHETIC  The advantage of colloids is that since they do not rapidly diffuse across the capillary membrane, they act to hold water in the intravascular space and maintain intravascular volume expansion for longer periods of time than crystalloids
  • 29.
    Water and Glucose These solutions are Hypotonic  Most common concentrations:  D5W – Fluid replacement and caloric supplementation  D50W – treats hypoglycemic (low blood sugar) in adults
  • 30.
    Water and Glucose Contraindications:  DO NOT use in HEAD INJURIES  Will cause cellular swelling  Precautions:  Volume overload  Electrolyte imbalance
  • 31.
    Whole Blood  Idealreplacement fluid if blood is being lost  Indications  Acute massive blood loss  Will resolve symptoms of hypovolemic shock and anemia
  • 32.
    VASSOPRESSOR AND IONOTROPICS NOT AS FIRST LINE THERAPY  Administration of this agents in absence of adequqte preload lead to decrease coronary perfusion and depletion of myocardial oxygen reserve  Noradrenaline – distributive shock  Ionotrops in - cardiogenic shock
  • 33.
    SEPTIC SHOCK  Severesepsis with cardiovascular organ dysfunction, i.e. hypotension (systolic blood pressure [SBP] < 5th centile  non-specific systemic inflammatory response to infection,trauma, burns, surgery etc.  Characterized by abnormalities in 2 or more of the following • body temperature• heart rate• respiratory function • peripheral leucocyte count
  • 34.
    SEPTIC SHOCK --management RESUSCITATION– ABC  FLUID THERAPY-- aggressive fluid resuscitation with crystalloids or colloids at 20 mls/kg as rapid IVpush over 5-10 mins. Can be repeated up to 60 mls/kg or more.  - correct hypoglycaemia and hypocalcaemia  IONOTROPES -- IV Dopamine 5 - 15 μg/kg min  IV Dobutamine 5 - 15 μg/kg/min  - for fluid refractory and dopamine/dobutamine refractory shock Adrenaline is given
  • 35.
     ANTIMICROBIAL-- IVantibiotics should be administered immediately after appropriate cultures are taken.  Start empirical, broad spectrum to cover all likely pathogens  antibiotic regime to be modified accordingly once C&S results
  • 36.
     RESPIRATORY SUPPORT-use PEEP and FIO2 to keep SaO2 > 90%, PaO2 > 80 mmHg  SUPPORTIVE THERAPY-  packed cells transfusion if Hb <10g%  - platelet concentrate transfusion if platelet count < 20 000  - if overt clinical bleeding, correct coagulopathy or DIVC
  • 37.
     - bicarbonatetherapy: give bicarbonate only in refractory metabolic acidosis,  - maintain normal electrolytes and blood sugar
  • 38.