ACCCN's Critical Care Nursing

628 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E



TABLE 23.2 Position and mobility restrictions in trauma patients

Type of injury Restrictions
Traumatic brain injury l Nurse head up 15–30 degrees.
l Side-lying as tolerated.
l Full tilt on bed if cervical spine not yet cleared of injury.
l Occasionally nursed flat if ICP problematic.
Facial trauma l Generally nurse in head-elevated position to reduce swelling, using either full bed tilt or back rest elevation.
Chest trauma l Nurse in varying positions from semi-Fowler to side-lying.
l Postural drainage (head down) usually beneficial if not contraindicated by other injuries (e.g. head or facial).
Abdominal trauma l Nurse in varying positions from semi-Fowler to side-lying.
l Preferable to have some degree of hip flexion when lying supine to reduce abdominal suture line tension.
Pelvic trauma l Position restrictions are dependent on severity of fracture(s), use of external fixateurs and degree of stabilisation.
l Some patients may sit out of bed and ambulate with external pelvis fixateur in situ.
l Position restrictions require regular review, as changed or loss of fixation may affect recovery.
Extremity trauma l Significant position restrictions may include limb elevation, avoidance of side-lying or limited movement.
ICP = intracranial pressure.


Additionally, hypothermia is a common contributor to l ensuring the patient is adequately covered during
the exacerbation of both acidosis and coagulopathy. 33-38 transport and hospital care
Acidosis has been discussed in earlier chapters so is l warm intravenous fluids
reviewed here only as it interacts with hypothermia and l using warm blankets or electrical warming blankets
coagulopathy in the trauma setting. Low cardiac output, l adjusting the temperature in the operating room
hypotension, hypoxia, hypothermia and rhabdomyolysis where feasible. 39
are common causes of acidosis in the trauma setting. The
increased recognition of the importance of this triad in In extreme cases of hypothermia internal methods of
the trauma setting has led to the development of damage rewarming, such as cardiopulmonary bypass and perito-
control surgery. The principle of this surgery is reviewed neal dialysis or lavage, might be utilised.
below. Coagulopathy

Hypothermia Coagulation is widespread in the trauma setting, and
Hypothermia is defined as a core temperature <35°C and ranges from a mild defect in coagulation function to life-
is associated with high morbidity and mortality. Even in threatening coagulopathy. Defects in coagulation may be
sub-tropical environments, hypothermia is identified in caused by dilution, hypothermia, acidosis, tissue damage
34,35
approximately 10% of major trauma cases during the or the effects of underlying disease.
prehospital or in-hospital phase of care. 36,39 Dilution results from the transfusion of either crystalloid
or colloid fluids, and occurs as the concentration of coag-
Uncontrolled causes of hypothermia can be endogenous ulation factors in the patient’s blood is diluted with the
or accidental. 33,34,37,39 Endogenous causes include meta- transfused fluid. It should be remembered that transfu-
bolic dysfunction with decreased heat production, or sion of red blood cells has the same effect, as whole
central nervous system dysfunction with insufficient ther- blood or packed cells have undergone some dilution and
moregulation such as in neurological trauma. Dermal have reduced viability of platelets. Hypothermia causes
38
dysfunction, such as a burn, is another endogenous cause coagulopathy because many of the enzymatic reactions
of hypothermia.
in coagulation are temperature-dependent. Platelet and
Accidental hypothermia can occur without thermoregula- thromboplastin function both decline with even moder-
tory dysfunction, and generally occurs in the trauma ate (34°C) hypothermia, while hypothermia stimulates
patient as a result of environmental exposure either at the fibrinolysis. 34,40
injury site or during transport to, or between, healthcare
facilities, as a result of large-volume fluid resuscitation or Acidosis reduces the activity of both the extrinsic and the
during prolonged surgical procedures. The pathophysio- intrinsic coagulation pathways, as well as platelet func-
logical changes associated with hypothermia vary depend- tion. This is particularly pronounced with a pH below
34
ing on the severity, and are outlined in Chapter 22. Of 6.8. Tissue damage causes endothelial disruption and
particular relevance, shivering leads to increased oxygen defibrination, which promote the systemic activation of
consumption and acidosis, and platelet dysfunction leads coagulation; this is particularly profound in patients with
to impaired clotting. 33,36,39 brain injury due to the high level of thromboplastin in
brain tissue. 34,37,38 The final cause of coagulopathy in
Measures to reduce the incidence of hypothermia – or trauma is the underlying disease present in many patients.
to correct it when it is present – in the trauma setting Patients may have a coagulation defect such as haemo-
include: philia or von Willebrand’s disease, or liver disease with

Trauma Management 629

resultant compromise to coagulation on an ongoing Nursing a patient who undergoes damage-control surgery
basis. Alternatively, patients may be taking anticoagu- requires recognition of the principles and aims of the
lants, such as aspirin or warfarin, as treatment for other surgery, as well as flexibility in care of the patient after
health conditions. 37,41 the initial surgery but before definitive surgery. In the
emergency department setting there is a need to under-
Treatment of coagulopathy should focus first on preven-
tion of coagulopathy and then on the treatment as take a rapid, systematic evaluation of the patient and
required. Prevention strategies include: 40 prepare him or her for rapid transfer to the operating
room. It is essential to implement all measures possible
l maintaining normothermia in critically injured to preclude the components of the trauma triad, while
patients through the use of blankets, warming devices, avoiding any delays to surgery. When the patient is admit-
and minimisation of exposure and theatre time ted to the ICU postoperatively, the standard mechanisms
l administering as little resuscitation fluid as is neces- for the treatment of hypothermia, acidosis and coagu-
sary to maintain adequate circulation lopathy, as discussed above, should be implemented.
l achieving control of haemorrhage as soon as possible, After damage-control surgery, patients may also have an
through techniques such as low-pressure resuscitation open abdomen with temporary dressings, or skeletal frac-
and damage-control surgery. tures with external fixateurs in situ.
There is a strong need to ensure that patients are not SKELETAL TRAUMA
overtransfused, and regular monitoring of coagulation
factors including haematocrit, platelet count, prothrom- Skeletal trauma involves injury to the bony structure of
bin time (PT), activated partial thromboplastin time the body. While skeletal injuries alone rarely result in the
(APTT), thrombin time (TT) and fibrinogen levels will patient being admitted to critical care, damage to sur-
assist in achieving this aim. The international normalised rounding blood vessels and nerves, as well as potential
ratio (INR) should be measured at the beginning of the complications such as fat embolism syndrome (FES)
process and repeated if abnormal. and rhabdomyolysis, may cause the patient to become
seriously ill. Patients with skeletal trauma who require
Treatment includes transfusion of platelets, fresh frozen admission to ICU include those with multiple injuries,
plasma (FFP) and cryoprecipitate, as well as the plasma severe pelvic fractures (often associated with significant
35
derivatives showing promise in this area of treatment. blood loss), long bone fractures (often associated with
While transfusion of platelets is specifically directed FES) and thoracic injuries such as flail segment. A small
towards increasing the circulating concentration of plate- number of people with crush injuries that cause signifi-
lets, administration of FFP is directed at increasing the cant damage to muscles, often resulting in rhabdomyoly-
levels of fibrinogen and other coagulation factors. Cryo- sis, also require admission to the ICU. 44,45
precipitate is made by freezing and thawing individual
units of FFP and collecting the precipitate, a process that Skeletal trauma is the form of trauma that causes the
concentrates fibrinogen, von Willebrand factor, factor highest number of patients to be admitted to hospital for
VIII and factor XIII. 24 hours or more, with approximately 50% of patients
28
experiencing a fracture as their main injury. Of those
patients admitted to an ICU, fractures are the second
Damage-control Surgery most common type of injury (after head injury), with
Damage-control surgery can be defined as a four-stage approximately 20% of patients experiencing this type of
procedure, involving early recognition of relevant patients injury.
and ‘rapid termination of an operation after control of
life-threatening bleeding and contamination followed by Pathophysiology
correction of physiological abnormalities and definitive Bone is composed of an organic matrix as well as bone
management’. 42,43 This approach to surgical correction of salts. The majority of the organic matrix is collagen fibres
traumatic injuries gained favour through the latter part of and the remainder is ground substance, a homogeneous
the 1990s and is intended to reduce the development gelatinous medium composed of extracellular fluid plus
46
of the triad of complications of hypothermia, acidosis proteoglycans. Calcium and phosphate are the primary
and coagulopathy. The intention is that surgery is initi- bone salts, although there are smaller amounts of magne-
ated rapidly, only the most rapid and simplest interven- sium, sodium, potassium and carbonate ions. These ions
tions that are required to stop bleeding and contamination combine to form a crystal known as hydroxyapatite.
are undertaken, then surgery is completed and the patient A fracture is simply defined as a break in the continuity
42
moved to definitive care, usually in the ICU. Care can of a bone. Fractures generally occur when there is force
then be undertaken to ensure that hypothermia, acidosis applied that exceeds the tensile or compressive strength
and coagulopathy do not develop or, if present, are of the bone. In patients sustaining a major injury (injury
rapidly reversed, thereby ensuring correction of physio- severity score [ISS] ≥16) fractures are the primary injury
logical abnormalities as quickly as possible. Definitive in more than 15% of cases, although many patients expe-
surgical correction of injuries is undertaken during the rience a fracture in addition to other serious injury result-
ensuing days when the patient is physiologically stable. ing in ICU admission. 28
Damage-control surgery can apply to a range of patients,
including those with abdominal, skeletal and thoracic Fractures are classified as either complete or incomplete.
trauma. A complete fracture is where the bone is broken all the

630 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

way through, while incomplete fractures only involve unit for assessment and treatment, including mechanical
part of the bone. Fractures are also classified according to ventilation.
the direction of the fracture line, and include linear, Internationally, there continues to be disagreement
oblique, spiral and transverse fractures.
regarding the pathophysiological changes associated with
A fracture causes disruption to the periosteum, blood FES, although there is general consensus on the following
vessels, marrow and surrounding soft tissue, resulting principles. It has been accepted that there is a mechanical
in a loss of mechanical integrity of the bone. Bone is component to the changes that take place in FES, where
one of only two sites (the other being the liver) that fat is physically forced into the venous system and causes
47
will reform itself, not forming scar tissue when it heals. physical obstruction of the vasculature. Although marrow
When a fracture occurs, there is initial bleeding and pressure is normally 30–50 mmHg, it can be increased
soft tissue damage around the site, with haematoma up to 600 mmHg during intramedullary reaming (the
formation within the medullary canal. The healing process where the medullary cavity of the bone is surgi-
sequence that follows a fracture depends on the type cally enlarged to fit a surgical implant such as a tibial
of fracture fixation that is used. When a fracture is fixed nail), consequently reaching a pressure significantly
49
in a method that eliminates the interfragmentary gap above pressures throughout the vasculature. A second
and provides stability to the site, such as in screwing theory, associated with the biochemical changes that
or wiring, primary healing takes place. When a fracture occur during trauma, proposes that trauma is associated
is fixed in a manner that reduces but does not eliminate with a higher level of circulating free fatty acids, which
movement around the fracture site, secondary healing cause destabilisation of circulating fats and/or direct tox-
takes place. 48 icity to specific tissues, including pulmonary and vascular
endothelium. 49
In primary healing, also referred to as direct union,
the haematoma that initially formed is eliminated by the
apposition of fracture ends during reduction. Once the Rhabdomyolysis
bone ends are intact, osteoclasts form cutting cones that Rhabdomyolysis is the breakdown of muscle fibres result-
in turn form new haversian canals across the fracture gap. ing in the distribution of the cellular contents of the
These contain blood vessels that are essential to primary affected muscle throughout the circulation, and occurs
bone healing. By 5–6 weeks after the fracture, osteoblasts during the reperfusion of injured muscle. The cellular
will fill the canals with osteons, which are the basic contents that are circulated include potassium, phos-
47
structure of the new bone. Although the bone is now phate, organic acids, myoglobin, creatine kinase and
44
formed, the strength and shape continues to develop over thromboplastin. Two phases of injury are essential for
coming weeks. the development of rhabdomyolysis: the first is when
muscle ischaemia occurs, and the second is with reperfu-
In contrast to primary healing, secondary healing is char- sion of the injured muscle. The length of time that muscle
acterised by an intermediate phase, where a callus of is ischaemic affects the development of rhabdomyolysis,
connective tissue is first formed and then replaced by with periods of less than 2 hours generally not producing
bone. 47,49 The secondary healing phase begins with an permanent damage, but periods above this time resulting
inflammatory phase in which the haematoma clots and in irreversible anatomical and functional changes. The
44
provides initial support, then inflammatory cells invade clinical sequelae of rhabdomyolysis include electrolyte
the haematoma to remove necrosed bone and debris. The abnormalities such as hypocalcaemia, hyperkalaemia and
reparative phase begins 1–2 weeks after the fracture and acidosis, hypovolaemia, acute renal failure and multi-
consists of immature woven bone being laid down and organ failure.
strengthened through a process known as mineralisation.
The final remodelling stage consists of replacement of the
woven bone by lamellar bone, through osteoblasts secret- Clinical Manifestations
ing osteoid that is mineralised and forms interstitial Common forms of skeletal trauma include the
lamellae. The remodelling of these structures occurs in following:
response to appropriate levels of mechanical loading l Long bone fractures. The long bones are the humerus,
during this phase. 47,48
radius, ulna, femur, tibia and fibula. Fractures of these
bones are serious and can carry a high level of morbid-
Fat embolism ity, especially if they involve a joint such as a trimal-
Fat embolism syndrome (FES) may occur in patients who leolar fracture of the ankle (distal tibia and fibula). In
have experienced a fracture of a long bone, particularly if many cases definitive surgical management is required,
multiple fractures or fractures to the middle or proximal with internal fixation.
parts of the femur are experienced. Fractures to the pelvis l Dislocations. All joints are at risk of traumatic dis-
can also lead to a fat embolism. Incidence of FES is low location, depending on the mechanism of injury. Dis-
(<1%). FES consists of fat in the blood circulation associ- locations can be limb-threatening if they cause
ated with an identifiable pattern of clinical signs and neurovascular compromise. Reduction of traumatic
symptoms that include hypoxaemia, neurological symp- dislocation is a medical emergency.
49
toms and a petechial rash. Patients generally present l Open fractures (compound). Any break in the skin
12–48 hours after they have experienced a relevant that communicates directly with the fracture is classi-
fracture and often require admission to a critical care fied as an open fracture. Open fractures carry a higher

Trauma Management 631

infection risk and require surgical treatment within l Fractures of the pelvis. The pelvis is the largest com-
8 hours. 50,51 bined bony structure in the body and serves to provide
l Traumatic amputation. Amputation refers to an avul- an essential supporting framework for ambulation
sion in which the affected limb or body appendage is and protection of pelvic organs. Major blood vessels
completely separated from the body. This can occur and nerves traverse the pelvic bones, supplying the
when a digit or extremity is sheared off by either lower limbs and pelvic organs. Therefore, injury to
mechanical or severing forces, for example amputa- any part of the pelvis is serious. The three bones that
tion of a thumb by a bandsaw. Traumatic amputations comprise the pelvic ring are the two innominate
vary in severity and ongoing compromise, with a bones (ilium and pubic rami) and the sacrum. Due
cleancut amputation more likely to be successfully to its reinforced structure, the amount of force
reattached than a crushed extremity. Criteria that required to fracture the pelvis is substantial. Fractures
inform the surgical decision-making process include of the pelvis can affect one or both sides of the pelvis,
the amount of tissue loss, location on the body at the and be stable or unstable. A variety of classification
connection site, damage to underlying and surround- systems exist to describe the severity of pelvic frac-
ing tissues, bones, nerves, tendons/muscles and tures, the most common being the Tile classification
vessels, and condition of the amputated part. (see Figure 23.2).



Tile A












A1 A2 A3
Avulsion injury Stable Transverse fractures of
Not involving the ring Minimal displacement sacrum or coccyx

Tile B












B1 B2 B3
Unilateral Lateral compression injury Bilaterally rotational instability
Internal rotation instability
Tile C












C1 C2 C3
Unilateral Bilateral Bilaterally vertically unstable
One side rotationally unstable
One side vertically unstable
FIGURE 23.2 Tile classification for pelvic fractures.
79

632 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

l Fractures of the spinal column. (see also Chapter 17). Given the potential for extensive blood loss, as well as
The spinal column includes all of the bony compo- the frequent close proximity of nerves and blood vessels
nents in the cervical, thoracic and lumbar vertebral to bones, neurovascular assessment of the patient with
regions. Fractures of the vertebra are common in skeletal trauma is essential (see Table 23.4).
trauma patients, but the actual incidence of fracture
without spinal cord injury in multitrauma patients is Collaborative practice: splinting
not well described. Not all fractures cause vertebral One of the major emergent management strategies for
column instability with the subsequent risk of spinal haemorrhage control in the patient with skeletal trauma
cord damage. A spine column fracture will be diag- is splinting. Splinting is a potentially lifesaving interven-
nosed as mechanically stable or unstable and this tion and is generally undertaken by nursing staff. The
will affect the positioning and possible activity of the purpose of splinting is to align and immobilise the bone,
patient. which alone has remarkable haemorrhage control
l Discoligamentous injuries of the spinal columns (see properties. Every fractured bone that has not undergone
also Chapter 17). The soft tissue components of the definitive orthopaedic management requires splinting.
spinal column include the spinal cord, the inter- Examples of intermediate stabilisation of fractures
vertebral discs and the spinal ligaments. An injury to include:
the spinal column can disrupt one or more of these
structures with or without fracture. These injuries can l Positioning of injured limbs. All patients who have
be highly unstable and the nurse must be vigilant with any form of splint in situ should not have the affected
spinal precautions and the fitting and management limb below the level of the patient’s body, and may
of the patient requiring a spine orthoses (refer to need to have it elevated to promote venous return and
Figure 23.1). minimise tissue oedema. In the ICU the trauma
Nursing Practice
There are several major considerations for the nurse man-
aging the critically ill patient with skeletal trauma. These TABLE 23.3 Potential blood loss caused by fractures 76
include appropriate assessment as well as application of
traction, management of any amputated parts and stabi- Fracture Blood loss (mL)
lisation of pelvic fractures and spine precautions. These Humerus 500–1500
latter aspects of care will be conducted in collaboration
with medical and allied health colleagues. Elbow 250–750
Radius/ulna 250–500
Independent practice
Pelvis 500–3000
Bones are very vascular structures and can be the cause
of substantial blood loss in the trauma patient. The Femur 500–3000
critical care nurse should therefore be cognisant of the Tibia/fibula 250–2000
potential for extensive blood loss in common fractures
(see Table 23.3). Ankle 250–1000




TABLE 23.4 Neurovascular observations of the skeletal trauma patient
Should be undertaken on all injured limbs both pre- and postoperatively as required
Observation Process Comments
Skin colour State the skin colour of the area inspected Pink: normal perfusion
as it compares with the unaffected part. Pale: reduced perfusion
NB: Distal limb pulses may be difficult to Dusky, purple or cyanotic discolouration: usually indicating
palpate in the injured limb; a warm significantly reduced perfusion
pink limb is a perfused limb.
Demarcated: a distinct line where the skin colour changes to
dusky (usually follows the vessel path)
Skin temperature to touch State the ambient temperature of the skin Normal: not discernibly cold to touch. Reduced skin
to touch as it compares with normally temperature indicates reduced perfusion.
perfused skin at room temperature.
Voluntary movement The patient should be able to move the It is important to assess range of motion where that is
non-immobilised distal part of any possible, provided this will not aggravate the injury.
injured limb (i.e. fingers and toes of a Reduced movement may indicate compromise to either the
plastered limb). nerve or blood supply to the limb.
Sensation The patient should be able to report Sensation should be assessed in nerve distributions (i.e. all
normal sensation to touch. fingers and toes). Reduced sensation may indicate
compromise to either the nerve or blood supply to the limb.

Trauma Management 633

patient will often be nursed flat, with the bed on tilt Collaborative practice: traumatic amputations
for a head-elevation position. In these circumstances, Traumatic amputation is the separation of a limb or
the injured dependent limb must be elevated on appendage from the body. During the prehospital phase
pillows so that it is no longer dependent. Care must it is hoped that any amputated body part will have been
be taken to ensure that elevation does not place pres- wrapped in a clean or sterile (if available) cloth. This
sure on any part of the limb: for example, a hand sack should then have been placed in a plastic, waterproof bag
made from a pillowcase tied to an IV pole should not and placed into an insulated cooler with ice. It is impor-
be used, as it places direct pressure on the path of tant that the ice does not come into direct contact with
the median nerve and can cause an iatrogenic the amputated part. When managed using these princi-
neurapraxia. ples, the amputated part may be viable for up to 6–12
l Wooden/air splints. These are padded appliances that hours before reattachment. Depending on any additional
are strapped to the injured limb. Ideally, no patient injuries, and the cardiovascular status of the patient,
should remain in wooden splints for longer than 4 surgery for limb salvage will be scheduled as soon as
hours, as pressure may build up on pressure points. possible.
l Plaster backslab. Limbs with fractures will often swell
as a physiological response to injury; a plaster back- Postoperative management will be guided by the type of
slab composed of layered Plaster of Paris is the pre- surgery that was performed, specifically whether or not
ferred treatment, as it accommodates swelling and can amputation occurred. Principles of postoperative care
easily be loosened by nursing staff at any time of day. include:
It is imperative that this be adequately padded within l appropriate positioning of the affected limb, usually
the limitations of providing structural support to the based on surgical orders
limb. Poorly made or ill-fitting backslabs can cause l frequent neurovascular observations, particularly
major complications, such as pressure sores or dis- observing for reperfusion injury, which manifests as
placement of fractures. an acute compartment syndrome or vascular trashing
l Traction. Traction may be required as part of fracture of distal vessels from a clot
management, and involves the application of a pulling l implementing changes in treatment initiated in
force to fractured or dislocated bones. There are three response to altered perfusion in a timely manner
types of traction: l psychological support to assist the patient in dealing
1. skeletal, where traction pins are anchored into the with the injury.
bone (i.e. Steinmann pin);
2. skin, where the body is gripped, as in the use of
slings and bandages;
3. manual, applied by a clinician pulling on a body Practice tip
part, such as in the reduction of dislocation. It may
also be applied to maintain the traction during Where there are any signs of deterioration of the reimplanted
such nursing care manoeuvres as log-rolling or part, communication should occur directly between the nursing
repositioning of the traction. staff and the surgical consultant to ensure timely implementa-
tion of changes to optimise salvage of the amputated part.
The principles of traction are to achieve the goal of align-
ment of bones whilst preventing complications. Remem-
ber that incorrectly-applied traction is painful and can
exacerbate the injury. The following should guide man-
agement of the patient with traction: Practice tip
1. The grip or hold on the body must be adequate For patients with amputations, on arrival in the emergency
and secure. department:
2. Provision for countertraction must be made. 1. Inspect the amputated part.
3. There must be minimal friction. 2. Clean with 0.9% saline solution and return to a clean plastic
4. The line and magnitude of the pull, once correctly bag wrapped in 0.9% saline-soaked gauze. Surround with
established, must be maintained. ice in a thermal cooler.
5. There must be frequent checks of the apparatus
and of the patient to ensure that: (a) the traction
set-up is functioning as planned; and (b) the Collaborative practice: pelvic stabilisation
patient is not suffering any injury as a result of the Pelvic fractures can be uncomplicated and require no
traction treatment.
surgical intervention, or they can be serious enough to be
the primary cause of death from exsanguination. Appro-
priate assessment and management of pelvic fractures is
Practice tip a major consideration for the management of any trauma
patient.
No patient should remain in a wooden splint longer than 4
hours. Wooden splints must be changed to a resting backslab The initial management of the patient with a fractured
that places the injured limb in anatomical fracture alignment. pelvis involves assessment and splinting. Assessment
should encompass the following two aspects: 45,51

634 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E






















FIGURE 23.3 Application of a pelvic binder (Courtesy SAM Medical Products).


1. haemodynamic status: to identify signs of ongoing
blood loss and determine fluid resuscitation
requirements
2. stability of pelvic ring: assessed with the aid of
clinical examination and diagnostic imaging. Pal-
pation and inspection of the anterior and posterior
pelvis for signs of trauma, including tenderness in
the conscious patient, is generally adequate. 45,51
The orthopaedic surgeon may elect to undertake further
clinical assessments incorporating ‘springing’ of the
pelvis, although it should be noted that this may aggra-
vate the injury. Nursing staff would not normally conduct
such assessment, unless under appropriate specialist
guidance in a setting such as remote area trauma nursing
or telehealth consultation.
Non-invasive pelvic binding, in the form of either a bed-
sheet or a proprietary pelvic binder, may make a signifi-
cant impact on patient morbidity and mortality. 45,51 Such 80
a manoeuvre will stabilise the pelvis and assist in approx- FIGURE 23.4 External fixateur: pelvis.
imating bleeding vessels, thereby assisting in haemostasis
(see Figure 23.3).
or weeks. Patients in external fixation may be permitted
Pelvic binders are temporary devices, 45,51 and ideally will
not be left in situ for longer than 4 hours. If a patient is to mobilise, although the extent of mobilisation will
to remain in the binder longer than 4 hours, nursing staff depend on the stability of the fracture. While the external
must take care to minimise pressure. Conscious patients fixateur is in place, the following nursing care is required:
should be advised to report signs of increasing pressure, l pin site care: usually cleaned with isotonic saline and
such as positional paraesthesia. Increasing abdominal covered with dry absorbent dressing; care should be
swelling may indicate a need to reposition the binder. taken to identify gaping or stretched skin around the
Position restrictions should be clarified by all members site, as this may require surgical intervention
of the healthcare team, especially if the patient will be in l analgesia: based on patient reports of pain and taking
the binder for a lengthy period. The patient may be able into account planned activities, such as mobilisation
to be log-rolled and side-lain with a pelvic binder in situ. and physiotherapy
Release of a pelvic binder should by undertaken only l mobilisation: based on stability of pelvis, and in con-
with caution and as part of definitive care (e.g. within the sultation with the surgeon
operating theatre), with all relevant members (particu- l patient education: particularly regarding the safety of
larly the orthopaedic or trauma surgeon) of the health- the procedure and mobilisation and rehabilitation
care team present. plans.
Invasive pelvic fixation uses an external fixateur (see Pelvic embolisation involves interventional radiology to
Figure 23.4) to achieve pelvic stabilisation. 45,51 The appli- control haemorrhage in patients with pelvic fractures.
cation of an external bridging frame (either anterior or Because of the large arteries that traverse the pelvis, arte-
posterior) to stabilise the pelvis may be an interim or rial bleeding can be the cause of substantial blood loss
definitive treatment measure that may be in situ for days in 10–20% of cases. 45,51 The timing of embolisation,

Trauma Management 635



TABLE 23.5 Spinal precautions 56

Action Rationale Aim Method
Head hold To maintain the cervical spine in Prevent flexion, extension and 1. Nurse holds head from head of bed – the head is held
a neutral position during any lateral head tilting during any firmly by placing one hand around the patient's jaw
position change movement. with fingers spread to cup the jaw and hold the
endotracheal tube as necessary. The forearm is used
to support side of the head
2. Nurse holds head from side of bed – nurse stands on
side of bed that the patient will be rolled towards.
One hand is placed firmly under the patient's occiput.
Ensure to be in a position to support the weight of
the head
The other hand holds the jaw and endotracheal tube as
necessary. The patient is rolled onto the forearm of
the nurse holding the head which completes the
biomechanical support for the head thus
immobilising the cervical spine during the rolling.
Log roll To maintain the entire spine in To prevent rotational torsion on The patient is rolled in one smooth motion with
anatomical alignment position the spinal column by assistants supporting the shoulder and pelvic girdles.
during any position change minimising twisting of the Another assistant supports the legs so the patient
craniocervical, cervico- moves in one plane
thoracic and thoracolumbar The patient is rolled in one smooth motion with the
junctions of the spinal column nurse holding the head issuing the command to start
and stop the manoeuvre.


particularly in relation to stabilisation, remains approximately 20% of road traffic crash injuries occurring
controversial. 45,51,55 to the chest, 30% of stabbing injuries occurring to the
chest and only 10–15% of assault and fall injuries occur-
54
Collaborative practice: spine orthoses ring to the chest. Associated mortality ranges from 4%
28,55
The cervical collar or orthosis is the most commonly used to 9%.
splint to immobilise the cervical spine. It commonly Pathophysiology
remains in situ for >24 hours in an ICU setting. This
particular type of splinting is associated with an increased The chest consists of the thoracic cavity and the organs
32
risk of pressure ulceration in immobile patients. Collar contained within. The thoracic cavity is made up of two
care is an essential component of critical care practice. structures, including a bony cavity consisting of the ribs,
Any dirt, grit, glass and road grime must be removed as sternum, scapulae and clavicles; and the second muscular
soon as possible from under the collar, particularly in the structure of the respiratory muscles and diaphragm. The
occipital regions. The patient should side-lie as much as organs contained in the chest include the lungs, airways,
possible and the collar should be removed while main- heart, blood and lymph vessels and oesophagus.
taining spinal precautions (see Table 23.5) and the under- Like all trauma, chest trauma can be penetrating or blunt
52
lying skin integrity assessed at least every 8 hours. Other in nature. Penetrating trauma, generally caused by blades
examples of spine orthoses include a halothoracic brace or bullets, results in damage to the structures and organs
and thoracolumbar/truncal anti-flexion bracing. in the chest, as well as disruption of the normal negative
intrapleural pressure resulting in a pneumothorax. Blunt
CHEST TRAUMA chest trauma generally occurs as a result of road traffic
Chest trauma is recognised as a severe, potentially life- crashes, falls and assaults or collisions.
threatening form of injury that may require admission to Chest trauma can be separated into injury to the thoracic
the critical care areas. Chest trauma may be blunt in structure, including the ribs and diaphragm; injury to the
nature, often being experienced during road traffic crashes lung, airways and associated tissue; injury to the heart
and can be associated with injuries to other areas of the and associated tissue; or injury to the vascular or digestive
body or penetrating in nature. It is often experienced system located in the chest.
during gunshot or stabbing injuries.

Chest trauma represents approximately 10% of injuries Description
that require admission to hospital for more than 24 Chest trauma covers a broad array of injuries and severity,
28
hours, although this proportion grows to over 15% and ranges from relatively minor injuries (e.g. abrasions
when only patients with major injury (injury severity and fracture of a single rib) to major, immediately life-
score >15) are considered. 28,53 Chest trauma also repre- threatening injuries (e.g. cardiac rupture or tension pneu-
sents approximately 15% of the injured patients requir- mothorax). Chest trauma is often associated with injuries
28
ing admission to the ICU. The incidence of chest trauma to other regions of the body, including the head, neck,
varies, depending on the external cause of the injury, with spine, abdomen and limbs. 57

636 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Chest trauma includes: side of the heart is most commonly injured, probably
as a result of the anterior placement of this side of the
l rib fractures: a very common form of chest trauma, heart in the thorax.
often a source of severe pain and often associated with l aortic injuries: generally, injuries to the brachioce-
other injuries such as haemothorax, pneumothorax phalic, left subclavian or right subclavian branches of
and pulmonary contusion. 57 the aorta and associated with high mortality at the
l flail chest: fractures to two or more ribs, in two or scene. 57
more places, resulting in a freely-moving section of l tracheobronchial injuries: tend to occur as a result of
the rib cage. Usually such fractures occur in the ante- direct blunt trauma and in close proximity to the
rior or lateral sections of the rib cage, where there is carina, but are relatively rare. 60
less muscle protection. The significant impact of this
injury is paradoxical movement of the flail segment Clinical Manifestations
during spontaneous ventilation, so that when a patient
inspires, the flail segment moves inwards with the Injuries to the thoracic cavity can manifest according to
negative intrapleural pressure instead of expanding the structures and systems involved (see Table 23.6).
with the rib cage. Compromised respiratory function When multiple organs and systems are involved, the com-
is caused by the increased work of breathing that this bined injuries pose an increased threat to life.
ineffective flail segment creates, as well as the con-
tused lung that normally occurs underneath the flail Nursing Practice
segment. 57 Given the underlying structures of heart, lungs and great
l diaphragmatic injuries: generally consist of diaphrag- vessels, chest trauma can cause rapid deterioration in the
matic rupture when there has been a significant rise in patient. Ongoing and thorough assessment, particularly
intra-abdominal pressure, usually with compression in relation to the signs and symptoms outlined in Table
injuries. When the rupture is sufficiently large, protru- 23.6, is essential. Other essential aspects of care include
sion of the abdominal contents into the thoracic patient positioning and management of pain relief.
space, resulting in respiratory compromise, is likely. 58
l pulmonary contusion: consists of bruising to the lung Independent practice: assessment
tissue, usually as a result of mechanical force. This Initial assessment in the emergency department should
bruising is followed by diffuse haemorrhage and inter- be conducted on an ongoing basis, with formal docu-
stitial and alveolar oedema, resulting in impaired gas mentation of these findings occurring every few minutes
exchange. 57,59 until stabilisation. The frequency of ongoing assessment
l pneumothorax: the accumulation of air in the pleural will then be based on the patient’s condition, but is likely
space. A pneumothorax may be closed (no contact to be needed every 15 minutes initially, reducing to
with the external atmosphere) or open (a communi- hourly with transfer to the critical care unit. Signs of chest
57
cating channel with the atmosphere). Closed pneu- trauma that represent life-threatening emergencies
mothoraces are generally caused by blunt chest trauma include the following.
and result from a fractured rib puncturing the lung
parenchyma. Open pneumothoraces generally occur l Cardiac tamponade: as blood collects in the pericar-
in the setting of penetrating trauma, where air is able dium, the venous return to the heart is impeded,
to move from the external atmosphere to the pleural resulting in reduced cardiac output. Signs of cardiac
space during inspiration. If not all of the inspired air tamponade include:
is able to escape during expiration, due to a tissue flap l elevated heart rate
or similar obstruction covering the opening, the l reducing pulse pressure, with falling systolic BP
volume of the pneumothorax will gradually expand and rising diastolic BP
and cause collapse of the adjacent lung, with resultant l increased preload (CVP and/or PCWP)
hypoxaemia. Where air is not able to escape at all from l distended neck veins
the pleural space, this is referred to as a tension pneu- l signs of reduced cardiac output, including lower
mothorax, and rapidly becomes a life-threatening level of consciousness, poor peripheral perfusion
event due to the increasing pressure on the lungs, and reduced urine output.
heart and trachea. l Tension pneumothorax: the lung or lungs collapse as
l haemothorax: the accumulation of blood in the the pleural space fills with air that cannot escape (see
pleural space. Blood may collect from the chest wall, Figure 23.5). As the volume of air grows with each
57
the lung parenchyma or major thoracic vessels. breath, the thoracic cavity contents are compressed or
Breath sounds are usually reduced on the side of the pushed against the opposite side of the chest. Signs of
haemothorax. Small haemothoraces (<200 mL blood) tension pneumothorax include:
may not be apparent on clinical or radiological inves- l elevated heart rate
tigation, although respiratory compromise is likely to l increased respiratory rate
be present. l decreased air entry, particularly over the affected
l cardiac trauma: encompasses a number of different lung
injuries, ranging from relatively mild bruising of the l tracheal deviation
heart muscle to rupture of the heart wall, septum or l distended neck veins
57
valves or damage to the coronary arteries. The right l surgical emphysema.

Trauma Management 637



TABLE 23.6 Clinical manifestations of chest trauma

System Manifestation Clinical signs and symptoms
Respiratory Any sign of respiratory compromise, noting Abnormal respiratory rate (<12 or >20 breaths/min)
l Airways that serial observations are an important Abnormal chest wall movement, including asymmetrical
l Lungs indicator of imminent decompensation chest wall expansion
l Diaphragm Reduced breath sounds
Obstructed airway
Hypoxia (<94%)
Hypercarbia
Apnoea
Dyspnoea
Orthopnoea
Crepitus/surgical emphysema
Cardiovascular Circulatory insufficiency resulting in decreased Abnormal heart rate (<60 or >100 beats/min)
l Heart tissue perfusion Dysrhythmia
l Great vessels In severe cases, Pulseless Electrical Activity (see Ch. 8)
Pulsus alternans
Decreased cardiac output
Lowered blood pressure (systolic <100 mm Hg)
Reduced peripheral perfusion
Confusion and reduced consciousness level
Gastrointestinal Perforation and contamination of mediastinum Crepitus
l Oesophageal rupture Haemopneumothorax
Pain
Cough
Stridor
Bleeding
Sepsis (late)
Systemic May occur in response to injury of a vessel that Varied depending on location, but may include:
l Air embolism traverses an air space; manifestations will l Focal neurological sign
vary depending on location and associated l Cardiac deterioration
injuries




Independent practice: positioning
Early mobilisation of the patient with chest trauma is
vital to prevent the complications of prolonged bedrest
and immobility. Patients should be nursed side-to-side
and in a variety of positions, including sitting upright.
The extent to which the patient can be mobilised is
dependent on other injuries. Patients should be mobil-
ised to sit out of bed as soon as they are conscious and
their injuries permit.
Care must be taken to accommodate the increased work
of breathing that is associated with injuries to the lungs.
Appropriate use of supplemental oxygen will assist the
patient’s exercise tolerance. Further, if the patient is
mechanically ventilated, additional mechanical support
(i.e. transient increase in pressure support) may be
applied to assist the patient’s exercise tolerance. Being
unable to catch their breath is a terrifying experience that
is likely to result in increased levels of anxiety for patients,
FIGURE 23.5 Right tension pneumothorax (Courtesy The Alfred, and should be avoided wherever possible.
Melbourne).

Independent practice: pain relief
Practice tip
The principles of managing pain in chest trauma patients
Unexplained hypotension in a patient with chest trauma may are similar to those for other patients, although the
indicate a tension pneumothorax; an urgent chest X-ray is potential severity of pain, particularly as a result of frac-
required for diagnosis. tured ribs, should not be underestimated. Effective pain
management in the chest trauma patient is a major

638 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

determinant of maintaining adequate spontaneous intrapleural pressure. Insertion of an intercostal catheter
breathing. Avoiding mechanical ventilation is a major drains the air and/or blood from between the pleura,
goal in the less-severe group of chest trauma patients, so resulting in reinstatement of the negative intrapleural
effective deep-breathing and coughing must be pro- pressure and reinflation of the underlying lung.
moted. Pain relief will normally include IV opioids, but A central principle in the treatment of chest trauma is the
may also include intercostal or epidural analgesia and use of the intercostal catheter (ICC) for chest drainage
non-steroidal anti-inflammatory agents in selected purposes. The principles of chest drainage include:
patients (see Chapter 7). Non-pharmacological means
such as the use of supplemental oxygen, use of cold l The lungs are encased in a potential space. The visceral
packs early and heat packs late in the treatment course, pleura attaches to the parietal pleura via surface
massage, relaxation and diversion techniques should also tension, creating a negative intrapleural pressure and
be considered. Providing and maintaining a comfortable attaching the lung to the chest wall. During inspira-
posture for the patient that includes the elevation and tion the rib cage moves out and the diaphragm con-
support of injured limbs has remarkable analgesic prop- tracts and moves down, increasing the size of the
erties. A confident, competent and efficient nurse that intrathoracic space. Air moves from an area of higher
engenders trust from both the patient and family is very pressure in the environment to an area of lower pres-
comforting. sure within the lungs along a pressure gradient.
l An intercostal catheter is inserted into the pleural
Collaborative practice space, passing between the ribs. The ICC is designed
to drain both air and fluid as required.
Caring for the patient with chest trauma requires a team
effort with input from nursing, medical and allied health l The drainage system and seal provides an ongoing
professionals. While the medical management is largely means of removing air and/or fluid from the pleural
directed towards attempting to correct the damage done space, while preventing air from the atmosphere enter-
by the trauma, the allied health interventions are largely ing via the ICC. The seal is provided by placing the
directed at minimising such complications as atelectasis distal end of the ICC under water (usually 2 cm). The
and ongoing problems with mobility. Nursing interven- catheter should not be placed under excessive levels
tions are essential to ensure patient comfort, minimise of water, as this creates resistance and will limit air
complications and promote healing of wounds through and fluid escaping from the pleural space.
such interventions as chest drainage and wound care. l Suction is often added to the drainage system to
promote drainage of fluid.
Collaborative practice: surgical Care of the chest trauma patient with intercostal drainage
management of injury is directed towards ensuring sterility and patency of the
system, assessing the amount and type of drainage, as
Surgical intervention in the chest trauma patient is gener- well as the impact on the patient (see Table 23.7). Addi-
ally limited to repair of tears and lacerations, for example tional considerations include the following:
repair of vessel injuries including aortic rupture, lung
lacerations, heart injuries including lacerations and val- l ICC may be positional, or alternatively haemo/
vular injury. A ruptured diaphragm or oesophageal per- pneumothoraces may be loculated. Repositioning of
foration will also be repaired surgically. either the patient or the catheter may be necessary.
l Side-lying or lifting the patient, especially with a
The emergency thoracotomy has proven beneficial in a
select group of patients with penetrating trauma and less frame, may kink or disconnect the ICC.
than 15 minutes of cardiopulmonary resuscitation; l Surgical emphysema around the site of the ICC may
however, it is generally recognised as not providing dislodge the tip of the catheter out of the pleural cavity
benefit in patients with blunt chest trauma. While dif- as the emphysema swells. Ongoing assessment, includ-
61
ferent techniques are used in different settings, the main ing a chest X-ray, will be required to confirm the posi-
access to the thoracic cavity is via a left thoracotomy, a tion of the ICC.
midline sternotomy or a ‘clam shell’ incision. Initial l Movement of the patient, including sitting upright,
assessment of the patient is used to determine the need will assist with fluid drainage; the volume of drainage
for a thoracotomy in either the emergency department or should be assessed after moving the patient.
the operating room. Nurses working in a trauma recep- l Monitoring of respiratory function should continue
tion facility that has the capacity for emergency thora- after removal of the ICC to detect recollection of air
cotomy should be familiar with the equipment and or fluid.
process for this procedure. Postoperative nursing care of
these patients should follow the same principles as those
for patients who have undergone routine cardiothoracic
surgery. Practice tip
Fresh, brightly-coloured blood drained from the ICC indicates
Collaborative practice: chest drainage continued active bleeding, while dark blood usually indicates
When injury to the pleura occurs, air or blood collects older blood that has been resting in the pleural space for some
between the two layers of the pleura, causing collapse of time.
the underlying area of lung and loss of the negative

Trauma Management 639

financial and social problems. Early referral of selected
TABLE 23.7 Assessment of chest drainage patients to allied health professionals has the potential
to significantly influence patient outcome.
Characteristic Description
ABDOMINAL TRAUMA
Water seal Ensure there is sufficient water in the
water seal chamber. Any organ or structure in the abdominal cavity can be
Bubbling Continued bubbling indicates an air leak. injured. Abdominal trauma presents unique challenges
to clinicians due to the abdominal cavity’s high diversity
Drainage Observe the nature and volume of fluid of organs and structures. The morbidity and mortality
exudate (NB: >1500 mL stat or
200/mL/hour for 2–4 hours; surgical associated with abdominal injuries are high, so the need
exploration may be required. for early, accurate diagnosis and treatment is paramount.
Abdominal trauma accounts for approximately 15% of
Patency Ensure the intercostal catheter is not
blocked, remove any blood clots. all trauma deaths, with haemorrhage being the major
cause in the first 48 hours. Latent trauma deaths after
Swinging Oscillation of fluid in the ICC confirms abdominal injury are usually related to sepsis and
patency, as this reflects the changes in
intrapleural pressure with respiration; complications.
such oscillation should continue even Recent advances in diagnostic and treatment techniques
when the lung has re-expanded.
for abdominal trauma have seen an increased emphasis
Suction If suction is ordered, check the on non-operative management for solid organ injury,
appropriate level is being delivered.
with more recent increases in the use of angioembolisa-
tion. These two clinical treatment innovations place an
emphasis on excellent patient monitoring and, in some
instances, higher ICU utilisation for selected cases. 62,63
Collaborative practice: ventilatory support
Ventilatory support is often required for patients with Patients who experience abdominal trauma as their main
chest trauma (see Chapter 15 for general principles). The injury comprise only 3–5% of injured patients requiring
following specific considerations apply: admission to ICU, although up to a quarter of trauma
28
patients experience some form of abdominal injury. Of
l Non-invasive ventilation: care should be taken based all patients who present to the emergency department
on associated injuries, with contraindications includ- with serious injury, approximately 15–20% have abdomi-
ing fractured base of skull or facial fractures. nal injury. 26
l Intubation: haemoptosis is relatively common in
patients with lung injury, and care must be taken to Pathophysiology
ensure removal of blood clots from the ETT. Heated, The abdominal cavity consists of a range of tissues and
humidified air and regular suctioning will assist with organ structures, including musculoskeletal, solid and
maintaining ETT patency. hollow organs, vessels and nerves. Musculoskeletal struc-
l Airway injury: initiation of positive pressure ventila- tures include the major abdominal muscle groups forming
tion in the chest trauma patient may identify damage the abdominal wall, as well as the lumbar vertebrae and
to a small airway that previously went unnoticed pelvis. Solid organs include the liver, spleen, pancreas,
(damage to a large airway will usually have been kidneys and adrenal glands (and ovaries in women).
detected early in the assessment phase). Treatment Hollow organs include the stomach, small and large
will depend on the severity and location of the rupture, intestines, gallbladder and bladder (and uterus in
but usually requires decompression of the pleura with women). Finally, the vessels and nerves include a complex
an ICC, possibly surgical intervention and advanced array of all abdominal blood vessels (arterial and venous),
respiratory support such as independent lung lymphatics, and nerves including neural plexuses and the
ventilation. spinal cord. Traumatic abdominal injuries are classified
l Use of tracheostomy: this may be required for patients as being extraperitoneal, intraperitoneal and/or retroperi-
with injury to the trachea and is managed using toneal. Importantly, a patient can have any mix or mul-
the same principles as with any patient with a tiples of these. The classification of injury guides clinical
tracheostomy.
decision making.
Collaborative practice: allied The pathophysiology of abdominal trauma is largely
health interventions related to the structure(s) injured. Careful serial assess-

Physiotherapy is generally required for chest trauma ments are essential to identify changing clinical manifes-
tations. The most common clinical manifestation of
patients. The primary aspects of care include chest phys- abdominal trauma is haemorrhage and/or signs of an
iotherapy, given the often extended episodes of mechani- acute abdomen, such as pain, tenderness, rigidity and
cal ventilation and bedrest that are required, as well bruising. Importantly, these are life-threatening signs and
as mobility exercises. Occupational therapy particularly require immediate surgical intervention.
offers benefits to the long-term ventilated patient in terms
of diversion activity, while social work is often beneficial The most significant sign of abdominal trauma in
for patients with long-term disability and ongoing the conscious patient is pain. Where hollow viscus

640 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

perforation has occurred, such as bruising across the area assessment and measurement techniques that exist, but
of the abdominal seatbelt, small bowel perforation may has been reported to be between 1% and 33%. 65
be present. These patients are characterised by pain out High IAP can have effects on multiple systems through-
of proportion to that expected with superficial abdominal out the body, as follows: 65,66
wall contusions. Other signs of abdominal trauma can be
related to the structure that has been injured. For example, l gut and hepatic effects: reduced blood flow to abdom-
haematuria demonstrates trauma to some part of the inal organs
urinary tract, including the kidneys. l renal effects: reduced renal blood flow and glomerular
filtration rate
Description l cardiovascular effects: decreased venous return through
The abdomen is susceptible to injury from a variety of pressure on the inferior vena cava and raised intratho-
external causes, both blunt and penetrating (see discus- racic pressure, leading to reduced cardiac output
sion of penetrating injuries below). A key aspect to l respiratory effects: where pressure on the abdominal
remember with any abdominal injury is that the superfi- side of the diaphragm increases abdominal resistance
cial injury does not always reflect what lies below. For to inspiration. In ventilated patients this is usually
example, it is not possible to be certain of the trajectory demonstrated by elevated peak inspiratory pressures,
that a bullet took after it passed through the skin. resulting in reducing tidal volume and minute volume
as the ventilator cycles off when either the preset pres-
Contusion/laceration sure is reached or pressure alarms are triggered
l central nervous system effects: reduced cerebral blood
Sudden deceleration of moving body tissues can result in flow due to the raised intracranial pressure from
laceration or haemorrhage into the tissues (contusion). impaired venous drainage. When this is coupled with
This is related to the tearing of the tissues that occurs due a lower cerebral perfusion pressure that results from
to inertia, or the tendency of tissues to resist changes in the reduced cardiac output, it is deleterious to the
speed or direction (e.g. to keep moving forwards when injured brain
the body has stopped moving, resulting in a tearing l cytokine response: activation of the stress response,
action to the tissues). Any structure in the abdomen is seen through raised interleukins IL-6 and IL-1 alpha,
susceptible to this type of injury. Commonly, the liver as well as tumour necrosis factor.
and spleen are the worst-affected organs, largely related
to a seatbelt injury in motor vehicle collisions. Laceration A high level of suspicion for ACS should be retained for
of a solid organ can be a minor injury that is appropri- all patients with abdominal trauma as well as those who
ately monitored and managed conservatively; alterna- have had abdominal surgery for other reasons. Clinical
tively, a similar injury can lead to exsanguination (e.g. a examination, looking for a distended and firm abdomen,
liver laceration into the hilum that involves the inferior is insensitive in the early stages of ACS; however, these
vena cava). Hollow viscus can be contused, as can the signs should be identified if ACS progresses to a late state.
mesentery and peritoneum. Proactive detection of ACS is more effectively carried out
through the use of routine IAP measurements in all
Perforation patients who have the potential to develop ACS. While
agreement as to the precise levels of IAP that indicate ACS
Full-thickness injury, or perforation, to a hollow viscus is yet to be achieved, there is widespread agreement that
organ is life-threatening. Perforation of the intestine can values above approximately 20 mmHg require investiga-
result in peritoneal soiling and ischaemic bowel. Small tion; and pressures above 25 mmHg, in association with
bowel injuries are particularly difficult to diagnose; if other clinically relevant findings such as firm or distended
diagnosis is delayed, morbidity can be severe. The abdom- abdomen and the systemic effects outlined above, often
inal seatbelt sign – in other words, bruising across the indicate a need for urgent surgery. 65,66
anterior abdominal wall that follows the path of the lap
and sash of the seatbelt – is a sentinel sign for hollow IAP can be measured directly by laparoscopy, but is more
64
viscus perforation. Importantly, patients with this type effectively measured on an ongoing basis, either intermit-
of abdominal trauma can present late (by days). If pre- tently or continuously, via an indirect technique of mea-
senting late, the usual clinical manifestations are pain, suring bladder pressures. IAP measurements are achieved
peritonitis and sepsis. 64 using an indwelling urinary catheter with a pressure
transducer or manometer levelled to the midaxillary line
Secondary injury: abdominal compartment and attached via a T piece to allow continuous sterile
67
syndrome (ACS) access. According to the World Society of the Abdomi-
The abdominal viscera are highly vascular and subject to nal Compartment Syndrome Guidelines, intermittent
67
measurements are obtained as follows:
vascular engorgement during massive fluid resuscitation.
Where this occurs, there is an acute rise in intra-abdominal 1. Lay the patient flat, or head-up if undergoing head
pressure (IAP). In severe cases, the IAP will rise to the injury management. If the IAP is measured with
point where cardiorespiratory function is compromised. the patient head-up, the level of elevation should
This is a surgical emergency and the abdominal cavity be documented to ensure that future measure-
requires decompression immediately. The incidence of ments are done with the patient in the same
ACS is difficult to determine because of the different position.

Trauma Management 641

2. The catheter is clamped and 25 mL (use consistent Where the patient has undergone a trauma laparotomy,
amount for all measurements) of room-temperature postoperative care is standard as for any patient who has
0.9% saline is infused into an empty bladder via undergone an abdominal surgical procedure. The specific
the indwelling urinary catheter. This will create the nursing care elements will depend on what organ has
static column of fluid for pressure measurement. been injured and the surgical procedure that has been
Higher infused volumes may create a falsely ele- undertaken to repair the injury. Careful attention must
vated intraabdominal pressure. be paid to those general nursing care elements that all
3. After 30–60 seconds of dwell time, the pressure is patients require (see Chapter 6).
measured via the transducer or manometer. Postoperative feeding and bowel care should be discussed
4. The catheter is unclamped to allow fluid to drain with the healthcare team and plans made early to avoid
out. It must be remembered to deduct the fluid delays and adverse events such as constipation (see
installation amount from any future urine output Chapter 19 for principles of feeding). A paralytic ileus is
measurements.
a common manifestation of the critically-ill abdominal
There is some evidence that accurate IAP measurements trauma patient. Ensuring that the gut is decompressed,
can be obtained on a continuous basis using a three-way with a functional enterogastric tube that is correctly posi-
catheter. The benefits of this method include the provi- tioned, is essential. Because constipation is a common
67
sion of a continuous measurement as well as the absence problem, early intervention and implementation of a
of instillation of additional fluid into the bladder. The bowel-care protocol for trauma should be considered (see
primary disadvantage is the potential for inaccuracy, Chapter 6).
depending on the volume of urine in the bladder.
Collaborative practice
Nursing Practice Collaborative practice for the care of patients after
Recent trends have seen an increasing use of nonoperative abdominal trauma includes effective diagnosis, surgical
care of patients with abdominal injury. In these patients, or radiological interventions, and associated care.
monitoring for deterioration is essential, as is the ability Damage-control surgery is now a mainstay in
to activate surgery and care for patients accordingly. management.
Diagnosis in the trauma setting consists of a thorough
Independent practice clinical assessment, the potential use of FAST, diagnostic
With the high use of nonoperative management tech- peritoneal lavage (DPL), abdominal computed tomogra-
niques for solid organ injury, the role of monitoring of phy (CT) and laparotomy or laparoscopy. Clinical assess-
patients with abdominal trauma is pivotal. Nurses must ment has the potential to reveal such clinical signs as skin
be cognisant of the clinical signs of abdominal injury, bruising, lacerations, signs of abdominal rigidity and
especially haemorrhage, and act on these immediately guarding. The various locations of clinical signs are clues
(see Table 23.8). Specific aspects of nursing care for to potential abdominal injury. The results of this phase
patients after abdominal trauma include pain manage- of the investigation will determine what additional diag-
ment, monitoring and postoperative care. Abdominal nostic tests are undertaken. FAST is rapidly becoming an
trauma patients will often experience severe pain, as a extension of the clinical assessment in abdominal trauma
result of both the primary trauma and any surgical inter- patients.
vention for repair (see Chapter 7).
Collaborative practice: diagnostic
Vital sign monitoring is a mainstay of nursing manage-
ment in patients with abdominal trauma, and all patients peritoneal lavage
should have appropriate monitoring (as outlined in The diagnostic peritoneal lavage (DPL) is a diagnostic
trauma reception). It is also essential that all patients procedure that can be undertaken rapidly to assess for
receive a urinalysis after incurring abdominal trauma in intraabdominal bleeding. It can identify the presence of
order to identify trauma to the urinary system. haemorrhage but gives no indication of its source. DPL





TABLE 23.8 Common signs of abdominal injury 83

Sign Description Suspected injury
Grey Turner’s sign Blueish discolouration of the lower abdomen and flanks Retroperitoneal haemorrhage
6–24 hours after onset of bleeding
Kehr’s sign Left shoulder tip pain caused by diaphragmatic irritation Splenic injury, although can be associated with any
intra-abdominal bleeding
Cullen’s sign Bluish discolouration around the umbilicus Pancreatic injury, although can be associated with any
peritoneal bleeding
Coopernail’s sign Ecchymosis of scrotum or labia Pelvic fracture or pelvic organ injury

642 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

may be performed on a patient with unexplained persis- appropriate treatment to control haemorrhage and repair
tent signs of shock (hypotension ± tachycardia); where organ injury (laparotomy). When this procedure is con-
the abdominal clinical examination and FAST is incon- sidered appropriate, rapid transit to the operating room
clusive; where there is a high index of suspicion of should be undertaken. As the consequences of missed or
intraabdominal injury; or alternative diagnostic evalua- delayed diagnosis of abdominal injury can be catastrophic
tion such as CT is unavailable. Disadvantages of the DPL for the patient, opening the peritoneal cavity to exclude
include the high level of invasiveness and associated injury in selected cases is a necessity.
complications, its inability to detect retroperitoneal inju-
ries, the high rate of non-therapeutic laparotomies and its
low specificity or high number of false-positive results. 22 Collaborative practice: embolisation
Interventional radiology is a treatment option in the
Prior to DPL, time permitting, the bladder should be
decompressed with an indwelling urinary catheter and management of abdominal trauma. Via an arterial
the stomach decompressed with an enterogastric tube. approach, the interventional radiologist can insert can-
The DPL procedure involves an incision below the umbi- nulae to identify arterial blushes (bleeders). Once identi-
licus, then a catheter passed into the peritoneal cavity and fied, the vessel can be ligated via mechanical coiling
aspirated to determine peritoneal contents. Differing or blocked chemically. Embolisation has been shown
results in terms of colour and volume indicate different to be effective and safe for a wide range of patients in
potential injuries. When blood, red blood cells, white the setting of splenic trauma, renal trauma and pelvic
62
blood cells, bacteria, faecal matter, bile or food particles trauma. The patient undergoing embolisation as a treat-
are aspirated, the peritoneal lavage is considered to be ment option for the control of haemorrhage requires
positive. 22 meticulous monitoring and an ability to respond imme-
diately to hypovolaemic shock should the bleeding
Collaborative practice: abdominal worsen.
computed tomography
Abdominal computed tomography (CT) is recognised as Collaborative practice: management of
having high sensitivity and specificity in the setting of the patient with an open abdomen
abdominal trauma and is therefore accepted as a diagnos-
tic mainstay in this group of patients, particularly for In cases of severe abdominal trauma, the abdominal
blunt trauma. The main exception to this is where the trauma patient may be returned to the ICU with an open
results of a FAST examination are positive and the patient abdomen, or laparostomy, covered with a temporary
is taken to surgery urgently. Abdominal CT is used less wound-closure system. There are various types of open
often in patients with penetrating trauma, primarily due abdominal dressings, but the principal aim of the dress-
to its lower sensitivity in diagnosing the hollow visceral ing is to provide a coverage for the contents of the peri-
22
injuries common in penetrating trauma. An important toneum if these are too swollen to fit beneath the closed
pitfall for CT imaging in abdominal trauma occurs when skin or where there is a need for repeated opening of the
40
the patient has arrived at the scanner so quickly after the abdomen. Ultimately, the aim is to close the skin as
injury that major blood loss is not apparent and the soon as possible, when the patient’s physiological status
extent of the injury is missed or underevaluated. A high normalises. It is possible for these abdominal dressings
index of suspicion in the setting of a negative CT and to cause a secondary ACS if they are too restrictive.
extensive abdominal trauma should remain, particularly The primary aims of managing a patient with an open
if signs of shock develop. abdomen include minimising complications of pro-
Debate currently exists as to the role of oral contrast in longed immobility, observing for signs of ongoing ACS,
the trauma patient who must remain supine and immo- restoring the patient’s physiology to normal and support-
bilised in a cervical collar. It is essential that nursing ing the patient and family through a psychologically-
assessment for the risk of aspiration be conducted, and distressing time. Understandably, both the patient and
to be prepared to manage the vomiting patient. Any their family can be distressed by the appearance of an
supine patient given radiographic contrast should not be open abdomen. There are no specific position restrictions
left unattended, and there should be sufficient staff avail- for a patient with an open abdomen, but haemodynamic
able at short notice to roll the patient onto their side if status is often labile so that care must be taken with side-
he/she vomits. The healthcare team should discuss the lying and hygiene care.
risk of vomiting prior to ordering the test so that an
informed decision can be made regarding the risk–benefit
ratio on an individual case basis. Oral contrast has been Specific Abdominal Injuries: Spleen
demonstrated to be highly effective in revealing hollow The spleen is the solid organ most commonly injured in
62
viscus injury, and therefore has a place in the diagnostic blunt trauma. Its location (under the ribs) also makes
evaluation of abdominal trauma. it vulnerable to secondary injury from fractured ribs.
Splenic injury should always be suspected in those
Collaborative practice: laparotomy/laparoscopy patients who have sustained a direct blow to the abdomen,
The role of diagnostic operations such as laparotomy/ as it is a large organ. Signs of splenic injury are generally
22
laparoscopy is well described in the literature, and is pain over the left upper quadrant. There may be no
essential to aid diagnosis (laparoscopy) and provide changes to vital sign parameters until the patient has

Trauma Management 643



TABLE 23.9 Spleen injury scale 62 TABLE 23.10 Liver injury scale 62

Grade* Injury description Grade* Injury description
I Haematoma Subcapsular, <10% surface area I Haematoma Subcapsular, <10% surface area
Laceration Capsular tear, <1 cm parenchymal depth Laceration Capsular tear, <1 cm parenchymal depth
II Haematoma Subcapsular, 10–50% surface area II Haematoma Subcapsular, 10%–50% surface area
Intraparenchymal, <5 cm in diameter Intraparenchymal, <10 cm in diameter
Laceration Parenchymal depth 1–3 cm not involving a Laceration Parenchymal depth 1–3 cm, <10 cm in length
trabecular vessel
III Haematoma Subcapsular, >50% surface area or expanding
III Haematoma Subcapsular, >50% surface area or expanding; Ruptured subcapsular or parenchymal
Ruptured subcapsular or parenchymal haematoma
haematoma Laceration Parenchymal depth >3 cm
Intraparenchymal haematoma >5 cm or
expanding IV Laceration Parenchymal disruption involving 25–75% of
Laceration Parenchymal depth >3 cm or involving hepatic lobe or 1–3 Couinaud’s segments
within a single lobe
trabecular vessels
V Laceration Parenchymal disruption involving >75% of
IV Laceration Laceration involving segmental or hilar vessels hepatic lobe or >3 Couinaud’s segments
producing major devascularisation (>25% within a single lobe
of spleen)
Vascular Juxtahepatic venous injuries; i.e. retrohepatic
V Laceration Completely shattered spleen vena cava/central major hepatic veins
Vascular Hilar vascular injury that devascularises spleen VI Vascular Hepatic avulsion
*Advance one grade for multiple injuries, up to grade III.
*Advance one grade for multiple injuries, up to grade III.




incurred significant circulating blood loss. Splenic injury seatbelt injuries and abdominal blows from an assault.
is categorised in a scale consisting of five levels; this scale The liver is also at risk of secondary injury from fractured
is designed to aid classification for management and ribs. Liver injuries are graded using the six-level liver
62
62
research purposes (see Table 23.9). injury scale (see Table 23.10). The treatment of liver inju-
ries is largely dependent on the nature of the injury or
The spleen has an immunological function that is not injuries to the liver itself, presence of concomitant inju-
well understood. After splenectomy, patients are at ries, premorbid status and overall injury severity. The
increased risk of infection and therefore require careful treatment options may also be guided by the services
education regarding lifelong risks. The role of immunisa- and expertise that your health agency can offer the
tion after splenectomy is very important, and the patient patient.
must be counselled regarding the necessity for follow-up
68
on immunisations. Prior to discharge from the hospital, The overwhelming aim of the management of liver inju-
the patient should be administered the first round of ries is to preserve liver function. This is achieved by
immunisations. The current recommendation for predis- controlling haemorrhage, resting the patient and close
charge immunisations include: monitoring. Most liver injuries can be managed non-
operatively. In these cases it is imperative that the patient
l pneumococcal vaccine
l meningococcal vaccines be closely monitored for signs of haemorrhage and that
l Haemophilus influenzae type B. 69 the capacity for laparotomy is available at short notice if
required. In some cases, embolisation may be considered
62
The patient will also be commenced on antibiotic pro- for arterial haemorrhage. Late complications of liver
phylaxis and should be advised to wear a medi-alert injury include infection, haematoma, bile leak and late
disk or card and consult specialist travel advice when haemorrhage.
travelling. 69
PENETRATING INJURIES
Specific Abdominal Injuries: Liver Trauma is broadly categorised according to whether the
The liver is a vital organ, with liver failure being a fatal external cause of injury was blunt or penetrating. Pene-
condition unless reversible. After the spleen, the liver is trating trauma refers to a mechanism of injury where the
the next most common solid organ injured. Any injury skin has been cut through the insertion of a foreign
to this highly vascular organ is serious and requires surgi- object. The most common examples include knife and
cal review. As the largest abdominal solid organ traversing gunshot wounds, although solid objects such as fences,
the midline, the liver is susceptible to injury from any signposts and tools can cause penetrating trauma. Pene-
external forces applied to the abdomen, for example trating trauma is significantly different from blunt trauma

644 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

in that the injury is largely localised to a single body maintain adequate perfusion to essential organs until
region. Exceptions to this may occur, for example, with definitive repair of the wound can be undertaken. 43
firearm wounds if there are multiple bullet-entry wounds l Psychosocial care of the patient and family. It is pos-
or multiple knife-stab sites. sible that patients with penetrating injury will need
specific psychosocial care, particularly when the injury
Care must be taken when caring for patients with pene-
trating injury to prevent injury to staff. This is particularly has occurred as a result of assault.
important when the patient presents with a knife in situ †
or a large, protruding foreign object in their body. It BURNS
should also be noted that some penetrating trauma Recent improvements in both shock and sepsis manage-
occurs as a result of a criminal act, and it is essential ment have resulted in patients with severe and extensive
to observe rules governing forensic evidence. Police burn injuries spending long periods of time in the critical
should be notified by the senior clinician involved in care environment. Burn injuries occur as a result of
providing care. thermal, electrical or chemical injury and cause both local
and systemic changes to a patient. An understanding of
Clinical Manifestations these changes will assist with planning appropriate care
The clinical manifestations of penetrating injuries are for this group of patients.
dependent on where in the body the penetrating injury In recent years, improved survival, reduced hospital
has occurred, the underlying organs and the amount of length of stay and a decrease in morbidity and mortality
force and dispersion caused by the injury. For example, a has been seen in burns patients. This is primarily due to
high-velocity bullet will cause substantial tissue damage a better understanding of burns pathophysiology and
in a wider area than just the bullet’s track. The clinical advancements in care that include improvements in
manifestations of penetrating trauma can be divided into resuscitation protocols, improved respiratory support,
two broad types: management of the hypermetabolic response, rigid infec-
tion control monitoring, early excision and burn wound
1. conspicuous: where the penetrating article is closure, use of skin substitutes and early nutritional
grossly visible (e.g. a shard of glass, a branch or a support.
knife). Care must be taken not to focus solely on
the visible cause of injury but to continue to under- Burn injuries are highly variable and individual injuries
take a systematic trauma assessment affect all ages and social groups. In general terms, assess-
2. inconspicuous: where the penetrating article is not ment is based on the size, depth and anatomical site of
immediately visible and may become apparent the injury, mechanism of injury and the presence of coex-
only during the systematic trauma assessment of isting conditions. The World Health Organization esti-
the patient (e.g. with gunshot wounds and projec- mates that more than 300,000 deaths are fire-related
tiles). In these injuries the visual signs on the exter- every year, the majority occurring in developing
nal skin may not reflect the catastrophic injury countries. 70
underlying it (e.g. ventricle lacerations or serious Burn injuries occur as a result of thermal, electrical or
vascular injury).
chemical injury and cause both local and systemic changes
to a patient. An understanding of these changes will assist
Nursing Practice with planning appropriate care for this group of patients.
Patients with penetrating injury will be cared for based All patients with a serious burn injury should be referred
on the severity and area of injury they have sustained. to a specialised burns unit that is staffed and equipped
Surgical intervention is usually more urgent than that appropriately to manage burns. The Australian and New
seen with blunt injury, as bleeding may be occurring from Zealand Burns Association (ANZBA) criteria outline
a ruptured organ or vessel either into a body cavity or which burns patients require treatment in a specialised
externally. For this reason, the incidence of procedures burns unit (see Box 23.1).
such as laparotomy and thoracotomy is high in patients
with a penetrating injury. PATHOPHYSIOLOGY
In the emergency setting the following considerations are The skin is the largest organ in the human body and
generally unique to the patient with a penetrating injury: accounts for 15% of its weight. The skin has multiple
purposes, including protection from infection, regulation
l Stabilise the foreign object. This may require padding of body heat and functioning as a vapour barrier.
and/or taping an object, for example a knife, to ensure
minimal movement and prevent further damage until The skin consists of three layers: the epidermis, the dermis
68
definitive care to remove the object. and subcutaneous tissue. The epidermis is the outer
l Care for the patient in a non-standard position. This layer, and is composed of stratified epithelial cells that
will be dependent on how and where any foreign protect against infection and conserve moisture. This
object is protruding from the body. For example, it layer is characterised by having regenerative ability. The
may be necessary to care for a patient in the side-lying dermis, as the middle layer, is between 1 and 4 mm thick,
or prone position until the object is removed.
l Minimal volume resuscitation. This describes the † This section has been prepared with the assistance of Yvonne Singer RN, Victorian
practice of only resuscitating a patient sufficiently to State Burns Education Program Coordinator, Victorian Adult Burns Service.

Trauma Management 645



BOX 23.1 Criteria for treatment in a TABLE 23.11 Systemic changes that occur with
specialised burn centre 77 burn injuries 71

l Burns greater than 10% of total body surface area (TBSA) System affected Pathophysiological change
l Burns to special areas: face, hands, feet, genitalia, perineum,
major joints Cardiovascular system l Increased capillary permeability
leading to capillary leak of
l Full-thickness burns greater than 5% of TBSA intravascular proteins and fluids to
l Electrical burns interstitial compartment
l Chemical burns l Peripheral and splanchnic
vasoconstriction
l Burns with an associated inhalation injury l Reduced myocardial contractility
l Circumferential burns of the limbs or chest l Systemic hypovolaemia due to
l Burns in the very young or very old above, plus fluid loss from burn
l Burns in people with preexisting medical disorders that Respiratory system l Bronchoconstriction
could complicate management, prolong recovery or l Adult respiratory distress syndrome
increase mortality
l Burns with associated trauma Metabolic system l Increased basal metabolic rate (up to
3 times normal)
l The possibility of non-accidental injury in children l Above, plus splanchnic
vasoconstriction, will lead to
catabolism if patient not fed early
and aggressively

Zone of Zone of Immunological system l Downregulation of immune response
coagulation stasis
Zone of
Epidermis hyperaemia
Dermis contribute to this stasis include microthrombus for-
mation, neutrophil adherence, fibrin deposition and
endothelial swelling. Tissue in this zone is potentially
Adequate Zone of Inadequate salvageable if sufficient resuscitation is achieved to
resuscitation coagulation resuscitation increase tissue perfusion. If insufficient resuscitation
occurs, or if there are additional insults of hypoten-
sion, infection or oedema, tissue within this zone may
convert to the zone of coagulation.
l Zone of hyperaemia: the outermost zone. It experi-
ences increased tissue perfusion as a result of local
Zone of stasis preserved Zone of stasis lost inflammatory response, which results in local vasodi-
lation and an increase in vascular permeability. Tissue
FIGURE 23.6 Zones of burn damage.
81
in this zone will usually recover, unless there are pro-
longed or severe periods of hypotension, infection or
oedema.
although thinner in the elderly and the very young. It is
composed of an outer papillary dermis and an inner Systemic changes
reticular dermis, and supplies nutrients to the epidermis. With a burn injury of >30% total burn surface area (TBSA)
The dermis contains all the accessory structures including microcirculation vessel wall integrity is altered resulting
blood vessels, nerve endings, the sweat and sebaceous in fluid and protein loss into the interstitium. The protein
glands and the hair follicles. The dermis itself does not loss results in a reduction in osmotic pressure which
have regenerative ability, but because the glands, vessels further insults circulating volume. Table 23.11 contains a
and follicles are lined with epidermis, burns that involve description of the changes to the cardiovascular, respira-
this layer may still regenerate. The innermost layer, the tory, metabolic and immunological systems that occur as
subcutaneous tissue, consists of adipose and connective a result of the release of cytokines and other inflamma-
tissue. This layer has no regenerative ability. tory mediators in response to the injury.
Local changes Inhalation injury
Local changes include the zones of coagulation, stasis and
hyperaemia (see Figure 23.6) and the specific changes are The presence of an inhalation injury will increase mortal-
71,72
outlined below. 71 ity and morbidity in people with a dermal burn injury.
Inhalation injury consists of three components that may
l Zone of coagulation: occurs at the point of maximum occur independently but often occur simultaneously, and
damage. Irreversible tissue loss occurs in this zone due include heat injury to the upper airways, effects of smoke
71
to coagulation of the constituent proteins. on the respiratory system and inhalation of toxic gases.
l Zone of stasis: surrounds the zone of coagulation and Diagnosis of an inhalation burn injury remains problem-
is an area of decreased tissue perfusion. Changes that atic, but it should be suspected if the injury was sustained

646 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

in a closed spaced as well as if there are facial burns,
singed nasal hairs or carbonaceous debris in the mouth
71
or pharynx or in the sputum. The specific changes are 9%
dependent on the type of substances inhaled at the time
of injury. In addition, the size of the smoke particles that
are inhaled will affect the location of any injury. If coarse
smoke particles are inhaled, these will primarily be
deposited in the upper tracheobronchial tree, whilst fine 18% 18%
smoke particles will usually be lodged in the alveoli.
Patients with inhalation burn injury will usually experi- Front
ence upper airway oedema and bronchospasm in the 9% 18% 9%
early stages, with the airway disease progressing to the 18%
small airways in subsequent days. 71,72,75 Back 9% Front
1% 9%
Clinical Manifestations 18%

The most prominent clinical manifestations of burn Back
injury are the dermal signs of injury. ANZBA categorise
burns as follows: 74 18% 18%
1. Epidermal burns are limited to injury to the epi-
dermis and tend to be very painful, with a common 14% 14%
example being sunburn. The skin is pink to red in
colour and remains intact. The surrounding tissues
may be oedematous and there is no blistering. This
burn injury will usually heal within 7 days.
2. Superficial partial-thickness burn injury involve A B
the epidermal and superficial dermal layers and are 78
generally red or mottled in appearance and the FIGURE 23.7 Diagram of the ‘rule of nines’ (A), adult; (B), child.
underlying skin will blanch with pressure, demon-
strating that perfusion is intact; blisters are a hall-
mark symptom. This degree of burn injury is very
painful and healing may take up to 14 days. There pinprick is lost. The coagulated dead skin of a full
is usually a lot of wound exudate in the first 72 thickness burn, which has a leathery appearance,
hours where the skin is broken. is called eschar.
3. Mid-dermal partial-thickness injuries extend a part
way into the dermis. They have a large zone of Assessment of the total body surface area
damaged non-viable tissue extending into the (TBSA) of burns
dermis, with damaged but viable tissue at the base. The extent of injury is best described using the percentage
Preservation of the damaged but viable tissue of the total body surface area that sustained burns. The
(particularly in the initial period following injury) measurement of burn surface area is important during
is pivotal to preventing burn wound progression. the initial management of people with burns for estimat-
As some of the nerve endings remain viable, pain ing fluid requirements and determining need for transfer
is present but is less severe when compared to to a burns service. Erythema should not be included
superficial burns. Similarly, as some of the capil- when calculating burn area.
laries remain viable, capillary return is present, There are several methods that provide a reproducible
albeit delayed. Blisters may be present and the estimation of the area of surface area burns. These are:
underlying dermis is a variable colour (pale to
dark pink). l Rule of Nines: for the adult population, the most
4. Deep partial-thickness burns extend into the deep widely known and easily applied method of estimat-
dermal layer. The tissue is a characteristic pink to ing TBSA is the ‘rule of nines’ (see Figure 23.7). The
pale ivory in appearance. It can also have a blotchy principle of this assessment method is that most areas
red base due to extravasation of red blood cells. of the body constitute 9% (or multiples of 9%) of
The underlying tissue does not blanch and the hair the TBSA.
is easily removed; sensation is reduced. These l Palmar surface: the surface area of a patient’s palm
burns usually take in excess of 3 weeks to heal and (including fingers) is about 1% total body surface
are managed with surgical excision and closure. area. This method of estimating TBSA is commonly
5. Full-thickness burns destroy both layers of skin taught in emergency medicine courses but is yet to be
(epidermis and dermis) and may penetrate more validated. The Palmar surface method can be used to
deeply into underlying structures. These burns estimate relatively small burns (<15% of total surface
have a dense white, waxy or even charred appear- area) or very large burns (>85%, when unburnt
ance. The sensory nerves in the dermis are destroyed skin is counted). For medium sized burns, it is
in a full thickness burn, and so sensation to inaccurate.

Trauma Management 647



TABLE 23.12 Acute nursing care after burn injury (first 24 hours)

Monitoring Minor burn injury (<10%) Major burn injury Critically ill
Fluid replacement Generally not fluid loaded. Fluid replacement as per relevant Major fluid replacement.
formula.
Need for intubation Supplemental oxygen therapy. Only if Supplemental oxygen therapy. Mandatory.
and mechanical airway burns are suspected or Intubation and mechanical
ventilation co-morbidities require it. ventilation may be required with
analgesia and in burns shock. Any
airway burn in this group requires
intubation.
Respiratory and Hourly TPR, BP, SpO 2 adapted according Continuous ECG, SpO 2 , temperature, Continuous invasive haemodynamic,
cardiovascular to patient status. urine output (hourly observations respiratory and urine output
observations if not continuously monitored). monitoring, including core
temperature.
Neurovascular Assess neurovascular status of Assess neurovascular status of Assess neurovascular status of
observations circumferential burns to chest and circumferential burns to chest and circumferential burns to chest and
limbs (including fingers and toes). limbs (including fingers and toes). limbs (including fingers and toes).
Analgesia Continuous, intermittent or patient- Continuous intravenous analgesia Continuous intravenous analgesia +
controlled (if patient capable) ±conscious sedation for dressings. sedation.
analgesia.
±conscious sedation for dressings.
Arterial blood gas, Baseline and as indicated by patient’s Baseline and as indicated by Baseline and minimum 4-hourly
serum potassium; condition. patient’s condition. depending on patient’s condition,
chloride and including temperature and
haemoglobin ventilatory requirements.
Haematology Baseline and as indicated by patient’s Baseline and as indicated by Baseline and as indicated by
condition. patient’s condition, noting that patient’s condition, noting that
more frequent assessment will be more frequent assessment will be
needed if coagulopathy is present. needed if coagulopathy is present.
Feeding Oral intake should be monitored and Enteral or oral intake should Enteral feeding should commence
encouraged. commence within 24 hours of within 24 hours of injury.
injury (note: burns of >20% TBSA
require enteral feeding).
General burn Primary debridement undertaken by Primary debridement undertaken by Primary debridement undertaken
dressings nursing staff with theatre nursing staff with theatre by nursing staff with theatre
debridement if indicated due to burn debridement if indicated due to debridement if indicated due to
depth. burn depth. burn depth.
Burn escharotomy as indicated (unlikely Burns echarotomy as indicated Burns escharotomy as indicated
unless circumferential injury). (likely with circumferential injury). (highly likely).






Nursing Practice minutes. This is most useful immediately after injury but
Care can be considered in two categories; the first is the can be instigated for 3 hours post-injury. The wound and
immediate priorities of care (outlined below) and includ- the patient should then be covered to reduce risk of hypo-
ing emergency principles, assessment and management thermia. Adequate analgesia must be provided early in
of airway, breathing and circulation, and minimisation of patient care.
hypothermia and hyperkalaemia. The second category of
care is that provided throughout the first 24 hours (see Airway
Table 23.12). Care of the burn patient beyond that time All patients with burn injury require supplemental
will follow the general principles for patients with com- oxygen. Facial burns or carbonaceous sputum (sputum
promise to one or more of the systems, with additional with signs of smoke or charcoal) may indicate a burn
considerations relating to wound care. injury to the airway. A carboxyhaemoglobin of >10%
within the first hour post-injury is strongly indicative of
Emergency principles of care inhalation injury. Classic signs of obstruction including
The patient should be removed from danger and the stridor, dyspnoea and hoarse voice warrant immediate
burning process should be stopped. The wound should intubation and should be considered early as worsening
then be cooled to minimise the burden of injury. ANZBA oedema can make intubation difficult. Airway stability is
recommend the application of cool running water for 20 mandatory for safe transfer. 71,72

648 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Breathing minimising exposure, warming fluids and warming the
Carbonaceous pulmonary secretions are a hallmark of patient’s environment. Warm blankets and heated humid-
airway injury. Dyspnoea and tachypnoea are signs of ified supplemental oxygen are also valuable adjuncts.
respiratory distress, while pulmonary oedema will often
ensue with airway burns. Hyperkalaemia
Cell destruction from the burn injury can result in high
Circulation serum potassium levels, which should be monitored
The massive interstitial and intracellular fluid shifts asso- closely. Metabolic acidosis will exacerbate the hyperkalae-
ciated with acute burn injury will deplete circulating mia, as intracellular exchange of hydrogen ions with
volume and result in shock if it remains uncorrected. potassium ions takes place.
Fluid resuscitation aims to anticipate and prevent rather
than treat shock. ANZBA guidelines recommend IV resus- Nutrition
citation in adults with burns >15% TBSA and children Supplemental feeding is mandatory and should com-
with burns >10% TBSA. mence as soon as possible following severe burn injuries
due to the hypermetabolism. Patients with >20% TBSA
Early intravenous cannulation (with two wide-bore can-
nulae) and the administration of high-volume fluids are unable to meet their nutritional requirements orally.
must begin immediately. ANZBA recommends crystalloid ANZBA recommends enteric feeding in adults with burn
solution in the first 24 hours. There are several fluid injury >20% and >10% TBSA in children.
replacement formulas, these are considered as a resuscita-
tion guideline with fluid administration being titrated to The Multitrauma Burns Patient
patient response. One of the most widely accepted resus- Burn is not always an isolated injury, and can occur in
citation formulas is the Modified Parkland formula, that the presence of other trauma (e.g. multitrauma). It is
recommends delivery of Hartmann’s solution at the rate essential to combine the principles of care of the burns
of 3–4 mL/kg/% TBSA over the first 24 hours commenc- patient with those of the relevant injury as outlined:
ing at the time of burn injury, with half the fluid admin- l Spinal injury: if the patient has potential spinal inju-
istered within the first 8 hours and the remainder over ries in addition to the burn, spinal precautions must
the next 16 hours. Time delays for implementation of be maintained; however, cervical collars should not be
fluid resuscitation should be corrected by increasing infu- used over a burnt neck or upper chest due to the
sion rates to reach targets. Fluid resuscitation should be potential for swelling and subsequent restriction. If a
guided by predetermined endpoints in combination with collar is used, changing to an appropriate size as the
fluid volumes dictated by the formula. Precise endpoints swelling worsens or goes down is essential.
for burns resuscitation remain debatable, at present l Skeletal injury: skin traction cannot be used in a
ANZBA recommends urine output of 0.5–1 mL/kg/hr in patient with burn injury over a limb that also has a
adults and 0.5–2 mL/kg/hr in children. skeletal fracture; this will necessitate early internal
Patients with circumferential full thickness burn injury fixation or the use of an external fixateur.
may require escharotomies due to the extensive oedema l Electrocution injuries: electrocution burns are largely
formation and the inelasticity of burn eschar. Delayed internal burns that potentially cause devastating mul-
capillary return, a cool limb and increased pain manifest tiple internal injuries. The electrical current causes a
earlier than loss of palpable pulse. burn at both the entry and exit sites. Where electrocu-
tion is confirmed or suspected the body must be
The use of invasive monitoring in the burns patient is inspected to identify all injuries. These may be in
controversial, as the relevant catheters often require inser- obscure places such as the hands and feet or even the
tion through a burn and therefore provide a portal of back and scalp. Close monitoring for cardiac damage
entry for infection. However, all serious burns patients and rhabdomyolysis is essential.
require an indwelling catheter for monitoring. Relevance
of other monitoring capability will be made on an indi- Burn Dressings
vidual patient basis, based on cardiovascular status, need
for inotropic support, extent of the burn and potential Mitigating infection is the primary aim of good burns
68
for infection. nursing. The greatest challenge is minimising the risk
for cross-contamination, and patients should be nursed
in a single room where possible. Burn dressings present
Minimising hypothermia a physical challenge, particularly when large areas of the
Skin is an essential component of the body’s natural body are affected.
thermoregulation mechanism, so loss of skin integrity, The traditional burn dressing in the ICU is undertaken as
coupled with such treatment strategies as cooling the a surgically clean technique. As part of the management
burn and administering high-volume fluid replacement, of the burn injury, there are a number of specific issues
exposure of wounds following injury and during dressing that require attention. The following is a guide to specific
changes places the patient at high risk of hypothermia. aspects of burn management:
Continuous temperature monitoring is essential, and
strategies to maintain normothermia should be imple- l Debridement: this refers to the excision of dead skin.
mented immediately and continuously. Strategies include Gentle scrubbing is generally used to remove loose

Trauma Management 649

tissue and burst blisters. Forceps and scissors may be l Skin substitutes: some products are available to
required to lift and remove smaller areas of tissue. cover partial-thickness wounds that provide a moist
Extensive areas of debridement will usually be under- environment that stimulates epithelialisation. These
taken in the operating room. are best reserved for ‘clean’ wounds. Some products
l Blisters: small blisters should be left intact, large blis- are able to act as full-thickness substitutes that provide
ters may be aspirated or deroofed during debride- wound closure, protection from mechanical trauma
ment, although it should be noted that evidence and bacteria and a vapour barrier. Once the new
regarding blister management is poor. Blisters over dermis is created the substitute is removed. 71
joints that are restricting movement should also be
debrided. SUMMARY
l Escharotomy: an escharotomy is undertaken to a limb
or side of the trunk for circumferential burns that are Care of the trauma patient presents the critical care nurse
contracting and creating vascular compromise to the with multiple challenges. With the introduction of
underlying and distal tissues. The escharotomy is an Trauma Systems the outcome and survival of injured
incision through the eschar, and does not involve patients has improved dramatically. The severity of injury,
opening muscle fascia. The escharotomy immediately and patient outcome, are dependent on effective prehos-
relieves the compression and is a limb/lifesaving sur- pital care, resuscitation, definitive surgical management
gical manoeuvre. The escharotomy is dressed as a burn on arrival at the hospital. Principles of resuscitation of
to prevent infection. the trauma patient are the same as that for all patients,
l Skin grafts: these are required to cover the skin defect. with a primary, secondary and tertiary survey being
They may be full-thickness or partial-thickness grafts, undertaken, and maintenance or correction of airway,
and may be harvested from the patient or, in some breathing and circulation taking precedence. Prevention
cases, obtained from a cadaver donor. Regardless of of the ‘trauma triad’ of hypothermia, acidosis and coagu-
the type of skin graft, nursing care remains the same, lopathy has the potential to significantly influence
with the aim being to maximise adherence. Specific patient outcome. Consideration of the specific injury,
nursing care of the graft site includes leaving the site with its resultant pathophysiological changes, is neces-
intact and immobilising the graft site, applying the sary to care effectively for patients with abdominal, chest,
appropriate wound care regimen, preventing shearing multiple or burn injuries. It is challenging work as trauma
injury to the graft site, and minimising the risk for patients are largely a young and healthy population
infection. With autografts, wound care will also be prior to injury and may experience significant ongoing
required for the donor site. 71 compromise.


Case study ‡

Chris was a 26-year-old, 120 kg, driver of a small sports car that ran l primary survey and associated resuscitation
a red light in rural Victoria. An oncoming delivery truck collided l intubation and mechanical ventilation
with the driver’s side at a high rate of speed. He was mechanically- l no cervical collar would fit him, so he was nursed with bilateral
trapped in the vehicle for over 80 minutes. On arrival of the emer- sandbag and head strapping
gency personnel his vital signs were as follows: l analgesia and sedation
l HR 110, RR not recorded, sBP 155 mmHg on palpation, GCS 15, l FAST exam gave a positive result
SpO 2 89% l CT of brain, cervical spine, chest, abdomen and pelvis.
l There was palpable surgical emphysema of the chest wall; a
tension pneumothorax was diagnosed. A pneumocath was Injuries included: C2 odontoid # (type 2) with 3.5 mm complete
inserted and an audible hiss was heard, with subsequent separation; a # R transverse process of C7 that extended into the
improvement in the patient’s vital signs. foramen transverserium; a # R transverse process of T1, bilateral rib
l IV cannula inserted with 1000 mL of Hartmann’s solution fractures with R sided flail segment in ribs 1–4, a # R pneumothorax
administered during extrication. Extrication was slow due to and sternal fracture. A Grade 3 Liver laceration, a fracture disloca-
the door of the car having to be removed and the patient’s tion of the R humeral head, right sided forearm degloving and
body habitatus, being 120 kg and 168 cm tall. scalp laceration injuries were also present.
l Chris met the major trauma triage criteria and was transferred In ICU the neurosurgical team documented that Chris was ‘not to
via helicopter, with a trauma team call activated prior to arrival. be moved’ as spinal stability could not be achieved due to the
When Chris arrived at the emergency department, a full team inability to fit an appropriate neck collar. A request was made for
was present to assess and treat him. This included a trauma an MRI, CT shoulder and angiogram to be completed before a
surgeon, emergency physician, trauma nurse leader, specialist halothoracic brace was to be fitted. After consultation with the
nurses and support staff. medical team 8 nurses log-rolled Chris with a head hold, and
placed a slide sheet and trauma spinal mat under him to facilitate
Treatment in the emergency department consisted of the movement between bed and radiology surfaces without further
following: movement.

‡ The authors acknowledge the assistance of Catherine Birch RN, Intensive Care Unit, The Alfred Hospital.

650 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E



Case study, Continued
Chris was ventilated in pressure control mode due to high peak embolised. Follow-up hematocrits were low but stable.
inspiratory pressures (PIPs). Sedation medication was increased to Follow-up CT showed no further increase in size of
facilitate ETT intolerance, and inotropes were required to maintain haematoma.
MAP goals. Continuous haemodynamic monitoring was required,
with target parameters within normal ranges. Serial ABGs, haemo- A surgical tracheostomy was performed due to prolonged ventila-
globin and coagulation profiles were also undertaken. tion wean, and allowed weaning of sedation. The Speech Pathol-
ogy department reviewed Chris and a Passy-Muir speaking valve
Teams involved in Chris’ care, and their reports, included: was used to assist him in communicating with his family.
l Cardiothoracic: flail chest, however no surgical intervention
required. Due to his size, a specialised chair that lay flat to allow transfer from
l Orthopaedics: # humerus, surgically fixed and placed in sling bed and is then moved into an upright position, allowed Chris to
with no internal rotation, and minimal external rotation for sit out of bed. Prior to surgical fixation of his spine CD was placed
dressings only. in a reverse Trendelenburg position to minimise axial loading on
l Plastics: degloving injuries, with a radial reverse forearm flap the C2 fracture when sitting to 30°.
performed. Prolonged bed rest, multiple skin folds and restricted movement
l Neurosurgery and orthotics: C2 # with Halothoracic brace contributed to a Grade 3 pressure area under Chris’ halothoracic
applied, posterior spinal fixation and reapplication of halo tho- brace and right shoulder. A treatment plan was developed that
racic brace for 3 weeks to provide further stabilisation. Inter- consisted of reducing the pressure by having the brace adjusted
mittently pre- and post-surgical fixation, Chris was noted to and regular dressings to debride the wound and provide an envi-
have absent movement in his lower limbs. Somato-Sensory ronment conducive to regranulation.
Evoked Potentials were undertaken which demonstrated bilat-
eral nerve conduction present. Chris’ girth precluded MRI A social worker met with Chris’ parents and his sister. Chris spent 4
investigation. weeks in ICU before being discharged to the ward and then to a
l Trauma Team: grade 3 liver laceration with positive FAST. As rehabilitation facility as he had significant muscle weakness due to
initial vital signs were stable, interventional radiology con- his myopathy from prolonged immobility. There was no ongoing
sulted for hepatic angiogram. A vessel of the hepatic artery was weakness as a result of spinal cord injury.




Research vignette

Ireland S, Endacott R, Cameron P, Fitzgerald M, Paul E. The incidence with a threefold independent risk of death: (OR (CI 95%)) 3.44
and significance of accidental hypothermia in major trauma – A (1.48–7.99), P = 0.04. Independent determinants for hypothermia
prospective observational study. Resuscitation 2011; 82(3): were prehospital intubation: (OR (CI 95%)) 5.18 (2.77–9.71),
300–306. P < 0.001, Injury Severity Score (ISS): 1.04 (1.01–1.06), P = 0.01,
Arrival Systolic Blood Pressure (ASBP) < 100 mmHg: 3.04 (1.24–
Abstract 7.44), P = 0.02, and wintertime: 1.84 (1.06–3.21), P = 0.03.
Background
Serious sequelae have been associated with injured patients who Of the 87 hypothermic patients who had repeat temperatures
are hypothermic (<35°C) including coagulopathy, acidosis, recorded in the Emergency Department, 77 (88.51%) patients had
decreased myocardial contractility and risk of mortality. a temperature greater than the recorded arrival temperature. There
was no change in recorded temperature for four (4.60%) patients,
Aim whereas six (6.90%) patients were colder at Emergency Depart-
Establish the incidence of accidental hypothermia in major trauma ment discharge.
patients and identify causative factors.
Conclusion
Method Seriously injured patients with accidental hypothermia have a
Prospective identification and subsequent review of 732 medical higher mortality independent of measured risk factors. For patients
records of major trauma patients presenting to an Adult Major with multiple injuries a coordinated effort by paramedics, nurses
Trauma Centre was undertaken between January and December and doctors is required to focus efforts toward early resolution of
2008. Multivariate analysis was performed using logistic regres- hypothermia aiming to achieve a temperature >35°C.
sion. Significant and clinically relevant variables from univariate
analysis were entered into multivariate models to evaluate deter- Critique
minants for hypothermia and for death. Goodness of fit was deter- All major trauma patients presenting for treatment of injury were
mined with the use of the Hosmer–Lemeshow statistic. enrolled into this prospective observational study. For this study,
the definition of major trauma is a surrogate of injury severity and
Main results risk of dying. However this criterion is not based on time critical
Overall mortality was 9.15%. The incidence of hypothermia was clinical criteria. Therefore this study design did have the propensity
13.25%. The mortality of patients with hypothermia was 29.9% of missing time-critical patients who had threat-to-life conditions

Trauma Management 651



Research vignette, Continued
that were reversed or did not result in death. The other major dying for those patients who were hypothermic on arrival to the
trauma criteria include the admission to ICU with ventilation or trauma centre in the study population. This was independent of
specified urgent surgery for intracranial, truncal, spine or pelvic measured risk factors. The researchers highlight a number of key
injury. points in their discussion that are supported with the results from
this sample population. Of particular note is the discussion around
The inclusion criteria included adults who presented with serious
injury and met the major trauma patient criteria as described by mitigating strategies for heat loss which was supported by this
the Victorian State Trauma System definition. Exclusions were study, with only a small number of patients failing to warm in the
those aged <18 years of age and all non-traumatic cardiac arrest ED. This supports the utility of nursing strategies to prevent heat
patients. It must be remembered that the state of Victoria in loss and facilitate patient warming.
Australia has a State-based trauma system that funnels all major Fundamentally, this is a well-designed and executed study,
trauma patients into two Level 1 adult trauma centres. With the however, limiting the study population to a predetermined major
caseload of The Alfred Hospital, this makes this study cohort a large trauma definition was a lost opportunity. While outcomes such as
and representative sample of major trauma across both an urban mortality, ICU length of stay (LOS) and hospital LOS are important
and rural settings. endpoints, this study missed an important subset of time-critical
minor trauma patients who present hypothermic. Using time-
The study identified hypothermia as a temperature <35°C on arrival critical status, such as trauma team activation, as inclusion criteria
to the trauma centre. The researchers also collected a variety of would have captured that subset of minor trauma patients. While
other parameters to help describe the nature and characteristics that group are not high users of ICU, they are high consumers of
of the hypothermic patient population. Mechanism of injury, pre- hospital services and subject to complications of injury such as
hospital time and prehospital intubations, mortality, ICU admis- infection, identified to be statistically significant in the hypother-
sion, the Injury Severity Score and length of stay were all included mic population. This study demonstrates the clinical significance
in the analysis. Data analysis consisted of both univariate and and incidence of accidental hypothermia in a major trauma popu-
multivariate analyses which incorporate many of the potential lation from an inclusive established state-based Trauma System.
confounders.
The implications for nursing are significant as over 10% of major
Of the 820 patients eligible for inclusion into the study, 732 were trauma patients have the potential to be hypothermic on arrival to
included for analysis. The enrolled population was representative the ED. This was irrespective of season or time of day. Nurses must
of the spectrum of injury including age and gender distributions. be vigilant in looking for, mitigating and reversing, hypothermia as
The key finding of this study was a threefold increase in risk of it is associated with a three-fold increased risk for death.




Learning activities

Learning activities 1–5 relate to the clinical case study. 6. Briefly describe the tenets on which all trauma systems are
1. Describe the implications of the type of accident experienced based.
by Chris for his likely injuries and treatment. 7. Undertake a trauma tertiary survey assessment, discussing the
2. Explain the rationale for pleural decompression and manage- process and findings with a senior clinical colleague.
ment of a pneumothorax in the early care of Chris. 8. Briefly describe why the mechanism of injury is important
3. Discuss the components of the ‘trauma triad’ and outline prac- information in diagnosing injuries.
tices that should be undertaken to prevent or ameliorate the 9. Describe why the patient’s positioning in the bed is an impor-
triad. tant consideration for trauma nursing care.
4. Identify the likely causes of Chris’ respiratory failure and agita- 10. What is ‘damage-control surgery’ and why is this so important
tion and discuss the various preventive and treatment to survival in trauma patients?
approaches that are available. 11. Describe the nursing observations of a patient with an inter-
5. Describe the practices that could be incorporated in Chris’ care costal underwater seal drainage system in situ.
to reduce his psychological distress.



NSW Trauma Management Guidelines, http://www.itim.nsw.gov.au/go/
ONLINE RESOURCES itim-trauma-guidelines
Royal Australasian College of Surgeons, www.surgeons.org
American College of Surgeons, www.facs.org Society of Trauma Nurses, www.traumanursesoc.org
Australasian College of Emergency Medicine, www.acem.org.au Victorian State Trauma System http://www.health.vic.gov.au/trauma/review99/
Australasian Trauma Society, www.atsoc.com.au index.htm
Australian and New Zealand Burn Association, http://www.anzba.org.au/ World Health Organization, http://www.who.int/topics/injuries/en/
Eastern Association for the Surgery of Trauma, www.east.org
An independent, non-profit organisation providing global education, information FURTHER READING
and communication resources for professionals in trauma and critical care,
www.trauma.org Moloney-Harmon PA, Czerwinski SJ. Nursing care of the paediatric trauma patient.
NSW Trauma System, http://www.itim.nsw.gov.au/index.cfm Cambridge: Elsevier; 2003.

652 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Langstaff D, Christie J. Trauma care: a team approach. Oxford: Butterworth- 27. Richards CF, Mayberry JC. Initial management of the trauma patient. Crit
Heinemann; 2000. Care Clin 2004; 20(1): 1–11.
McQuillan K, Whalen E, Flynn-Makick, M. Trauma nursing: from resuscitation 28. Aitken LM, Lang JH, Bellamy N. Queensland Trauma Registry: description of
through rehabilitation, 4th edn. Philadelphia: Saunders; 2008. serious injury throughout Queensland, 2003. Herston: Centre of National
Research on Disability and Rehabilitation Medicine; 2004.
29. National Trauma Registry Consortium (Australia and New Zealand).
REFERENCES National Trauma Registry report, 2002. Herston: NTRC; 2004.
30. Department of Human Services.Victorian State Trauma Outcome Registry
1. New Zealand Health Information Service. Selected morbitity data for publicly and Monitoring Group. Victorian State Trauma Registry: 1 July 2002–30 June
funded hospitals 2000/01. Wellington: Ministry of Health; 2004. 2003, summary report. Melbourne: Department of Human Services; 2004.
2. Peden M, McGee K, Krug E. Injury: a leading cause of the global burden of 31. Hadley MN, Walters BC, Grabb PA, Oyesiku NM, Przybylski GJ et al. Guide-
disease. Geneva: World Health Organization; 2002. lines for the management of acute cervical spine and spinal cord injuries.
3. Bonnie RJ, Fulco CE, Liverman CT. Reducing the burden of injury: advancing Clin Neurosurg 2002; 49: 407–98.
prevention and treatment. Washington: National Academy Press; 1999. 32. Jacobson T, Tescher A, Miers A, Downer L. Improving practice: efforts to
4. Australian Institute of Health and Welfare (AIHW). Australia’s Health, 2010. reduce occipital pressure ulcers. J Nurs Care Qual 2008; 23(3): 283–8.
Canberra: AIHW; 2010. 33. Kheirbek T, Kochanek A, Alam H. Hypothermia in bleeding trauma: a friend
5. Tobias M. The burden of disease and injury in New Zealand. Wellington: or foe? Scand J Trauma, Resusc Emerg Med 2009; 17: 65–80.
Ministry of Health; 2001. 34. Hess J, Brohi K, Dutton RP, Hauser CJ, Holcomb JB et al. The coagulopathy
6. Mathers C, Vos T, Stevenson, C. The burden of disease and injury in Australia. of trauma: a review of mechanisms. J Trauma 2008; 65(4): 748–54.
Canberra: Australian Institute of Health and Welfare; 1999. 35. D’Angelo MR, Dutton RP. Management of trauma-induced coagulopathy:
7. Mock C et al. Guidelines for trauma quality improvement programmes. Geneva: trends and practices. AANA 2010; 78: 35–40.
World Health Organization; 2009. 36. Langhelle A, Lockey D, Harris T, Davies G. Body temperature of trauma
8. Mann NC, Mullins RJ, Hedges JR, Rowland D, Arthur M et al. Mortality patients on admission to hospital: a comparison of anaesthetised and non-
among seriously injured patients treated in remote rural trauma centers anaesthetised patients. Emerg Med J 2010, DOI: 10.1136/emj.2009.086967.
before and after implementation of a statewide trauma system. Medical Care 37. Frith D, Brohi K. The acute coagulopathy of trauma shock: clinical relevance.
2001, 39(7): 643–53. Surgeon 2010; 8(3): 159–63.
9. Hoyt DB, Coimbra R. Trauma systems. Surgical Clinics of N America 2007; 38. Clement N, Tennant C, Muwanga C. Polytrauma in the elderly: predictors
87: 21–35. of the cause and time of death. Scand J Trauma Resusc Emerg Med 2010; 18:
10. Cameron PA, Gabbe BJ, Cooper DJ, Walker T, Judson R, McNeil J. A statewide 26.
system of trauma care in Victoria: effect on patient survival. Med J Aust 2008; 39. Ireland S, Endacott R, Cameron P, Fitzgerald M, Paul E. The incidence and
189(10): 546–50. significance of accidental hypothermia in major trauma – A prospective
11. Liberman M, Mulder DS, Jurkovich GJ, Sampalis JS. The association between observation study. Resuscitation 2011; 82(3): 300–306.
trauma systems and trama center components and outcom in a mature 40. Larson CR, White CE, Spinella P, Jones JA, Holcomb JB et al. Association of
regionalized trauma system. Surgery 2005; 137(6): 647–58. shock, coagulopathy and initial vital signs with massive transfusion in
12. Moore L, Hanley JA, Turgeon AF, Lavoie A. Evaluation of the long-term trend combat casualties. J Trauma 2010; 69(Suppl1): S26–32.
in mortality from injury in a mature inclusive trauma system. World J Surg 41. Ganter M, Pittet J. New insights into acute coagulopathy in trauma patients.
2010; 34: 2069–75. Best Pract Res Clin Anaesthesiol 2010; 24: 15–25.
13. Nirula R, Maier R, Moore E, Sperry J, Gentiello L Scoop and run to the 42. Fabian, T. Damage control in trauma: laparaotomy wound management
trauma center or stay and play at the local hospital: hospital transfer’s effect acute to chronic. Surg Clin N Am 2007; 87(1): 73–93.
on mortality. J Trauma 2010; 69: 595–601. 43. Duchesne JC, Kimonis K, Marr AB, Rennie KV, Wahl G et al. Damage control
14. Brown JB, Stassen NA, Bankey PE, Sangosanya AT, Cheng JD, Gestring ML. resuscitation in combination with damage control laparotomy: a survival
Helicopters and the civilian trauma system: national utilization patterns advantage. J Trauma 2010; 69(1): 46–52.
demonstrate improved outcomes after traumatic injury. Trauma 2010; 69(5): 44. Bosch X, Poch E, Grau J. Rhabdomyolysis and acute kidney injury. New Eng
1030–36. J Med 2009; 361(1): 62–72.
15. Shepherd MV, Trethewy CE, Kennedy J, Davis L. Helicopter use in rural 45. Williams-Johnson J, Williams E, Watson H. Management and treatment of
trauma. Emerg Med Australas 2008; 20(6): 494–9. pelvic and hip injuries. Emerg Med Clin North Am 2010; 28(4): 841–59.
16. Cherry R, King TS, Carney DE, Bryant P, Cooney RN. Trauma team activation 46. Guyton AC, Hall JE. Textbook of medical physiology. Philadelphia: WB Saun-
and the impact on mortality. JTrauma 2007; 63(2): 326–30. ders; 2011.
17. Kouzminova N, Shatney C, Palm E, McCullough M, Sherck J. The efficacy of 47. Pape H, Marcucio R, Humphrey C, Colnot C, Knobe M, Harvey EJ. Trauma-
a two-tiered trauma activation system at a level I trauma center. J Trauma induced inflammation and fracture healing. J Orthop Trauma 2010; 24(9):
2009; 67(4): 829–33. 522–5.
18. Zalstein S, Danne P, Taylor D, Cameron P, McLellan S, Fitzgerald M et al. 48. Jagodzinski M, Krettek C. Effect of mechanical stability on fracture healing–
The Victorian major trauma transfer study. Injury 2010; 41(1): 102–9. an update. Injury 2007; 38(S1): S3–10.
19. Garwe T, Cowan LD, Neas BR, Sacra JC, Albrecht RM. Directness of transport 49. Akhtar S. Fat embolism. Anesthesiology Clin 2009; 27(3): 533–50.
of major trauma patients to a level I trauma center: a propensity-adjusted 50. Lenarz CJ, Watson JT, Moed BR, Israel H, Mullen JD, Macdonald JB. Timing
survival analysis of the impact on short-term mortality. J Trauma; 2010, DOI: of wound closure in open fractures based on cultures obtained after debride-
10.1097/TA.0b013e3181e243. ment. J Bone Joint Surg Am 2010; 92(10): 1921–6.
20. Nocera N, Schoettker P. NEWS Checklist (Abstract). Aust Emerg Nurs 2001; 51. Fulkerson E, Egol K. Timing issues in fracture management: a review of
4(2): 31. current concepts. Bulletin of the NYU Hospital for Joint Diseases 2009; 67(1):
21. Inaba K, Branco BC, Lim G, Russell K, Teixeira, PGR, Lee K et al. The increas- 58–67.
ing burden of radiation exposure in the management of trauma patients. 52. Consortium for Spinal Cord Medicine. Early acute management in adults with
J Trauma; 2010, DOI: 10.1097/TA.0b013e3181ebb4d4. spinal cord injury: a clinical practice guideline for health-care providers. Washing-
22. Rozycki GS, Root HD. The diagnosis of intrabdominal visceral injury. ton DC: Paralyzed Veterans of America; 2008.
J Trauma 2010; 68(5): 1019–23. 53. Department of Human Services (Victoria). Victorian State Trauma Registry, 1
23. Gaarder C, Kroepelien CF, Loekke R, Hestnes M, Dormage J, Naess PA. July 2002-30 June 2003. Melbourne: Department of Human Services; 2004.
Ultrasound performed by radiologist – confirming the truth about FAST in 54. NSW Department of Health. NSW Trauma Minimum Data Set, 2003. Sydney:
trauma. J Trauma 2009; 67(2): 323–9. NSW Department of Health; 2004.
24. Kanz KG, Paul AO, Lefering R, Kay MV, Kreimeier U et al. Trauma manage- 55. Kulshrestha P, Munushi I, Wait R. Profile of chest trauma in a level I trauma
ment incorporating focused assessment with computed tomography in center. Trauma 2004; 57(3): 576–81.
trauma (FACTT) – potential effect on survival. J Trauma Manag Outcomes 56. The Alfred Hospital. Spinal Clearance Management Protocol, Updated 1.6.06.
2010; 4: 4. Victoria: The Alfred Hospital; 2006.
25. Delprado A. Trauma systems in Australia. Trauma Nursing 2007; 14: 93–7. 57. Keel M, Meier C. Chest injuries – what is new? Curr Opin Crit Care 2007;
26. Kohn MA, Hammel JM, Bretz SW, Stangby A. Trauma team activation criteria 13(6): 674–9.
as predictors of patient disposition from the emergency department. Acad 58. Lopez P, Arango J, Gallup TM, Cohn SM, Myers J et al. Diaphragmatic inju-
Emerg Med 2004; 11(1): 1–9. ries; what has changed over 20-year period? Am Surg 2010; 76(5): 512–16.

Trauma Management 653

59. Raghavendran K, Notter RH, Davidson BA, Helinski JD, Kunkel SL, Knight 70. World Health Organization. The WHO plan for burn prevention and care.
PR. Lung contusion: inflammatory mechanisms and interaction with other Geneva: WHO; 2008.
injuries. Shock 2009; 32(2): 122–30. 71. Grunwald T, Garner W. Acute burns. Plast Reconstr Surg 2008; 121(5): 311.
60. Schneider T, Volz K, Dienemann H, Hoffmann H. Incidence and treatment 72. Latenser BA. Critical care of the burn patient: the first 48 hours. Crit Care
modalities of tracheobronchial injuries in Germany. Interact Cardiovasc tho- Med 2009; 37(10): 2819–26.
racid Surg 2009; 8(5): 571–6. 73. Sheridan RL, Tompkins RG. What’s new in burns and metabolism. J Am Coll
61. Soreide K, Petrone P, Asensio J. Emergency throacotomy in trauma: rationale, Surg 2004; 198(2): 243–63.
risks and realities. Scand J Surg 2007; 96(1): 4–10. 74. Edgar D, Katsu A, eds. Burn survivor rehabilitation: principles & guidelines for
62. Holden A. Abdomen–Interventions for solid organ injury. Injury 2008; the allied health professional. Albany Creek: Australian & New Zealand Burns
39(11): 1275–89. Association; 2007.
63. Peitzman AB, Richardson JD. Surgical treament of injuries to the solid 75. Cancio LC. Airway management and smoke inhalation injury in the burn
abdominal organs: a 50-year perspective from the Journal of Trauma. patient. Clin Plast Surg 2009; 36(4): 555–67.
J Trauma 2010; 69(5): 1011–21. 76. McQuillan K, Whalen E, Flynn-Makic M, eds. Trauma nursing: from resuscita-
64. Alsayali M, Atkin C, Winnett J, Rahim R, Niggemeyer LE, Kossmann T. Man- tion through rehabilitation. Philadelphia: Saunders; 2008.
agement of blunt bowel and mesenteric injuries: experience at the Alfred 77. Australian and New Zealand Burn Association. Referral criteria to a burn unit.
Hospital. Eur J Trauma Emerg Surg 2009; 35(5): 482–8. [Cited April 2011]. Available from: http://www.anzba.org.au/index.php?
65. Rizoli S Mamtani A, Scarpelini S, Kirkpatrick AW. Abdominal compartment option=com_content&view=article&id=51&Itemid=58.
syndrome in trauma resuscitation. Curr Opin Anaesthesiol 2010; 23(2): 78. Newberry L, ed. Sheehy’s emergency nursing: principles and practice, 5th edn.
251–7. St Louis: Mosby; 2003.
66. Cheatham M, Safcsak K. Is the evolving management of intra-abdominal 79. Kozin S, Bertlet A. Pelvis and acetabulum. In: Kozin S, Bertlet A, eds. Hand-
hypertension and abdominal compartment syndrome improving survival? book of common orthopaedic fractures, 2nd edn. Chester: Medical Surveillance;
Crit Care Med 2010; 38(2): 402–7. 1992.
67. Malbrain M, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M et al. Results 80. Maher AB, Salmond SW, Pellino TA. Orthopedic nursing, 2nd edn. Philadel-
from the international conference of experts on intra-abdominal hyperten- phia: WB Saunders; 1998.
sion and abdominal compartment syndrome. I. Definitions. Intens Care Med 81. Hettiaratchy S, Dziewulski P. ABC of burns: pathophysiology and types of
2006; 32(11): 1722–32. burns. BMJ 2004; 328(7453): 1427–9.
68. Langley JM, Dodds L, Fell D, Langley GR. Pneumococcal and influenza 82. Hoffman JR, Mower WR, Wolfson AB, Todd KH, Zucker MI. Validity of a set
immunization in asplenic persons: a retrospective population based cohort of clinical criteria to rule out injury to the cervical spine in patients with
study 1990–2002. BMC Infectious Diseases 2010; 10: 219. blunt trauma. New Eng J Med 2000; 343(2): 94–9.
69. Victorian Spleen Registry. Recommendations for the prevention of infection in 83. Eckert KL. Penetrating and blunt abdominal trauma. Crit Care Nurse Q 2005;
asplenic or hyposplenic patients 2010. Victoria: The Alfred Hospital; 2010. 28(1): 41–59.

24 Resuscitation







Trudy Dwyer
Jennifer Dennett


management, rhythm recognition, administration of
Learning objectives medications and post resuscitation care. Resuscitation
involves many moral and ethical issues, such as family
After reading this chapter, you should be able to: presence during resuscitation, deciding when to cease or
l identify the clinical assessment used to identify sudden initiate resuscitation, and near-death experiences.
cardiac arrest (SCA).
l outline the role of the chain of survival in the management BACKGROUND
of SCA.
l outline the management of common arrhythmias Coronary heart disease (CHD) is the leading cause of
associated with SCA. death in most industrialised countries, with over half of
1-3
l describe the use of advanced airway adjuncts and these being due to sudden cardiac arrest (SCA). Despite
advances in CHD management, survival outcome figures
indications for use in SCA. from SCA remain poor. Survival after SCA is dependent
4-6
l discuss indications, actions and routes of administration of on the presenting rhythm, early defibrillation, effective
medications used in advanced life support. cardiopulmonary resuscitation and advanced life sup-
l describe the appropriate care of persons experiencing SCA port. Because the presenting rhythm with the majority
6
including specific circumstances such as the pregnant of witnessed SCAs is ventricular fibrillation, bystander
woman, electrical injuries and drowning. cardiopulmonary resuscitation and early defibrillation
l discuss current research in resuscitation. are the major interventions influencing outcome after
SCA. 2,6-7 It is possible that the number of ventricular
fibrillation/ventricular tachycardia (VF/VT) arrests is actu-
ally higher than reported, as often by the time the cardiac
Key words arrest team arrives the patient’s rhythm has deteriorated
to asystole. 8
resuscitation
cardiopulmonary resuscitation INCIDENCE/AETIOLOGY OF CARDIAC ARRESTS
advanced life support The prevalence of CHD varies worldwide, thus estimates
of the incidence of SCA are difficult to obtain. In Austra-
lia, CHD is the leading cause of disease burden (9%) and
INTRODUCTION accounts for 16.5% of all deaths. 9,10 There are many
factors that contribute to cardiac arrest. In adults, the
The continuum of critical illness for an individual can most common cause of cardiac arrest is a primary cardiac
11
span the period before and beyond hospital admission. event, with coronary artery disease accounting for up to
Resuscitation is often required outside the critical care 90% of all victims. 12,13 CHD is the most likely cause of
environment, and the ‘cardiac arrest’ team has evolved to death in those over 35 years of age, compared to non-
use a more proactive, early-intervention approach, utilis- cardiac causes such as drowning, acute airway obstruction
ing a range of systems and instruments to detect deterio- or trauma for people less than 35 years of age. 13
ration in patients’ clinical status (see Chapter 3). It is well While causes of cardiac arrest are numerous, most often
recognised that improved outcomes from cardiac arrest it is associated with ventricular fibrillation triggered by an
are dependent on early recognition and initiation of the acutely ischaemic or infarcted myocardium or primary
‘chain of survival’. This chapter introduces the resuscita- electrical disturbance. Causes of cardiac arrest may be
3
tion systems and processes in both the prehospital and separated into two categories, primary and secondary, as
the in-hospital settings. The chain of survival provides a displayed in Table 24.1.
framework for the management of the person experienc-
ing cardiac arrest and resuscitation in specific circum- Acute myocardial infarction (AMI) is the most common
stances. The chapter expands on the final link in the precursor to cardiac arrest. In victims of trauma, drug
654 chain, advanced life support, to outline advanced airway overdose and drowning, the predominant cause of cardiac

Resuscitation 655

as standardised recording of outcome data did not exist,
TABLE 24.1 Causes of cardiac arrest resuscitation endeavours could not be compared mean-
19
ingfully between countries. Consequently, the Inter-
Primary causes Secondary causes national Liaison Committee on Resuscitation (ILCOR)
was formed in 1992 to promote global discussion and
Acute myocardial infarction Cessation of breathing
Cardiomyopathy Airway obstruction consistency of guidelines between these international
19
Electrical shock (low- and high-voltage) Severe bleeding resuscitation councils. The AHA, ARC, NZRC, ERC and
Congenital heart disease (e.g. prolonged Hypothermia ILCOR guidelines are subject to constant review and
Q-T) Metabolic disturbance modification based on emerging scientific data. Guide-
Drugs Electrical disturbance lines and recommendations are classified according to
Trauma
Neuromuscular disease scientific evidence. The most recent substantive guide-
20
lines from ILCOR were published in October 2010, with
the ARC and NZRC guidelines published in January 2011.
arrest is asphyxia. Cardiac arrest in children is rare and While it is recognised there are differences between the
even more rarely sudden, 14,15 with the common causes various councils, this chapter primarily reports on the
being trauma, congenital heart disease, long QT syn- ARC and NZRC recommendations.
drome, drug overdose, hypoxia and hypothermia. The
most common arrhythmia in infants is bradycardia, and
the prognosis is especially poor if asystole is present. 14,16 SURVIVAL OF OUT-OF-HOSPITAL ARRESTS
Despite recent advances in resuscitation and technology,
PATHOPHYSIOLOGY the survival rate for out-of-hospital cardiac arrest (OHCA)
6
remains poor. Factors associated with higher rates of
In sudden cardiac arrest with cardiac origin, it is believed mortality for adults are: age over 80 years, unwitnessed
that myocardial ischaemia leads to ventricular irritability arrest, delays before commencing CPR, defibrillation
and the progression from ventricular tachycardia to ven- response times longer than 8 minutes, and non-
17
tricular fibrillation (VF) and ultimately asystole. After ventricular tachycardia/fibrillation rhythm. The outcome
21
the onset of VF (in animal studies), carotid arterial blood statistics for children after OHCA are similarly poor.
14
flow continues for approximately 4 minutes even in the Marked differences in the inclusion criteria and outcome
absence of cardiac compressions, as coronary perfusion definitions may, however, also explain the wide varia-
pressure (the pressure gradient between the aorta and the tions in survival rates from cardiac arrests. In recogni-
21
17
right atrium) falls over this period. This initial phase tion of these variations, the Utstein guidelines were
is characterised by minimal ischaemic injury, and it is developed and implemented to consistently document,
during this time that defibrillation is most likely to result monitor and compare out-of-hospital cardiac arrests.
in the restoration of a perfusing rhythm, while initiation These guidelines:
of effective cardiac compressions will increase the coro-
nary perfusion pressure. 17 l establish uniform terms and definitions for out-of-
hospital resuscitation
Progression of the cardiac arrest beyond 4 minutes results l establish a reporting template for resuscitation studies
in accumulation of toxic metabolites, depletion of high- to ensure comparability
energy phosphate stores, and the initiation of ischaemic l define time points and time intervals relating to
cascades. A high probability of irreversible cellular cardiac resuscitation
17
injury exists where a cardiac arrest extends for longer than l define clinical items and outcomes that emergency
10 minutes, and the return of a spontaneous circulation medical systems should gather
17
during this period may initiate a reperfusion injury (see l develop methods for describing resuscitation systems.
Chapter 11 for further discussion).
RESUSCITATION SYSTEMS SURVIVAL FROM IN-HOSPITAL ARRESTS
AND PROCESSES In-hospital resuscitation, as with OHCA, have survival
Many factors such as age, pres-
22,23
rates of around 20%.
Since the rediscovery of the effectiveness of closed-chest ence or absence of morbidity before or during the hospi-
cardiopulmonary resuscitation (CPR) in 1960 and its tal admission, absence of ‘not-for-resuscitation’ orders,
subsequent widespread adoption, CPR has saved the lives asystole and non-ICU location contribute to the low
18
of many, potentially ensuring years of productive life. in-hospital survival rates. 24,25
As CPR quickly became one of the most widely-used and
researched procedures, voluntary coordinating bodies MANAGEMENT
13
developed throughout the world. Organisations such as
the European Resuscitation Council (ERC), the American The overall aim of managing a patient in arrest is the
Heart Association (AHA), the New Zealand Resuscitation prompt restoration of a spontaneous perfusing rhythm
Council (NZRC), the Heart and Stroke Foundation of with minimal neurological dysfunction. It is well recog-
Canada, and the Southern African and Australian Resus- nised that successful outcome from cardiac arrest is
citation Councils (ARCs) established practice guidelines dependent on several key factors: (a) early recognition of
to improve standards in resuscitation, and coordinated cardiac arrest; (b) immediate effective CPR, (c) optimis-
resuscitation activities on a national basis. 19,20 However, ing response times, and (d) early defibrillation. 26,27 The

656 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

probability of an unsuccessful outcome grows with the always been adequate when a cardiac arrest occurs in the
length of time taken to restore spontaneous circulation. hospital, from the point of view of early recognition,
timeliness or availability of equipment or staff. 24,25 The
CHAIN OF SURVIVAL traditional cardiac arrest team responded to the seriously
To optimise a person’s chance of survival, the ‘chain of ill, but the patient was often not salvageable by the time
27
survival’ strategy has been developed, that represents the cardiac arrest team arrived. Two-thirds of in-hospital
the sequence of four events that must occur as quickly as cardiac arrests are potentially avoidable, with up to 84%
possible: early recognition, early CPR, early defibrillation of all in-hospital cardiac arrests demonstrating evidence
and postresuscitation care (see Figure 24.1). These time- of deterioration in the 6 to 8 hours preceding the arrest. 29,30
sensitive, sequential actions must occur to optimise a Consequently, in recent years there has been a move to
cardiac arrest victim’s chances of survival. Communities implement rapid response teams (RRT) that facilitate the
with integrated links along this chain have demonstrated early recognition and rapid management of critically ill
higher survival rates after OHCA than those with deficien- patients, for example the medical emergency team (MET),
cies in these links. 2 the patient-at-risk team (PART) and physiological track
and trigger systems (TTS) such as the medical early-
EARLY RECOGNITION OF CARDIAC ARREST warning system (MEWS) 31-33 (see Chapter 3 for further
The chain of survival begins with early recognition of a discussion). These teams replace the traditional cardiac
medical emergency and the activation of the medical arrest team by responding to a calling criteria based pri-
calling system. 2,28 However, the chain of survival has not marily on abnormal vital signs (see Table 24.2).


Chain of survival


Post resuscitation care
Early recognition and call for help Early CPR
Early Defibrillation



- to restore quality of life

- to prevent cardiac arrest

- to restart the heart
- to buy time
FIGURE 24.1 Chain of survival (Courtesy Koninklijke Philips Electronics NV).




TABLE 24.2 Early calling criteria
Children
Area Adults 0–12 months 1–8 years
Airway Threatened Threatened Threatened
Breathing All respiratory arrests All respiratory arrests All respiratory arrests
Respiratory rate <5 RR <20 RR <15
Respiratory rate >27 32 RR >50 RR >35
Grunting respirations
Circulation All cardiac arrests All cardiac arrests All cardiac arrests
Pulse rates <40 Pulse rates <70 Pulse rates <50
Pulse rates >140 Pulse rates >180 Pulse rates >160
Systolic BP <90 Systolic BP <50 Systolic BP <60
Capillary return >5 seconds
Marked pallor
Neurology Sudden fall in the level of Floppy Floppy
consciousness (fall in the Glasgow Unresponsive Unresponsive
Coma Scale score of ≥2 points) Depressed conscious level Depressed conscious level
Repeated or prolonged seizures Prolonged seizures Prolonged seizures
Other Any patient you are seriously Any patient you are seriously Any patient you are seriously
worried about who does not fit worried about who does not fit worried about who does not fit
the above criteria the above criteria the above criteria

Resuscitation 657

17
Early warning system calling criteria are widely displayed more anterior and acutely angled. The airway of an
around the hospital and the RRT is activated in the same infant is also more cartilaginous and can be easily
manner as the cardiac arrest team, ultimately resuscitat- occluded when the neck is hyperextended; in addition,
34
ing patients earlier. Recent reviews of the literature and the large tongue can easily fall back to obstruct the
40
meta-analyses show that in clinically unstable patients, pharynx. Hence, the head of an infant should be main-
early access – including early recognition and interven- tained in the neutral position, whereas a child aged 1–8
tion by a MET/rapid response system – can reduce the will require the ‘sniffing position’ with varying degrees
incidence of cardiac arrests outside ICUs, however there according to age. The chin-lift and head-tilt manoeuvres
are inconsistent findings regarding their impact on inten- may be used in children to obtain the appropriate amount
sive care admission rates and lowering hospital mortality of positioning for age. Jaw thrust may be used if head-tilt/
40
rates. 35-37 To further facilitate earlier activation of the RRTs chin-lift is contraindicated. Do not use the finger sweep
family and patients have been provided with a means to to clear the airway of an infant, as this may result in
activate the team on a patient’s behalf. 38 damage to the delicate palatal tissues and cause bleeding,
which can worsen the situation. Use of finger sweep can
BASIC LIFE SUPPORT force foreign bodies further down into the airway.
40
When a patient is identified as in potential or actual Suction is more useful for removing vomitus and
arrest, a primary and secondary survey should be con- secretions.
ducted in the DRSABCD sequence: 39
l Danger. Check for danger (hazards or risks or safety)
l Responsive. Check for response (if responsive/
unconscious) Practice tip
l Send. Send for help Infants are obligatory nose-breathers, so it is always important
l Airway. Open the airway. Airway assessment is under- to clear the nostrils.
taken to establish a patent airway while maintaining
cervical spine support (if injury is suspected)
l Breathing. Check breathing. Breathing includes the
assessment and establishment of breathing, noting Breathing
rate, pattern, chest movement and tissue oxygenation
l CPR. Start CPR. Give 30 chest compressions (almost To assess for the presence of breathing, look, listen and
two compressions/second) followed by two breaths. feel for breath sounds for no more than 10 seconds. If the
l Defibrillation. Attach an automated external defibril- person is unresponsive with absent or abnormal breath-
lator as soon as available and follow its prompts. ing, call for help and compressions should be com-
menced immediately. Agonal gasps are not to be
Continue CPR until responsiveness and normal breath- considered as normal breathing. Typically, the arterial
ing return. Ideally, these interventions are performed blood will remain saturated with oxygen for several
simultaneously or in rapid sequence and will take no minutes following the cardiac arrest and as cerebral and
longer than 60–90 seconds to complete. This systematic myocardial cell oxygenation is limited more by the
approach correlates closely with the principles of basic absence of cardiac output as opposed to the reduced
life support (BLS), in that where a life-threatening abnor- PaO 2 , effective compressions are more important than
mality is detected, immediate intervention is required rescue breaths. 27
before further assessment (see Figure 24.2).
Airway CPR
Recognition of airway obstruction includes listening for Individuals should commence cardiac compressions if
inspiratory (stridor), expiratory or grunting noises. The the victim is unconscious, unresponsive, not moving
work of breathing can be assessed by the respiratory rate, and not breathing normally. Where possible, change
intercostals, subcostal or sternal recession, use of acces- the person delivering the compressions every two
sory muscles, tracheal tug or flaring of the alae nasi. minutes. Pulse check by lay rescuers and health profes-
Nasal flaring is especially evident in infants with respira- sionals in BLS is not recommended. Assessment of effec-
tory distress. Noisy breathing is obstructed breathing, tive chest compression by healthcare professionals may
but the volume of the noise is not an indicator of the be made by continuous end tidal CO 2 (ETCO 2 ) moni-
severity of respiratory failure. Should obstruction to air toring. For CPR to be effective the patient should be
flow be detected, then the airway should be opened flat, supine and on a firm surface. The chest should be
using three manoeuvres: the head-tilt, chin-lift and jaw compressed in the midline over the lower half of the
thrust. The ARC recommends assessing a person’s airway sternum, which equates to the ‘centre of the chest’, at
without turning them onto the side unless the airway is a depth of more than 5 cm (in adults) and at a rate
obstructed with fluid (vomit or blood) or submersion of 100 compressions per minute for adults, infants and
injuries. 39 children, with the rate rising to 120/min for the
27
newborn. CPR should be initiated when the heart rate
The airway of the infant differs from that of the older is 60 beats/min for the neonate, infant and the small
child or adult in that the infant has a large head and child and 40 beats/min for the large child. Performed
tongue, small mouth, and the larynx is narrower, shorter, correctly, external cardiac compressions (ECC) can

658 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E
















































































39
FIGURE 24.2 Basic life support flow chart.

Resuscitation 659

produce a systolic blood pressure peak of 60–80 mmHg generally held belief is that ECC alone is better than no
(in adults) and a cardiac output of 20–30% of normal. 27,41 CPR at all. 46-48
With external chest compressions it takes time to reach
optimal levels of coronary perfusion pressure and, ulti- Devices to augment compression
49
mately, bloodflow. Any interruption to chest compres- As ECC supplies only 30% of normal cardiac output
sions therefore decreases the coronary perfusion pressure and 15% of normal cerebral blood flow, there is a great
42
and resultant blood flow, ultimately reducing survival. need to find ways to improve ECC. While no circulatory
After 30 compressions open the airway and give two adjunct is currently recommended, several are being
breaths. 43 routinely used in the preadmittance and in-hospital
20
Survival potentially improves when an individual receives settings. A few of the recent devices are outlined in
a higher number of chest compressions during CPR, even Table 24.4.
if the person receives fewer ventilations. Because of this, Given the limited available information on the outcome
it is recommended that a 30 : 2 compression-to-ventila- of any of these devices and the absence of evidence to
tion ratio is used in adults, children and infants regardless demonstrate these devices are superior to conventional
of the number of rescuers, and 3 : 1 for neonates. Having manual CPR, no device is currently recommended as a
noted this, in the advanced life support paediatric setting, routine substitute for manual CPR. 20
the compression ratio changes to 15 : 2 and a ratio of 3 : 1
for the newborn with any number of rescuers (see Table
24.3). Studies note that the average person may not only Practice tip
be reluctant to initiate mouth-to-mouth resuscitation
44
but will also take eight seconds to deliver one breath. CPR should commence if the patient is unconscious, unrespon-
45
When a rescuer is reluctant to perform rescue breaths, sive, not moving and not breathing, even if the patient is taking
external cardiac compression (ECC) without expired the occasional gasp.
air resuscitation (EAR) should be encouraged, as the





TABLE 24.3 CPR for adults, children and infants

Age Airway Compression (CPR) 1 or 2 person
Infants <1 year Jaw support or chin-lift (no Two fingers or two overlying thumbs on 30 : 2
head-tilt) the lower end of the sternum with hands PALS 15 : 2
encircling the chest, 100 beats/min
Younger child: 1–8 years Head-tilt more than infants but less heel of one hand, 100 beats/min 30 : 2
than adults PALS 15 : 2
Older child: 9–14 years Head-tilt two hands, 100 beats/min 30 : 2
PALS 15 : 2
Adult Head-tilt two hands, 100 beats/min 30 : 2
PALS = paediatric advanced life support.





TABLE 24.4 Augment compression devices

Device Description
Active compression–decompression (ACD-CPR) l utilises a small portable device to compress and decompress the chest (‘plunger method’)
l enhances ventilation and venous return by raising the negative intrathoracic pressure
139
which facilitates venous return, thus priming the heart for subsequent compressions.
Interposed abdominal compression combined l least technical device
(IAC) with CPR (IAC-CPR) l the abdomen is compressed (midway between the xiphisternum and the umbilicus)
alternately with the rhythm of chest compression
l results in increased resistance in the descending aorta, thus raising the coronary
perfusion pressure 140
l receives the highest recommendation 140
Non-invasive automated chest compression l utilises a load-distributing band (LDB) to compress the anterior chest 141
device (AutoPulse) l the device is built around a backboard that contains a motor.
l the motor tightens or loosens LDB around the patient’s chest.
l has demonstrated better coronary perfusion when compared to manual CPR 141

660 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Defibrillation After checking for a pulse, the AED requires only four
While CPR has been associated with improved survival steps to operate: turn power on, place self-adhesive elec-
to discharge from hospital, it cannot be substituted for trodes on a victim’s chest, rhythm analysis follows (hands-
the definitive treatment of early defibrillation. It is thought off period), then (if advised by the machine) press the
that CPR will supply sufficient oxygen to the brain and shock button. The AED will automatically interpret
heart until defibrillation is available. Ultimately, despite the cardiac rhythm and if VF/VT is present, will advise the
the most effective CPR, the single-most important cause operator to provide a shock. This ‘hands-off’ period may
of decreased prognosis in pulseless VT/VF cardiac arrests result in significant interruptions to chest compressions
55
is a delay in electrical defibrillation. 3 and adversely impact patient survival. The combined
preshock and the postshock pause ideally should be less
53
Praecordial thump than 5 seconds. This can be achieved by continuing
compressions while the defibrillator is charging and
A praecordial thump is a single, sharp blow delivered resuming chest compressions immediately after the deliv-
with a clenched fist to the midsternum of a victim’s chest ery of the shock. Biphasic AEDs are safe, easy to use and
7
from a height of 25–30 cm above the sternum. The are effective for detecting and classifying arrhythmias
mechanical energy generated by the praecordial thump (sensitivity 100%, specificity 97%). FAEDs are pro-
may generate a few joules, and therefore if applied within grammed to assess the rhythm, charge the defibrillator
the first few seconds of onset of a shockable rhythm, but and deliver shocks without user intervention.
it has a very low success rate at converting VF/VT to a
perfusing rhythm. 50,51 Because of the very low success rate Successful defibrillation and survival to discharge is
and the brief period for application, delivery of the thump inversely related to the time from onset of ventricular
must not delay accessing help or a defibrillator. Only situ- fibrillation to defibrillation. For every minute that passes,
56
ations where the VF arrest is witnessed and monitored the probability of survival decreases 5–10%, so resusci-
and a defibrillator is not immediately on hand (i.e. criti- tation bodies place great emphasis on early defibrillation.
cal care environments) would the delivery of the praeco- To facilitate early defibrillation, ILCOR endorses the
rdial thump be appropriate. 20 concept of non-medical individuals being authorised,
53
educated and encouraged to use defibrillators. This
Electrical defibrillation public access to early defibrillation has seen the place-
ment of defibrillators on aircraft, in casinos and cricket
Defibrillation is the passage of a current of electricity grounds, with non-medical personnel such as police,
through a fibrillating heart to simultaneously depolarise flight attendants, security guards, family members and
the mass of myocardial cells and allow them to repolarise even children successfully initiating early defibrilla-
uniformly to an organised electrical activity. There are tion. 57,58 The effectiveness of training non-traditional out-
52
two defibrillator modes for delivery of electrical energy: of-hospital first responders to use the AED has improved
monophasic and biphasic waveforms. Monophasic defi- survival to discharge rates. Similarly, in-hospital cardiac
20
brillators are no longer manufactured, however they are arrests also occur in any area, and all healthcare workers
still available in clinical settings. Monophasic defibrilla- should be capable of initiating early defibrillation. The
53
tors operate by the current travelling in one direction ARC notes that while BLS does not have to include the
from one paddle through the heart to the opposite use of adjunctive equipment, the use of AEDs by persons
paddle. 52,53 In comparison, the biphasic defibrillator’s with education in their use is supported and should be
current travels in one direction through the heart for a taught. Figure 24.3 outlines the integration of defibrilla-
predetermined time, then reverses. tion with BLS.



Practice tip
Practice tip
Effective BLS can slow the loss of amplitude and waveform of
VF. Interruptions to effective CPR should be kept to a minimum. Remember, when using a monophasic defibrillator for AF car-
dioversion, the use of hand-held paddles is preferable to the
use of self adhesive pads. 59
There are two types of external defibrillators: the manual
external defibrillator (MED), and the automatic external
defibrillator (AED). The AED can be either fully auto- For 90% of people in VF, return of a perfusing rhythm
matic (FAED) or semiautomatic (SAED). The MED will occur after a single shock. However it is rare that a
requires the user to be able to immediately and accurately pulse will be palpable with the perfusing rhythm, hence
recognise arrhythmias and make the decision whether to the immediate resumption of chest compressions in the
53
initiate defibrillation or not. In comparison, the AED postshock period is supported. Failure to successfully
automatically detects and interprets the rhythm without convert VF after the single-shock strategy may indicate the
relying on the user’s recognition of arrhythmias. AEDs need for a period of effective CPR (30 : 2) for 2 min and
53
can be operated in both manual and semiautomatic rhythm reanalysis, then shock if indicated. A single
mode. When using an AED, the user determines whether shock strategy is now recommended for all patients in
54
the person is unresponsive, not breathing and pulseless. cardiac arrest requiring defibrillation for VF or pulseless

Resuscitation 661




Advanced Life Support
for Adults

During CPR
Start CPR Airway adjuncts (LMA / ETT)
30 compressions: 2 breaths Oxygen
Minimise Interruptions Waveform capnography
IV / IO access
Plan actions before interrupting compressions
(e.g. charge manual defibrillator)
Attach Drugs
Defibrillator / Monitor Shockable
nd
* Adrenaline 1 mg after 2 shock
nd
(then every 2 loop)
rd
* Amiodarone 300 mg after 3 shock
Non Shockable
* Adrenaline 1 mg immediately
nd
(then every 2 loop)
Assess Non
Shockable
Rhythm Shockable
Consider and Correct
Hypoxia
Hypovolaemia
Shock Hyper / hypokalaemia / metabolic disorders
Hypothermia / hyperthermia
Tension pneumothorax
Tamponade
CPR CPR Toxins
for 2 minutes for 2 minutes Thrombosis (pulmonary / coronary)
Return of
Spontaneous Post Resuscitation Care
Circulation? Re-evaluate ABCDE
12 lead ECG
Treat precipitating causes
Re-evaluate oxygenation and ventilation
Temperature control (cool)
Post Resuscitation Care
December 2010
62
FIGURE 24.3 Advanced life support flow chart.

39
VT. Not all the electrical energy delivered during defi- suitable for use in children older than 8 years. Ideally, for
brillation will traverse the myocardium. Table 24.5 out- children between 1 and 8 years paediatric pads and an
63
lines some of the common factors contributing to the AED with paediatric capability should be used. These
success or failure of defibrillation. Studies have demon- pads also are placed as per the adult methodology. If the
strated that lower-energy biphasic defibrillators are asso- AED does not have a paediatric mode or paediatric pads
24
ciated with greater first-shock efficacy, require lower then the standard adult AED and pads can be used.
joules, cause less myocardial dysfunction and increase Defibrillation of infants less than one year of age is not
return of spontaneous circulation when compared with recommended. 53
the monophasic defibrillator. 60,61 The optimum defibril- The importance of early, uninterrupted chest compres-
lation energy level is that which sufficiently abolishes the sions and early defibrillation are well promulgated in the
arrhythmia to enable the return of an organised rhythm, ILCOR guidelines. As determining the length of time
12
53
with minimal myocardial damage. The recommended from collapse is difficult to accurately estimate, it is
first shock for a monophasic defibrillator is 360 J and imperative rescuers perform chest compressions until the
200 J for biphasic defibrillators. Other biphasic energy defibrillator is both available and charged. 64,65
levels may be used providing there is relevant clinical data
for a specific defibrillator that suggests that an alternative
energy level provides adequate shock success (ARC & ADVANCED LIFE SUPPORT
62
NZRC Guideline 11.4). If the initial shock is unsuccess- Basic life support can provide around 20–30% of normal
ful, subsequent shocks should be delivered at the above cardiac output and a fraction of inspired oxygen (FiO 2 )
61
doses or higher energy levels may be selected. In chil- of 0.1–0.16. Consequently, a significant number of
dren, it is recommended 4J/kg for the initial and sub- patients rely on the provision of advanced life support
sequent shocks for both biphasic and monophasic (ALS) for survival. ALS extends BLS to provide the knowl-
53
defibrillators. Standard adult AEDs and pads are edge and skills essential for the initiation of early

662 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E



TABLE 24.5 Factors contributing to the success or failure of defibrillation

Success Failure Precautions
l Early defibrillation l Inadequate contact with the chest (Excessive chest l Place defibrillation electrodes at least 8 cm away
(<4 min) hair) from ECG electrodes, or implantable medical devices
l Presenting l Faulty positioning of the paddles pacemakers, vascular access devices
rhythm (VT/VF) l Synchronise button in the on position, flat battery or l Remove medication patches, wipe the area before
fractures lead applying defibrillation electrodes
l Positioning over bone/fat or breast tissue l Do not defibrillate unless all clear of the bed/patient
l Drying out of gel conduction pads l Do not charge/discharge paddles in the air
l Patient factors: acidosis, hypoxia, electrolyte imbalance, l Do not have the patient in contact with metal
drug toxicity, hypothermia l Do not allow oxygen to flow onto the patient during
l Time of respiration (best delivered at end-expiration) delivery of the shock (at least 1 m from the patient)
l PEEP and auto-PEEP (air-trapping) should be minimised l Ensure the chest is dry
l Paddles/electrodes too small (8–12 cm electrodes for l Do not use electrode gels and pastes as these can
adults) spread between the paddles and potentially spark.





Advanced Life Support
for Infants and Children

During CPR
Start CPR Airway adjuncts (LMA / ETT)
15 compressions: 2 breaths Oxygen
Minimise Interruptions Waveform capnography
IV / IO access
Plan actions before interrupting compressions
(e.g. charge manual defibrillator to 4 J/kg)
Attach Drugs
Defibrillator / Monitor Shockable
* Adrenaline 10 mcg/kg after 2nd shock
(then every 2nd cycle)
* Amiodarone 5 mg/kg after 3rd shock
Non Shockable
* Adrenaline 10 mcg/kg immediately
(then every 2nd cycle)
Assess Non
Shockable
Rhythm Shockable Consider and Correct
Hypoxia
Adrenaline 10 mcg/kg Hypovolaemia
Shock (4 J/kg) (immediately then Hyper/hypokalaemia/metabolic disorders
every 2nd loop) Hypothermia/hyperthermia
Tension pneumothorax
Tamponade
CPR CPR Toxins
for 2 minutes for 2 minutes Thrombosis (pulmonary/coronary)
Return of
Spontaneous Post Resuscitation Care
Circulation? Re-evaluate ABCDE
12 lead ECG
Treat precipitating causes
Re-evaluate oxygenation and ventilation
Temperature control (cool)
Post Resuscitation Care
December 2010
62
FIGURE 24.4 Advanced life support for infants and children flowchart.
treatment and stabilisation of people post-cardiac arrest. and ALS. The ARC and NZRC algorithm for management
Advanced skills traditionally include defibrillation, of cardiopulmonary arrest (see Figures 24.3 and 24.4)
advanced airway management and the administration of outlines the two decision paths of therapy in ALS: (a)
resuscitation drugs. While BLS is generally initiated prior defibrillation and CPR for pulseless VT/VF (shockable);
to ALS, where a defibrillator and a person trained in its and (b) identifying and treating the underlying cause for
use are available, defibrillation takes precedence over BLS non-VT/VF (non shockable).

Resuscitation 663

Advanced Airway Management used with either the face mask or other adjunct airway
16
A person with signs of acute respiratory distress should devices such as LMA, Combitube or ETT. Having noted
be administered oxygen at the highest possible concen- this, there is currently no evidence to suggest that the use
tration. Initially during CPR, whenever possible, admin- of automated ventilators during cardiac arrest are more
16
43
ister the highest possible oxygen concentration. Oxygen beneficial than bag–valve–mask devices.
should never be withheld for fear of adverse effects, as Rhythm
rescue breaths provide an inspired oxygen concentration There is an association between the initial cardiac arrhyth-
of only 15–18%. The administration of oxygen alone mias and survival to discharge after SCA. Cardiac arrest
does not result in adequate ventilation, and as such the rhythms can be divided into two subsets:
establishment of an effective airway is paramount. Airway
management is essential in the performance of CPR, and 1. ventricular fibrillation (VF) and pulseless ventricu-
may be administered using a variety of techniques. The lar tachycardia (VT)
choice of advanced airway adjunct is determined by the 2. non-VF/VT incorporating asystole and pulseless
availability of equipment and experienced personnel (see electrical activity (PEA).
Table 24.6 and Chapter 15): The most common arrhythmias observed in SCA are
l oropharyngeal (Guedel’s) airway pulseless VT and VF, with 60–85% of all patients initially
6
l nasopharyngeal airway presenting with these lethal arrhythmias. PEA occurs as
67
l laryngeal mask airway the initial rhythm in approximately 13–22% of cases;
l oesophageal–tracheal Combitube when witnessed by emergency personnel in the prehos-
68
l endotracheal intubation pital setting, it has been documented as high as 50%.
l tracheostomy. Asystole is the most common arrest arrhythmia in chil-
dren, because their hearts respond to prolonged severe
While endotracheal tube (ETT) is considered the ‘gold hypoxia and acidosis by progressive bradycardia leading
standard’ for airway management in a cardiac arrest, as it to asystole. 53
protects the airway, assists effective ventilation, ensures
delivery of high concentrations of oxygen and eases suc- Ventricular fibrillation and pulseless
tioning, no studies have found that ETT use during a cardiac ventricular tachycardia
20
arrest increases survival. It is vital that CPR not be inter- As previously noted, the only intervention shown to
rupted for more than 10 seconds during attempts at endo- unequivocally improve long-term survival after a VF or
tracheal intubation. Waveform capnography should be pulseless VT arrest is prompt and effective BLS, uninter-
20
12
applied to confirm the ETT placement. The ETCO 2 may rupted chest compressions and early defibrillation. VT
12
also be used to monitor the quality of the CPR. Given the and VF rhythms are displayed in Figures 24.5 and 24.6.
limitations noted in Table 24.6, a variety of adjunct airway/ Energy levels and subsequent shocks are equivalent for
ventilation management devices, such as bag–mask ven- both VF and pulseless VT.
tilation (BMV) and supraglottic airway devices (SADs)
such as laryngeal mask airway (LMA), the classic laryngeal Non-VF/VT
mask airway (cLMA), the oesophageal–tracheal Combi- Non-VF/VT arrhythmias include pulseless electrical activ-
tube (ETC) and the I-gel are available. When an LMA- ity and asystole. Pulseless electrical activity (PEA) or elec-
Fasttrach is in place, it can be used to guide the passage of tromechanical dissociation (EMD) reflects a dissociation
bougies, introducers, a bronchoscope or an ETT into the between the heart’s electrical and mechanical activities,
trachea. The benefit of the SADs is that they are easily and the two terms are used interchangeably. It is impor-
inserted without interruption to chest compressions. tant to note that PEA/EMD may present as any rhythm
66
Currently, there is no evidence to support the routine use normally compatible with a pulse (e.g. sinus rhythm,
of any particular advanced adjunct airway devices. Health- sinus tachycardia/bradycardia). PEA is characterised by a
care professionals trained to use supraglottic airway stroke volume insufficient to produce a palpable pulse,
devices (e.g. LMA) may consider their use for airway man- despite adequate electrical activity. PEA often follows
69
agement during cardiac arrest and as a backup or rescue defibrillation of VF and has a survival rate of 0–6%.
68
airway in a difficult or failed tracheal intubation. Management of PEA includes identifying and correcting
Once an airway has been established, continue chest com- reversible causes, summarised as the 4 Hs and 4 Ts in
pressions without interruption for ventilation. Ventilate the Table 24.7.
lungs at a rate of approximately 10 breaths a minute and an Careful confirmation of asystole (see Figure 24.7) on two
inspiratory time of 1 sec with sufficient volume to produce leads and the absence of a palpable pulse are essential
a normal chest rise. Ventilation adjuncts may include: when making the decision to manage asystole. When an
l a simple face mask with filter and oxygen connector out-of-hospital arrest has an initial rhythm of asystole,
20
(preintubation) survival to discharge is as low as 2%.
l bag–valve–mask systems Medications Administered During
l ventilators. Cardiac Arrest
If available, automated ventilators can be used. These Resuscitation drugs can be administered during a cardiac
may be set to deliver a tidal volume of 6–7 mL/kg at a arrest using a variety of routes including peripheral and
rate of 10 breaths/min. The automated ventilator may be central veins, or intraosseous (IO). Administration by the

664 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E




































Practice considerations Incorrect size or placement may contribute to airway obstruction by pushing the tongue back into the pharynx. Unlike adult insertion, the insertion of the oropharyngeal airway in infants and young children is inserted right-way-up; a tongue depressor or laryngoscope should be used to aid insertion. 40 Use with caution in patients with head injuries. With the exception of infant’s head-tilt, jaw support or jaw thrust is still necessary when























Adjuncts used during resuscitation Description Conforms to the curve of the palate, moving the tongue forwards away from the posterior pharyngeal wall. 40 Sizes from 000–5. Soft tube inserted into the nasopharynx. A self-inflating bag that may be connected to a face mask, LMA or ETT. The LMA consists of a tube with an elliptical cuff fitted at the distal end that inflates in the hypopharynx around the posterior perimeter of the larynx. The LMA is inserted orall
















TABLE 24.6 Airway type Oropharyngeal (Guedel’s) airway Nasopharyngeal airway Bag–valve–mask (BVM) systems Laryngeal mask airway (LMA) Oesophageal– tracheal Combitube (ETC) Laryngeal tube (LT) I-gel Endotracheal tube (ETT)

Resuscitation 665


















FIGURE 24.5 Ventricular tachycardia.















FIGURE 24.6 Ventricular fibrillation.

















FIGURE 24.7 Asystole.


(adults) of an isotonic solution followed by at least 1
TABLE 24.7 Causes of pulseless electrical activity 7 minute of continuous external cardiac compressions.
Where there is difficulty accessing a peripheral vein,
The four Hs The four Ts selected medications may be administered via an IO
20
route. Tracheal administration of medication is no
l Hypoxia l Tamponade
l Hypovolaemia l Tension pneumothorax longer recommended as the dose delivered is unpredict-
l Hypo/hyperthermia l Toxins/poisons/drugs able and the optimal dose is unknown. 20
l Hypo/hyperkalaemia and metabolic l Thrombosis:
disorders pulmonary/coronary Intraosseous infusion involves the insertion of a metal
needle with trocar (usually utilising a drill) into the
bone marrow and provides a rapid, safe and reliable
70
central venous route remains the optimal method, but access to the circulation. The marrow sinusoids of
the decision to access peripheral versus central cannula- long bones are a non-collapsible venous system in
tion will depend on the skill of the operator. Peripheral direct connection with the systemic circulation, allowing
venous cannulation is the quickest and easiest method, drugs to reach the central circulation as quickly as medi-
71
however, the patient in cardiac arrest may have inacces- cations injected into central veins. Intraosseal access
20
sible peripheral veins. Should a decision be made to is safe and effective for use in patients of all age
insert a central line during a cardiac arrest, this must groups. 72,73 General blood specimens such as biochem-
not take precedence over defibrillation attempts, CPR istry values, blood cultures, haemoglobin and cross-
or airway maintenance. Medications inserted into a match studies can also be taken from the marrow at
peripheral line should be flushed with at least 20 mL cannulation. 17

666 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

administrated in a cardiac arrest. However, it could be
Practice tip considered in adult patients with proven or suspected
12
pulmonary embolism or acute thrombotic aetiology.
Attempts at peripheral cannulation in children should be Effective CPR should be continued for at least 60–90
aborted after 2 minutes and an intraosseous needle inserted. minutes following the administration of the fibrinolytic
medication as there is evidence in these situations of
good neurological outcome and survival after following
extended periods of CPR. 80
Vasopressors such as adrenaline and vasopressin have
been used as adjuncts in cardiac arrests to improve the During the arrest, strategies should be initiated to prevent
success of CPR. While there is no evidence that shows the development of serious periarrest arrhythmias. When-
that the routine use of any vasopressor during a cardiac ever possible, arterial blood gases, serum electrolytes and
arrest will increase survival to discharge from hospital a 12-lead ECG should be obtained to assist with deter-
12
adrenaline is still recommended. Adrenaline has been mining the precise rhythm and appropriate medical inter-
16
demonstrated to increase the return of spontaneous cir- ventions. The presence or absence of adverse signs and
12
culation but not survival to hospital discharge. The symptoms will dictate interventions. Adverse factors may
optimal dose of adrenaline in the prehospital and include clinical evidence of:
in-hospital setting remains unclear. Current recommen- l low cardiac output (unconscious, unresponsive, sys-
dations propose that adrenaline 1 mg should be admini- tolic BP <90 mmHg, increased sympathetic activity)
stered for VT/VF following the second shock and then l reduced diastolic filling time (excessive tachycardia,
every second loop thereafter. For asystole and electrome- e.g. heart rates of >150/min, wide complex tachycar-
chanical dissociation (EMD) administer 1 mg of adrena- dia and supraventricular tachycardia)
line in the initial loop then every second loop (ARC & l excessive bradycardia (heart rates of <40/min)
62
NZRC guideline 11.5) (see Table 24.8). Studies have l raised end-diastolic filling pressure (presence of pul-
reported that vasopressin produced no overall change in monary oedema or raised jugular venous pressures)
survival after cardiac arrest when compared with l reduced coronary blood flow (chest pain).
adrenaline. 74-76 Currently there is no evidence to support
or refute the use of vasopressin as an alternative to or in Interventions can broadly be divided into three options
combination with adrenaline. for immediate treatment:
The optimal role and exact benefit of antiarrhythmic 1. antiarrhythmics (refer to periarrest in Table 24.8)
medications in cardiac resuscitation is yet to be fully 2. electrical cardioversion
elucidated, but they have very little, if any, role to play in 3. cardiac pacing.
12
the treatment of cardiac arrests. The common antiar- Common periarrest arrhythmias and interventions are
rhythmic drugs include amiodarone, lignocaine, magne- covered in Chapter 11. Antiarrhythmic interventions such
sium, atropine and calcium (see Table 24.8). While no as medications, physical manoeuvres and electrical thera-
antiarrhythmic has been shown to improve survival to pies may be proarrhythmic. 16
discharge, recent trials have demonstrated that amioda-
rone is superior to lignocaine and placebo in improving Fluid Resuscitation
survival to hospital admission for people with refractory
77
VF in out-of-hospital cardiac arrests. The efficacy of IV Fluid resuscitation may be considered if hypovolaemia is
amiodarone in the setting of VT and VF is 51–100%. If suspected as a possible cause of the cardiac arrest. 0.9%
78
after the third shock, the VT/VF has not reverted then a sodium chloride or Hartmann’s solution are recom-
bolus injection of 300 mg of amiodarone is recom- mended as a rapid infusion in the initial stages of resus-
mended and 150 mg for recurrent or refractory VT/VF. citation (at least 20 mL/kg). There is no evidence to
12
Lignocaine (1 mg/kg) may be used as an alternative if support the routine administration of fluids during a
20
amiodarone is not available or cannot be used, but the cardiac arrest in the absence of hypovolaemia.
12
two should not be used together. There is no evidence
of improved survival with the use of atropine in a cardiac Pacing
arrest with asystole or PEA. Calcium chloride has little During a cardiac arrest, temporary cardiac pacing may be
20
use in the management of arrhythmias unless caused by required for sustained symptomatic bradycardia unre-
hyperkalaemia, hypocalcaemia or hypermagnesaemia, or sponsive to medical intervention. Two types of temporary
an overdose of calcium channel-blocking drugs. Sodium cardiac pacing are utilised during a cardiac arrest: trans-
bicarbonate is no longer administered routinely, as it may venous (invasive) and transcutaneous (external, non-
cause hypernatraemia, hyperosmolality and intracellular invasive) pacemakers. As most current defibrillators have
acidosis from the rapid ingress of CO 2 generated from its the capacity to pace, transcutaneous pacemakers are gen-
dissociation. Bicarbonate is recommended if the cardiac erally used in an arrest situation.
arrest is associated with hyperkalaemia or tricyclic anti-
depressant overdose. 12 Ultrasound Imaging
There is insufficient data for the routine use of magne- Ultrasound imaging has shown to have some benefit on
79
sium in cardiac arrests, except if torsades de pointes is the detection and diagnosis of reversible causes of arrest
12
suspected. Thrombolytics should not be routinely including cardiac tamponade, pulmonary embolism,

Resuscitation 667


Continued







Adverse events Tachyarrhythmias; hypertension; coronary vasoconstriction; increased myocardial oxygen consumption. Vasodilation and hypotension, bradycardia, heart block. May have negative inotropic effects. Use with caution in renal failure. Avoid use in torsades de pointes and other causes of prolonged Q-T. Toxicity, slurred speech, psychosis, altered level of consciousness, muscle twitching, seizures and coma. Hypotension, heart bloc









VF and pulseless VT 10 mcg/kg after the 2nd shock then after every second cycle. PEA and asystole 10 mcg/kg immediately, then every second Initial dose of 5 mg/kg bolus over 2 minutes, which may be repeated to a maximum of 300 mg. Periarrest: IV infusion 5–15 µg/kg/ min as continuous infusion (max Initial dose of 1 mg/kg IV or IO.







Paediatric cycle. of 1.2 g in 24 h).

Dose

VF and pulseless VT 1 mg after the 2nd shock then after every second cycle. PEA and asystole 1 mg in the initial cycle, then every Initial bolus dose of 300 mg in 20 mL dextrose. A further 150 mg could be considered for refractory cases. Periarrest: An infusion of 15 mg/kg over 24 hours may be commenced. Bolus of 1 mg/kg at a rate of 25–50 mg/min. Periarrest: May be followed by an additional bolus of









Adults second cycle 0.5 mg/kg.







Medications (ARC & NZRC Guideline 11.5) 62 Indications VF and pulseless VT resistant to the three initial counter shocks. PEA and asystole. VT/VF refractory to three shocks. Polymorphic VT and wide complex tachycardia of uncertain origin. Control of haemodynamically stable VT when cardioversion unsuccessful (in the presence of LV dysfunction). Adjunct to electrical cardioversion of SVT. Prophylaxis of recurrent VF/VT. VF and pulseless VT whe




















TABLE 24.8 Action Adrenaline is a catecholamine that increases aortic diastolic pressure and coronary artery perfusion by producing arteriolar vasoconstriction. It may facilitate defibrillation by improving myocardial blood flow during CPR. Traditionally the first-line medication for the treatment of VF and refractory VT, adrenaline has not demonstrated improved outcomes after cardiac arrest and has been associated with postresuscitation my

668 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E











Adverse events Hypotension with rapid administration. Use with caution if renal failure present. Muscle weakness, paralysis and respiratory failure. Tachycardia and excitement. Calcium is incompatible with a range of medications and may precipitate in IV lines. Tissue necrosis with extravascation may occur. Should not be routinely administered. Alkalosis, hypernatraemia, hyperosmolality, paradoxical cerebral acidosis, depressed card








IV or IO bolus of 0.1–0.2 mmol/kg. Maybe followed by an infusion of 0.3 mmol/kg over 4 hours. 0.2 mL/kg 10% calcium chloride, or 0.7 mL/kg 10% calcium 0.5–1 mmol/kg via IV or IO administered over 2–3 min. 0.03–0.07 mmol/kg via slow administration IV or IO. Periarrest: 0.2 mmol/kg/hr as a continuous infusion; dilute with at least 50 times its volume and mix well, as can be fatal. 0.2–0.5 mmol/kg/h to a maximum of 1 mmol/kg if hypo








Paediatric gluconate via IV

Dose







Bolus of 5 mmol. Periarrest: May be followed by infusion of 20 mmol infused over 4 hours. A bolus dose of 5–10 mL 10% calcium chloride (6.8 mmol). A bolus dose of 1 mmol/kg administered over 2–3 min. As NaHCO 3 is incompatable with many medications, it should be administered by a separate line or flushed before and after administration. 5 mmol via slow bolus. ARC & NZRC = Australian Resuscitation Council and New Zealand Resuscita



Adults





Torsades de pointes with or without a pulse; cardiac arrest associated with digoxin toxicity. Failure of defibrillation and adrenaline to reverse VF and Documented hypokalaemia or hypomagnesaemia. Hypocalcaemia, hyperkalaemia, overdose of calcium blockers. Correcting a metabolic acidosis (pH <7.1), or base deficit of ≤10 or after 15 min; pre-existing hyperkalaemia; tricyclic antidepressant overdose and urinary alkalinisation in ov




Indications pulseless VT. acidosis. toxicity.









TABLE 24.8, Continued Action Magnesium is a major intracellular cation resulting in smooth muscle relaxation and membrane stabilisation. Calcium is essential to nerve and muscle impulse formation and excitation. Sodium bicarbonate (NaHCO 3 ) is an alkaline agent that may be used to correct an acidosis. Routine administration of sodium bicarbonate for treatment of in-hospital and out of hospital cardiac arrest is not recommended. Potassium i

Resuscitation 669

83
pneumothorax, aortic dissection or hypovolaemia. Place- airways secondary to oedema or swelling. Defibrillation
ment of the probe at the sub-xiphoid position prior to energy, drug doses and administration are in accordance
stopping for planned rhythm assessment will facilitate with ALS guidelines. 87
views within 10 sec and minimise chest compression If maternal cardiac arrest occurs in the labour ward,
20
interruptions. While the use of imaging has not been operating room or emergency department and BLS and
shown to improve outcome, absence of heart motion on ALS measures are unsuccessful, the uterus should be
sonography during resuscitation is highly predictive of emptied by surgical (scalpel) intervention within 4–5
death. 20
minutes. Maternal resuscitation may not be possible
87
Special Considerations until the fetus is removed. Successful resuscitations have
occurred after prompt surgical intervention. Refer to
87
Whilst not common, there are some clinical presenta- Chapter 26 for additional information about critical
tions that require special considerations in a cardiac arrest illness and pregnancy.
scenario: these include pregnancy, electrical injuries and
drowning. The principles of airway, breathing and circula- Electrical injuries
tion remain the same, although modifications must be Electrical burn injuries (EBIs) and lightning injuries are
made because of the physiological changes that occur.
similar in that they occur infrequently, commonly cause
Pregnancy widespread acute and delayed tissue damage, and can
arrest the heart and respiratory centre. Burn injuries are
In 2008, there was an estimated 342,900 maternal deaths discussed in Chapter 23. This section focuses on the
81
worldwide. Precipitants included pulmonary embolism, cardiac arrest situation. High-voltage electrocution is
trauma, peripartum haemorrhage, amniotic fluid embo- associated with a high incidence of cardiac abnormalities,
lism, eclamptic seizure, congenital and aquired cardiac including arrhythmias, prolongation of the QT interval,
disease, myocardial infarction, subarachnoid haemor- ST and T wave changes, and myocardial infarction. The
83
82
rhage and cerebral aneurysm. Regardless of the aetio- most common cause of death with lightning injury is
logy, resuscitation following cardiac arrest in late cardiac arrest due to VF or asystole or respiratory arrest.
88
pregnancy is often unsuccessful. Hence, timely delivery Because of the potential for cardiac injuries, all patients
by caesarean section in the setting of maternal cardiac should be admitted for cardiac monitoring.
arrest may save both infant and mother.
A lightning strike may result in asystole followed by spon-
The principles of airway, breathing and circulation remain taneous return of circulation. If ventilation is initiated
the same, but modifications must be made because of the early and severe hypoxia does not ensue, a patient’s
physiological changes that occur with normal preg- chance of recovery should be better. Initial response of
88
83
nancy. A number of factors may need to be considered BLS should always begin with D (danger), that is, avoid-
when resuscitating a pregnant woman. Any situation that ance of injury to the rescuer. Ensure that the environment
affects haemodynamic status will be exacerbated in a is safe for rescuers by disconnecting the electrical supply,
supine position, as autocaval compression may result in where possible, without touching the patient. Where
84
a fall in cardiac output of up to 25%. The mother may high-voltage lines (power lines) are in contact with the
be placed in the left lateral tilt (15 degrees) or supine with person or the vehicle, no attempt should be made to
a pillow under the right buttock, to displace the uterus extricate the person from the vehicle until the situation
from the inferior vena cava, facilitating venous return and is deemed safe by an authorised electricity supply person.
83
cardiac output. Often the angle of the tilt is overesti- Once the environment is safe, commence BLS resuscita-
mated potentially reducing the quality of the chest com- tion. The neck and spine should be protected, as there
85
pressions. The uterus may also be manually and gently may be trauma.
displaced to the left to remove caval compression. 83
In lightning victims, emphasis is on the immediate resus-
While ventilation : compression ratios remain the same citation of those who appear unresponsive. Respiratory
for a pregnant woman, chest compression may be com- arrest may be prolonged due to paralysis of the medullary
plicated by flaring of the ribs, raised diaphragm, obesity respiratory centre; if not corrected, cardiac arrest second-
and breast hypertrophy. 83 ary to hypoxia ensues. Fixed, dilated pupils should not

The superior displacement of stomach contents by the be used as a poor prognosis of outcome, as victims can
gravid uterus and a relaxed cardiac sphincter contribute benefit from prolonged resuscitation without major
to an increased risk of gastric aspiration in the pregnant sequelae. 88
woman. 83,86 Because of this increased risk, cricoid pres-
sure should be applied until after the airway is protected Drowning
87
by a cuffed tracheal tube. Tracheal intubation should be General issues in managing drowning presentations are
86
attended to early, utilising a short-handled laryngoscope discussed in Chapter 22. This section focuses on resusci-
87
or with a blade mounted at more than 90 degrees, as tation of a cardiorespiratory arrest. Hypoxia and acute
airway anatomy is altered with the larynx more anterior lung injury (ALI) from drowning results in respiratory
and superior, while pharyngeal mucosa is slightly oede- arrest which, if not corrected may proceed to a cardiac
86
matous and friable. A tracheal tube a size smaller than arrest. 89,90 A patient’s emotional state, associated diseases,
one normally chosen for a similar size non-pregnant previous hypoxia and water temperature all influence this
woman may be chosen because of potential narrower progression. 83

670 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

The primary goal of initial intervention is the relief of resuscitation team will vary between organisations, but
83
hypoxaemia and restoration of cardiovascular stabil- generally the team should possess the following skills: 94
ity. 89,90 Resuscitation of drowning victims follows BLS l advanced airway management and intubation skills
guidelines, with commencement as soon as practical. l intravenous access skills including central venous
Rescue breathing may commence while the victim is still access
83
in the water, provided it is safe for the rescuer. As drown- l defibrillation and external pacing abilities
ing victims may have swallowed considerable amounts of l medication administration skills
water, vomiting and aspiration of gastric contents can be l postresuscitation skills.
a major problem during resuscitation. To minimise the
risks of inhalation, abdominal compression, the Heim- As members of a resuscitation team in the hospital gener-
lich manoeuvre and attempts to drain water from the ally do not work together but come from all areas of the
lungs are not recommended. Instead the victim should hospital, the team should have a designated leader. The
be placed on the side for the initial assessment of airway team leader gives direction and guidance, assigns tasks
63
and breathing. Cardiac arrest in these victims is second- and makes clinical decisions without directly performing
ary to hypoxia, so compression-only CPR is likely to be specific procedures. 16,94 The leader should engender the
83
less effective and should be avoided. Once experienced team’s trust. Where leaders initiate structure within the
personnel arrive, ALS and administration of oxygen arrest team, members not only work together better, they
should be initiated. The principles of respiratory support also perform the tasks of resuscitation more quickly and
94
and ventilation are discussed in Chapter 11, and treat- more effectively. The leader nominates the roles of arrest
ment of the sequelae of a drowning victim is discussed team members. Roles of team members include airway
in Chapter 16. management, chest compression, medication administra-
tion (including IV access), documentation of events and
Evaluation During Resuscitation care of family members. The team leader should be
responsible for postresuscitation transfer, documenta-
Maintenance of an effective cardiac output during CPR tion, communicating with family members and health-
is evaluated by palpating the carotid or femoral pulse care professionals and debriefing of the team. 94
in adults (brachial in children); this was once the ‘gold
standard’ for assessing circulation. However, neither lay- The resuscitation scenario is both complex and stressful
persons nor professionals can rapidly (in less than 10 sec) for all participants. Often, participants express feelings
and accurately perform this step. Pulse checks are not that too many people are involved, with no one person
recommended for evaluation after defibrillation until 2 in control. Unfortunately, the concept of the multidisci-
minutes of CPR have been performed, regardless of the plinary team, where all members’ contributions are
95
rhythm postdefibrillation. equally respected, is often not evident in the literature.
In addition, while nurses already present at a cardiac
The use of capnometry as a non-invasive technique for arrest in the hospital setting may be willing and compe-
monitoring CPR’s effectiveness is recommended. As tent to perform CPR, they may be prevented from doing
12
partial pressure of end-tidal carbon dioxide (PetCO 2 ) so because of the arrival of the cardiac arrest team. 96,97
concentration correlates with pulmonary bloodflow
during CPR, the adequacy of resuscitation efforts is evalu-
ated by measuring this parameter. PetCO 2 also correlates FAMILY PRESENCE DURING
with cardiac output, return of spontaneous circulation AN ARREST
(ROSC) and outcomes in cardiac arrest. A mean PetCO 2
91
of 17 mmHg or above has been associated with survival The practice of family members witnessing resuscitation
from cardiac arrest, while a mean PetCO 2 <10 mmHg is has over time become more evident, both in practice and
associated with poor outcomes. A rise in PetCO 2 during in the literature. This shift in practice has been attributed
CPR may indicate the return of spontaneous circula- to increasing patient autonomy and the presence of
98
80
tion. Conversely, experimental studies have demon- family at a cardiac arrest in popular television shows.
strated that cardiac arrest from massive pulmonary This has contributed to public support, family members
embolism is associated with an extremely low PetCO 2 requesting – and expecting – to be present. 99,100 However,
92
readings during CPR. Having noted this, hyperventila- the issue of whether the family should be present during
tion during CPR is not recommended and may be a cardiac arrest remains controversial. Proponents argue
harmful. Similarly, animal studies indicate that hyper- the importance of family being with loved ones during
ventilation is associated with raised thoracic pressure, their last moments, as this shortens the period of grieving
98
decreased coronary and cerebral perfusion and reduced and provides closure. Indeed, professional resuscitation
return of spontaneous circulation. Clinical studies show bodies recommend that family should be afforded the
that rescuers consistently hyperventilate patients during opportunity to be present. However, translating these rec-
a cardiac arrest. 93 ommendations into practice varies within health care
personnel. Commonly cited is concern that the family
ROLES DURING CARDIAC ARREST may interrupt the work of the resuscitation team, the
ethical and medico–legal implications, or concern about
Resuscitation teams should be organised to ensure offending the family. 101-103 Contrary to these beliefs, there
that the individual skills of each member are used effec- is limited evidence that family interfere with the perfor-
94
tively and efficiently. The exact composition of the mance of the resuscitation team. 101,104,105

Resuscitation 671

Conflicting evidence exists as to the psychological effects
of such an event on the family. Effects have been docu- BOX 24.1 Cooling techniques postcardiac
98
mented as ranging from no adverse effects through to arrest 107-109
expressions of distress, haunting consequences and
106
trauma. Where families are provided the option of External:
being present, a staff member should be identified to l Cooling blankets/pads, ice packs, wet towels, fanning and
have sole responsibility of supporting the family. cooling helmets
CEASING CPR Internal:
l IV administration of saline (30 mL/kg at 4°C over 30 minutes
The decision to cease CPR is often difficult; continuing to achieve a 1.5°C fall in core temperature)
CPR beyond 30 minutes without return of spontaneous l IV heart exchange device
circulation (ROSC) is usually futile unless the arrest was l Peritoneal and pleural lavage (not generally used)
compounded by hypothermia, submersion in cold water,
lightning strike, drug overdose or other identified and
treatable conditions such as intermittent VF/VT. Pro-
16
longed resuscitation of greater than 60 minutes may be of body temperature, identification and treatment of
made for a severely hypothermic, child victim of near- acute coronary syndromes and optimisation of mechani-
drowning. Pupillary signs should not be used as a predic- cal ventilation are a few of the targeted objectives of care
tor of outcome in infants and children, as 11–33% of (ARC & NZRC Guideline 11.8). 62
children with non-reactive pupils have survived long-
17
term after CPR. It is important to have eliminated all ROLE OF HYPOTHERMIA IN ADULTS AFTER
causes as far as possible. CARDIAC ARREST
Termination of resuscitation is a multifactorial process, During cardiac arrest, prolonged global ischaemia
influenced by provider comfort and experience, patient coupled with inadequate reperfusion during the immedi-
prognosis, desires previously expressed, wishes and ate postresuscitation period can lead to severe cerebral
112
values, the culture of the hospital, the EMS or emergency hypoxic injury. Induced moderate hypothermia (28–
department, protocols and resource issues, and national 32°C) has been used in open-heart cardiac surgery since
113
and international guidelines that reflect changing stan- the 1950s to protect the brain against global ischaemia.
dards of care, resource availability, global interpretations One randomised control trial and other studies have
107
of utility and emerging science. With scientific advances shown that cooling patients postcardiac arrest provides
and evidence-based protocols becoming more widely significant survival benefit as well as improved cardiac
implemented, current impressions of termination deci- and neurological function. 113-115 Prospective randomised
107
sions will change over time. It is appropriate to invite studies have demonstrated that mild hypothermia (32–
suggestions from team members, to ensure that all 34°C) increases the rate of favourable neurological
members are comfortable with a decision to stop the outcome in comatosed adult patients resuscitated after
16
resuscitation attempt. Ultimately, terminating CPR is out-of-hospital cardiac arrest (OHCA) due to VF. 114,115 A
equivalent to a determination of death, and must be variety of cooling techniques are described in Box 24.1.
made by a physician. In some out-of-hospital circum- Therapeutic cooling consists of the induction, mainte-
stances it may be the paramedical staff that make this nance and rewarming phases. ILCOR recommends
116
decision regarding stopping CPR. Prospectively validated that unconscious adult patients with spontaneous cir-
termination of resuscitation rules such as the ‘basic life culation after OHCA should be cooled to 32–34°C for
support termination of resuscitation rule’ are recom- 12–24 hours if the initial rhythm was VF. This cooling
mended to guide termination of prehospital CPR in may also be beneficial for other rhythms or in-hospital
adults. 24 113
cardiac arrest. It is important to note that shivering
POSTRESUSCITATION PHASE must be prevented during this phase (ARC & NZRC
62
Guideline 11.8).
The aim of postresuscitation care is the maintenance of Persistent hyperglycaemia following cardiac arrest has
cerebral and myocardial perfusion and the return of a been associated with poor neurological outcome. Moni-
patient to a state of best possible health. Resuscitation toring of blood sugar levels and treatment of hypergly-
does not cease with the return of spontaneous circula- caemia (>10 mmol/L) with insulin is recommended in
tion. However, the ROSC after cardiac arrest does not the post cardiac arrest period. 117
always equate to a positive outcome for the patient. Mor-
tality rates following in-hospital cardiac arrests vary NEAR-DEATH EXPERIENCES
between 67 and 71%. 108,109 This high mortality rate has
been attributed to multiple organs that are involved with With the rise in survival rates after a critical illness, there
109
whole of body ischaemia during cardiac arrest. The are increasing numbers of documented near-death
reperfusion responses that occur following successful (NDEs) and out-of-body (OBEs) experiences. 118,119 Near-
110
resuscitation is termed postcardiac arrest syndrome. death has been described as unusual experiences during
118
Coordinated care and specific interventions initiated in a close brush with death. Experiences have typically
111
the postarrest phase can influence outcomes. Control included memories of bright tunnels of light, deceased

672 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

relatives, out-of-body sensations, feelings of presence of and outcomes after CPR strongly influences their prefer-
deity and peace. 120,121 These experiences may vary between ences. 129 Most patients, and indeed healthcare workers,
131
cultures: Euro-Americans may report a golden colour commonly hold unrealistic expectations of CPR success,
light where as Tibetans may report a clear light. 122 People and will often reverse their preference for commencing
report the experiences as pleasant, and they have resulted CPR once they are informed of the true probability
in positive life changes for the individual. After-effects of of survival and functional status after resuscitation. 129
an NDE include absence of fear of death, more spiritual Regardless of this, healthcare workers continue to dem-
view of life, less regard for material wealth and/or a onstrate a reluctance to discuss CPR options with patients.
heightened chemical sensitivity. 119,120 The incidence of Despite open discussion, poor documentation and com-
NDEs after cardiac arrest is reported at 6–18%, 118,123 with munication can result in CPR being inappropriately
the frequency generally being higher in people under 60 commenced. 132 Approximately one-third of patients suc-
119
years of age. Hence, an awareness of the incidence of cessfully resuscitated have subsequently stated that they
133
NDEs, the cultural differences and needs of the person did not want to be resuscitated. Conversely, and con-
with a reported NDE are essential postcardiac arrest. 120,124 trary to medical and nursing opinions, some people
choose CPR even when they have a terminal illness, coma
LEGAL AND ETHICAL or serious disability. 129
CONSIDERATIONS Standardised orders for limitations on life-sustaining
treatments (e.g. DNAR, POLST) should be considered
Burgeoning technology in the 1960s enabled the support to decrease the incidence of futile resuscitation attempts
of oxygenation and circulation for people whose illnesses and to ensure that adult patient’s wishes are honoured.
would have been lethal just a few years before. Enthusi- These orders should be specific, detailed, transferable
asm for restoration of life led healthcare workers to rou- across healthcare settings, and easily understood. Pro-
tinely initiate CPR for all patients who died in hospital. 125 cesses, protocols and systems should be developed that
Unfortunately, this led to inappropriate resuscitation fit within local cultural norms and legal limitations
attempts and the realisation of the economic, medical to allow providers to honour patient’s wishes about
and ethical burden to society when survivors had a resul- resuscitation efforts. With the exception of a zero sur-
24
tant poor quality of life. 126 In the 1970s, growing concern vival rate there remains no formal consensus on DNAR
about inappropriate application of CPR and patient’s decision-making practices or the termination of resuscit-
rights led authors to suggest means of forgoing resuscita- tion. While researchers have attempted to develop prog-
127
tion and involving patients in decision making. Tradi- nostic indicators for cardiac arrest outcome, moralists
tionally, the decision to initiate or withhold CPR was would argue that the use of such prognostic tools alone
often made by the treating medical team in the absence reflect utilitarianism, 133 and should never be used in
of the patient or family. 128
isolation of the input of the patient and healthcare
Hospitals responded by developing procedures for with- team. 134
holding CPR through the documentation of ‘do not
attempt to resuscitate’ (DNAR) orders, physician orders SUMMARY
for life-sustaining treatment (POLST), advance directives Outcomes for patients after in-hospital sudden cardiac
or living wills 128 (see Chapter 5). For patients or their arrest remain poor. Successful management of a patient
surrogates to meaningfully participate in decision making following SCA depends largely on the timely implemen-
about CPR, they must have some understanding of sur- tation of the chain of survival. Nurses should understand
vival rates and adverse effects associated with CPR. 129 the role of the chain of survival in the resuscitation of the
Consequently, much debate has ensued over the right of person following cardiac arrest. The chain emphasises the
a person to forgo treatment. 125
importance of early recognition and intervention, con-
Research proposes that while patients want to be involved tinuous uninterrupted compressions and the early use of
in CPR decision making and want some form of advance the defibrillator as a BLS skill. Despite the plethora of
directive, their knowledge is limited and often derived research on the topic of resuscitation, there is much we
from television dramas. 128,130 Understanding of morbidity still do not know.


Case study

Thomas was brought into the Emergency Department (ED) at to leave the department. His respiratory rate was 40 with an
1500hrs suffering an acute asthma attack. The paramedics were audible wheeze and a heart rate was 130 beats per minute (sinus
called to his home by Thomas’ mother. Thomas was a 42-year-old tachycardia).
man with an intellectual disability who lived at home with his
elderly mother as his carer. The paramedics stated that they had Thomas was treated for an acute asthma attack in the ED with
inserted intravenous cannula, administered oxygen and salbuta- oxygen, continuous salbutamol nebulisers, ipratropium bromide
mol by nebuliser times three (once on arrival to his home and twice nebuliser and IV hydrocortisone. General screening bloods were
during transport to the ED). On assessment, Thomas was unable to obtained including an arterial blood gas and urea and electrolytes.
speak in sentences and was thrashing around the trolley wanting Non-invasive ventilation with positive end expiratory pressure

Resuscitation 673



Case study, Continued
(PEEP) and pressure support was initiated. However, Thomas hypothermia/hyperthermia, tension pneumothorax, tamponade,
became increasingly anxious, frightened, trying to get off the ED toxins, thrombosis.
trolley and continually attempting to remove the mask.
After every second loop of CPR Thomas was given 1 mg of IV
At this stage Thomas had an altered conscious state, was adrenaline. Each cycle equated to 2 minutes of CPR (5 sets of 30
exhausted, tachycardic, tachypnoeic and hypoxic. It was evident com pressions and 2 breaths). Compressions continued during all
that Thomas was failing and was in need of sedation, paralysis, interventions in order to minimise interruptions to CPR.
intubation and mechanical ventilation. There was some discus- During the simultaneous ALS interventions, it became evident that
sion regarding the extent of Thomas’ disability issues and Thomas was ventilating only one lung, his trachea was displaced
whether intubation and ventilation was suitable. It was decided to the right and lung sounds were absent from the left chest. In
that in the absence of an advance directive or ‘do not resuscitate’ view of his acute asthma attack and subsequent mechanical ven-
(DNR) order that a continuation of resuscitation was appropriate tilation it was clear that Thomas was suffering a tension pneumo-
and proper. thorax that resulted in PEA and cardiopulmonary arrest. An urgent

The decision to intubate was made, consent was gained from chest X-ray was ordered, but in the meantime a 16 gauge IV
his mother and Thomas was sedated and paralysed and intu- cannula was inserted in the second intercostal space on the left
bated with a size 8 mm endotracheal tube (ETT). Following his side of the anterior chest. Thomas’ chest was decompressed and
intubation Thomas was ventilated on pressure control (SIMV an underwater seal chest drain was set up to be inserted. This inser-
mode) with a rate of 28 and an inspiratory/expiratory (I : E) ratio tion resulted in Thomas’ tension pneumothorax being successfully
of 1 : 4. During insertion of an arterial line Thomas was noted resolved.
to be pulseless with a sinus rhythm on the monitor. A diagnosis Four minutes into the arrest, return of spontaneous circulation was
of pulseless electrical activity (PEA) was made and CPR was achieved and compressions were ceased, and the resuscitation
commenced immediately at a compression ventilation ratio of effort moved to postresuscitation therapy. The aims of this therapy
30 : 2. were to continue respiratory support, maintain cerebral perfusion,
treat and prevent cardiac arrhythmias and determine and treat the
Thomas was given 1 mg of adrenaline intravenously and CPR at a cause of the arrest.
rate of 100 compressions per minute was continued for two
minutes. During this time two main focuses of resuscitation were Thomas was admitted to the ICU, intubated, mechanically venti-
implemented simultaneously, implementation of advanced life lated, sedated and paralysed. Therapeutic hypothermia was insti-
support interventions and discovery and treatment of potential tuted as per the ICU’s guideline. A cooling kit was placed on
causes of arrest. The interventions applied were making sure that Thomas and he was given intravenous ice cold saline 30 mL/kg
the ETT placement was accurate and both lungs were ventilated over 30 minutes. His core temperature was maintained at 32–34 C
°
(waveform capnography was attached); ensuring Thomas was for 24 hours. After 24 hours, Thomas was gradually warmed to a
given 100% oxygen via the ETT, confirming appropriate function- normal core temperature. Thomas remained in the ICU for 8 days
ing IV access. Potential causes of the arrest were considered, and postresuscitation care continued to ensure the best possible
hypoxia, hypovolaemia, hyper/hypokalaemia/metabolic disorders, outcome for him.





Research vignette

Kory P, Weiner J, Mathew J, Fukunaga M, Palmero V, Singh B et al. primary emphasis on speed. The main endpoints were the time
A rapid, safe, and low-cost technique for the induction of mild intervals between return of spontaneous circulation (ROSC),
therapeutic hypothermia in post-cardiac arrest patients. Resuscita- initiation of hypothermia (IH), and achievement of target tem-
tion 2011; 82(1): 15–20. perature (TT).
Abstract Results
Aim of study 65 patients underwent MTH during a 3-year period. All patients
The benefits of inducing mild therapeutic hypothermia (MTH) in reached target temperature. Median ROSC–TT was 134 min.
cardiac arrest patients are well established. Timing and speed of Median ROSC–IH was 68 min. Median IH–TT was 60 min. IH–TT
induction have been related to improved outcomes in several cooling rate was 2.6 °C/h. Complications were similar to that of
animal trials and one human study. We report the results of an other large trials. 31% of this mixed population of IHCA and OHCA
easily implemented, rapid, safe, and low-cost protocol for the patients recovered to a Pittsburgh cerebral performance score
induction of MTH. (CPC) of 1 or 2.
Methods Conclusion
All in-hospital cardiac arrest (IHCA) and out-of-hospital cardiac A protocol using a combination of core and surface cooling modal-
arrest (OHCA) patients admitted to an intensive care unit meeting ities was rapid, safe, and low cost in achieving MTH. The cooling
inclusion criteria were cooled using a combination modality of rate of 2 °C/hour was superior to most published protocols. This
rapid, cold saline infusion (CSI), evaporative surface cooling, and method uses readily available equipment and reduces the need for
ice water gastric lavage. Cooling tasks were performed with a costly commercial devices.

Research vignette, Continued
Critique Performance Category (CPC). This scale rates patients from 1
The use of therapeutic hypothermia as a modality to improve (normal) through to 5 (certified brain-dead) and has been used as
159
mortality and morbidity in out of hospital cardiac arrest has been a comparable outcome measure in similar recent studies. This
147
well recognised in the literature since 2002. The International study noted that 31 percent of participants had a CPC score of 1
Liaison Committee on Resuscitation (ILCOR) published an advisory or 2. While the Australian experience has not been discussed,
statement in 2003 recommending the implementation of thera- generalisation to the Australian context should be made with
peutic hypothermia. The American Heart Association (AHA) and caution.
148
the European Resuscitation Council (ERC) also published thera- Whilst the researchers claim that their modality of therapeutic
peutic hypothermia guidelines following the ILCOR 2005 con- hypothermia is rapid, safe and low cost, they highlight that the
149
sensus on science and treatment recommendations, and these major barrier inhibiting the uptake of this treatment is technical
150
were updated and republished in 2010. However, as pointed difficulties. The researchers attribute these difficulties to the cost
out in this paper, the uptake of therapeutic hypothermia across of commercial equipment required to rapidly and effectively
the world has been slow and reasons for this have included the implement therapeutic hypothermia. This cost is underexplored in
cost of equipment used for cooling. 151-156 When referring to these this study; it is eluded that all devices are expensive and therefore
statements of utilisation, the reader should be aware that the unattainable by many hospitals. The researchers then state that
Australian experience has not been discussed and therefore gen- their method is labour -intensive, however the cost comparison of
eralisation of the Australian context cannot be made. Further, the labour as opposed to use of the various devices is not explored.
as the authors note, the use of a single study site limits the The insertion and confirmation of nasograstric tube (NGT) occurred
generalisability of the findings.
by auscultation and aspiration of gastric fluid. Evidence cautions
The ILCOR statement on therapeutic hypothermia states that intra- against the use of litmus paper, auscultation and bubbling to
venous ice cold fluids (30 mL/kg) can safely initiate therapeutic confirm NGT placement, with pH testing and X-ray confirmation
161
hypothermia and the use of ice packs and/or cooling blankets and preferred. Thus, the reader should be aware that the use of ice-
150
pads can maintain temperature control. In this study, therapeutic water gastric lavage is not supported by ILCOR and that there are
hypothermia was initiated at 40 mL/kg; the authors do not state inherent risks of NGT misplacement. Replication of the study
why they used a higher fluid volume than recommended by ILCOR. without the ice-water gastric lavage cooling technique will likely
Similarly, the use of ice-water gastric lavage in the study has not be beneficial.
been recommended by ILCOR. Other reported methods of non- The benefits of initiating mild therapeutic hypothermia following
invasive cooling not recommended by ILCOR, but evident in the an OHCA or IHCA are well documented in the literature. The
literature, includes the trans-nasal insertion of an evaporative authors rightly note that transferring this evidence into practice
coolant into the nasopharynx. 157-159
has not been seen and cite the ease of cooling processes as
Various methods have been documented for recording and moni- its potential barrier. In the study, the researchers report a redu-
toring the core temperature, including involving the bladder, ction in the ROSC to initiation of hypothermia time (257 to 132
160
rectum, pulmonary artery and oesophagus. While pulmonary minutes) with targeted education, raising clinical awareness
artery catheters are considered to be ‘gold standard’, the use of through lectures and wide distribution of cooling protocols.
minimally-invasive monitoring such as oesophageal temperature Other studies have also found an increase in the therapeutic
monitoring is considered to be optimal. Temperature monitor- hypothermia following the implementation of a standardised
159
ing using the bladder and the rectum should be interim measures protocol. 162,163
only as there is typically is a ‘temperature lag time’ behind the core
temperature. In addition, variability of measurements occurs with The mix of patients in this study also needs consideration. Defini-
the flow of urine presence and faeces around the catheter. Con- tive data on benefit has been primarily based on out-of-hospital
sistent with ILCOR recommendations, re-warming commenced cardiac arrest (OHCA) with ILCOR only highlighting two studies
150
after 24 hours, however the authors state that the recommended that included both OHCA and in-hospital cardiac arrests (IHCA).
rate is no more than 0.5 °C/h. ILCOR makes no mention of the rate The researchers in this study had predominately IHCA patients
of rewarming and the researchers reference this rate to Scandina- (n = 40) whereas OHCA patients were of lower numbers (n =
vian Clinical Practice. The researchers in the study achieved a 25). This study is important as it adds weight to the supportive
44
re-warming rate of 0.18 °C/h. evidence for therapeutic hypothermia for all patients suffering
cardiac arrest who remain comatose post return of spontaneous
Cognitive preservation was measured as an outcome measure circulation. Interestingly the IHCA group had better neurological
in the current study using the Glasgow-Pittsburg Cerebral outcomes overall when compared with the OHCA group.



Learning activities

All learning activities relate to the case study. 4. Discuss the pathophysiology of PEA in relation to the case
1. Discuss the management of this patient in relation to the ALS study.
flowchart. 5. Outline the role of therapeutic hypothermia in post arrest care.
2. Discuss the ethical issues of consent and limitations of treat- 6. Outline the postresuscitation management that is related to
ment as related to the case study. this case study.
3. Identify potential causes of PEA.

Resuscitation 675

ONLINE RESOURCES 24. Soar J, Mancini M, Bhanji F et al. On behalf of the Education, Implementa-
tion, and Teams Chapter Collaborators. Part 12: Education, implementation,
American Heart Association (AHA), http://www.americanheart.org and teams: 2010 international consensus on cardiopulmonary resuscitation
Australian Resuscitation Council (ARC), http://www.resus.org.au and emergency cardiovascular care science with treatment recommenda-
Center for Pediatric Emergency Medicine (CPEM), http://www.med.nyu.edu/ tions. Resuscitation 2010; 81: e288–330.
peder/cpem 25. Smith G. In-hospital cardiac arrest: Is it time for an in-hospital ‘chain of
European Resuscitation Council (ERC), http://www.erc.edu prevention’? Resuscitation 2010; 81(9): 1209–11.
International Liaison Committee on Resuscitation (ILCOR), http://www.ilcor.org/ 26. Hajbaghery M, Mousavi G, Akbar H. Factors influencing survival after
en/home in-hospital cardiopulmonary resuscitation. Resuscitation 2005; 66(3):
New Zealand Resuscitation Council (NZRC), http://www.nzrc.org.nz 317–21.
The Regional Emergency Medical Services Council of New York City, http://www. 27. Koster R, Baubin M, Bossaert L et al. European Resuscitation Council Guide-
nycremsco.org/default.asp. lines for Resuscitation 2010 Section 2. Adult basic life support and use of
automated external defibrillators Resuscitation 2010; 81(10): 1277–92.
REFERENCES 28. Brindley P, Simmonds M, Gibney R. Medical emergency teams: Is there
M.E.R.I.T? Can J Anaesthes 2007; 54(5): 389–91.
29. Kause J, Smith G, Prytherch D, Parr M, Flabouris A, Hilman K. A comparison
1. Rubart M, Zipes D. Mechanisms of sudden cardiac death. J Clin Investigation of antecedents to cardias arrests, deaths and emergency intensive admissions
2005; 115(9): 2305–15. in Australia and New Zealand, and the United Kingdom – The ACADEMIA
2. Meyer A, Cameron P, Smith K, McNeil J. Out-of-hospital cardiac arrest. eMJA study. Resuscitation 2004; 62(2): 275–82.
2000; 172: 73–6. 30. Considine J, Botti M. Who, when and where? Identification of patients at
3. Ali S, Antezano S. Sudden Cardiac Death. South Med J 2006; 99(5): risk of an in-hospital adverse event: implications for nursing practice. Int J
502–10. Nurs Res 2004; 10(1): 21–31.
4. Rea T, Eisenberg M, Sinibaldi G. Incidence of EMS-treated out-of-hospital 31. DeVita M, Smith G, Adam S et al. Identifying the hospitalised patient in
cardiac arrest in the United States. Resuscitation 2004; 63(1): 17–24. crisis: A consensus conference on the afferent limb of Rapid Response
5. Atwood C, Eisenberg M, Herlitz J. Incidence of EMS-treated out-of-hospital Systems Resuscitation 2010; 81(4): 375–82.
cardiac arrest in Europe. Resuscitation 2005; 67(1): 75–80. 32. Lee A, Bishop G, Hillman K, Daffurn K. The medical emergency team.
6. Holmgren C, Bergfeldt L, Edvardsson N et al. Analysis of initial rhythm, Anaesth Intens Care 1995; 23(2): 183–6.
witnessed status and delay to treatment among survivors of out-of-hospital 33. Prytherch D, Smith G, Schmidt P, Featherstone P. ViEWS – Towards a
cardiac arrest in Sweden. Heart and Education in Heart 2010; 96(22): national early warning score for detecting adult inpatient deterioration Resus-
1826–30. citation 2010; 81(8): 932–7.
7. Rea T, Pearce R, Raghunathan T. Incidence of out-of-hospital cardiac arrest. 34. Hillman K. Critical care without walls. Curr Opinion Crit Care 2002; 8(6):
Am J of Cardiol 2004; 93: 1455–60. 594–9.
8. Waalewijn R, Nijpels MA, Tijssen JG, Koster RW. Prevention of deterioration 35. Massey D, Aitken L, Chaboyer W. Literature review: do rapid response
of ventricular fibrillation by basic life support during out-of-hospital cardiac systems reduce the incidence of major adverse events in the deteriorating
arrest. Resuscitation 2002; 54(1): 31–6. ward patient? J Clin Nurs 2010; 19(23–24): 3260–73.
9. Herlitz J, Engdahl J, Svensson L, Young M, Angquist K-A, Holmberg S. Can 36. Chan P, Jain R, Nallmothu B, Berg R, Sasson C. Rapid response teams: a
we define patients with no chance of survival after out-of-hospital cardiac systematic review and meta-analysis. Archives of Internal Med 2010; 170(1):
arrest? Heart Lung 2004; 90: 1114–18. 18–26.
10. Australian Institute of Health and Welfare (AIHW). Australia’s health 2010. 37. Laurens N, Dwyer T. The effect of Medical Emergency Teams on patient
Australia’s health series no. 12. Canberra: AIHW; 2010. outcome: A review of the literature. Int J Nurs Prac 2010; 16(6): 533–44.
11. Muller D, Agrawal R, Arntz H. How sudden is sudden cardiac death? Circula- 38. Ray EM, Smith R, Massie S et al. Family alert: Implementing direct family
tion 2006; 114: 1146–50. activation of a pediatric rapid response team. Joint Comm J on Quality &
12. Deakin C, Nolan J, Soar J. European Resuscitation Council Guidelines for Patient Safety 2009 35(11): 575–80.
Resuscitation 2010. Section 4. Adult advanced life support. Resuscitation 2010; 39. Australian Resuscitation Council and New Zealand Resuscitation Council
81(10): 1305–52. (ARC NRC). Airway: Guideline 4. Available at: http://www.resus.org.au/.
13. Herlitz J, Svensson L, Engdahl J. Characteristics of cardiac arrest and resus- 40. Mackway-Jones K, Molyneux E, Phillips B, Wieteska K. Advanced paediatric
citation by age group: an analysis from the Swedish Cardiac Arrest Registry. life support: the practical approach, 4th edn. Blackwell Publishing; 2005.
Am J Emerg Med 2007; 25(9): 1025–31. 41. Wyllie J, Perlman J, Kattwinkel J et al. On behalf of the Neonatal Resuscita-
14. Dickson E, Anders N. Infant resuscitation. Curr Anaesthetics Crit Care 2004; tion Chapter Collaborators. Part 11: Neonatal resuscitation: 2010 Interna-
15: 53–60. tional consensus on cardiopulmonary resuscitation and emergency
15. Atkins DL, Everson-Stewart S, Sears GK et al. Epidemiology and outcomes cardiovascular care science with treatment recommendations. Resuscitation
from out-of-hospital cardiac arrest in children: the Resuscitation Outcomes 2010(10); 81: e260–87.
Consortium Epistry – Cardiac Arrest. Circulation 2009; 119(11): 1484–91. 42. Berg R, Saunders A, Kern K, Hilwig R, Heidenreich J, Porter M. Adverse
16. Rosen K, Sinz E, Casto J. Basic and advanced life support, acute resuscitation, hemodynamic effects of interrupting chest compressions for rescue breath-
and cardiac resuscitation. Curr Opin Anaesthesiol 2001; 14(2): 177–8. ing during cardiopulmonary resuscitation for ventricular defibrillation
17. Frenneaux M. Cardiopulmonary resuscitation: some physiological consider- cardiac arrest. Circulation 2001; 104(20): 2465–70.
ations. Resuscitation 2003; 58(3): 259–65. 43. Nolan J, Hazinski M, Billi J et al. Part 1: Executive summary: 2010 Interna-
18. Ballew K. Cardiopulmonary resuscitation: recent advances. BMJ 1997; tional consensus on cardiopulmonary resuscitation and emergency cardio-
314(7092): 1462–6. vascular care science with treatment recommendations. Resuscitation 2010;
19. Cummins R, Chamberlain D, Hazinski M, Nadkarni V, Kloeck W, Kramer E. 81(1 Suppl1): e1–25.
Recommended guidelines for reviewing, reporting, and conducting research 44. Dwyer T. Psychological factors inhibiting family member’s confidence to
on in-hospital resuscitation: the in-hospital ‘Utstein style’ Circulation 1997; initiate CPR. Prehospital Emerg Care 2008; 12 April(2): 157–61.
95(8): 2213–39. 45. Assar D, Chamberlain D, Colquhoun M, Donnelly P, Handley A et al. Ran-
20. Nolan J, Soar J, Zideman D et al. European Resuscitation Council Guidelines domised controlled trial of staged teaching for basic life support: skill acqui-
for Resuscitation 2010. Section 1. Executive summary. Resuscitation 2010; sition at bronze stage. Resuscitation 2000; 45(1): 7–15.
81(10): 1219–76. 46. Koster R, Sayre M, Botha M et al. Part 5: Adult basic life support: 2010 Inter-
21. Petrie D, De Maio V, Stiell I. Factors affecting survival after prehospital national consensus on cardiopulmonary resuscitation and emergency car-
asystolic cardiac arrest in basic life support-defibrillation system OPALS diovascular care science with treatment recommendations. Resuscitation
Study Group. Canadian J of Emerg Med 2001; 3(3): 113–18. 2010; 81(10): e48–70.
22. Meaney P, Nadkarni V, Kern K, Indik J, Halperin H, Berg R. Rhythms and 47. Iwami T, Kawamura T, Hiraide A et al. Effectiveness of bystander-initiated
outcomes of adult in-hospital cardiac arrest. Crit Care Med 2010; 38(1): cardiac-only resuscitation for patients with out-of-hospital cardiac arrest.
101–8. Circulation 2007; 116(2): 900–7.
23. Genardi M, Cronin S, Thomas L. Revitalizing an established rapid response 48. Bobrow B, Spaite D, Berg R et al. Chest compression-only CPR by lay rescuers
team [Evaluation study]. DCCN 2008; 27(3): 104–9. and survival from out-of-hospital cardiac arrest. JAMA 2010; 304(3): 1447–54.

676 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

49. Delguercio L, Feins N, Cohn J, Coomaraswamy R, Wollman S, State D. tion in the emergency department: A prospective, randomized study.
Comparison of blood flow during external and internal cardiac massage in Resuscitation 2010; 81(8): 994–9.
man. Circulation 1965; 31 (Suppl1): 171–80. 74. Wenzel V, Krismer A, Arntz H, Sitter H, Stadlbauer K, Lindner K. European
50. Pellis T, Kette F, Lovisa D et al. Utility of pre-cordial thump for treatment of Resuscitation Council Vasopressor during Cardiopulmonary Resuscitation
out of hospital cardiac arrest: a prospective study. Resuscitation 2009; 80(1): Study Group: a comparison of vasopressin and epinephrine for out-of-hos-
17–23. pital cardiopulmonary resuscitation. New England J Med 2004; 350: 105–13.
51. Haman L, Parizek P, Vojacek J. Precordial thump efficacy in termination of 75. Stiell G, Hebert P, Wells G. Vasopressin versus epinephrine for in hospital
induced ventricular arrhythmias. Resuscitation 2009; 80(1): 14–16. cardiac arrest: a randomised controlled trial. Lancet 2001; 358: 105–9.
52. Wilson R, Gwinnutt C. Recent advances in cardiopulmonary resuscitation. 76. Aung K, Htay T. Vasopressin for cardiac arrest: a systematic review and meta-
Curr Anaesth Crit Care 2004; 15(6): 418–26. analysis. Archives of Internal Med 2005; 165: 17–24.
53. Deakin C, Nolan J, Sunde K, Koster R. European Resuscitation Council 77. Kudenchuk P, Cobb L, Copass M, et al. Amiodarone for resuscitation after
Guidelines for Resuscitation 2010 Section 3. Electrical therapies: Automated out-of-hospital cardiac arrest due to ventricular fibrillation. New England J of
external defibrillators, defibrillation, cardioversion and pacing. Resuscitation Med 1999; 341: 871–8.
2010; 81(10): 1293–1304. 78. Lunxian T, Hu X, Qing H. Intravenous amiodarine for the treatment of
54. Dwyer T, Mosel Williams L, Jacobs I. Benefits and use of shock advisory ventricular tachycardia and ventricular fibrillation. Cochrane Database of
defibrillators in-hospitals. Int J Nurs Prac 2004; 10(2): 86–92. Systematic Reviews 2003(2). CD004195.
55. vanAlem AP, Sanou BT, Koster RW. Interruption of cardiopulmonary resus- 79. Allegra J, Lavery R, Cody R. Magnesium sulfate in the treatment of refractory
citation with the use of the automated external defibrillator in out-of-hos- ventricular fibrillation in the prehospital setting. Resuscitation 2001; 49(3):
pital cardiac arrest. Annals of Emerg Med 2003; 42(4): 449–57. 245–9.
56. Cummins R, Sanders A, Mancini E, Hazinski M. In-Hospital Resuscitation 80. Sehra R, Underwood K, Checchia P. End tidal CO 2 is a quantitative measure
– A statement for healthcare professionals from the American Heart Associa- of cardiac arrest. Pacing Clin Electrophysiolgy 2003; 26(1): 515–17.
tion Emergency Cardiac Care Committee and the Advanced Cardiac Life 81. Hogan M, Foreman K, Naghavi M. Maternal mortality for 181 countries,
Support, Basic Life Support, Pediatric Resuscitation, and Program Adminis- 1980–2008: a systemic analysis of progress towards Millennium Develop-
tration subcommitties. Circulation 1997; 95(8): 2211–12. ment Goal 5. Lancet 2010; 375(9726): 1609–23.
57. Valenzuela T, Roe D, Nichol Clark L. Outcomes of rapid defibrillation by 82. Lewis G. The Confidential Enquiry into Maternal and Child Health
security officers after cardiac arrest in casinos. New England J of Med 2000; (CEMACH). Saving Mothers’ Lives: Reviewing maternal deaths to make mother-
343(17): 1206–9. hood safer, 2003–005. The seventh report of the confidential enquiries into mater-
58. Grundry J, Comess K, De Rook F, Jorgenson D, Brady G. Comparison of nal deaths in the United Kingdom. London: CEMACH; 2007.
naive sixth-grade children with trained professionals in the use of an auto- 83. Soar J, Perkins G, Alfonzo A et al. European Resuscitation Council Guide-
matic external defibrillator. Circulation 1999; 100(16): 1703–7. lines for Resuscitation 2010 Section 8. Cardiac arrest in special circum-
59. Sunde K, Jacobs I, Deakin C, Hazinski M, Kerber R et al on behalf of Defibril- stances: Electrolyte abnormalities, poisoning, drowning, accidental
lation Chapter Collaborators. Part 6: Paediatric 2010 International consensus hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma,
on cardiopulmonary resuscitation and emergency cardiovascular care science pregnancy, electrocution Resuscitation 2010; 81(10): 1400–33.
with treatment recommendations. Resuscitation 2010; 81s: e71–85. 84. Cardosi R, Porter K. Cesarean delivery of twins during maternal cardiopul-
60. Hess EP, Atkinson EJ, White RD. Increased prevalence of sustained return of monary arrest. . Obstet Gynecol 1998; 94(4): 695–9.
spontaneous circulation following transition to biphasic waveform defibril- 85. Jones SJ, Kinsella SM, Donald FA. Comparison of measured and estimated
lation. Resuscitation 2008; 77(1): 39–45. angles of table tilt at Caesarean section. Brit J Anaesthetics 2003; 90(1):
61. Morrison L, Dorian P, Long J et al. Out-of-hospital cardiac arrest rectilinear 86–7.
biphasic to monophasic damped sine defibrillation waveforms with 86. Luppi C. Cardiopulmonary resuscitation: pregnant women are different.
advanced life support intervention trial (ORBIT). Resuscitation 2005; 66(2): AACN Clin Iss Adv Pract Acute Crit Care 1997; 8(4): 574–85.
149–57. 87. Morris S, Stacey M. Resuscitation in pregnancy. BMJ 2003; 327(7426):
62. Australian Resuscitation Council and New Zealand Resuscitation Council 1277–80.
(ARC & NZRC). The Australian Resuscitation Council Online. Available 88. Zafrena K, Durrerc B, Herryd J, Bruggere H. Lightning injuries: prevention
from: http://www.resus.org.au/. and on-site treatment in mountains and remote areas: official guidelines of
63. de Caen A, Kleinman M, Chameides L et al. On behalf of the Paediatric Basic the International Commission for Mountain Emergency Medicine and the
and Advanced Life Support Chapter Collaborators. Part 10: Paediatric basic Medical Commission of the International Mountaineering and Climbing
and advanced life support: 2010 International consensus on cardiopulmo- Federation (ICAR and UIAA MEDCOM). Resuscitation 2005; 65(3):
nary resuscitation and emergency cardiovascular care science with treatment 369–72.
recommendations. Resuscitation 2010; 81(2): e213–59. 89. Layon A, Modell J. Drowning update. Anesthesiology 2009; 110: 1390–1401.
64. Christenson J, Andrusiek D, Everson-Stewart S. Chest compression fraction 90. Salomez F, Vincent J. Drowning: a review of epidemiology, pathology, treat-
determines survival in patients with out-of-hospital ventricular fibrillation. ment and prevention. Resuscitation 2004; 63(3): 261–8.
Circulation 2009; 120(13): 1241–7. 91. Frakes M. Measuring end-tidal carbon dioxide: clinical applications and
65. Chan P, Krumholz H, Spertus J et al. Automated external defibrillators and usefulness. Crit Care Nurse 2001; 21(5): 23–37.
survival after in-hospital cardiac arrest JAMA 2010; 304(19): 2129–36. 92. Cortney D, Watts J, Kline J. End tidal CO 2 is reduced during hypotension
66. Gatward M, Thomas J, Nolan J, Cook T. Effect of chest compressions on the and cardiac arrest in a rat model of massive pulmonary embolism. Resuscita-
time taken to insert airway devices in a manikin. Brit J Anaest 2008; 100: tion 2002; 53(1): 83–91.
351–6. 93. Aufderheide T, Sigurdsson G. Hyperventilation-induced hypotension during
67. Herlitz J, Bang A, Alsen B, Aune S. Characteristics and outcome among cardiopulmonary resuscitation. Circulation 2004; 109(16): 1960–65.
patients suffering from in hospital cardiac arrest in relation to whether the 94. Cooper S, Wakelam A. Leadership of resuscitation teams: ‘lighthouse leader-
arrest took place during office hours. Resuscitation 2002; 53(1): 127–33. ship. Resuscitation 1999; 42(1): 27–45.
68. De Maio V, Stiell J, Wells G, Spaite D. Cardiac arrest witnessed by emergency 95. Meerabeau L, Page S. I’m sorry if I panicked you: Nurses’ accounts of team-
medical services personnel: descriptive epidemiology, prodromal symptoms, work in cardiopulmonary resuscitation. J Interprofessional Care 1999; 13(1):
and predictors of survival. Annals of Emerg Med 2000; 35(2): 138–46. 29–35.
69. Rosborough J, Deno D. Electrical therapy for post defibrillatory pulseless 96. Dwyer T, Mosel Williams L. Nurses’ behaviour regarding CPR and the theo-
electrical activity. Resuscitation 2004; 63(1): 65–72. ries of reasoned action and planned behaviour. Resuscitation 2002; 52(1):
70. Wenzel V, Lindner KH, Augenstein S et al. Intraosseous vasopressin improves 85–90.
coronary perfusion pressure rapidly during cardiopulmonary resuscitation 97. Dwyer T, Mosel Williams L, Mummery K. Defibrillation beliefs of rural
in pigs. Crit Care Med 1999; 27(8): 1565–9. nurses: Focus group discussions guided by the theory of planned
71. Duncan A. The critically ill child. In: Bersten A, Soni N, Oh T, eds. Oh’s behaviour. Int Electronic J Rural Remote Health Research, Education, Practice
intensive care manual. Oxford: Butterworth-Heinemann; 2003. and Policy 2005; 5(322). Available from: http://www.rrh.org.au/articles/
72. Shavit Y, Hoffmann R, Galbraith A, Waisman Y. Comparison of two mechan- showarticlenew.asp?ArticleID=322.
ical intraosseous infusion devices: a pilot, randomized crossover trial. Resus- 98. MacLean D, Guzzetta C, White C, Fontaine D, Eichhorn D, Meyers T. Family
citation 2009; 80(9): 1029–33. presence during cardiopulmonary resuscitation and invasive procedures:
73. Leidel B, Kirchhoff C, Braunstein V, Bogner V, Biberthaler P, Kanz K. Com- Practices of critical care and emergency nurses. J of Emerg Nursing 2003;
parison of two intraosseous access devices in adult patients under resuscita- 29(3): 208–21.

Resuscitation 677

99. Mazer M, Cox L, Capon J. The public’s attitude and perception concerning 124. Daffin C. Near death experiences ‘must be taken seriously’. Nursing Standard
witnessed cardiopulmonary resuscitation. Crit Care Med 2006; 34(12): 2002; 16(17): 9–13.
2925–8. 125. Lynn J. Regulating hearts and minds: the mismatch of law, custom and
100. Ong M, Chung W, Mei J. Comparing attitudes of the public and medical resuscitation decisions. J Am Geriatric Society 2003; 51(10): 45–52.
staff towards witnessed resuscitation in an Asian population. Resuscitation 126. Landry F, Parker J, Phillips Y. Outcome of cardiopulmonary resuscitation in
2007; 73(1): 103–8. the intensive care setting. Archives of Internal Med 1992; 152(11): 2305–8.
101. Miller H, Stiles A. Family Presence During Resuscitation and Invasive Proce- 127. Rabkin M, Gillerman G, Rice N. Orders not to resuscitate. New Engl J of Med
dures: The Nurse Experience. Qualitative Health Research 2009; 19(10): 1976; 295(12): 364–72.
1431–42. 128. Kerridge I, Pearson S, Rolfe I, Lowe M. Decision making in CPR: attitudes of
102. Newton A. Witnessed resuscitation in critical care: The case against. Intens hospital patients and health care professionals. Med J Aust 1998; 169:
Crit Care Nursing 2002; 18(3): 146–50. 128–31.
103. Boyd R, White S. Does witnessed cardiopulmonary resuscitation alter per- 129. Kerridge I, Pearson S, Rolfe I, Lowe M, McPhee J. Impact of written informa-
ceived stress in accident and emergency staff? Euro J of Emerg Med 2000; 7(1): tion on knowledge and preferences for cardiopulmonary resuscitation. 2.
51–3. eMJA 1999; 171: 239–44.
104. Weslien M, Nilstun T, Lundqvist A, Fridlund B. Narratives about resuscita- 130. Harris D, Willoughby H. Resuscitation on television: Realistic or ridiculous?
tion: Family members differ about presence. Euro J of Cardiovasc Nurs 2006; A quantitative observational analysis of the portrayal of cardiopulmonary
5(1): 68–74. resuscitation in television medical drama Resuscitation 2009; 80(11):
105. Schmidt B. Review of Three Qualitative Studies of Family Presence During 1275–9.
Resuscitation. The Qualitative Report 2010; 15(3): 731–6. 131. Heyland D, Frank C, Groll D. Understanding cardiopulmonary resuscitation
106. Fulbrook P, Albarran J, Latour J. An European survey of critical care decision making: perspectives of seriously ill hospitalised patients and
nurses’ attitudes and experiences of having family members present family members. Chest 2006; 130(2): 419–28.
during cardiopulmonary resuscitation Int J Nurs Studies 2005; 45(5): 132. Giles H, Moule P. ‘Do not attempt resuscitation’ decision-making: a study
557–67. exploring the attitudes and experiences of nurses. Nursing Crit Care 2004;
107. Larkin G. Termination of resuscitation: the art of clinical decision making. 9(3): 115–22.
Curr Opin Crit Care 2002; 8(3): 224–9. 133. Hayward M. Cardiopulmonary resuscitation: are practitioners being realis-
108. Nadkarni V, Larkin G, Peberdy M. First documented rhythm and clinical tic? Brit J Nurs 1999; 8(12): 810–14.
outcome from in-hospital cardiac arrest among children and adults. JAMA 134. Fritz Z, Fu J. Ethical issues surrounding do not attempt resuscitation orders:
2006; 295(1): 50–57. decisions, discussions and deleterious effects. J Med Ethics 2010; 36(10):
109. Nolan J, Laver S, Welch A, Harrison D, Gupta U, Rowan K. Outcome follow- 593–7.
ing admission to UK intensive care units after cardiac arrest: a secondary 135. Smith R, Hickey B, Santamaria J. Automated external defibrillators and
analysis of the ICNARC Case Mix Programme Database. Anaesthesia 2007; survival after in-hospital cardiac arrest: early experience at an Australian
62(12): 1207–16. teaching hospital. Crit Care Resusc 2009; 11(4): 261–5.
110. Nolan J, Neumara R, Adriea C et al. Post-cardiac arrest syndrome: Epidemi- 136. Forcina M, Farhat A, O’Neil W, Haines D. Cardiac arrest survival after imple-
ology, pathophysiology, treatment, and prognostication: A Scientific State- mentation of automated external defibrillator technology in the in-hospital
ment from the International Liaison Committee on Resuscitation; the setting. Crit Care Med 2009; 37(4): 1229–36.
American Heart Association Emergency Cardiovascular Care Committee; 137. Zafari A, Zarter S, Heggen V et al. A program encouraging early defibrillation
the Council on Cardiovascular Surgery and Anesthesia; the Council on Car- results in improved in-hospital resuscitation efficacy. J Am Coll Cardiol 2004;
diopulmonary, Perioperative, and Critical Care; the Council on Clinical 44(4): 846–52.
Cardiology; the Council on Stroke (Part 1). Int Emerg Nurs 2009; 17(4): 138. Haines D. Automated external defibrillators and the law of unintended
203–25. consequences. JAMA 2010; 304(19): 2178–9.
111. Binks A, Nolan J. Post-cardiac arrest syndrome. Minerva Anestesiol 2010; 76: 139. Kern K, Morley P, Babbs C. Use of adjunctive devices in cardiopulmonary
362–8. resuscitation. Annals of Emerg Med 2001; 37(4 Suppl): S568–77.
112. Negovsky V. Postresuscitation disease. Crit Care Med 1988; 16(10): 942–6. 140. Hickey R. Recent developments and emerging concepts in cardiopulmonary
113. Nolan J, Morley P, Hoek T, Hickey R. Therapeutic hypothermia after cardiac cerebral resuscitation. Clinic Pediatr Emerg Med 2004; 5: 217–23.
arrest: an advisory statement by the Advanced Life Support Task Force of the 141. Timerman S, Cardoso L, Ramires J, Halperin H. Improved hemodynamic
International Liaison Committee on Resuscitation. Resuscitation 2003; 57(3): performance with a novel chest compression device during treatment of
231–5. in-hospital cardiac arrest. Resuscitation 2004; 61(3): 273–80.
114. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypother- 142. Hand H. Cardiopulmonary resuscitation: the laryngeal mask airway. Emerg
mia to improve the neurological outcome after cardiac arrest. New England Nurse 2002; 10(104): 31–7.
J Med 2002 346(8): 557–63. 143. Cook T, Strube P, Lees M, Millar J, Baskett P. Randomised crossover compari-
115. Bernard S, Gray T, Buist M, Jones B, Silvester W, Gutteridge G. Treatment of son of the proseal with the classic laryngeal mask airway in unparalysed
comatose survivors of out-of-hospital cardiac arrest with induced hypother- anaesthetised patients. Br J Anaesth 2002; 88(4): 527–32.
mia. New Eng J Med 2002; 346(8): 557–63. 144. Kette F, Reffo I, Giordani G, Buzzi F, Borean V et al. The use of laryngeal tube
116. Poldermann K, Herold I. Therapeutic hypothermia and controlled normo- by nurses in out-of-hospital emergencies: preliminary experience. Resuscita-
thermia in the intensive care unit: practical considerations, side effects, and tion 2005; 66(1): 21–5.
cooling methods. Crit Care Med 2009; 37(3): 1101–20. 145. Tiah L, Wong E, Chen M, Sadarangani S. Should there be a change in teach-
117. Australian Resuscitation Council and New Zealand Resuscitation Council ing of airway management in the medical school curriculum? Resuscitation
(ARC NRC). Post-resuscitaion therapy in adult advanced life support: Guide- 2005; 64(1): 87–91.
line 11.7. Available from: http://www.resus.org.au/. 146. Kette F, Reffo I, Giordani G et al. The use of laryngeal tube by nurses in out-
118. Greystone B. Incidence and correlates of near-death experiences in a cardiac of-hospital emergencies: Preliminary experience Resuscitation 2005; 66(1):
care unit. Gen Hosp Psychiat 2003; 25(4): 269–76. 21–2.
119. Van Lommel P, van Wees R, Meyers V, Elfferich I. Near-death experience in 147. Bernard S, Gray T, Buist M, Jones B, Silvester W, Gutteridge G. Treatment of
survivors of cardiac arrest: a prospective study in the Netherlands. Lancet comatose survivors of out-of-hospital cardiac arrest with induced hypother-
2001; 358(15): 2039–45. mia. New Eng J Med 2002; 346(8): 557–63.
120. James D. What emergency department staff need to know about near-death 148. Nolan J, Morley P, Hoek T, Hickey R. Therapeutic hypothermia after cardiac
experiences. Top Emerg Med 2004; 26(1): 29–34. arrest: an advisory statement by the Advanced Life Support Task Force of the
121. Parnia S, Fenwick P. Near death experiences in cardiac arrest: vision of a International Liaison Committee on Resuscitation. Resuscitation 2003; 57(3):
dying brain or versions of a new science of consciousness. Resuscitation 2002; 231–5.
52(1): 5–11. 149. American Heart Association. American Heart Association Guidelines for
122. Belanti J, Perera M, Jagadheesan K. Phenomenology of Near-death Experi- Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part
ences: A Cross-cultural Perspective. Transcultural Psychiatry 2008; 45(1): 7.5: Postresuscitation Support Care. Circulation 2005; 112(5): 84–8.
121–33. 150. Morrison L, Deakin C, Morley P, Callaway C, Kerber R, Kronick S. Part 8:
123. Parina S, Waller D, Yeates R, Fenwick P. A qualitative and quantitative study Advanced life support: 2010 International Consensus on Cardiopulmonary
of the incidence, features and aetiol-ogy of near death experiences on cardiac Resuscitation and Emergency Cardiovascular Care Science with Treatment
arrest survivors. Resuscitation 2001; 48(2): 149–56. Recommendations. Circulation 2010; 122: S345–421.