Shock and blood

CHAPTER

2 transfusion

LEARNING OBJECTIVES

To understand: • Appropriate monitoring and end points of

• The pathophysiology of shock and ischaemia– resuscitation
reperfusion injury • Use of blood and blood products, the benefits
• The different patterns of shock and the principles and risks of blood transfusion
and priorities of resuscitation

INTRODUCTION release. These mechanisms lead to injury of the capillary

endothelial cells. These, in turn, further activate the immune
Shock is the most common and therefore the most important and coagulation systems. Damaged endothelium loses its integ-
cause of death of surgical patients. Death may occur rap- rity and becomes ‘leaky’. Spaces between endothelial cells allow
idly due to a profound state of shock, or be delayed due to the fluid to leak out and tissue oedema ensues, exacerbating cellular
consequences of organ ischaemia and reperfusion injury. It is hypoxia.
important therefore that every surgeon understands the patho-
physiology, diagnosis and priorities in management of shock and
Systemic
haemorrhage.
Cardiovascular
SHOCK As preload and afterload decrease, there is a compensatory
baroreceptor response resulting in increased sympathetic activity
Shock is a systemic state of low tissue perfusion which is inad- and release of catecholamines into the circulation. This results
equate for normal cellular respiration. With insufficient delivery in tachycardia and systemic vasoconstriction (except in sepsis –
of oxygen and glucose, cells switch from aerobic to anaerobic see below).
metabolism. If perfusion is not restored in a timely fashion, cell
death ensues. Respiratory
The metabolic acidosis and increased sympathetic response
Pathophysiology result in an increased respiratory rate and minute ventilation
Cellular to increase the excretion of carbon dioxide (and so produce a
As perfusion to the tissues is reduced, cells are deprived of compensatory respiratory alkalosis).

PART 1 | PRINCIPLES
oxygen and must switch from aerobic to anaerobic metabolism.
The product of anaerobic respiration is not carbon dioxide but Renal
lactic acid. When enough tissue is underperfused, the accumu- Decreased perfusion pressure in the kidney leads to reduced
lation of lactic acid in the blood produces a systemic metabolic filtration at the glomerulus and a decreased urine output. The
acidosis. renin–angiotensin–aldosterone axis is stimulated, resulting in
As glucose within cells is exhausted, anaerobic respiration further vasoconstriction and increased sodium and water reab-
ceases and there is failure of sodium/potassium pumps in the cell sorption by the kidney.
membrane and intracellular organelles. Intracellular lysosomes
release autodigestive enzymes and cell lysis ensues. Intracellular Endocrine
contents, including potassium are released into the blood stream. As well as activation of the adrenal and renin–angiotensin
systems, vasopressin (antidiuretic hormone) is released from the
Microvascular hypothalamus in response to decreased preload and results in
As tissue ischaemia progresses, changes in the local milieu result vasoconstriction and resorption of water in the renal collecting
in activation of the immune and coagulation systems. Hypoxia system. Cortisol is also released from the adrenal cortex contrib-
and acidosis activate complement and prime neutrophils, result- uting to the sodium and water resorption and sensitizing the cells
ing in the generation of oxygen free radicals and cytokine to catecholamines.

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 14 SHOCK AND BLOOD TRANSFUSION

Table 2.1 Cardiovascular and metabolic characteristics of shock.

Hypovolaemia Cardiogenic Obstructive Distributive

Cardiac output Low Low Low High

Vascular resistance High High High Low
Venous pressure Low High High Low
Mixed venous saturation Low Low Low High
Base deficit High High High High

Ischaemia–reperfusion syndrome Cardiogenic shock

During the period of systemic hypoperfusion, cellular and organ Cardiogenic shock is due to primary failure of the heart to
damage progresses due to the direct effects of tissue hypoxia and pump blood to the tissues. Causes of cardiogenic shock include
local activation of inflammation. Further injury occurs once myocardial infarction, cardiac dysrhythmias, valvular heart
normal circulation is restored to these tissues. The acid and disease, blunt myocardial injury and cardiomyopathy. Cardiac
potassium load that has built up can lead to direct myocardial insufficiency may also be due to myocardial depression due to
depression, vascular dilatation and further hypotension. The endogenous factors (e.g. bacterial and humoral agents released
cellular and humoral elements activated by the hypoxia (com- in sepsis) or exogenous factors, such as pharmaceutical agents or
plement, neutrophils, microvascular thrombi) are flushed back drug abuse. Evidence of venous hypertension with pulmonary or
into the circulation where they cause further endothelial injury systemic oedema may coexist with the classical signs of shock.
to organs such as the lungs and the kidneys. This leads to acute
lung injury, acute renal injury, multiple organ failure and death. Obstructive shock
Reperfusion injury can currently only be attenuated by reducing In obstructive shock there is a reduction in preload due to
the extent and duration of tissue hypoperfusion. mechanical obstruction of cardiac filling. Common causes of
obstructive shock include cardiac tamponade, tension pneumo-
Classification of shock thorax, massive pulmonary embolus or air embolus. In each case,
There are numerous ways to classify shock, but the most com- there is reduced filling of the left and/or right sides of the heart
mon and most clinically applicable is one based on the initiating leading to reduced preload and a fall in cardiac output.
mechanism (Summary box 2.1).
All states are characterised by systemic tissue hypoperfusion Distributive shock
and different states may coexist within the same patient. Distributive shock describes the pattern of cardiovascular
responses characterising a variety of conditions, including septic
Summary box 2.1 shock, anaphylaxis and spinal cord injury. Inadequate organ
perfusion is accompanied by vascular dilatation with hypoten-
Classification of shock sion, low systemic vascular resistance, inadequate afterload and
■ Hypovolaemic shock a resulting abnormally high cardiac output.
■ Cardiogenic shock In anaphylaxis, vasodilatation is due to histamine release,
■ Obstructive shock while in high spinal cord injury there is failure of sympathetic
outflow and adequate vascular tone (neurogenic shock). The
PART 1 | PRINCIPLES

■ Distributive shock
■ Endocrine shock cause in sepsis is less clear but is related to the release of bacterial
products (endotoxin) and the activation of cellular and humoral
components of the immune system. There is maldistribution of
Hypovolaemic shock blood flow at a microvascular level with arteriovenous shunting
Hypovolaemic shock is due to a reduced circulating volume. and dysfunction of cellular utilization of oxygen.
Hypovolaemia may be due to haemorrhagic or non-haemorrhag- In the later phases of septic shock there is hypovolaemia from
ic causes. Non-haemorrhagic causes include poor fluid intake fluid loss into interstitial spaces and there may be concomitant
(dehydration), excessive fluid loss due to vomiting, diarrhoea, myocardial depression, complicating the clinical picture (Table
urinary loss (eg. diabetes), evaporation, or ‘third-spacing’ where 2.1).
fluid is lost into the gastrointestinal tract and interstitial spaces,
as for example in bowel obstruction or pancreatitis. Endocrine shock
Hypovolaemia is probably the most common form of shock, Endocrine shock may present as a combination of hypovolaemic,
and to some degree is a component of all other forms of shock. cardiogenic or distributive shock. Causes of endocrine shock
Absolute or relative hypovolaemia must be excluded or treated include hypo- and hyperthyroidism and adrenal insufficiency.
in the management of the shocked state, regardless of cause. Hypothyroidism causes a shock state similar to that of neuro-

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 Shock 15

Table 2.2 Clinical features of shock.

Compensated Mild Moderate Severe

Lactic acidosis + ++ ++ +++

Urine output Normal Normal Reduced Anuric
Conscious level Normal Mild anxiety Drowsy Comatose
Respiratory rate Normal Increased Increased Laboured
Pulse rate Mild increase Increased Increased Increased
Blood pressure Normal Normal Mild hypotension Severe hypotension

genic shock due to disordered vascular and cardiac responsive- urine output and the patient may exhibit mild anxiety. Blood
ness to circulating catecholamines. Cardiac output falls due to pressure is maintained although there is a decrease in pulse pres-
low inotropy and bradycardia. There may also be an associated sure. The peripheries are cool and sweaty with prolonged capil-
cardiomyopathy. Thyrotoxicosis may cause a high-output car- lary refill times (except in septic distributive shock).
diac failure.
Adrenal insufficiency leads to shock due to hypovolaemia and Moderate shock
a poor response to circulating and exogenous catecholamines. As shock progresses, renal compensatory mechanisms fail, renal
Adrenal insufficiency may be due to pre-existing Addison’s dis- perfusion falls and urine output dips below 0.5 mL/kg per hour.
ease or be a relative insufficiency due to a pathological disease There is further tachycardia, and now the blood pressure starts to
state, such as systemic sepsis. fall. Patients become drowsy and mildly confused.
Severity of shock Severe shock
Compensated shock In severe shock, there is profound tachycardia and hypotension.
As shock progresses, the body’s cardiovascular and endocrine Urine output falls to zero and patients are unconscious with
compensatory responses reduce flow to non-essential organs to laboured respiration.
preserve preload and flow to the lungs and brain. In compen-
sated shock, there is adequate compensation to maintain central Pitfalls
blood volume and preserve flow to the kidneys, lungs and brain. The classic cardiovascular responses described (Table 2.2) are
Apart from a tachycardia and cool peripheries (vasoconstriction, not seen in every patient. It is important to recognise the limita-
circulating catecholamines), there may be no other clinical signs tions of the clinical examination and to recognise patients who
of hypovolaemia. are in shock despite the absence of classic signs.
However, this cardiovascular state is only maintained by
reducing perfusion to the skin, muscle and gastrointestinal Capillary refill
tract. There is a systemic metabolic acidosis and activation of Most patients in hypovolaemic shock will have cool, pale
humoral and cellular elements within the underperfused organs. peripheries, with prolonged capillary refill times. However, the
Although clinically occult, this state will lead to multiple organ actual capillary refill time varies so much in adults that it is not
failure and death if prolonged due to the ischaemia–reperfusion a specific marker of whether a patient is shocked, and patients
effect described above under Ischaemia–reperfusion syndrome. with short capillary refill times may be in the early stages of
Patients with occult hypoperfusion (metabolic acidosis despite shock. In distributive (septic) shock, the peripheries will be

PART 1 | PRINCIPLES
normal urine output and cardiorespiratory vital signs) for more warm and capillary refill will be brisk, despite profound shock.
than 12 hours have a significantly higher mortality, infection
rate and incidence of multiple organ failure (see below under Tachycardia
Multiple organ failure). Tachycardia may not always accompany shock. Patients who
are on beta-blockers or who have implanted pacemakers are
Decompensation unable to mount a tachycardia. A pulse rate of 80 in a fit young
Further loss of circulating volume overloads the body’s compen- adult who normally has a pulse rate of 50 is very abnormal.
satory mechanisms and there is progressive renal, respiratory Furthermore, in some young patients with penetrating trauma,
and cardiovascular decompensation. In general, loss of around where there is haemorrhage but little tissue damage, there may
15 per cent of the circulating blood volume is within normal be a paradoxical bradycardia rather than tachycardia accompa-
compensatory mechanisms. Blood pressure is usually well main- nying the shocked state.
tained and only falls after 30–40 per cent of circulating volume
has been lost. Blood pressure
It is important to recognise that hypotension is one of the last
Mild shock signs of shock. Children and fit young adults are able to main-
Initially there is tachycardia, tachypnoea, a mild reduction in tain blood pressure until the final stages of shock by dramatic

Thomas Addison, 1799–1860, physician, Guy’s Hospital, London, UK, described the effects of disease of the suprarenal capsules in 1849.

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 16 SHOCK AND BLOOD TRANSFUSION

increases in stroke volume and peripheral vasoconstriction. and ventilation. Once ‘airway’ and ‘breathing’ are assessed and
These patients can be in profound shock with a normal blood controlled, attention is directed to cardiovascular resuscitation.
pressure.
Elderly patients who are normally hypertensive may present Conduct of resuscitation
with a ‘normal’ blood pressure for the general population but Resuscitation should not be delayed in order to definitively
be hypovolaemic and hypotensive relative to their usual blood diagnose the source of the shocked state. However, the timing
pressure. Beta-blockers or other medications may prevent a and nature of resuscitation will depend on the type of shock and
tachycardic response. The diagnosis of shock may be difficult the timing and severity of the insult. Rapid clinical examination
unless one is alert to these pitfalls. will provide adequate clues to make an appropriate first determi-
nation, even if a source of bleeding or sepsis is not immediately
Consequences identifiable. If there is initial doubt about the cause of shock, it
is safer to assume the cause is hypovolaemia and begin with fluid
Unresuscitatable shock resuscitation, and then assess the response.
Patients who are in profound shock for a prolonged period of In patients who are actively bleeding (major trauma, aortic
time become ‘unresuscitatable’. Cell death follows from cellular aneurysm rupture, gastrointestinal haemorrhage), it is coun-
ischaemia and the ability of the body to compensate is lost. terproductive to institute high-volume fluid therapy without
There is myocardial depression and loss of responsiveness to fluid controlling the site of haemorrhage. Increasing blood pressure
or inotropic therapy. Peripherally there is loss of the ability to merely increases bleeding from the site while fluid therapy cools
maintain systemic vascular resistance and further hypotension the patient and dilutes available coagulation factors. Thus opera-
ensues. The peripheries no longer respond appropriately to vaso- tive haemorrhage control should not be delayed and resuscita-
pressor agents. Death is the inevitable result. tion should proceed in parallel with surgery.
This stage of shock is the combined result of the severity of Conversely, a patient with bowel obstruction and hypovol-
the insult and delayed, inadequate or inappropriate resuscitation aemic shock must be adequately resuscitated before undergoing
in the earlier stages of shock. Conversely, when patients present surgery otherwise the additional surgical injury and hypovolae-
in this late stage, and have minimal responses to maximal ther- mia induced during the procedure will exacerbate the inflam-
apy, it is important that the futility of treatment is recognised matory activation and increase the incidence and severity of
and valuable resources are not wasted. end-organ insult.

Fluid therapy
Multiple organ failure
In all cases of shock, regardless of classification, hypovolaemia
As techniques of resuscitation have improved, more and more and inadequate preload must be addressed before other therapy
patients are surviving shock. Where intervention is timely is instituted. Administration of inotropic or chronotropic agents
and the period of shock is limited, patients may make a rapid, to an empty heart will rapidly and permanently deplete the
uncomplicated recovery. However, the result of prolonged sys- myocardium of oxygen stores and dramatically reduce diastolic
temic ischaemia and reperfusion injury is end-organ damage and filling and therefore coronary perfusion. Patients will enter the
multiple organ failure. unresuscitatable stage of shock as the myocardium becomes
Multiple organ failure is defined as two or more failed organ progressively more ischaemic and unresponsive to resuscitative
systems (Summary box 2.2). attempts.
First-line therapy, therefore, is intravenous access and
administration of intravenous fluids. Access should be through
Summary box 2.2 short, wide-bore catheters that allow rapid infusion of fluids
as necessary. Long, narrow lines, such as central venous cath-
Effects of organ failure eters, have too high a resistance to allow rapid infusion and
■ Lung: Acute respiratory distress syndrome are more appropriate for monitoring than fluid replacement
■ Kidney: Acute liver insufficiency therapy.
Clotting: Coagulopathy
PART 1 | PRINCIPLES

■
■ Cardiac: Cardiovascular failure Type of fluids
There is continuing debate over which resuscitation fluid is best
for the management of shock. There is no ideal resuscitation
There is no specific treatment for multiple organ failure. fluid, and it is more important to understand how and when to
Management is supporting of organ systems with ventilation, administer it. In most studies of shock resuscitation there is no
cardiovascular support and haemofiltration/dialysis until there is overt difference in response or outcome between crystalloid solu-
recovery of organ function. Multiple organ failure currently car- tions (normal saline, Hartmann’s solution, Ringer’s lactate) or
ries a mortality of 60 per cent; thus prevention is vital by early colloids (albumin or commercially available products).
aggressive identification and reversal of shock. Furthermore, there is less volume benefit to the administration

RESUSCITATION
Alexis Frank Hartmann, 1898–1964, paediatrician, St Louis, MO, USA, described
Immediate resuscitation manoeuvres for patients presenting in the solution; should not be confused with the name of Henri Albert Charles Antoine
Hartmann, French surgeon, who described the operation that goes by his name.
shock are to ensure a patent airway and adequate oxygenation

Sidney Ringer, 1835–1910, Professor of Clinical Medicine, University College Hospital, London, UK.

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 Resuscitation 17

of colloids than had previously been thought, with only 1.3 times
Summary box 2.3
more crystalloid than colloid administered in blinded trials. On
balance, there is little evidence to support the administration of
Monitoring for patients in shock
colloids, which are more expensive and have worse side-effect
profiles. Minimum
Most importantly, the oxygen carrying capacity of crystalloids ■ ECG
and colloids is zero. If blood is being lost, the ideal replacement ■ Pulse oximetry
fluid is blood, although crystalloid therapy may be required while ■ Blood pressure
awaiting blood products.
■ Urine output
Hypotonic solutions (dextrose etc.) are poor volume expand- Additional modalities
■ Central venous pressure
ers and should not be used in the treatment of shock unless the ■ Invasive blood pressure
deficit is free water loss (eg. diabetes insipidus) or patients are ■ Cardiac output
sodium overloaded (eg. cirrhosis). ■ Base deficit and serum lactate

Dynamic fluid response

The shock status can be determined dynamically by the cardio-
vascular response to the rapid administration of a fluid bolus. In
total, 250–500 mL of fluid is rapidly given (over 5–10 minutes)
and the cardiovascular responses in terms of heart rate, blood
pressure and central venous pressure are observed. Patients can Cardiovascular
be divided into ‘responders’, ‘transient responders’ and ‘non- Cardiovascular monitoring at a minimum should include con-
responders’. tinuous heart rate (ECG), oxygen saturation and pulse waveform
Responders have an improvement in their cardiovascular and non-invasive blood pressure. Patients whose state of shock
status which is sustained. These patients are not actively losing is not rapidly corrected with a small amount of fluid should have
fluid but require filling to a normal volume status. central venous pressure monitoring and continuous blood pres-
Transient responders have an improvement which then sure monitoring through an arterial line.
reverts to the previous state over the next 10–20 minutes. These
patients have moderate ongoing fluid losses (either overt haem- Central venous pressure
orrhage or further fluid shifts reducing intravascular volume). There is no ‘normal’ central venous pressure (CVP) for a
Non-responders are severely volume depleted and are likely shocked patient, and reliance cannot be placed on an individual
to have major ongoing loss of intravascular volume, usually pressure measurement to assess volume status. Some patients
through persistent uncontrolled haemorrhage. may require a CVP of 5 cmH2O, whereas some may require a
CVP of 15 cmH2O or higher. Further, ventricular compliance
can change from minute to minute in the shocked state, and
Vasopressor and inotropic support CVP is a poor reflection of end diastolic volume (preload).
Vasopressor or inotropic therapy is not indicated as first-line CVP measurements should be assessed dynamically as
therapy in hypovolaemia. As discussed above, administration response to a fluid challenge (see above). A fluid bolus (250–
of these agents in the absence of adequate preload rapidly leads 500 mL) is infused rapidly over 5–10 minutes.
to decreased coronary perfusion and depletion of myocardial The normal CVP response is a rise of 2–5 cmH2O which
oxygen reserves. gradually drifts back to the original level over 10–20 minutes.
Vasopressor agents (phenylephrine, noradrenaline) are indi- Patients with no change in their CVP are empty and require
cated in distributive shock states (sepsis, neurogenic shock) further fluid resuscitation. Patients with a large, sustained rise in
where there is peripheral vasodilatation, and a low systemic CVP have high preload and an element of cardiac insufficiency
vascular resistance, leading to hypotension despite a high cardiac or volume overload.
output. Where the vasodilatation is resistant to catecholamines
Cardiac output

PART 1 | PRINCIPLES
(e.g. absolute or relative steroid deficiency) vasopressin may be
used as an alternative vasopressor. Cardiac output monitoring allows not only assessment of
In cardiogenic shock, or where myocardial depression com- the cardiac output but also the systemic vascular resistance
plicated a shock state (e.g. severe septic shock with low cardiac and, depending on the technique used, end diastolic volume
output), inotropic therapy may be required to increase cardiac (preload) and blood volume. Use of invasive cardiac monitoring
output and therefore oxygen delivery. The inodilator dob- using pulmonary artery catheters is becoming less frequent as
utamine is the agent of choice. new non-invasive monitoring techniques, such as Doppler ultra-
sound, pulse waveform analysis and indicator dilution methods,
provide similar information without many of the drawbacks of
Monitoring more invasive techniques.
The minimum standard for monitoring of the patient in shock Measurement of cardiac output, systemic vascular resistance
is continuous heart rate and oxygen saturation monitoring, fre- and preload can help distinguish the types of shock present
quent non-invasive blood pressure monitoring and hourly urine (hypovolaemia, distributive, cardiogenic), especially when they
output measurements. Most patients will need more aggressive coexist. The information provided guides fluid and vasopressor
invasive monitoring, including central venous pressure and inva- therapy by providing real-time monitoring of the cardiovascular
sive blood pressure monitoring (Summary box 2.3). response.

Christian Johann Doppler, 1803–1853, Professor of Experimental Physics, Vienna, Austria, enunciated the Doppler principle in 1842.

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 18 SHOCK AND BLOOD TRANSFUSION

Measurement of cardiac output is desirable in patients who Mixed venous oxygen saturation
do not respond as expected to first-line therapy, or who have The per cent saturation of oxygen returning to the heart from
evidence of cardiogenic shock or myocardial dysfunction. Early the body is a measure of the oxygen delivery and extraction by
consideration should be given to instituting cardiac output mon- the tissues. Accurate measurement is via analysis of blood drawn
itoring on patients who require vasopressor or inotropic support. from a long central line placed in the right atrium. Estimations
can be made from blood drawn from lines in the superior vena
Systemic and organ perfusion cava, but these values will be slightly higher than those of a
Ultimately, the goal of treatment is to restore cellular and organ mixed venous sample (as there is relatively more oxygen extrac-
perfusion. Ideally, therefore, monitoring of organ perfusion tion from the lower half of the body). Normal mixed venous
should guide the management of shock. The best measures of oxygen saturation levels are 50–70 per cent. Levels below 50 per
organ perfusion and the best monitor of the adequacy of shock cent indicate inadequate oxygen delivery and increased oxygen
therapy remains the urine output. However, this is an hourly extraction by the cells. This is consistent with hypovolaemic or
measure and does not give a minute-to-minute view of the cardiogenic shock.
shocked state. The level of consciousness is an important marker High mixed venous saturations (>70 per cent) are seen in
of cerebral perfusion, but brain perfusion is maintained until the sepsis and some other forms of distributive shock. In sepsis, there
very late stages of shock, and hence is a poor marker of adequacy is disordered utilization of oxygen at the cellular level, and arte-
of resuscitation (Table 2.3). riovenous shunting of blood at the microvascular level. Thus less
Currently, the only clinical indicators of perfusion of the oxygen is presented to the cells, and those cells cannot utilise
gastrointestinal tract and muscular beds are the global measures what little oxygen is presented. Thus, venous blood has a higher
of lactic acidosis (lactate and base deficit) and the mixed venous oxygen concentration than normal.
oxygen saturation. Patients who are septic should therefore have mixed venous
oxygen saturations above 70 per cent; below this level, they are
Base deficit and lactate not only in septic shock but also in hypovolaemic or cardiogenic
Lactic acid is generated by cells undergoing anaerobic respira- shock. Although the SvO2 level is in the ‘normal’ range, it is
tion. The degree of lactic acidosis, as measured by serum lactate low for the septic state, and inadequate oxygen is being supplied
level and/or the base deficit, is sensitive for both diagnosis of to cells that cannot utilize oxygen appropriately. This must be
shock and monitoring the response to therapy. Patients with a corrected rapidly. Hypovolaemia should be corrected with fluid
base deficit over 6 mmol/L have a much higher morbidity and therapy, and low cardiac output due to myocardial depression
mortality than those with no metabolic acidosis. Furthermore, or failure should be treated with inotropes (dobutamine), to
the duration of time in shock with an increased base deficit is achieve a mixed venous saturation greater than 70 per cent
important, even if all other vital signs have returned to normal (normal for the septic state).
(see occult hypoperfusion below under End points of resuscita- New methods for monitoring regional tissue perfusion and
tion). oxygenation are becoming available, the most promising of
These parameters are measured from arterial blood gas analy- which are muscle tissue oxygen probes, near-infrared spec-
ses, and therefore the frequency of measurements is limited and troscopy and sublingual capnometry. While these techniques
they do not provide minute-to-minute data on systemic per- provide information regarding perfusion of specific tissue beds,
fusion or the response to therapy. Nevertheless, the base deficit it is as yet unclear whether there are significant advantages over
and/or lactate should be measured routinely in these patients existing measurements of global hypoperfusion (base deficit,
until they have returned to normal levels. lactate).

Table 2.3 Monitors for organ/systemic perfusion.

Clinical Investigational

Systemic perfusion Base deficit

PART 1 | PRINCIPLES

Lactate
Mixed venous oxygen saturation
Organ perfusion
Muscle – Near-infrared spectroscopy
Tissue oxygen electrode
Gut – Sublingual capnometry
Gut mucosal pH
Laser Doppler flowmetry
Kidney Urine output –
Brain Conscious level Tissue oxygen electrode
Near-infrared spectroscopy

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 Haemorrhage 19

End points of resuscitation patients develop ATC within minutes of injury and it is associ-
It is much easier to know when to start resuscitation than when ated with a four-fold increase in mortality. It is likely that ATC
to stop. Traditionally, patients have been resuscitated until they exists whenever there is the combination of shock and tissue
have a normal pulse, blood pressure and urine output. However, trauma (e.g. major surgery). ATC is the component of trauma-
these parameters are monitoring organ systems whose blood flow induced coagulopathy (TIC) which is ultimately multifactorial
is preserved until the late stages of shock. A patient therefore (Figure 2.1).
may be resuscitated to restore central perfusion to the brain, Ongoing bleeding with fluid and red blood cell resuscitation
lungs and kidneys and yet continue to underperfuse the gut and leads to a dilution of coagulation factors which worsens the coag-
muscle beds. Thus activation of inflammation and coagulation ulopathy. In addition, the acidosis induced by the hypoperfused
may be ongoing and lead to reperfusion injury when these organs state leads to decreased function of the coagulation proteases,
are finally perfused, and ultimately multiple organ failure. resulting in coagulopathy and further haemorrhage. The reduced
This state of normal vital signs and continued underperfusion tissue perfusion includes reduced blood supply to muscle beds.
is termed ‘occult hypoperfusion’. With current monitoring tech- Underperfused muscle is unable to generate heat and hypother-
niques, it is manifested only by a persistent lactic acidosis and mia ensues. Coagulation functions poorly at low temperatures
low mixed venous oxygen saturation. The duration patients and there is further haemorrhage, further hypoperfusion and
spend in this hypoperfused state has a dramatic effect on out- worsening acidosis and hypothermia. These three factors result
come. Patients with occult hypoperfusion for more than 12 hours in a downward spiral leading to physiological exhaustion and
have two to three times the mortality of patients with a limited death (Figure 2.1).
duration of shock. Medical therapy has a tendency to worsen this effect.
Resuscitation algorithms directed at correcting global per- Intravenous blood and fluids are cold and exacerbate hypother-
fusion end points (base deficit, lactate, mixed venous oxygen sat- mia. Further heat is lost by opening body cavities during surgery.
uration) rather than traditional end points have been shown to Surgery usually leads to further bleeding and many crystalloid
improve mortality and morbidity in high-risk surgical patients. fluids are themselves acidic (e.g. normal saline has a pH of 6.7).
However, it is clear that despite aggressive regimens, some Every effort must therefore be made to rapidly identify and stop
patients cannot be resuscitated to normal parameters within 12 haemorrhage, and to avoid (preferably) or limit physiological
hours by fluid resuscitation alone. More research is underway to exhaustion from coagulopathy, acidosis and hypothermia.
identify the pathophysiology behind this and investigate new
therapeutic options. Definitions
Revealed and concealed haemorrhage
HAEMORRHAGE Haemorrhage may be revealed or concealed. Revealed haemor-
Haemorrhage must be recognised and managed aggressively to rhage is obvious external haemorrhage, such as exsanguination
reduce the severity and duration of shock and avoid death and/ from an open arterial wound or from massive haematemesis from
or multiple organ failure. Haemorrhage is treated by arresting a duodenal ulcer.
the bleeding – not by fluid resuscitation or blood transfusion. Concealed haemorrhage is contained within the body cavity
Although necessary as supportive measures to maintain organ and must be suspected, actively investigated and controlled. In
perfusion, attempting to resuscitate patients who have ongoing trauma, haemorrhage may be concealed within the chest, abdo-
haemorrhage will lead to physiological exhaustion (coagulopa- men, pelvis, retroperitoneum or in the limbs with contained
thy, acidosis and hypothermia) and subsequently death. vascular injury or associated with long-bone fractures. Examples
of non-traumatic concealed haemorrhage include occult gas-
Pathophysiology trointestinal bleeding or ruptured aortic aneurysm.
Haemorrhage leads to a state of hypovolaemic shock. The
combination of tissue trauma and hypovolaemic shock leads to Primary, reactionary and secondary haemorrhage
the development of an endogenous coagulopathy called acute Primary haemorrhage is haemorrhage occurring immediately due
traumatic coagulopathy (ATC). Up to 25 per cent of trauma to an injury (or surgery). Reactionary haemorrhage is delayed

PART 1 | PRINCIPLES
haemorrhage (within 24 hours) and is usually due to dislodge-
ment of clot by resuscitation, normalisation of blood pressure
and vasodilatation. Reactionary haemorrhage may also be due
to technical failure, such as slippage of a ligature.
Trauma Shock Secondary haemorrhage is due to sloughing of the wall of a
vessel. It usually occurs 7–14 days after injury and is precipitated
ATC by factors such as infection, pressure necrosis (such as from a
Haemorrhage drain) or malignancy.
Fibrinolysis Inflammation Hypothermia Acidaemia Surgical and non-surgical haemorrhage
Genetics Loss, dilution Surgical haemorrhage is due to a direct injury and is amenable
to surgical control (or other techniques such as angioembolisa-
TRAUMA-INDUCED tion). Non-surgical haemorrhage is the general ooze from all raw
COAGULOPATHY (TIC) surfaces due to coagulopathy and cannot be stopped by surgical
means (except packing). Treatment requires correction of the
Figure 2.1 Trauma-induced coagulopathy. coagulation abnormalities.

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