General principles of shock

SHOCK:
General principles, Classification & Management
PREPARED BY DR. DAWIT ALEMAYEHU(OSR I)
MODERATD BY DR. ZEGENE TAYE(CONSULTANT ORTHOPEDIC SURGEON)
1

OBJECTIVE
 To develop an understanding of the definition and pathophysiology of shock.
 To develop an understanding and overview of the different types of shock.
 To develop a systematic approach to the detection and management of shock.
PREPARED BY DR. DAWIT ALEMAYEHU
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OUTLINE
 INTRODUCTION
 DEFINITION
 PATHOPHYSIOLOGY
 STAGES OF SHOCK
 CLASSIFICATION
 CLINICAL PRESENTATION
 SEVERITY OF SHOCK
 APPROACH TO THE PATIENT IN SHOCK
 MONITORING AFTER TREATMENT
 CONSEQUENCES OF UNTREATED SHOCK
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INTRODUCTION
 Shock is the most common and therefore the most important cause of death among surgical
patients.
 Death may occur rapidly as a result of a profound state of shock or be delayed, resulting from the
consequences of organ ischaemia and reperfusion injury.
 It is important, therefore, that every surgeon understands the pathophysiology and diagnosis of
shock and haemorrhage, as well as the priorities for their management.
 Average adult (70 kg male) has an estimated 4.7 - 5 L of circulating blood
 Average child (2-10 years old) has an estimated 75 - 80 ml/kg of circulating blood
4

DEFINITION
 Shock is a systemic state of low tissue perfusion, which is inadequate for normal cellular
respiration.
 With insufficient delivery of oxygen and glucose, cells switch from aerobic to anaerobic
metabolism.
 If perfusion is not restored in a timely fashion, cell death ensues.
5

PATHOPHYSIOLOGY
 Cellular
 As perfusion to the tissues is reduced, cells are deprived of oxygen and must switch from aerobic to
anaerobic metabolism.
 The product of anaerobic respiration is not carbon dioxide but lactic acid.
 When enough tissue is underperfused, the accumulation of lactic acid in the blood produces systemic
metabolic acidosis.
 As glucose within cells is exhausted, anaerobic respiration ceases and there is failure of the
sodium/potassium pumps in the cell membrane and intracellular organelles.
 Intracellular lysosomes release autodigestive enzymes and cell lysis ensues.
 Intracellular contents, including potassium, are released into the bloodstream.
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 Microvascular
 As tissue ischaemia progresses, changes in the local milieu result in activation of the immune and
coagulation systems.
 Hypoxia and acidosis activate complement and prime neutrophils, resulting in the generation of oxygen
free radicals and cytokine release.
 These mechanisms lead to injury of the capillary endothelial cells.
 These in turn further activate the immune and coagulation systems.
 Damaged endothelium loses its integrity and becomes ‘leaky’.
 Spaces between endothelial cells allow fluid to leak out and tissue oedema ensues, exacerbating cellular
hypoxia.
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STAGES OF SHOCK
 Regardless of the type of shock, there is a physiologic continuum.
 Shock begins with an inciting event, such as a focus of infection (eg, abscess) or an injury (eg,
gunshot wound).
 Preshock
 Preshock is also referred to as warm shock or compensated shock.
 It is characterized by rapid compensation for diminished tissue perfusion by various homeostatic
mechanisms.
 As an example, compensatory mechanisms during preshock may allow an otherwise healthy adult to be
asymptomatic despite a 10 percent reduction in total effective arterial blood volume.
 Tachycardia, peripheral vasoconstriction, and either a modest increase or decrease in systemic blood
pressure may be the only clinical signs of shock.
11

 Shock
 During shock, the compensatory mechanisms become overwhelmed and signs and symptoms of organ
dysfunction appear.
 These include tachycardia, dyspnea, restlessness, diaphoresis, metabolic acidosis, oliguria, and cool
skin.
 The signs and symptoms of organ dysfunction typically correspond to a significant physiologic
 Examples include
 a 20 to 25 percent reduction in effective arterial blood volume in hypovolemic shock,
 a fall in the cardiac index to less than 2.5 L/min/m2 in cardiogenic shock, or
 activation of innumerable mediators of the systemic inflammatory response syndrome (SIRS) in distributive shock.
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 End-organ dysfunction
 Progressive end-organ dysfunction leads to irreversible organ damage and patient death.
 During this stage, urine output may decline further (culminating in anuria and acute renal failure),
decreases the cardiac output and alters cellular metabolic processes, and restlessness evolves into
obtundation, and coma.
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CLASSIFICATION OF SHOCK
 There are SIX main types of shock that
can be grouped into two pathogenic
groups:
 Vasoconstrictive – hypovolaemic,
Traumatic and cardiogenic shock
 Vasodilative – septic, neurogenic and
anaphylactic shock.
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Hypovolaemic shock
 Hypovolaemia is probably the most common form of shock and is to some degree a component of
all other forms of shock.
 Hypovolaemic shock is caused by a reduced circulating volume.
 Hypovolaemia may be due to haemorrhagic or non-haemorrhagic(Fluid loss- induced) causes.
 Non- haemorrhagic causes include
 poor fluid intake (dehydration) and
 excessive fluid loss because of vomiting, diarrhoea, urinary loss (e.g. diabetes), evaporation and ‘third-
spacing’, in which fluid is lost into the gastrointestinal tract and interstitial spaces, as for example in bowel
obstruction or pancreatitis.
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Relate to adults and children over the age of 12

Traumatic Shock
 The systemic response after trauma, combining the effects of soft tissue injury, long bone fractures,
and blood loss, is clearly a different physiologic insult than simple hemorrhagic shock.
 The hypoperfusion deficit in traumatic shock is magnified by the proinflammatory activation that
occurs following the induction of shock.
 Examples of traumatic shock include small volume hemorrhage accompanied by soft tissue injury
(femur fracture, crush injury), or any combination of hypovolemic, neurogenic, cardiogenic, and
obstructive shock that precipitate rapidly progressive proinflammatory activation.
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 Treatment of traumatic shock is focused on
 correction of the individual elements to diminish the
cascade of proinflammatory activation, and
 prompt control of hemorrhage, adequate volume
resuscitation to correct O2 debt,
 débridement of nonviable tissue, stabilization of bony
injuries, and appropriate treatment of soft tissue injuries.
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Initial management algorithm
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Cardiogenic shock
 Cardiogenic shock is due to primary failure of the heart to pump blood to the tissues.
 Causes of cardiogenic shock include
 myocardial infarction,
 valvular heart disease,
 cardiac dysrhythmias,
 Blunt myocardial injury or penetrating injury (e.g. fracture of the sternum) and
 cardiomyopathy.
 Cardiac insufficiency may also be caused by myocardial depression resulting from endogenous
factors (e.g. bacterial and humoral agents released in sepsis) or exogenous factors, such as
pharmaceutical agents or drug abuse.
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Obstructive shock
 In obstructive shock there is a reduction in preload because of mechanical obstruction of cardiac
filling.
 Common causes of obstructive shock include
 cardiac tamponade,
 tension pneumothorax,
 massive pulmonary embolus and
 air embolus.
 In each case there is reduced filling of the left and/or right sides of the heart leading to reduced
preload and a fall in cardiac output.
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Distributive shock
 There is maldistribution of blood flow at a microvascular level with arteriovenous shunting and
dysfunction of the cellular utilization of oxygen.
 Distributive shock describes the pattern of cardiovascular responses characterizing a variety of
conditions including septic shock, anaphylaxis and Neurogenic shock
 Inadequate organ perfusion is accompanied by vascular dilatation with hypotension, low systemic
vascular resistance, inadequate afterload and a resulting abnormally high cardiac output.
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A, Septic shock
 Number one cause of intensive care unit (ICU) death(Mortality 50%)
 This results from the entry of toxins into the circulation, which poison the Vasoconstrictive mechanisms
within the blood vessels.
 The profound vasodilatation that results dramatically reduces afterload; even with a normal circulating blood
volume and raised cardiac output, the patient’s blood pressure falls and the pulse pressure widens (e.g.
110/70 → 90/30).
 Oxygen consumption increases and, despite the high cardiac output, tissue perfusion and oxygenation are
reduced, and organ damage results.
 The toxins can also damage the myocardium and cause capillary leakage, complicating the presentation with
elements of cardiogenic and hypovolaemic shock.
23

B, Neurogenic shock
 Neurogenic shock is produced by high spinal cord injury, which disrupts the sympathetic nerves controlling
vasoconstriction.
 Usually injury occurs in T4 – 8 region
 The peripheral vasculature relaxes and becomes profoundly dilated, reducing pre-load and afterload.
 Even with a raised cardiac output, the patient cannot maintain an adequate blood pressure and shock
ensues.
 Neurogenic shock is not caused by an isolated head injury and is different from ‘spinal shock’, which is a
temporary flaccidity following spinal damage.
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 Since neurogenic shock is always related to traumatic spinal cord damage, it is likely to coexist with
a degree of hypovolaemia from associated trauma.
 CLINICAL SMPTOMS- Bradycardia, hypotension ,Extremities warm
 Treat with IV Norepinephrine or Dopamine drip(vasoconstrictors) and volume
 Avoid overinfusion (risk of pulmonary edema, CHF)
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C, Anaphylactic shock
 This is a type of allergic reaction.
 Exposure to an antigen to which an individual has previously been sensitized triggers off a cascade reaction.
 The mast cells degranulate and release large quantities of histamine into the bloodstream.
 Other vasoactive substances are released, and profound vasodilatation is caused.
 Massive capillary leakage results in sudden oedema, which with loss of fluid into the bowel causes
hypovolaemia.
 (1 mm depth of oedema across the body surface equates to a 1.5 L fluid loss.)
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 This picture is complicated by other effects such as bronchospasm.
 Anaphylaxis can be triggered by many common antigens such as shellfish or peanuts.
 Of particular significance to the hospital practitioner are allergies drugs, particularly to penicillin
antibiotics (which are now commonly given to open fracture patients immediately or very soon after
the injury is recognized), chlorhexidene and latex.
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Endocrine shock
 Endocrine shock may present as a combination of hypovolaemic, cardiogenic and distributive shock.
 Causes of endocrine shock include hypo- and hyperthyroidism and adrenal insufficiency.
 Hypothyroidism causes a shock state similar to that of neurogenic shock as a result of disordered
vascular and cardiac responsiveness to circulating catecholamines.
 Cardiac output falls because of low inotropy and bradycardia.
 There may also be an associated cardiomyopathy.
 Adrenal insufficiency leads to shock as a result of hypovolaemia and a poor response to circulating
and exogenous catecholamines.
 IT may result from pre-existing Addison’s disease or it may be a relative insufficiency caused by a
pathological disease state such as systemic sepsis.
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CLINICAL PRESENTATION
 The clinical presentation varies according to the type of shock, its cause, and its stage of
presentation.
 Several features are common among all types of shock (cardinal findings), while other features may
suggest a particular type of shock (suggestive findings).
 Cardinal findings — Cardinal features of shock include hypotension, oliguria, abnormal mental
status, metabolic acidosis, and, in some patients, cool and clammy skin.
 Hypotension – Hypotension occurs in the majority of shock patients. It may be absolute hypotension (eg,
systolic blood pressure <90 mmHg) or relative hypotension (eg, a drop in systolic blood pressure >40
mmHg).
 Relative hypotension explains, in part, why a patient may be in shock despite having a high or normal blood pressure.
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 Oliguria – Oliguria may be due to shunting of renal blood flow to other vital organs, intravascular volume
depletion, or both.
 When intravascular volume depletion is a cause, it may be accompanied by orthostatic hypotension, poor skin
absent axillary sweat, or dry mucous membranes.
 Change in mental status – The continuum of mental status changes frequently encountered in shock
begins with agitation, progresses to confusion or delirium, and ends in obtundation or coma.
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 Cool, clammy skin – Potent vasoconstrictive mechanisms compensate for decreased tissue perfusion by
redirecting blood from the periphery to the vital organs, thereby maintaining coronary, cerebral, and
splanchnic perfusion.
 Not all patients with shock have cool and clammy skin, however.
 Patients with early distributive shock or terminal shock may have flushed, hyperemic skin.
 The former occurs prior to the onset of compensatory vasoconstriction, while the latter is due to failure of compensatory
vasoconstriction.
 Metabolic acidosis – Metabolic acidosis develops as shock progresses, reflecting decreased clearance of
lactate by the liver, kidneys, and skeletal muscle.
 Lactate production may increase due to anaerobic metabolism if shock progresses to circulatory failure and tissue
hypoxia, which can worsen the acidemia.
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 Suggestive findings ;- These findings are neither sensitive nor specific.
 Hypovolemic shock –
 Physical manifestations may include decreased skin turgor (in younger patients), dry skin, dry axillae,
tongue, or dry oral mucosa.
 In addition, patients may have postural hypotension, decreased jugular venous pressure, or
central venous pressure.
 There may be anemia, or the amylase and lipase may be elevated.
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 Cardiogenic shock – Depending upon the cause of the cardiogenic shock, patients may report dyspnea,
chest pain, or palpitations.
 Many patients have a history of cardiovascular disease.
 Lung examination may reveal diffuse crackles and cardiac examination may reveal a new murmur, gallops, or soft
sounds.
 The jugular venous pressure and central venous pressure may be increased, while the distal arterial pulses may be
diminished.
 There may be evidence of pulmonary congestion or pulmonary edema on a chest radiograph, as well as recent or
current ischemia on an electrocardiogram.
 Cardiac enzymes may be elevated.
 An echocardiogram may demonstrate the etiology.
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 Distributive shock –
 Depending upon the cause of the distributive shock, patients may report dyspnea,
productive cough, dysuria, hematuria, chills, myalgias, rashes, fatigue, malaise, headache,
photophobia, pain, or a recent ingestion.
 There may be fever, tachypnea, tachycardia, leukocytosis, an abnormal mental status, or
flushing.
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SEVERITY OF SHOCK
 Compensated shock
 As shock progresses the body’s cardiovascular and endocrine compensatory responses reduce flow to non-
essential organs to preserve preload and flow to the lungs and brain.
 Apart from a tachycardia and cool peripheries (vasoconstriction, circulating catecholamines) there may be
no other clinical signs of hypovolaemia.
 However, this cardiovascular state is only maintained by reducing perfusion to the skin, muscle and
gastrointestinal tract.
 Patients with occult hypoperfusion (metabolic acidosis despite normal urine output and cardiorespiratory
vital signs) for more than 12 hours have a significantly higher mortality rate, infection rate and incidence of
multiple organ failure
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 Decompensation
 Further loss of circulating volume overloads the body’s compensatory mechanisms and there is
renal, respiratory and cardiovascular decompensation.
 In general, loss of around 15% of the circulating blood volume is within normal compensatory
 Blood pressure is usually well maintained and only falls after 30–40% of the circulating volume has been
lost.
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 Mild shock
 Initially there is tachycardia, tachypnoea and a mild reduction in urine output and the patient may exhibit mild
anxiety.
 Blood pressure is maintained although there is a decrease in pulse pressure.
 The peripheries are cool and sweaty with prolonged capillary refill times (except in septic distributive shock).
 Moderate shock
 As shock progresses, renal compensatory mechanisms fail, renal perfusion falls and urine output dips below 0.5
ml /kg/hr.
 There is further tachycardia and now the blood pressure starts to fall.
 Patients become drowsy and mildly confused.
 Severe shock
 In severe shock there is profound tachycardia and hypotension.
 Urine output falls to zero and patients are unconscious with laboured respiration.
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Pitfalls
 The classic cardiovascular responses are not seen in every patient.
 It is important to recognize the limitations of the clinical examination and to recognize patients who
are in shock despite the absence of classic signs.
1. Capillary refill
 Most patients in hypovolaemic shock will have cool, pale peripheries with prolonged capillary refill times;
 however, the actual capillary refill time varies so much in adults that it is not a specific marker of whether a
patient is shocked, and patients with short capillary refill times may be in the early stages of shock.
 In distributive (septic) shock the peripheries will be warm and capillary refill will be brisk despite profound
shock.
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2. Tachycardia
 Tachycardia may not always accompany shock.
 Patients who are on β-blockers or who have implanted pacemakers are unable to mount a tachycardia.
 A pulse rate of 80 in a fit young adult who normally has a pulse rate of 50 is very abnormal.
3. Blood pressure
 It is important to recognise that hypotension is one of the last signs of shock.
 Children and fit young adults are able to maintain blood pressure until the final stages of shock by dramatic
increases in stroke volume and peripheral vasoconstriction. (These patients can be in profound shock with a
normal blood pressure.)
 Elderly patients who are normally hypertensive may present with a ‘normal’ blood pressure for the general
population but be hypovolaemic and hypotensive relative to their usual blood pressure.
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APPROACH TO THE PATIENT IN SHOCK
• ABCDE
• Airway
• control work of Breathing
• optimize Circulation
• assure adequate oxygen Delivery
• achieve End points of resuscitation
 Goals for patient
 Assurance of adequate tissue perfusion
 Restoration of normal or baseline BP
 Return/recovery of organ function
 Avoidance of complications from
prolonged states of hypoperfusion
43

 ABCs
 Cardiorespiratory monitor
 Pulse oximetry
 Supplemental oxygen
 IV access
 ABG, labs
 Foley catheter
 Vital signs including rectal temperature
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Airway
 Determine need for intubation but remember: intubation can worsen
hypotension
 Sedatives can lower blood pressure
 Positive pressure ventilation decreases preload
 May need volume resuscitation prior to intubation to avoid hemodynamic
collapse
45

Control Work of Breathing
 Respiratory muscles consume a significant amount of oxygen
 Tachypnea can contribute to lactic acidosis
 Mechanical ventilation and sedation decrease WOB and improves
survival
46

Optimizing Circulation
• Isotonic crystalloids
• Titrated to:
• CVP 8-12 mm Hg
• Urine output 0.5 ml/kg/hr (30 ml/hr)
• Improving heart rate
• May require 4-6 L of fluids
• No outcome benefit from colloids
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Maintaining oxygen Delivery
 Decrease oxygen demands
Provide analgesia and anxiolytics to relax muscles and avoid
shivering
 Maintain arterial oxygen saturation/content
 Give supplemental oxygen
 Maintain Hemoglobin > 10 g/dL
 Serial lactate levels or central venous oxygen saturations to assess tissue
oxygen extraction
48

• Do you remember how to quickly
estimate blood pressure by pulse?
60
80
70
90
• If you palpate a pulse,
you know SBP is at
least this number
49

ENDPOINTS OF RESUSCITATION
 It is much easier to know when to start resuscitation than when to stop.
 Traditionally patients have been resuscitated until they have a normal pulse, blood pressure and
urine output;
 Therefore, a patient may be resuscitated to restore central perfusion to the brain, lungs and kidneys
and yet the gut and muscle beds continue to be underperfused.
 Thus, activation of inflammation and coagulation may be on-going and, when these organs are finally
perfused, it may lead to reperfusion injury and ultimately multiple organ failure.
50

 This state of normal vital signs and continued underperfusion is termed occult hypoperfusion
(OH).
 With current monitoring techniques it is manifested only by a persistent lactic acidosis and low mixed
venous oxygen saturation level.
 The duration that patients spend in this hypoperfused state has a dramatic effect on outcome.
 Patients with OH for more than 12 hours have a two to three times higher mortality rate than that of
patients with a limited duration of shock
 Resuscitation algorithms directed at correcting global perfusion endpoints (base deficit, lactate,
mixed venous oxygen saturation) rather than traditional endpoints have been shown to improve
mortality and morbidity in high-risk surgical patients;
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Goal directed approach
1. Urine output > 0.5 mL/kg/ hr
2. CVP 8-12 mmHg
3. MAP 65 to 90 mmHg
4. Central venous oxygen
concentration > 70%
5. Wedge pressure = 10 to 12
mmHg
6. Cardiac index > 3 L/min/m2
7. Blood lactate < 4 mmol/L
8. Base deficit -3 to +3 mmol/L
9. PH 7.35-7.45
52

CONDUCT OF RESUSCITATION
 Resuscitation should not be delayed in order to definitively diagnose the source of the shocked
state;
 however, the timing and nature of resuscitation will depend on the type of shock and the timing and
severity of the insult.
 Rapid clinical examination will provide adequate clues to make an appropriate first determination,
even if a source of bleeding or sepsis is not immediately identifiable.
 If there is initial doubt about the cause of shock it is safer to assume the cause is hypovolaemia
and begin with fluid resuscitation, followed by an assessment of the response.
53

 In patients who are actively bleeding (major trauma, aortic aneurysm rupture, gastrointestinal
haemorrhage) it is counterproductive to institute high-volume fluid therapy without controlling
the site of haemorrhage.
 Increasing blood pressure merely increases bleeding from the site, and fluid therapy cools the patient and
dilutes available coagulation factors.
 Thus, operative haemorrhage control should not be delayed and resuscitation should proceed in parallel
with surgery.
54

Peripheral venous cannulation
 Intravenous access must be secured at the earliest opportunity; this can be very difficult in later
stages of shock.
 The size of the cannula is important because of its effect on flow, which is directly proportional to
the fourth power of the radius of the cannula (Poiseuille’s Law); halving the radius of a cannula
reduces the flow rate by a factor of 16 .
 Flow is also reduced as cannula length is increased.
55

 Clearly it is difficult, if not impossible, to keep up with major
haemorrhage without a minimum of two short large-bore
cannulae.
 Hence, the ATLS® guideline for in-hospital trauma cannulation is
insertion of two cannulae, minimum size 16-gauge, but preferably 14-
gauge, into large peripheral veins, typically in the antecubital fossae.
 Catastrophic haemorrhage may require the insertion of a large-bore,
8-gauge resuscitation cannulae into a large vein such as the femoral
vein and use of a rapid infusor to deliver a massive transfusion of
blood and plasma under pressure.
56

Infusion Rates
Access Gravity Pressure
18 g peripheral IV 50 mL/min 150 mL/min
8.5 Fr CV cordis 200 mL/min 450 mL/min
57

Fluid therapy
 In all cases of shock, regardless of classification, hypovolaemia and inadequate preload must be
addressed before other therapy is instituted.
 Initial bolus of 2 L of crystalloid that can be repeated once if vital signs are not restored to normal
 Patients who respond well to fluid resuscitation likely had a 10% to 20% blood volume deficit; patients who
do not respond have a higher volume deficit.
 As the second bolus is being given, blood should be obtained.
 Administration of inotropic or chronotropic agents to an empty heart will rapidly and permanently
deplete the myocardium of oxygen stores and dramatically reduce diastolic filling and therefore
coronary perfusion.
58

Type of fluids
 There is no ideal resuscitation fluid and it is more important to understand how and when to
administer them.
 In most studies of shock resuscitation there is no overt difference in response or outcome
between crystalloid solutions (normal saline, Hartmann’s solution, Ringer’s lactate) and colloids
(albumin or commercially available products).
 Most importantly, the oxygen-carrying capacity of crystalloids and colloids is zero.
 If blood is being lost, the ideal replacement fluid is blood, although crystalloid therapy may be required
while awaiting blood products.
 Hypotonic solutions (e.g. dextrose) are poor volume expanders and should not be used in the
treatment of shock unless the deficit is free water loss (e.g. diabetes insipidus) or patients are
sodium overloaded (e.g. cirrhosis).
59

Choice of replacement fluid
 Colloid (theoretical benefits )
 more rapid plasma volume expansion
 lesser risk of pulmonary edema
 solutions have been associated with
coagulopathy , kidney injury
 Lower volume of colloid is needed to have
the same therapeutic end point.
 (1L of crystalloid=250ml of colloid)
 Crystalloid : generally preferred
 are equally effective as colloid in expanding
the plasma volume
 hyperchloremic acidemia develops as a result
of replacement of the bicarbonate in shed
blood with chloride
 balanced electrolyte solutions (e.g., lactated
Ringer's) results in less of a bicarbonate deficit
 are much less expensive
60

 The current standard in severely injured patients
 Initial resuscitation-limited to keep SBP around 80 to 90 mmHg.
 To prevent hypothermia , acidosis, coagulopathy(“ bloody vicious cycle” or “lethal triad”)
 Control of hemorrhage is achieved in the operating room
 Damage control surgery : arrest hemorrhage, control sepsis, protect from further injury
 minimize of heat loss
61Damage control resuscitation

 accomplished with blood products and limited crystalloids
 consists of transfusion with red blood cells, fresh frozen plasma (FFP), and platelet
units given in equal number
 Platelets should be transfused in the bleeding patient to maintain counts above
50 × 109/L.
 data also support the use of antifibrinolytic agents(tranexamic acid )
62

 Indication ( timing of institution) for damage
control surgery
1. Temperature ≤ 34˚C
2. BP<70
3. PH ≤ 7.2
4. PT and PTT double their normal value
5. RBCs transfused ≥ 10 units
6. Intra operative blood loss> 2 L
7. Transfusion of >1500 of RBC during initial
resuscitation
8. Serum bicarbonate ≤ 15 mEq/L
9. Transfusion of ≥ 4,000 mL blood
10. Transfusion of ≥ 5,000 mL blood and blood
products
11. Intraoperative volume replacement ≥ 12,000
mL
12. Clinical evidence of intraoperative
coagulopathy
63

Dynamic fluid response
 The shock status can be determined dynamically by the cardiovascular response to the rapid
administration of a fluid bolus.
 In total, 250–500 ml of fluid is rapidly given (over 5–10 min) and the cardiovascular responses in
terms of heart rate, blood pressure and central venous pressure (CVP) are observed.
 Patients can be divided into ‘responders’, ‘transient responders’ and ‘nonresponders’.
64

 Responders show an improvement in their cardiovascular status, which is sustained.
 These patients are not actively losing fluid but require filling to a normal volume status.
 Transient responders show an improvement but then revert to their previous state over the next
10–20 min.
 These patients either have moderate on-going fluid losses (either overt haemorrhage or further fluid
shifts reducing intravascular volume).
 Non-responders are severely volume depleted and are likely to have major on-going loss of
intravascular volume, usually through persistent uncontrolled haemorrhage.
65

Intraosseous infusion
 Venous access can be difficult in the hypovolaemic child
 Indications:- Major trauma , Extensive burns ,Cardiopulmonary arrest ,Septic shock
 If difficulty experienced then intraosseous route can be used as an alternative
 Medullary canal in a child has a good blood supply
 Drugs and fluids are absorbed into venous sinusoids of red marrow
66

 Red marrow replaced by yellow marrow after 5 years
of age
 Less effective in older children
 Systemic drug levels are similar to those achieved via
the intravenous route
 Technique is generally safe with few complications
67

Vasopressor and inotropic support
 Vasopressor or inotropic therapy is not indicated as first-line therapy in hypovolaemia.
 Vasopressor agents (phenylephrine, noradrenaline) are indicated in distributive shock states
(sepsis, neurogenic shock), in which there is peripheral vasodilatation and a low systemic vascular
resistance, leading to hypotension despite a high cardiac output.
 When the vasodilatation is resistant to catecholamines (e.g. absolute or relative steroid deficiency),
vasopressin may be used as an alternative vasopressor.
 In cardiogenic shock or when myocardial depression complicates a shock state (e.g. severe septic
shock with low cardiac output), inotropic therapy may be required to increase cardiac output and,
therefore, oxygen delivery.
 The inodilator dobutamine is the agent of choice.
68

BLOOD OPTIONS
 O negative blood (universal donor)
 Type specific blood
 Cross-matched blood
 transfuse in 1:1:1 ratio (red blood cells: platelets: plasma)
69

• History
• Recent illness
• Fever
• Chest pain, SOB
• Abdominal pain
• Comorbidities
• Medications
• Toxins/Ingestions
• Recent hospitalization or
surgery
• Baseline mental status
• Physical examination
• Vital Signs
• CNS – mental status
• Skin – color, temp, rashes, sores
• CV – JVD, heart sounds
• Resp – lung sounds, RR, oxygen sat, ABG
• GI – abd pain, rigidity, guarding, rebound
• Renal – urine output
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Further Evaluation
• Labs:
• CBC
• Chemistries
• Lactate
• Coagulation studies
• Cultures
• ABG
• CT of head/sinuses
• Lumbar puncture
• Wound cultures
• Acute abdominal series
• Abdominal/pelvic CT or US
• Cortisol level
• Fibrinogen, FDPs, D-dimer
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MONITORING
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A, Cardiovascular
 As a minimum, cardiovascular monitoring should include continuous heart rate
[electrocardiogram (ECG)], oxygen saturation and pulse waveform and non-invasive blood
pressure.
 Patients whose state of shock is not rapidly corrected with a small amount of fluid should have
CVP monitoring and continuous blood pressure monitoring through an arterial line.
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B, Central venous pressure
 There is no ‘normal’ CVP for a shocked patient, and reliance cannot be placed on an individual
pressure measurement to assess volume status.
 Further, ventricular compliance can change from minute to minute in the shocked state, and CVP
is a poor reflection of end-diastolic volume (preload).
 CVP measurements should be assessed dynamically as the response to a fluid challenge.
 A fluid bolus (250–500 ml) is infused rapidly over 5–10 min.
 The normal CVP response is a rise of 2–5 cmH2O, which gradually drifts back to the original level over 10–
20 min.
 Patients with no change in their CVP are empty and require further fluid resuscitation.
 Patients with a large, sustained rise in CVP have high preload and an element of cardiac insufficiency or
volume overload.
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C, Cardiac output
 Cardiac output monitoring allows an assessment of not only the cardiac output but also the
systemic vascular resistance and, depending on the technique used, end-diastolic volume
(preload) and blood volume.
 Invasive cardiac monitoring using pulmonary artery catheters is becoming less frequent as new
non-invasive monitoring techniques such as Doppler ultrasound, pulse waveform analysis and
indicator dilution methods provide similar information without many of the drawbacks of more
invasive techniques.
 Measurement of cardiac output, systemic vascular resistance and preload can help distinguish the
types of shock that are present (hypovolaemia, distributive, cardiogenic), especially when they
coexist.
 Measurement of cardiac output is desirable in patients who do not respond as expected to first-
line therapy or who have evidence of cardiogenic shock or myocardial dysfunction.
75

D, Systemic and organ perfusion
 Ideally, monitoring of organ perfusion should guide the management of shock.
 The best measures of organ perfusion and the best monitor of the adequacy of shock therapy
remain the urine output;
 however, this is an hourly measure and does not give a minute-to-minute view of the shocked state.
 The level of consciousness is an important marker of cerebral perfusion, but brain perfusion is
maintained until the very late stages of shock and, hence, is a poor marker of adequacy of
resuscitation.
 Currently, the only clinical indicators of perfusion of the gastrointestinal tract and muscular beds
are the global measures of lactic acidosis (lactate and base deficit) and the mixed venous oxygen
saturation.
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Base deficit and lactate
 Lactate
 is generated by conversion of pyruvate to lactate by LDH in the setting of insufficient O2.
 Lactic acid is generated by cells undergoing anaerobic respiration.
 indirect marker of tissue hypoperfusion
 lactate less than 2.5
 Elevated serum lactate is an indirect measure of the O2 debt,
 The degree of lactic acidosis, as measured by the serum lactate level and/or the base deficit,
is a sensitive tool for both the diagnosis of shock and the monitoring of the response to
therapy.
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Base deficit
 is the amount of base in millimoles that is required to titrate 1 L of whole blood to a pH of 7.40 with the
sample fully saturated with O2 at 37°C (98.6°F) and a partial pressure of CO2 of 40 mmHg.
 usually is measured by arterial blood gas analysis in clinical practice
 Base deficit can be stratified into
 mild (3–5 mmol/L),
 moderate (6–14 mmol/L), and
 severe (15 mmol/L) categories,.
 Higher mortality with worsening base deficit in patients with trauma.
 the frequency of organ failure increased with greater base deficit.
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 Patients with a base deficit of over 6 mmol /L have much higher morbidity and mortality rates
than those with no metabolic acidosis.
 Further, the duration of time in shock with an increased base deficit is important, even if all other
vital signs have returned to normal .
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 These parameters are measured from arterial blood gas analyses and, therefore, the frequency of
measurements is limited and they do not provide minute-to-minute data on systemic perfusion or
the response to therapy.
 Nevertheless, the base deficit and/or lactate should be measured routinely in these patients until
they have returned to normal levels.
80

 Mixed venous oxygen saturation
 The percentage saturation of oxygen returning to the heart from the body is a measure of the oxygen
delivery and extraction by the tissues.
 Accurate measurement is via analysis of blood drawn from a long central line placed in the right atrium.
 Estimations can be made from blood drawn from lines in the superior vena cava but these values will be
slightly higher than those of a mixed venous sample (as there is relatively more oxygen extraction from
the lower half of the body).
 Normal mixed venous oxygen saturation levels are 50–70%.
 Levels below 50% indicate inadequate oxygen delivery and increased oxygen extraction by the cells.
 This is consistent with hypovolaemic or cardiogenic shock.
81

 High mixed venous saturation levels (> 70%) are seen in sepsis and some other forms of
distributive shock.
 In sepsis there is disordered utilisation of oxygen at the cellular level and arteriovenous shunting of blood
at the microvascular level.
 Thus, less oxygen is presented to the cells, cells cannot utilise what little oxygen is presented and venous
blood has a higher oxygen concentration than normal.
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 Levels lower than this indicate that the patient is not only in septic shock but also in hypovolaemic
or cardiogenic shock.
 Although the mixed venous oxygen saturation level is in the ‘normal’ range, it is low for the septic state
and inadequate oxygen is being supplied to cells that cannot utilise oxygen appropriately.
 This must be corrected rapidly.
 Hypovolaemia should be corrected with fluid therapy and low cardiac output caused by myocardial
depression or failure should be treated with inotropes (dobutamine) to achieve a mixed venous saturation
level of > 70% (normal for the septic state).
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CONSEQUENCES
 Unresuscitatable shock
 Patients who are in profound shock for a prolonged period of time become ‘unresuscitatable’.
 Cell death follows from cellular ischaemia, and the ability of the body to compensate is lost.
 There is myocardial depression and loss of responsiveness to fluid or inotropic therapy.
 Peripherally there is loss of the ability to maintain systemic vascular resistance and further hypotension
ensues.
 The peripheries no longer respond appropriately to vasopressor agents.
 Death is the inevitable result.
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 Multiple organ failure
 When intervention is timely and the period of shock is limited, patients may make a rapid, uncomplicated
recovery; however, the result of prolonged systemic ischaemia and reperfusion injury is end-organ
damage and multiple organ failure.
 Multiple organ failure is defined as two or more failed organ systems .
 There is no specific treatment for multiple organ failure.
 Management is by supporting organ systems with ventilation, cardiovascular support and
haemofiltration/dialysis until there is recovery of organ function.
 Multiple organ failure currently carries a mortality rate of 60%.
 Thus, prevention is vital by early aggressive identification and reversal of shock.
85

REFERENCE
1. BAILEY & LOVE’S SHORT PRACTICE of SURGERY 25TH EDITION(2008)
2. SHWARTZ PRINCIPLES OF SURGERY 9TH EDITION
3. TINTINALLIS EMERGENCY MEDICINE A COMPREHENSIVE STUDY GUIDE 8TH EDITION
4. UPTODATE 21.2
5. ORTHOBULLET 2017
6. AAOS COMPREHENSIVE ORTHOPAEDIC REVIEW (2015)
7. AAOS ORTHOPEDIC REVIEW COURSE(2011)
8. APLEY 10TH EDITION(2017)
9. MILLER’S REVIEW OF ORTHOPAEDICS 7TH EDITION (2016)
10. ORTHOTEERS
11. INTERNET
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General principles of shock

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