5. Shock: Diagnosis
• Diagnosis easy if overt volume loss or
haemodynamic instability
• Diagnosis challenging if loss is occult or
at a slow pace
• Investigations
• CBC
• ABG/VBG
• BUN, creatinine
• ECG
• CVP
6.
7.
8. General approach to
management of shock
• ABC management
• IV access
• Correction of oxygen debt
• Control of fluid loss
• Gastric decompression
• Urinary catheterisation
16. Fluid Resuscitation:
Crystalloids Vs Colloids?
• Question remains unanswered
• “…it is the dose, not the choice of fluid
that is the real issue – and the proper
dose of any drug is enough…”
17. Treatment of Hypovolemic
Shock: Fluid Resuscitation
Crystalloids
• Isotonic
• Ringer’s Lactate
• 0.9% saline
• Hypertonic
saline
• With Dextrose
• Without Dextrose
Colloids
Albumin
Low-molecular
weight Dextran
Hydroxyethyl
starch
Fresh frozen
plasma
Human Albumin
18. Fluid Resuscitation:
Crystalloids
Advantages
• Inexpensive
• Readily
available
• Freely mobile
across
capillaries
• No risk of
transfusion
reaction
Disadvantages
• Increased Clot
disruption
• Dilutional
coagulopathy
• Dilutional
anemia
• Metabolic
acidosis
• Hypothermia
19. Fluid Resuscitation: Colloids
Advantages
• Less water
administered
i.e. more
resuscitation
per ml
• Less decrease
in oncotic
pressure
• Acid buffer
(FFP)
Disadvantages
Expensive (Albumin,
FFP)
Cross infection (FFP)
Increase interstitial
oncotic pressure
22. Fluid Resuscitation: When to
Add Blood?
• Do not delay resuscitation while waiting for
blood to be grouped and arrive
• If estimated loss > 20% blood volume
consider blood transfusion.
• Whole blood is ideal
• Keep Hb between 7 and 9 gm/dL
• MTP-1:1:1
23. Points to Remember When
Giving Blood
• Always use youngest possible blood
• Use fully cross-matched blood
• Guard against hypothermia if giving large
volumes
• Do not transfuse large amount of packed
RBC’s alone
• Consider auto-transfusion e.g. blood
retrieved from peritoneal cavity
24. Fluid Resuscitation: How
Much?
• Depends on estimated volume loss,
clinical picture and CVP monitoring
• Rule of thumb: 3ml of crystalloid for every
ml of blood lost e.g. 70kg patient in Class
III shock has lost almost 1500 ml of blood
and needs 4500 ml of crystalloids for
volume replacement
25. Fluid Resuscitation: Rate
• Restore volume deficit in minutes to hours
not hours to days
• Start fluids stat and do not wait for lab
results or for blood
“Cardiac arrest due to low Hb is very unusual,
but cardiac arrest due to hypovolemia is
relatively common”
• In young patients transfuse at the most
rapid convenient rate
• In elderly give repeated small boluses
28. Fluid Resuscitation: End
Points
• Bedside recognition of return to normal
circulation
• Warm extremities
• Normal or improved mental status
• Pulse rate <100 / min
• Normal BP or rising BP
• Urine output >0.5ml / kg / hr
• Resolution of acidosis
• CVP returns to normal ??
30. Acidosis
• Treat underlying cause of shock
• Correction of PH
• THAM (tromethamine tris hydrodymethyl
aminomethane)- lean body weight (kgs)xbase
deficit(mmol/l)
31. Acidosis
• Treat underlying cause of shock
• Correction of PH
• THAM (tromethamine tris hydrodymethyl
aminomethane)- lean body weight (kgs)xbase
deficit(mmol/l)
38. Adjuvant Therapy
• Vasopressors
• Epinephrine
• Nor-epinephrine
• Dopamine
• Dobutamine
• Positioning
• Not head-down but elevate only both legs
• Pulmonary support (O2 by face mask)
• Analgesics – small doses by intravenous
route
39. Vasopressors
• Vasopressor therapy initially to target a mean arterial
pressure (MAP) of 65 mm Hg Norepinephrine as the
first choice vasopressor
• Epinephrine (added to and potentially substituted for
norepinephrine) when an additional agent is needed to
maintain adequate blood pressure
• Vasopressin 0.03 units/minute can be added to
norepinephrine (NE) with intent of either raising MAP
or decreasing NE dosage
41. Damage control surgery
• Principles
• Initial homeostasis and packing
• Control of contamination
• Correction of acidosis, coagulopathy and
hypothermia
• Definitive surgery within 24 hrs
42. Phases of DCS
• Stage I- Prehospital & Hospital
• Rapid evaluation
• CXR, Pelvis X-Ray,ICD Insertion
• Damage control resuscitation
• Permissive hypotension
• 20-30 mins
43. Phases of DCS
• Stage II-Damage control laparotomy
• Control hemorrhage
• Prevent contamination
• Avoid further injuries
44. Phases of DCS
• Stage III-Resuscitation
• Reverse the sequel of hypotension
• Physiological and biochemical restoration
• Adequate Oxygen delivery
• Agressive core rewarming
• Correction of coagulopathy
• Phase IV- Definitive surgery
47. Future Of Resuscitation
The ideal blood substitute would do the following:
• Deliver oxygen
• Require no compatibility testing
• Have few side effects
• Have prolonged storage capabilities
• Persist in the circulation
• Be cost-effective
49. PITFALLS: DIAGNOSIS AND
MANAGEMENT OF SHOCK
Normal BP: Occult shock
Inadequate volume resuscitation
Volume to vasopressor mismatch
Resuscitation fluid replaces volume but no inherent pro
survival property
Shock is defined as inadequate perfusion to maintain normal organ function. With prolonged anaerobic metabolism, tissue acidosis and O2 debt accumulate. Thus, the goal in the treatment of shock is restoration of adequate organ perfusion and tissue oxygenation. Resuscitation is complete when O2 debt is repaid, tissue acidosis is corrected, and aerobic metabolism is restored.
Shock in a trauma patient or postoperative patient should be presumed to be due to hemorrhagic until proven otherwise.
The clinical signs of shock may be evidenced by agitation, cool clammy extremities, tachycardia, weak or absent peripheral pulses, and hypotension.
* Hypotension (due to hypovolaemia, perhaps
followed by myocardial insufficiency)
* Skin pallor (vasoconstriction due to
catecholamine release)
* Tachycardia (due to catecholamine release)
* Confusion, aggression, drowsiness, and coma
(due to cerebral hypoxia and acidosis)
* Tachypnoea (due to hypoxia and acidosis)
* General weakness (due to hypoxia and
acidosis)
* Thirst (due to hypovolaemia)
* Reduced urine output (due to reduced
perfusion).
The diagnosis and treatment of shock must occur almost simultaneously. For most trauma patients, treatment is instituted as if the patient has hypovolemic shock, unless there is clear evidence that the shock state has a different cause.
base deficit is associated with hypovolemia and impaired tissue perfusion, a base deficit does not accurately identify an elevated serum lactate concentration or shock.
However, worsening base deficit is associated with increasing morbidity.
Cultures as clinically appropriate before antimicrobial therapy if no significant delay (> 45 mins) in the start of antimicrobial(s)
At least 2 sets of blood cultures (both aerobic and anaerobic bottles) be obtained before antimicrobial therapy with at least 1 drawn percutaneously and 1 drawn through each vascular access device, unless the device was recently (<48 hrs) inserted
inferior vena cava diameter, inferior vena cava inspiratory collapse, and the ratio of internal jugular vein height to width and found that maxi- mal inferior vena cava diameter was better able to differentiate a central venous pressure < 10 mm Hg from a central venous pressure > 10 mm Hg versus the other 2 measures.
when to use: uncontrolled bleeding
small bolus of 250ml crystalloid to maintain SBP-90mmhg, MAP-65mmhg,
Controversy-TBI, target SPB - 110mmhg
Proinflammatory- RL
NS- abdominal compartment
Metabolic acidocis ( dilution of bicarbonate buffers) , hyperchloremic non anion gap metabolic acidosis
plasmalyte- low Cl and additional gluconate and mg(renal failure)
Further investigations showed that when the lactate in LR was replaced with other sources of energy that could be better used by the mitochondria, the inflammatory aspects were attenuated. One such novel fluid was ketone Ringer’s solution
L lactate- intermediate in mammalian tissue
D lactate- methylyoxal glycosylate to lactic acid
D lactate- highly pro inflammatory, neuropsychotic disturbances
HTS- reduces inflammatory response and imunosupression (immunomodulator), less volume compared to NS
Use fully cross-matched blood unless impending lethal exsanguination; then use type ‘O’ blood; in girls & women of childbearing age give ‘O’ negative blood
Whole blood- no pulmonary problems,or coagulation problem
in lack of blood aggressive use of FFP,
decreased perfusion causing lactic acidosis, and consumptive coagulopathy.
the resuscitation injury from the amount and type of fluid infused contributing to hypothermia if the fluid is not warmed and dilutional coagulopathy.
The 50-mL ampule of sodium bicarbonate has 1 mEq/ mL—in essence, similar to giving a hypertonic concentration of sodium, which quickly draws fluid into the vascular space. Given its high sodium concentration, a 50-mL bolus of sodium bicarbonate has physiologic results similar to 325 mL of normal saline or 385 mL of LR. Essentially, it is like giving small doses of HTS. Sodium bicarbonate quickly increases CO2 levels by its conversion in the liver, so if the minute ventilation is not increased, respiratory acidosis can result.
THAM (trometamol; tris-hydroxymethyl aminomethane) is a biologically inert amino alcohol of low toxicity, which buffers carbon dioxide and acids in vitro and in vivo. decreased co2 production
At 37 degrees C, the pK (the pH at which the weak conjugate acid or base in the solution is 50% ionised) of THAM is 7.8, making it a more effective buffer than bicarbonate in the physiological range of blood pH.
accepting a proton, generating bicarbonate and decreasing the partial pressure of carbon dioxide in arterial blood (paCO2)
Hypothermia
Coagulopathy due to reduced enzymatic activity
Enhancing fibrinolytic activity
Platelet aggregation dysfunction( inhibition of TXB2 inhibition
factor IX and thromboplastin is most affected
Induced hypothermia is vastly different from spontaneous hypothermia, which is typically from shock, inadequate tissue perfusion, or cold fluid infusion.
It takes 1 kcal to raise the temperature of 1 liter of water by 1°C.
However, we are not made of pure water, and blood has a specific heat coefficient of 0.87. Thus, the human body as a whole has a specific heat coefficient of 0.83. Therefore, it actually takes 62.25 kcal (75 kg × 0.83) to raise body temperature by 1° C.
Induced hypothermia is vastly different from spontaneous hypothermia, which is typically from shock, inadequate tissue perfusion, or cold fluid infusion.
It takes 1 kcal to raise the temperature of 1 liter of water by 1°C.
However, we are not made of pure water, and blood has a specific heat coefficient of 0.87. Thus, the human body as a whole has a specific heat coefficient of 0.83. Therefore, it actually takes 62.25 kcal (75 kg × 0.83) to raise body temperature by 1° C.
It works with tissue factor and activated platelets. with tissue injury, TF is released at high levels at the site of injury, as are activated platelets. Theoretically, because rFVIIa targets the site of tissue injury, it is ideal in surgery.
Reduces need for massive blood transfusion
For example, if a patient had blunt injuries to the spleen and a femur fracture and was infused rFVIIa, the drug would work predominantly at the site of injury but would not create a systemic state of throm- botic or embolic problems.
PCC actually has many factors (factors II, VII, IX, X) in it, including variable amounts of factor VIIa,
TXA- Tranexamic acid (TXA) is a synthetic analogue of the amino acid lysine. Antifibrinolytic
Time dependent action- survival advantage when given early
CRASH 2 trial(Clinical Randomization of an Antifibrinolytic in Significant Haemorrhage)
Placebo Vs 1gm/10min+1gm/hr
-reduced death due to haemorrhage
-No significant increase in clots
- reduced 30 days hospital mortality
Fibrinogen + platelet primary substitute for clot formation
Reduced fibrinogen associated with increased mortality
consider if Fibrinogen <1gm/L
The definition of shock is inadequate tissue perfusion,
Blood delivers oxygen by red cells, which contain hemoglobin. The simple calculation of oxygen delivery (DO2) is the cardiac output (CO) multiplied by the content of oxygen carried by a volume of blood (CaO2):
The average hemoglobin carries 1.34 mL of oxygen per gram, depending on the arterial hemoglobin (Hgb) oxygen saturation (SaO2) of the red cell. In addition, a minor amount of oxygen is dissolved in plasma. This amount is calculated by multiplying the solubility constant 0.003 times the partial pressure of oxygen in the arterial blood (PaO2). The CaO2 of arterial blood is calculated as follows:
In states of hemorrhage and resuscitation, the stroke volume is affected by infusion of fluids. As blood volume is decreased, it will ultimately affect stroke volume and is compensated by an increase in heart rate.
Oxygen consumption (VO2) by cells is calculated by subtract- ing the content of oxygen in the venous system (CvO2) from delivered oxygen content in the arterial blood (CaO2):
To optimize oxygen delivery, one of the most efficient ways, according to past calculations, was to add hemoglobin. If the hemoglobin level increased from 8.0 to 10 g/dL, by transfusing 2 units of blood, oxygen delivery would increase by 25%. Blood transfusions were part of the optimization process because they also increased wedge pressure and LVED volume and thus cardiac output, but it was rarely noted that transfusions placed patients on the flat part of the consumption curve.
Vasopressors should only be initiated with/after adequate resuscitation is provided
with crystalloids, colloids, and/or blood products.
Vasopressors are not recommended in the initial stabilization of hemorrhagic shock.
Permissive hypotension may be employed until bleeding is controlled in patients
requiring emergent surgical intervention.
Epinephrin-a,b1,b2-2-10ug/min, CO & SVR increses
NE- a,b1, SVR markdly increses increasing CO, 2-20ug/min
Dop- 0.3-5ug/kg/min dop rec,5-10ug/kg/min- positive ionotropic b1, 10ug/kg/min a1mediated vasoconstriction
High dose of pressor agents worsen flow at the capillary bed and tends to increase lactate level
High dose of pressor agents worsen flow at the capillary bed and tends to increase lactate level
Aims to restore physiology at the expense of anatomical reconstruction
On going Damage control resuscitation
Peri hepatic packing
baloon catheter temponad
Splenectomy
pancreatic packing and drainage
Bile drainage
Cieliac axix and spleenic artery ligation
Common hepatic artery ligation
Aorta,SMA, common iliac and internal iliac - intraluminal shunting/ grafting
renal artery nephrectomy
Tensly disdended abdomen
inadequate ventilation, elevated peak expiratory airway pressure, oliguria anuria,hypoxia
IAP >20 mmhg
Sudden release of pressure lead to ischemic repercussion injury,acidosis, vasodilatation,
It was shown that neutrophils are activated after a 40% blood volume hemorrhage when followed by resuscitation with LR.
The type and amount of fluids directly caused inflammation. All the artificial fluids used to raise BP could cause the inflammatory sequelae of shock.
In contrast to volume expanders, blood substitutes refer to fluids that can carry oxygen.
In contrast to volume expanders, blood substitutes refer to fluids that can carry oxygen.
HBOC- source of HB- discarded human blood, bovine, transgenic E.colino communicable pathogen,no abo rh antigen, universally compatible, short half life, free radical generation, immunosuppression, repercussion injury
PFC-biologically inert, dissolves large quantity on oxygen and co2 than plasma. immiscible in water, linear relationship to o2 partial pressure