Manual Icu

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Royal Adelaide Hospital

Intensive Care Unit

Medical Manual

2010 Edition

Website: http://icuadelaide.com.au/
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Foreword

Welcome to Intensive Care.

This manual has been written to facilitate the daily running of the RAH Intensive Care
Unit. It is by no means the definitive answer to all intensive care protocols and
procedures, nor is it designed to be a textbook.

A standardised approach to management is desirable for optimal patient care and safety,
improving communication and understanding between members of the ICU team and
associated specialties. This approach provides a common platform for staff who come
from different countries and training backgrounds.

The manual outlines various Protocols, which represent a standard approach to practice
within the Unit. These have been derived from the available literature, clinical
experience and where appropriate, cost-effectiveness. Guidelines designed to assist in
clinical management are included but patient management will ultimately depend upon
the clinical situation.

Assistance is always available from the Duty Consultant and senior nursing staff. Use
your time in the Unit to get the most out of the large clinical caseload. Ask questions
about clinical problems, equipment and procedures with which you are unfamiliar.
There are numerous textbooks, journals and references available in the Unit.

This manual has undergone numerous changes, with contributions from many of the
ICU staff and from other specialty services within the hospital. The contents of this
manual are produced from the consensus views of the senior medical staff and were
accurate at the time of publication.

A/Prof Robert Young
Director
2010 11
th
Edition

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CONTENTS

CONTENTS ........................................................................................................................ 3
PART 1 - ADMINISTRATION ............................................................................................. 6
A. Staffing - Royal Adelaide Hospital ICU ............................................................... 6
B. Rostering and Job Descriptions ............................................................................. 8
Table: Team Duties .............................................................................................. 8
Table: Registrar Shifts ....................................................................................... 10
C. Orientation .......................................................................................................... 11
D. Weekly Programme ............................................................................................. 12
Table: Weekly Unit Programme ........................................................................ 12
E. Admission and Discharge Policies ...................................................................... 13
F. Care for Patients Discharged from ICU for Terminal Care. ............................... 15
G. Clinical Duties in the ICU ................................................................................... 16
H. Documentation .................................................................................................... 19
I. Consent in ICU ................................................................................................... 21
J. ICU Ward Rounds ............................................................................................... 22
K. Clinical Duties Outside of the Intensive Care Unit ............................................. 23
L. Hospital Emergencies ......................................................................................... 28
M. Research in ICU .................................................................................................. 29
N. Information Technology in ICU .......................................................................... 30
PART 2 - CLINICAL PROCEDURES ................................................................................. 31
A. Introduction ......................................................................................................... 31
B. Procedures ........................................................................................................... 31
C. Peripheral IV catheters ........................................................................................ 32
D. Arterial Cannulation ............................................................................................ 33
E. Central Venous Catheters .................................................................................... 34
F. Urinary Catheters ................................................................................................ 36
G. Epidural Catheters ............................................................................................... 37
H. PICCO Catheters ................................................................................................. 37
Table: PiCCO Values and Decision Tree ........................................................... 38
I. Pulmonary Artery Catheters ................................................................................ 39
Table: Standard Haemodynamic Variables ........................................................ 41
J. Pleural Drainage .................................................................................................. 42
K. Endotracheal Intubation ...................................................................................... 44
L. Weaning Guidelines ............................................................................................ 49
Flowchart: Ventilation Weaning Protocol .......................................................... 50
M. Extubation ........................................................................................................... 51
N. Emergency Surgical Airway Access ................................................................... 52
O. Fibreoptic Bronchoscopy .................................................................................... 53
P. Tracheostomy ...................................................................................................... 54
Q. Pericardiocentesis................................................................................................ 57
R. Intra-aortic balloon counterpulsation .................................................................. 58
S. Cardiac Pacing .................................................................................................... 61
T. Oesophageal Tamponade Tubes ......................................................................... 64
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U. Extracorporeal Membrane Oxygenation .............................................................. 65
PART 3 - DRUGS AND INFUSIONS .................................................................................... 66
A. Policy ................................................................................................................... 66
B. Principles of drug prescription in Intensive Care ................................................ 67
C. Cardiovascular Drugs .......................................................................................... 67
Table: Cardiovascular effects of inotropes ......................................................... 68
Table: Inotropic Agents Used in ICU ................................................................. 69
Table: Vasopressors ............................................................................................ 70
Table: Antihypertensive & Vasodilator Agents .................................................. 71
Table: Antiarrhythmic Agents ............................................................................ 74
Table: Thrombolytics ......................................................................................... 76
Table: Antiplatelet Agents .................................................................................. 77
D. Respiratory Drugs ................................................................................................ 78
Table: Bronchodilators ....................................................................................... 79
E. Sedation, Analgesia and Muscle Relaxants ......................................................... 80
Table: Sedation Levels ....................................................................................... 80
Table: Sedatives / Analgesics ............................................................................. 82
Table: Muscle Relaxants .................................................................................... 84
F. Anticoagulation ................................................................................................... 85
Table: HITS Probability Score 4T Score ...................................................... 88
Table: Anticoagulants ......................................................................................... 89
Table: Heparin Infusion Protocol ....................................................................... 90
Table: Lepirudin Infusion Protocol .................................................................... 90
Table: Age Adjusted Warfarin Loading Protocol* ............................................. 91
G. Endocrine Drugs .................................................................................................. 92
Flowchart: Blood Glucose Management in ICU ................................................ 93
Table: Insulin Infusion Protocol ......................................................................... 93
Flowchart: Insulin Protocol for Patients Discharged from ICU ......................... 94
Table: Steroid Doses / Relative Potencies .......................................................... 96
H. Renal Drugs - Diuretics ..................................................................................... 97
Table: Diuretics .................................................................................................. 98
I. Gastrointestinal Drugs ......................................................................................... 99
Table: GI Drugs ................................................................................................ 100
J. Antibiotics ......................................................................................................... 101
Table: Vancomycin Dosing Schedule .............................................................. 104
Table: Antibiotic Infusion Schedules ............................................................... 105
Table: Peri-operative Antibiotic Prophylaxis ................................................... 107
Table: Perioperative Endocarditis Prophylaxis ................................................. 108
Table: Empirical Antibiotics ............................................................................ 109
Table: Antibiotics for Specific Organisms ....................................................... 111
PART 4 - FLUIDS AND ELECTROLYTES ........................................................................ 112
A. Principles of Fluid Management in Intensive Care............................................ 112
B. Nutrition ............................................................................................................ 114
Flowchart: Nutritional Therapy Protocol .......................................................... 116
Table: Average daily requirements ................................................................... 118
Table: Baxter TPN Solution Options ................................................................ 119
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C. Blood Component Therapy ............................................................................... 120
Table: Guidelines for the management of an elevated INR ............................. 126
Table: Xigris Dosing Schedule ........................................................................ 129
Table: Blood Transfusion Reactions ................................................................ 131
D. Guidelines for the Management of Electrolytes ................................................ 132
Table: Classification of Lactic Acidosis .......................................................... 140
PART 5 - CLINICAL MANAGEMENT ............................................................................. 143
A. Cardiopulmonary Resuscitation ........................................................................ 144
Flowchart: Basic Life Support ......................................................................... 144
Flowchart: Advanced Life Support .................................................................. 145
Flowchart: Paediatric Cardiorespiratory Arrest ............................................... 146
B. Induced Hypothermia Post Cardiac Arrest ........................................................ 147
C. Failed Intubation Drill ....................................................................................... 148
D. Respiratory Therapy .......................................................................................... 150
Table: Oxygen Delivery Devices ...................................................................... 150
E. Management of Cardiothoracic Patients ........................................................... 167
F. Renal Failure ..................................................................................................... 171
Diagram: CVVHDF Circuit ............................................................................. 177
G. Neurosurgical protocols .................................................................................... 180
Flowchart: Cerebral Perfusion Pressure Algorithm .......................................... 183
World Federation of Neurosurgeons Classification .......................................... 184
H. Microbiology Protocols ..................................................................................... 189
I. Drug overdose ................................................................................................... 197
Flowchart: Approach to the unconscious, undetermined overdose ................... 200
Graph: Modified Rumack-Matthew Nomogram .............................................. 202
Table: N-Acetylcysteine Administration ......................................................... 203
K. Bites and Envenomation ................................................................................... 211
K. Limitation of Therapy ....................................................................................... 211
L. Brain Death and Organ Donation ...................................................................... 212

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PART 1 - ADMINISTRATION

A. Staffing - Royal Adelaide Hospital ICU

1. Consultant Medical Staff

Director A/Prof Rob Young
Deputy Director Dr Peter Sharley

Director of Research A/Prof Marianne Chapman

Supervisor of Training Dr Nick Edwards

Consultants Dr Stuart Baker
Dr David Clayton
Dr Adam Deane
Dr David Evans
Dr Mark Finnis
A/Prof Arthas Flabouris
Dr Ken Lee
Dr Matt Maiden
Dr Stuart Moodie
Dr Richard Newman
Dr Richard Strickland
Dr Mary White
Dr Gerald Wong
Dr Alex Wurm

2. Senior Nursing Staff

Nursing Director: Mr Ian Blight

Clinical Services Coordinators: Ms Deb Herewane
Ms Ros Acott
Ms Tracey Cramey
Mr Steve Wills

Nurse Managers: Ms Ali Coventry
Ms Heather Pile

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3. Administrative Staff

Administrative Manager Ms Emma Przibilla

Team Leader / Roster Manager Ms Sherridan Clark

Unit Secretary Ms Kristina Gabell

Ward Clerks Ms Ann Kerr
Ms Lisa Migliaccio

4. Registrars

a) Three levels of registrars are rostered in the unit:
i) Senior Registrars: An advanced trainee in the College of Intensive Care
Medicine program (or equivalent training program) who has completed or
near completed training. This person may take first call at night and the
position gives experience of responsibility at a consultant level. The Senior
Registrars also help manage the registrar roster, coordinate registrar
presentations, coordinate simulator sessions and contribute to Unit
teaching activities.
ii) Senior Trainees: Usually trainees in the College of Intensive Care
Medicine (or equivalent) training program, who are rostered according to
seniority and experience.
iii) Junior Trainees/RMOs: Vocational trainees, trainees in other programs
(e.g. surgical, physician training, etc) or residents in general rotations.
b) Portfolios are determined by experience and rostering requirements.
c) All registrars, except SRs, will rotate through Units A, B and C.
d) Training positions at Royal Adelaide Hospital:
i) Intensive Care Positions
+ The College of Intensive Care Medicine (was the Joint Faculty of
Intensive Care Medicine, ANZCA) has accredited the RAH as a C24
Unit for training for the fellowship in intensive care (FCICM).
+ Registered trainees may undertake their full 24 months of core
training, required to complete advanced CICM training, in this ICU.
+ Registrars not enrolled in the above training scheme but wishing to
gain further postgraduate experience in intensive care may apply for
these positions. Applications including a current c.v. should be
forwarded to Dr Alex Wurm. (alex.wurm@health.sa.gov.au)
+ Trainees enrolled in formal training programs are given priority of
appointment.
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ii) Positions for non-intensive care trainees
+ Rotations of registrars in these positions are made from the respective
specialty based training programs at the RAH.
+ Anaesthesia trainees: 1 position (3 or 6 month term).
+ Physician trainees: 1 position (3 or 6 month term).
+ Surgical trainees: 1 position (3 or 6 month term).
+ Emergency Medicine trainees: 2 positions (3 or 6 month term).

iii) Supervisors of Training at Royal Adelaide Hospital:
+ Intensive Care: Dr Nick Edwards
+ Medicine: Dr S M Guha
+ Anaesthesia: Dr I Banks
+ Surgery: Mr P G Devitt
+ Emergency Medicine: Dr R Dunn

B. Rostering and Job Descriptions

Table: Team Duties
0800 - 1900
ICU Team A
Beds 1-12
Consultant Team A Manages Unit A
Senior Registrar A Manages Unit A, TPN
Registrar A1 (D1) Beds 1-6.
Registrar A2 (D2) Beds 7-12.
ICU Team B
Beds 12-24
Consultant Team B Manages Unit B
Senior Registrar B Manages Unit B
Registrar B1 (D3) Beds 13-18
Registrar B2 (D4) Beds 19-24
ICU Team C
Beds 25-34
Consultant Team C Manages Unit C
Registrar C1 (D5)
Unit C, Beds 25-34.
Registrar C2 (D6)
Duty Intensivist
Speed Dial 1650
Bed management, Ward consults
D7 registrar Consults, Code blue, TPN
Teaching Consultant Undergraduate and postgraduate teaching

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1830 - 0830
ICU 1
st
On-Call
Consultant
Attends evening handover round.
On-call for any problems overnight.
ICU 2
nd
On-Call
Consultant
Backs-up ICU 1
st
on-call when required.
Night Registrar 1 (N1) Beds 1-12
Night Registrar 4 (N4)
Consults, Code blue calls.
Oversees beds 1-34, allocates workload
Senior Registrar 1 First Consultant call Wednesday and Saturday
Senior Registrar 2 First Consultant call Thursday and Sunday
NB: The allocation of responsibilities overnight is at the discretion of the registrars
present and should be established by mutual agreement between the registrars and
consultant on call.

1. Roster Guidelines

a) Rosters are primarily designed to meet training and patient care requirements,
taking into account overall staff numbers and skill-mix.
b) In addition, award requirements, occupational health & safety considerations,
and individuals preferences and requests are taken into account.
c) The system is not infallible if there is a problem with any aspect of the roster,
please notify the ICU secretary as soon as possible.
d) Each roster covers a 4 week period, with the working week commencing on a
Wednesday.
e) Rosters are usually posted two weeks in advance.
f) Where possible you will be rostered more than two days-off following night
duty.
g) The rostering system utilises a wide variety of different codes as set out in the
following table:

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Table: Registrar Shifts
Abbr Shift Description Times & Meal Breaks Hrs
SR Senior Registrar
08:00-18:00
1x 30min meal break
9.5
D8 Day shift: report to DI
D1,2 Day shift Unit A
08:00-19:00
1x 30min meal break
10.5
D3,4 Day shift Unit B
D5,6 Day shift Unit C
D7 Day shift: consults & Code blue
N1 Night shift Unit A
18:30-08:30
2x 30min meal breaks
13.0
N2 Night shift Unit B
N3 Night shift Unit C
N4 Night shift: consults & Code blue
A Annual, Study, Exam, Conference leave
@ Request

2. Requesting Shifts

a) Particular shifts or days off can be entered on a request roster sheet that is
posted on the pin-up board opposite the medical staff pigeon holes.
b) The request sheet is collected on the date indicated on the top of the sheet.
c) Requests should also be discussed with the ICU secretary.
(phone 8222 5325 or email: sherridan.clark@health.sa.gov.au).
d) Some things to bear in mind when requesting shifts:
i) Requests can significantly complicate the roster and you should therefore
exercise some restraint and not request your entire roster.
ii) If you need to request several shifts please indicate in red, which two are
the most important and priority will be given to these requests.
iii) Requests cannot be granted if they disadvantage other staff, compromise
skill-mix, or overall staffing numbers necessary for the shift.

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3. Changing/Swapping Shifts

a) If you wish to change a shift after the roster has been posted, you may do so
with the following guidelines:
i) Once the roster is posted, the onus is on the individual to arrange any shift
swaps and these must occur within the same roster period.
ii) You should first endeavour to swap the shift with someone in the same
skill group so that the skill-mix is maintained for the shift.
iii) You must speak to the ICU Secretary for approval (phone 82225325 or
email: sherridan.clark@health.sa.gov.au) and then note changes on the
rosters posted in the ward and on the medical pin-up board.

4. Annual Leave

a) Annual leave for medical staff is on a first come - first served basis, so book
leave as soon as possible.
b) Only 3 registrars can be on leave at any one time, so before filling in an
application form check that leave is available with the ICU secretary.
c) Please contact the ICU Secretary if you have any questions or concerns about
your roster at anytime.
d) Leave is in accordance with the SA Salaried Medical Officers Award (5 weeks
annual and 1 week study leave) and registrars are required to forward a signed
copy of leave requests to the Senior Registrar for rostering purposes.

5. Sick Leave

a) If you are sick and unable to attend work, please contact both:
i) The Duty Intensivist by day, or
Senior Registrar at night (SD: 1650), and
ii) The Roster Manager - Mon-Fri (09:00-16:00)
b) If you can, predict an expected day or night of return to work.
c) Mark your pay sheet accordingly as sick leave

C. Orientation

1. Registrars commencing duty within the unit at the main RMO changeover dates will
undergo a half-day orientation program.

2. This will include sessions from:
a) The Director of ICU (or delegate)
b) The Director of Research
c) Infectious Diseases / Clinical Microbiology
d) The Acute Pain Service
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D. Weekly Programme

Table: Weekly Unit Programme
Monday Tuesday Wednesday Thursday Friday
08:00 Handover round Handover round Handover round Handover round Handover round

09:00
Bedside round
Bedside round
Bedside round
Bedside round
Bedside round

10:00

11:00
ICU Grand Round ICU Grand Round

12:00
ICU X-ray meeting

Consultant meeting
13:00

Bedside round

14:00
Simulator Training Simulator Training

15:00
Audit Journal Club
Clinical Teaching
(trainees)
Trainee Tutorial
BICMed Course
junior registrar
tutorial
(non-trainees)

16:00

Registrar tutorial
(all registrars)

17:00

18:30 Handover round Handover round Handover round Handover round Handover round

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E. Admission and Discharge Policies

1. Admissions Policy
a) Patients are managed by the ICU staff during their stay in ICU.
b) Admission is reserved for patients with actual or potential vital organ system
failures, which appear reversible with the provision of ICU support.
c) All admissions, including transfers and retrievals, must be approved by the
Duty Intensivist (SD: 1650).
d) Retrievals must be discussed with the Consultant when the SR is on 1
st
call.
e) Resuscitation or admission must not be delayed in imminently life threatening
cases, unless specific advanced directives exist and are clearly documented.
f) Such admissions should be discussed with the Duty Intensivist ASAP.
g) Patients are admitted to ICU under the bed-card of the original or taking clinic.
h) Patients admitted via the retrieval service must be admitted under a parent clinic,
who should be notified of the patients admission to the ICU.
i) Clinics requesting elective postoperative surgical beds should book the bed at least
one day in advance and must confirm bed availability with the Duty Intensivist on
the day of surgery, prior to anaesthesia commencing.
j) Admission disputes must be referred to the Duty Intensivist.

2. Discharge Policy:
a) All discharges should be:
i) Approved by the responsible ICU consultant.
ii) Discussed with the parent clinic prior to patient transfer, including any
ongoing or potential problems.
iii) Transferred In hours
+ i.e. prior to 18:00 - unless specifically approved by a consultant.
b) A discharge summary must be completed and a copy filed in the case-notes.
c) All patients on insulin protocols should be referred to the Endocrine Unit prior to
discharge (preferably the day before)
d) Patients discharged on TPN must be entered in the TPN folder in Unit A.
e) Notify the Acute Pain Service of patients discharged under their care.
f) Withdrawal or limitation of therapy is a consultant responsibility.
g) Treatment limitation/non-escalation directives must be discussed with the patient
or patients family, the parent clinic and clearly documented prior to discharge.
h) Referral to the Palliative Care should occur pre-discharge where indicated.

3. Deaths Policy:
a) The duty ICU consultant must be informed of all unexpected deaths.
b) The duty ICU registrar must ensure:
i) A death certificate is completed or the Coroner notified
ii) The parent clinic or duty intern is notified
iii) Referring doctors (i.e. GPs, other specialists / hospitals) are notified.
c) Where indicated, consent for a post-mortem should be obtained from relatives as
soon as possible.
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d) The Coroner must be notified in all cases where death is:

i) A death in custody, e.g. police, corrections, mental health detention.
ii) A death by unusual, unexpected, unnatural, violent or unknown cause.
iii) A death during, as a result of or within 24 hours of a surgical, invasive or
diagnostic procedure, including the administration of an anaesthetic for the
carrying out of the procedure. The following procedures are excluded:
+ The giving of an intravenous injection
+ The giving of an intramuscular injection
+ Intravenous therapy
+ The insertion of a line or cannula
+ Artificial ventilation
+ Cardio-pulmonary resuscitation
+ Urethral catheterisation
+ The insertion of a naso-gastric tube
+ Intra-arterial blood gas collection
+ Venipuncture for blood collection for testing
+ Subcutaneous injection or infusion
iv) The term anaesthetic means a local or general anaesthetic and includes a
sedative or analgesic.
v) A death within 24 hours of being discharged from a hospital or having
sought emergency treatment at a hospital.
vi) A death of a person under a protected person order under the Aged or
Infirm Persons Property Act 1940 or the Guardianship and
Administration act 1993.
vii) A death in the course or as a result or within 24 hours of a person receiving
medical treatment to which consent for that treatment has been given under
Part 5 of the Guardianship and Administration act, 1993.
viii) A death of a child subject to a custody or guardianship order under the
Childrens Protection Act 1993.
ix) A death on an aircraft or vessel with a place in South Australia as its place
of disembarkation.
x) A patient death in an approved treatment centre under the Mental Health
Act 1993.
xi) A resident death in a supported residential facility licensed under the
Supported Residential Facilities Act.
xii) A death in a hospital or treatment facility for the treatment for a drug
addiction.
xiii) If no certificate as to the cause of death has been given to the Registrar of
Births, Deaths and Marriages.

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F. Care for Patients Discharged from ICU for Terminal Care.

1. Preparation for discharge.
a) For the families of dying patients, moving from a familiar environment will add
a level of anxiety and uncertainty, even if it will be to a quieter setting.
b) Handover to the ward treating team should be as comprehensive as possible,
including a social as well as medical history.
c) Families should be supported to accept that there may still be uncertainty about
the patients course and the timing of death.
d) Families should be reassured that the focus will be on maintaining comfort.
e) Levels of ongoing active support for the patient, e.g. IV or subcutaneous fluids
should be clarified between ICU staff, the Ward team and family members.

2. Symptom management in terminal care.
a) Physical symptoms that should be considered in planning ongoing care are:
i) Pain either spontaneous or on movement
ii) Agitation, restlessness
iii) Respiratory tract secretions
iv) In a conscious patient there may be other symptoms
e.g. nausea and vomiting, dyspnoea
v) Prevention of seizures may be a relevant issue
b) If the patient is requiring either analgesia or sedation in ICU, these should be
continued on discharge to the ward.
i) Opioid infusions can be continued as subcutaneous infusions via a pump
(e.g. Graseby or equivalent)
ii) If sedation is required, midazolam can be administered via subcutaneous
route as a continuous infusion, with an opioid if already in use.
c) If the patient has not required regular opioid or sedation in ICU, the following
PRN orders should be in place prior to discharge:
i) For pain:
+ Opioid nave patient - e.g. morphine 2.5-5mg s.c. 2 hrly prn
+ Opioid tolerant - dose guided by background usage
ii) For agitation, restlessness:
+ Midazolam 2.5mg - 5mg s.c. 1 hrly prn
iii) For management of secretions:
+ Hyoscine hydrobromide 400 g s.c. 3-4 hourly prn
+ Atropine 600 g s.c. 3-4 hourly prn

3. Where appropriate, formal consult and involvement of the Palliative Care Service is
encouraged.

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G. Clinical Duties in the ICU

1. Infection Control in ICU

a) Prevention and containment of nosocomial infection is a fundamental principle of
effective medical practice.
b) The critically ill patient is highly vulnerable to nosocomial infection, which results
in significant morbidity, prolonged length of hospital stay, increased cost and
attributable mortality.
c) It is the responsibility of every member of the health care team to ensure
compliance with Hospital and Unit infection control policies. This may include
reminding senior colleagues or visiting teams to conform to basic issues such as
hand-washing or additional precautions.
d) Hand-hygiene remains the only established method of effective infection control
and must be strictly performed by all members of the health care team:
i) Aqium hand gel must be used by all staff:
+ Every time they enter or exit a patients cubicle
(defined as the line of the door or curtain of bed space.)
+ Before wearing gloves
+ Before and after patient contact
+ Before and after contact with a patients environment
ii) Hand wash with soap where:
+ Contact with blood or body fluids
+ Hands are visibly soiled
+ After removing gloves
iii) Hand wash with chlorhexidine:
+ Prior to clinical procedures
+ After contact with patients with multi-resistant organisms
e) Gloves
i) Disposable gloves must be worn for all contact with patients bodily fluids,
dressings and wounds.
ii) Gloves must be disposed of within the patient cubicle on leaving
f) Plastic aprons are to be worn:
i) With gross physical contact with the patient (e.g. patient turns)
ii) For additional precautions (see below)
g) Additional precautions:
i) The following patients require additional precautions:
+ Infection or colonisation with:
a. Methicillin Resistant Staph. Aureus
b. Vancomycin Resistant Enterococcus
c. Multiresistant gram negatives
d. Clostridium difficile
+ Burns
+ Febrile neutropenia
+ Immunosuppressed patients as directed by Infection Control
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ii) Unit C patients who are infective risks will normally be managed in either
Unit A or B.
iii) An Additional Precautions sign is placed outside cubicles of patients
identified as infective risks:
+ Red sign = patient has multi-resistant organism
+ Blue sign = patient is immunocompromised
iv) New disposable gowns and gloves must be used for each person entering
the cubicle and disposed of within the cubicle upon leaving.
v) Consumable stock within the cubicle should be kept to a minimum.
vi) Notify appropriate staff if patients are transported to theatre, for diagnostic
procedures, or for ambulance transport.
vii) Once the patient has been transferred or discharged, the area should remain
vacant until terminally cleaned in accordance with RAH policy.
viii) Environmental swabbing in Intensive Care is conducted as required by
Infection Control staff.
h) Aseptic technique
i) Aseptic technique is to be used for all patients undergoing major invasive
procedures (refer to procedures section).
ii) This includes:
+ Hand disinfection: surgical scrub with chlorhexidine for >1 minute
+ Sterile barrier: full gown, mask, hat, gloves and sterile drapes.
+ Skin prep with chlorhexidine 2% in 70% alcohol: let the skin dry.
i) Sharps disposal
i) The person performing the procedure is responsible for disposal of all
sharps (needles, blades) using the sharp disposal containers.
ii) Nursing staff are not responsible for disposal of sharps after a medical
procedure.
j) Traffic control
i) Movement of people through the unit should be kept to a minimum. This
applies equally to visiting clinics and large numbers of relatives.
ii) All visitors are expected to conform to the above infection control
measures and should be tactfully reminded or instructed when necessary.
k) Nominated isolation/quarantine rooms for highly contagious patients:
i) Rooms 3, 4, 5 & 6 - shared air-conditioning
ii) Rooms 21 & 22 - sealed, independent, negative pressure A/C units.

2. Guidelines for admission of a new patient to ICU

a) Handover from the referring doctor. Obtain as much information as possible.
b) Primary survey:
i) Ensure adequate airway, breathing and place the patient on a FiO
2
= 1.0 until
a blood gas is done.
ii) Check circulation and venous access.
c) Notify the duty consultant.
d) Secondary survey: fully examine the patient.
e) Document essential orders:
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i) Ventilation
ii) Sedation / analgesia
iii) Drugs, infusions
iv) Fluids
f) Outline the management plan to the nursing staff.
g) Secure appropriate basic monitoring/procedures:
i) SpO
2

ii) ECG
iii) Arterial line
iv) IDC, nasogastric tube
v) CVC for the majority
h) Basic investigations as indicated:
i) Routine biochemistry, blood picture and coagulation studies
ii) Group and screen.
iii) Septic screen/microbiology.
iv) Arterial blood gas
v) ECG
vi) CXR (after placement of appropriate lines)
i) Advanced investigations: CT, angiography, MRI, etc
j) Advanced monitoring where indicated: e.g. PA catheter, ICP, PiCCO.
k) Document in case notes. (See below)
l) Notify the parent clinics of patients admitted directly to ICU
NB: this applies particularly to patients who have been retrieved.
m) Clinic Interns and RMOs should clerk hospital admissions direct to ICU.
n) Inform and counsel relatives.

3. Daily management in ICU.

a) Daily investigations:
i) Routine blood tests (U&E, LFT, Mg, Hb, WCC, Plts, ABG) are ordered on
the daily flow chart and signed for on the 11:00 am fluid round.
ii) Coagulation studies, drug levels or other tests are requested as required and
may also be requested on the daily flow chart.
iii) The night duty nurses take the bloods at 06:00 and complete the request form,
which must be signed by the night registrar.
iv) Registrars are responsible for taking blood specimens:
+ When nursing staff request assistance.
+ For blood transfusion - the requesting registrar must ensure that the
labelling of the request form and the specimen matches the patients
wristband.
v) Chest x-rays are ordered after the morning handover round via OACIS.
+ Routine daily chest x-rays are not performed in ICU
+ Chest x-rays are performed
a. On admission to ICU (beds 1-24)
b. Following invasive procedures:
i. Endotracheal intubation
19
ii. Complicated percutaneous tracheostomy
iii. CVC placement (subclavian or jugular)
iv. Nasogastric or IABP placement
c. Suspected pneumothorax
d. At the discretion of the attending doctor
b) Handover ward rounds are at 08:00 and 18:30. These are brief business rounds to
handover essential information to the next team (either day or night) and are
attended by the duty consultant, team registrars and senior nursing staff.
c) Liaison with parent clinics is essential to ensure continuity of management.
Clinics must be informed of significant changes in a patients condition or the
requirement for specialist investigations or interventions.
d) Complex investigations (e.g. CT, MRI scans) and procedures should be authorised
by the duty consultant and discussed with the parent clinic where appropriate.

H. Documentation

The following guidelines are designed to facilitate the recording of clear, relevant
information that is essential for continuity of care, audit and medico-legal review.

Entries should establish a balance, being concise but still accurately recording all
relevant information and events.

Specific documentation required by ICU registrars includes:

1. Admission note for all patients admitted to ICU (Units A, B & C)
2. Daily entry in case notes during admission.
3. Handover summary
4. Discharge summary
5. Death certificates.

1. Admission Notes

a) All patients admitted to Units A & B must have a detailed admission summary.
i) The admitting clinic must be notified, by the admitting registrar, and
invited to record an admission summary for patients admitted directly to
ICU. This is to ensure that clinics are aware when a patient has been
admitted under their bedcard.
ii) The admission note should incorporate all relevant aspects of the patients
medical history, clinical examination and results of appropriate
investigations.
b) Complicated Unit C patients require the same level of detail as Unit A & B
patients.

20
c) Routine postoperative short stay patients in Unit C do not need detailed
admission notes. In these patients record:
i) Relevant operative & anaesthetic details
ii) Significant comorbidities and history
iii) Anticipated problems
iv) Procedures e.g. epidural, invasive monitoring, TPN

2. Daily case-note entries

a) A daily entry must be made in the case notes.
i) Notes are most efficiently recorded after the 11:00 ward round so that
current results and management plans are recorded
b) Additional notes must be made for the following:
i) Significant changes in physical condition necessitating changes in
management, e.g. renal failure requiring dialysis.
ii) Invasive procedures, e.g. laparotomy, tracheostomy, PAC/CVC insertion
iii) Results of specific investigations or tests, e.g. CT scans, endocrine tests
iv) Changes in policy, e.g. non-escalation of treatment, advance directives.

3. Handover summary

a) Due to the large number of complex patients, an ongoing handover summary
should be established for each patient
b) This facilitates ease of handover between day and night resident staff and for the
duty consultant staff.
c) This is not a formal casenote, nor does it take the place of a thorough review of
each patient and their casenotes. Meant to be an aide-mmoire to be updated
each shift.
d) This is stored in a specific ICU database available on the PCs in the ICU.

4. Discharge summary

a) All patients transferred from ICU (Units A/B/C) require a Medical Transfer
Summary (MR 42) form completed.
b) This is a single page document outlining all relevant transfer information.
c) The original should be filed in the case notes and a photocopy placed in the
marked box in the Unit B station for filing by the secretary.
d) The duty registrar on the day of transfer is responsible for completing the form.
e) Incomplete or missing summaries will be forwarded to the responsible registrar
for completion.
f) Short term Unit C patients do not require detailed discharge summaries, only
pertinent information relating to their stay.

21
5. Death certificates

a) The following forms need to be completed:
i) RAH Notification and Certification of Death (MR 150.2)
+ all patients including those reported to the Coroner
ii) Death Certificate ("the yellow form")
+ do not complete this for deaths reported to the Coroner
iii) First Medical Certificate
+ do not complete this for deaths reported to the Coroner
b) Deaths notifiable to the Coroner:
i) Contact the Coroners office and provide preliminary demographic details
of the deceased.
ii) The Coroners office will then fax the Medical Practitioners Deposition
form for you to complete and return by fax.
iii) File the original deposition in the patients case-notes.

I. Consent in ICU

1. Competent patients:

a) All competent patients undergoing invasive procedures should have a standard
RAH consent form (MR: 60.16) completed and signed by the patient.

2. Incompetent patients (sedation, coma or encephalopathy):

a) Third party consent is not necessary for routine ICU procedures, including:
i) endotracheal intubation
ii) arterial lines
iii) central venous lines
iv) pulmonary artery catheters
v) transvenous pacing wires
vi) underwater seal drains
vii) jugular bulb catheters
viii) intra-aortic balloon counterpulsation
ix) oesophageal tamponade tubes
x) bronchoscopy
b) However, relatives should be informed prior to the procedure if present.
c) The indications, conduct and complications of the procedure should be
documented in the casenotes.
d) Major invasive procedures such as percutaneous tracheostomy, coronary
angiography, permanent pacemaker insertion or major surgical procedures
require completion of a consent form:
i) Emergency procedures signed by two doctors
ii) Non-urgent procedures by third party consent (next-of-kin).
e) Ultimate responsibility for consent lies with the operator performing the
procedure. ICU staff are not responsible for consent for procedures performed
outside of ICU, e.g. surgical tracheostomy, or PICC lines placed in radiology
22
f) A person, not necessarily next-of-kin, who has been nominated by the patient as
a medical power of attorney may sign or refuse consent on behalf of the patient.
g) Relatives should always be informed of any non-routine procedures and the
consent issue explained, irrespective of the presence or absence of a medical or
legal power of attorney.
h) If relatives cannot be contacted, emergency life saving treatment should
proceed immediately, with discussion with the Duty Consultant.

J. ICU Ward Rounds

1. Grand rounds held on Mondays and Fridays are an integral feature of the running of
the unit. This is an open, multi-disciplinary meeting to discuss management issues and
is a valuable teaching forum. Current x-rays and investigation results are displayed via
computer projection.

2. The ward round is attended by:
a) Team A, B, C and Duty ICU consultants and all floor registrars
b) An infectious diseases consultant
c) Senior nursing staff
d) Physiotherapists
e) A pharmacist
f) A dietician
g) Invited clinics when appropriate
h) Medical students

3. Registrars are expected to present their allocated patients at this round and to actively
participate in the discussion.

4. Presentations at this round should be of a standard suitable for a fellowship
examination:
a) Presentation should take no more than 5 minutes.
b) Emphasise the relevant and pertinent issues only:
i) Patient details and demographics.
ii) State day of ICU admission (e.g. Day 6 ICU).
iii) Diagnosis or major problems.
iv) Relevant pre-morbid history pertinent to this admission.
v) Relevant progress and events in ICU
(deterioration/improvement, procedures, investigations).
vi) Current clinical status (system by system).
vii) Outline features on daily pathology and radiology.
viii) Current plan of management:
+ Medications
+ Further investigations / procedures
+ Discharge planning & prognosis

23
5. Bedside patient rounds

a) Are held daily, including grand-round days, at the discretion of the duty consultant.
b) Team consultants and registrars review each patients condition.
c) Unit A&B flowcharts are re-written daily and include orders for ventilation,
procedures, medications, infusions and fluid therapy.
i) To ensure all aspects of patient care have been considered, the
FATDOGS algorithm should be considered in all patients:
- F - Feeding & fluids
- A - Analgesia & sedation
- T - Thromboprophylaxis
- D - Drugs therapeutic & usual
- O - Oxygen & ventilation
- G - Glucose control
- S - Sit out of bed
ii) You need to either write up each one of these each day or have a reason
why you have not.
d) Printed stickers should be used for routine medications and infusions.
e) All orders must be signed by a doctor.
f) Requests for routine blood tests are made on the chart.
g) Patients transferred to Unit C or to the wards must have the hospital blue
folder completed. As a general rule, all medication orders are re-written and
fluid or nutrition orders for the next 24 hours are prescribed. Patients started on
TPN should have their details entered in the TPN folder kept in Unit A.
h) Similarly, Unit C patients have their charts reviewed, however all medications
and fluids are recorded on the hospital blue treatment folders.

K. Clinical Duties Outside of the Intensive Care Unit

1. Policy regarding outside consults:

a) NB: The Unit must not be left unattended at any time to attend outside calls.
(i.e. at least one registrar must remain on the floor)
b) The consults and code-blue/trauma pagers are carried by the Consults Registrar
(D7) during the day and Night Registrar 4 overnight (this may be modified at
the discretion of the 1
st
on-call consultant / senior registrar).
c) All consults should be addressed as soon as possible.
d) If the ICU workload is heavy, refer ward consults to the DI, who will delegate
appropriately.
e) Notify the senior nurse and fellow registrar(s) when leaving the floor.
f) The following duties accompany the Consults pager (pager no #89 1122*):
i) Ward consults
ii) Requests for Total Parenteral Nutrition (refer to DI)
iii) Requests for retrieval (refer to MedStar)

24
g) The following duties accompany the Emergency pager (#33)
i) Code blue calls |
ii) Escalated MET calls | *see (4) below.
iii) Trauma (P1) resuscitation
+ Trauma pages are subdivided into levels
+ Attendance by the ICU registrar is only required for Level 1 calls.
h) All consults/MET calls potentially requiring admission to ICU must be
discussed with the Duty Intensivist (DI).

2. Ward Calls

a) Consults regarding potential admissions from the general wards, theatre, ED.
b) Pre-operative consults for potential or booked surgical patients.
c) Advice regarding fluid and electrolyte management, oxygen therapy, sedation and
analgesia (usually referred to APS).
d) Review as requested patients in the:
i) Spinal Injuries Unit with potential respiratory failure.
ii) Burns Unit for airway / breathing assessment, IV access or resuscitation.
e) Requests for venous access:
i) Requests must come from registrar level or above and after reasonable
attempts have been made to obtain IV access.
ii) Radiology provide a PICC line service in working hours.
iii) CVCs are not to be inserted on ward patients.
f) Requests for TPN.

3. Total Parenteral Nutrition (TPN)

a) ICU provides a TPN service for the hospital.
b) Requests for TPN are elective (i.e. Mon to Fri: 0800-1800) and should be made
according to recommended indications.
c) Requests are made via the DI or consults registrar.
d) The TPN Folder is kept in the Unit A ward station.
e) The Team A Senior Registrar and Consultant will manage:
i) Initial consultation with the requesting clinic.
ii) Recording TPN patients in the TPN Folder.
iii) Insertion of a PICC catheter.
iv) Daily:
+ Review of electrolytes and fluid balance,
+ Review of the central venous catheter/PICC,
+ Prescription of TPN orders vitamins / trace elements,
+ Issue a request form for serum electrolytes.
+ Use pink labels from ICU & leave a spare for labelling of specimen tubes
- this ensures priority in the lab
f) The Unit A Senior Registrar is responsible for TPN on the weekends.
g) Refer to the section on nutrition in the clinical protocols for indications &
complications.

25
4. Code Blue & MET Calls

a) The RAH medical emergency code is 33#.
i) Upon dialling 33#, switchboard automatically page the following people:
+ ICU registrar
+ ICU equipment nurse
+ Medical registrar
b) These calls are divided into:
i) Code Blue *all calls must be attended immediately
+ Cardiac &/or respiratory arrest (actual or impending)
+ Threatened airway
+ Major haemorrhage
ii) MET calls
+ Significant clinical deterioration (see MET criteria)
+ MET calls are not routinely attended by ICU Registrars.
+ The ICU Registrar should remain immediately available if a MET call
has been activated, so that assistance can be provided to the MET team if
required (e.g. avoid starting procedures such as CVC insertions if the
MET pager has activated).
c) When 33 is displayed on the pager:
i) Dial 33# on an internal phone.
ii) Switchboard will then state the location of the arrest.
iii) Clearly state who you are (i.e. ICU registrar) and go to the location.
d) Ensure that the ICU staff know where you are going and that the Unit is not left
unattended.
e) At the emergency:
i) This hospital follows the Australian Resuscitation Council guidelines for
cardiopulmonary resuscitation (refer to flowcharts for basic and advanced life
support in the clinical protocols)
ii) The ICU/resuscitation registrar is responsible for initial assessment, securing
the airway and establishing effective ventilation.
iii) Basic life support is done by attending nursing and medical staff and may be
directed by either ICU or medical registrar.
iv) Advanced life support is directed by the more senior registrar present. This is
usually the ICU registrar.
v) Depending on the outcome of the Code Blue, the patient may be admitted to
ICU, CCU or remain on the ward according to standard admission policies.
vi) As a general rule, it is better to admit a patient if previous details are not
immediately available than to prematurely abandon resuscitation.
vii) Document your involvement with the resuscitation in the casenotes.
viii) The home team should be involved or at least informed of their patients
condition, including when resuscitation is unsuccessful.

26
5. Trauma Calls

a) As in cardiac arrest, a 33# call is activated for trauma patients who meet
specified trauma criteria. (Refer to trauma directives.)
b) Trauma pages will appear as 2 Levels:
i) Level 1: major trauma requiring immediate attendance / airway support
ii) Level 2: trauma requiring full assessment in ED/Resus.
c) The following people are paged and the level response detailed on the pager:
i) ICU/resuscitation registrar
ii) Trauma Service registrar
iii) Accident and emergency registrar
d) On receiving a Level 1 call the ICU registrar should proceed directly to Resus in
the Emergency Department (ED)
e) Ensure that ICU staff know where you are going and that the Unit is not left
unattended.
f) At the trauma resuscitation:
i) This hospital follows the Early Management of Severe Trauma (RACS)
guidelines.
ii) The team leader is designated by the current Trauma Service Directive (found
on the wall in Resus).
iii) Role of the ICU registrar:
+ Primarily as a backup for acute life threatening situations in the event that
sufficiently experienced personnel are not available in Resus.
+ If anaesthetic staff are present in Resus, there is no requirement for ICU
registrars to attend the resuscitation unless specifically requested by these
personnel or the Trauma Director.
+ If anaesthetic staff are not immediately available, the following role is
indicated until appropriate personnel arrive:
a. Initial airway assessment and management.
b. Establishing effective ventilation
c. Assistance with vascular access and restoration of circulation.
d. Other acute interventions (e.g. UWSD) as required
+ Once anaesthetic & trauma team members are present and the situation is
under control, return to ICU: do not leave ICU unattended for lengthy
periods of time.
+ If prolonged resuscitation is anticipated, call in the ICU or Trauma
Consultant and/or delegate to the anaesthetic/resuscitation registrars if
necessary.
+ Transportation of trauma patients to CT scan, angiography etc is the
responsibility of the emergency anaesthetic staff.
+ ICU registrars must not do prolonged intra-hospital transports for trauma
patients without approval by the duty ICU consultant.
27
iv) General principles:
+ Document your involvement with the resuscitation in the casenotes
+ Once the primary survey is completed, proceed to the secondary survey
and order the appropriate investigations - generally all patients need
lateral C-spine, chest and pelvis X-rays, group and cross-match. This is
coordinated by the Trauma team leader.
+ In critically ill patients, ensure that a suitably qualified person (in terms of
resuscitative skills) remains with the patient at all times. This is
mandatory if the patient is transported from Resus (e.g. to radiology,
ICU, theatre).
+ Notify ICU staff of pending admissions.
+ Demarcation disputes are referred to the duty Trauma Consultant.

6. Retrieval Requests

a) Requests for consultation may originate from a number of sources. Namely,
i) The DI phone (SD: 1650)
ii) Other ICU telephones
iii) ICU registrar pager
iv) Other clinics who have been consulted by outside medical officers.
b) All retrieval requests should be referred immediately to the state retrieval
service, MedStar on 82224222.
c) All requests from MedStar for the transfer of patients to the Royal Adelaide
Hospital must be referred to the on-call ICU consultant.

7. Intrahospital transportation of Intensive Care patients

a) All transports must be authorised by the duty ICU consultant.
b) The transport/investigation must be considered in the best interests of the patient.
c) All ventilated and potentially unstable transports need a medical escort.
d) Stable, self-ventilating patients may be transported by an ICU RN
e) If ICU nursing staff are concerned, then a medical escort is required.
f) At no stage must the unit be left uncovered.
g) If the Unit is busy, or transports clash with ward rounds, other personnel may be
deployed to do the transport. This is coordinated by the duty ICU consultant.
h) As a general rule, ICU staff are responsible for transportation of ICU patients.
i) Anaesthesia is responsible for transport of the following ICU patients:
i) Trauma resuscitation patients
ii) Patients to and from theatre
iii) Patients to and from hyperbaric medicine.
j) The transport of patients undergoing prolonged investigations or treatments, (e.g.
MRI, angiographic embolisation, invasive radiological procedures, TIPS) should
be discussed with the Duty ICU consultant and Duty Anaesthetist (SD 1175)

28
k) Guidelines
i) Registrars must familiarise themselves with transport monitors, portable
ventilators and infusion pumps.
ii) Inform and discuss the transport with the nursing staff as soon as possible.
iii) Patients must be appropriately monitored during the transport and
observations recorded on the flow chart.
iv) Document any problems which may occur during transport.
v) Ensure that the results of investigations performed (e.g. CT scans etc) are
recorded in the case notes by the appropriate person.

L. Hospital Emergencies

1. The emergency number is 33# : state the nature and location of emergency

2. Fire
a) A copy of the hospital emergency procedures (fire, smoke, bomb-threat) is kept in
the P4A and P4C nursing stations.
b) The chief fire and emergency officer is the overall controller during a fire or smoke
emergency (code red).
c) Become familiar with the location of fire exits, extinguishers and blankets in the
Unit.
i) Unless a fire is small and easily contained do not attempt to fight the fire
yourself.
ii) Remove yourself from the immediate vicinity of the fire, alerting other staff
members as indicated, and position yourself behind the automatic fire doors.
iii) The MFS has a 3 minute response time to the RAH.
iv) Wait for the arrival of the Fire Chief and assist in any patient
movement/evacuation only as indicated by the Fire Chief.
d) Role of medical staff:
i) There is no place for heroic action. Ensure your own safety first.
ii) Wait for the arrival of the MFS.
iii) Assist in patient assessment/management under the coordination of the Fire
Chief.
iv) In the event of a significant fire / smoke hazard, staff will only re-enter the
danger zone in the immediate company of a MFS fire-fighter, with
appropriate breathing apparatus.

29
M. Research in ICU

1. Personnel:
a) Director of Research A/Prof. Marianne Chapman
b) Clinical Research Manager Stephanie OConnor
c) Research nurses Justine Rivett, Danila Peake

2. Statistical and computing advice is available through ICU Research from the
University of Adelaide (Dept. Public Health).

3. Members of the medical and nursing staff are encouraged to become involved in
research during their stay in the Unit. Registrars are expected at least to obtain
consent for ongoing studies as part of their responsibilities within the unit.
Knowledge of these studies can be obtained from either the Director of Research or
the Clinical Research Manager. Further involvement is encouraged and there are
supports within the unit to facilitate research to occur.

4. There are broadly 3 types of research projects occurring in the unit:
a) Drug company sponsored projects
b) Locally initiated projects (supported by funding from a)
c) Studies performed with the ANZICS Clinical Trials Group (see below).

5. Completed research projects should be presented at either a local or interstate
scientific meeting. Some funding is available for both nurses and medical staff who
present work at any meeting.
a) Applications should be made to the Coordinator of Research.
b) Eligible meetings include, but are not limited to:
i) ANZICS / ACCCN Annual Scientific Meeting - held in October.
+ Abstracts must be sent by July.
+ Free papers/posters
+ Prizes are awarded for:
a. Best medical and nursing free papers
b. Best medical and nursing reviews
c. Best poster
d. Best paper by a FCICM trainee (Matt Spence Medal).
ii) CICM ASM: free papers. Annual - June.
iii) Thoracic Society of Australia and New Zealand: Annual - March.
iv) ICE (Institute of Continuing Education), ACCCN Conference. Annual
May.
c) Further details can be obtained from the Director of Research and the Clinical
Research Manager.

30
6. Most projects require prior RAH Research Ethics Committee approval:
a) Submission dates and a pro forma may be obtained from the Clinical Research
Manager.
b) If the study involves drug administration then it must first go to the
Investigational Drugs Subcommittee.
c) A copy of the ethical approval letter and protocol must be given to the Clinical
Research Manager. The Clinical Research Manager will also keep details of
progress of research projects.

7. Further information:
a) Facilities are available in the Adelaide University Department of Anaesthesia
and Intensive Care for laboratory work. There is an animal laboratory
performing predominantly pharmacokinetic & pharmacodynamic studies.
Resource persons: Prof Guy Ludbrook or Dr Matt Maiden.
b) ICU database. We have a database extending back many years containing data
on all intensive care patients (excluding Unit C). This includes demographics,
illness severity scores and outcomes. We also have access to a national
database. We also collect other data locally. Resource person: Dr Mark Finnis.
c) ANZICS Clinical Trials Group. There is a national clinical trials group to
facilitate multicentre trials in Australia. The group is open to all interested
parties and proposals for multicentre trials can be presented for consideration.
Meetings twice per year April and October. Resource person: A/Prof. Marianne
Chapman.

N. Information Technology in ICU

a) All consultant and registrar offices and the Registrar Teaching Room are
equipped with PCs, connected to the RAH local area network (LAN).
b) Facilities available through the LAN include:
i) Intranet e-mail accounts
ii) WWW browsing facilities (available on application).
iii) Intranet resources, which are being continuously expanded:
+ UpToDate

+ An extensive range of electronic text books
+ Internal telephone and Australian business directories
+ Medline via OVID
+ ICU Handover Database
iv) On application registrars will be allocated a username, which will carry
with it an Internet e-mail account for the duration of their stay.
c) In addition, many of the consultants have access to the University of Adelaide,
including Barr-Smith Library resources.
d) The Unit has an internet presence at http://www.icuadelaide.com.au/
e) NB: Use of hospital computers to access inappropriate material is not tolerated.
RAH guidelines detail appropriate use.

31

PART 2 - CLINICAL PROCEDURES

A. Introduction

1. Registrars are encouraged to become proficient in all Intensive Care procedures.
2. Invasive procedures should be authorised by a senior registrar or the duty ICU
consultant.
3. Adequate familiarisation and supervision with unfamiliar procedures is essential:
there is always someone available to help.
4. The relative risk vs. benefit of all procedures must be carefully considered.
5. Do not persist if you are having difficulty with the procedure: call for help
6. Consent for procedures: *refer to Administration / Consent
a) Competent patients undergoing invasive procedures should have a standard
RAH Consent Form (MR:60.16) completed and signed by the patient
b) Third party consent is not necessary for incompetent patients undergoing
routine ICU procedures.
c) Major ICU procedures, such as percutaneous tracheostomy or
enterogastrostomy, require third party or two-doctor consent.
7. Indications, conduct and any complications of the procedure should be clearly
documented in the case notes, in addition to a consent form if this is completed.
8. Discuss the planned procedure with the attending ICU nursing staff and allow
sufficient time for setting up of trays and equipment.
9. Remember: the nursing staff have extensive experience with these procedures.
10. It is the responsibility of the operator to discard all sharps used in the procedure and
to ensure that they are placed in a sharps disposal container.

B. Procedures

1. Registrars are expected to become proficient in all routine procedures.
2. Specialised procedures are done either by the Duty Consultant or strictly under
consultant supervision.
3. Guidelines for the listed routine and specialised procedures are outlined in the
following sections.

32
Routine ICU procedures

1. Endotracheal intubation
2. Peripheral venous catheterisation
3. Central venous catheterisation / PICC line insertion
4. Arterial cannulation
5. Pulmonary artery catheterisation
6. Urinary catheterisation
7. Lumbar puncture
8. Epidural catheterisation
9. Underwater seal drain insertion
10. Pleurocentesis
11. Peritoneocentesis
12. Nasogastric tube insertion

Specialised ICU procedures

1. Percutaneous tracheostomy
2. Fibreoptic bronchoscopy
3. Transvenous pacing
4. Pericardiocentesis
5. Oesophageal tamponade tube insertion
6. Intra-aortic balloon counterpulsation
7. Extracorporeal Membrane Oxygenation

C. Peripheral IV catheters

1. Indications:
a) First line IV access for resuscitation, especially blood transfusion
b) Stable patients where a CVC is no longer necessary
2. Management protocol:
a) Remove/replace all resuscitation lines inserted in unsterile conditions.
b) Generally avoid peripheral IV use in ICU patients and remove if not in use.
c) Use local anaesthesia in awake patients.
d) Aseptic technique:
i) Handwash with AVAGARD
(chlorhexidine 2%) or
MEDISPONGE
(chlorhexidine 4%) + gloves

ii) Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol)
e) Dressing: adhesive occlusive (Opsite
or equivalent)
f) Change / remove all peripheral lines after 48 hours.
g) Avoid lower-limb placement in patients with vascular disease.
3. Complications
a) Infection
b) Thrombosis
c) Extravasation in tissues

33
D. Arterial Cannulation

1. Indications:
a) Routine measurement of systemic blood pressure in ICU
b) Multiple blood gas and laboratory analysis
c) Measurement of BP during transport of patients in hostile environments

a) Remove and replace lines inserted in unsterile conditions as soon as possible.
b) Brachial and femoral arterial lines should be changed as soon as radial or
dorsalis pedis arteries are available.
c) Aseptic technique:
i) Handwash with AVAGARD
MEDISPONGE
(chlorhexidine 4%) + sterile gloves

ii) Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol)
d) Local anaesthesia in awake patients.
e) Cannulae:
i) Arrow
radial or femoral kits (Seldinger technique).

ii) 20G Insyte
.
iii) Single lumen 20G CVC for femoral arterial lines.
f) Insertion sites in order of preference:
radial > dorsalis pedis > femoral > brachial
g) The femoral artery may be the sole option in the acutely shocked patient.
h) Secure with a StatLock
device.
i) There is no optimal time for an arterial line to be removed or changed.
j) IA cannulae are changed/removed in the following settings:
i) Invasive IA line is no longer necessary.
ii) Distal ischaemia
iii) Mechanical failure (overdamped waveform, inability to aspirate blood)
iv) Evidence of unexplained systemic infection
v) Evidence of local infection
k) Measurement of pressure:
i) Transducers should be zeroed each nursing shift
ii) Zero reference = the mid-axillary line, 5
th
intercostal space
l) Maintenance of lumen patency
i) Continuous pressurised (Intraflo
) saline flush at 3ml/hr.

3. Complications
a) Infection
b) Thrombosis
c) Digital ischaemia
d) Vessel damage / aneurysm
e) Haemorrhage / disconnection

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E. Central Venous Catheters

NB: Registrars should be familiar with the interpretation and limitations of
haemodynamic variables derived from central catheters (CVC, PICCO and PAC) in
critically ill patients.

1. Indications:
a) Standard IV access in ICU patients:
i) Vasoactive infusions
ii) Fluid administration (including elective transfusion)
iii) TPN, hypertonic solutions (amiodarone, nimodipine, etc.)
b) Monitoring of right atrial pressure (CVP)
c) Venous access for:
i) Pulmonary artery catheterisation (PAC)
ii) Continuous renal replacement therapy (CVVHDF), plasmapheresis.
iii) Jugular bulb oximetry.
iv) Transvenous pacing.
d) Resuscitation
i) Large bore peripheral IV line(s) are 1
st
line.
ii) Standard lumen CVCs are not appropriate for acute volume resuscitation.
iii) Consider using a PAC sheath if central access is required and adequate
peripheral access is unobtainable.

2. Management protocol: (applies to all types of CVC):
a) Types:
i) The default CVC for all ICU patients is a Cook
antimicrobial
impregnated (rifampicin/minocycline) 7F 15 or 20cm 3-lumen catheter.
ii) Non-impregnated catheters inserted outside the ICU should be changed to
an impregnated catheter according to clinical indication.
iii) Dolphin Protect
catheters are used for CVVHDF and plasmapheresis

iv) Pulmonary artery catheter sheath (part of the PAC kit)
v) Dress non-impregnated catheters with BioPatch

b) Sites:
i) Subclavian is the preferred site for routine stable patients, followed by
internal jugular.
ii) Femoral access is preferable where:
+ Dolphin Protect
/ CVVHDF
+ Limited IV access (burns, multiple previous CVCs),
+ A thoracic approach is considered hazardous:
a. Severe respiratory failure from any cause (PaO
2
/FiO
2
< 150)
b. Hyper-expanded lung fields (severe asthma, bullous disease)
c. Coagulopathy (see below)
+ Inexperienced staff requiring urgent access, where supervision is not
immediately available.
35
c) Coagulopathic patients:
i) INR > 2.0 or APTT > 50s correct with FFP and/or
prothrombinex
ii) INR 1.5-2.0 or APTT 40-50s correct with FFP, or
use IJ or femoral approach
iii) Platelets < 50,000 transfuse 1 pack (5
U
) platelets
iv) Failure to increment platelet count after transfusion avoid subclavian
v) Uncontrolled coagulopathy femoral approach or PICC
vi) Check patient anatomy with ultrasound prior to the procedure.
d) Technique policy
i) Use local anaesthesia in awake patients.
ii) Strict aseptic technique at insertion:
+ Handwash with AVAGARD
MEDISPONGE
(chlorhexidine 4%)
+ Sterile barrier: gown, sterile gloves, mask, hat
sterile drapes (CVC - Patient Cover)
+ Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol)
iii) Seldinger technique or ultrasound guided insertion Sonosite

iv) U/sound guided insertion is preferred where:
+ There is an increased complication risk (e.g. bleeding, pneumothorax)
+ Large bore catheter insertion.
+ Distorted patient anatomy.
v) CVC Catheter lengths:
+ 15cm - right subclavian or internal jugular
+ 20cm - left subclavian or internal jugular, either side femoral
vi) Secure all lines with a StatLock
device or suture
vii) Dressing: non occlusive dressing
viii) Flush all lumens with saline.
ix) Transduce pressure ASAP post-insertion to exclude arterial placement.
x) Check CXR prior to use, except in urgent circumstances
e) Maintenance
i) Routine IV administration set change at 7 days.
ii) Daily inspection of the insertion site and clinical examination for infection
irrespective of insertion duration.
iii) Catheters remain as long as clinically indicated and are changed when:
+ Evidence of systemic infection
a. New, unexplained fever or |WCC
b. Deterioration in organ function
c. Positive blood culture by venipuncture with likely organisms
(S. epidermidis, candida spp.), and/or
+ Evidence of local infection - inflammation or pus at insertion site.
iv) Guidewire exchanges are actively discouraged. They may be indicated in
the following situations, only after discussion with a consultant:
+ Mechanical problems in a new catheter (leaks or kinks)
+ Difficult or limited central access (e.g. burns).
36
v) Maintenance of lumen patency
+ Central venous catheters (pre-printed on the patient flowsheet)
a. Flush unused lumens with 1ml normal saline 8 hourly
+ Vascath: into each lumen 8 hourly (printed sticker)
a. Withdraw 2ml and discard.
b. Flush with 2ml normal saline.
c. Flush 1.5ml solution (5000
U
heparin/3ml = 2500
U
/lumen).
d. NB: Each lumen has its internal volume printed on it.

3. Complications:
a) At insertion
i) Arterial puncture haematoma, thrombosis, embolism
ii) Pneumothorax, haemothorax, chylothorax
iii) Neural injury (phrenic, brachial plexus, femoral nn.)
b) Passage of wire/catheter
i) Arrhythmias
ii) Wire embolism - if this occurs, notify senior staff immediately
iii) Perforation of SVC / RA - tamponade
c) Presence of catheter
i) Catheter infection: rates increase under the following conditions:
+ Size of catheter - thicker catheters (PAC, Vascaths)
+ Site of catheter - femoral > internal jugular > subclavian sites
+ Number of lumens
+ Nature of fluid through catheters - TPN or dextrose solutions
ii) Thrombosis, HITS secondary to heparin
iii) Catheter / Air embolism
iv) Knotting of catheters (esp. PAC)
v) Pulmonary infarct / arterial rupture (PAC)

NB: Where CVC insertion presents a significant risk in a non-urgent
situation, consider insertion of a PICC line as an alternative.

F. Urinary Catheters

1. Standard in all ICU patients
a) Aseptic technique at insertion.
i) Hand disinfection: surgical scrub with chlorhexidine for >1 minute
ii) Sterile barrier: gloves and sterile drapes.
iii) Skin prep: chlorhexidene 1%
b) Local anaesthesia gel in all patients.
c) Only Biocath
TM
catheters should be inserted in ICU & changed 6 weekly.
d) Standard Foley catheters should be changed to a Biocath
TM
after 14 days.
e) Silastic catheters should be changed after 1 month.
f) Remove catheters in anuric patients and perform intermittent catheterisation
weekly, or as indicated.
37
G. Epidural Catheters

1. Indications
a) Post-operative pain relief (usually placed in theatre)
b) Analgesia in chest trauma.

a) Notify the Acute Pain Service of any epidural placed in ICU.
b) Epidural cocktails should follow the Acute Pain Service protocols
c) Strict aseptic technique at insertion.
d) Daily inspection of the insertion site. The catheter should not be routinely
redressed, except under the advice of the APS.
e) Leave in for a maximum of 5 days and then remove.
f) Remove if:
i) Not in use for > 24 hours, or
ii) Clinical evidence of unexplained sepsis, or
iii) Positive blood culture by venipuncture with likely organisms
(S. epidermidis, candida).
g) Heparin/Warfarin Protocol (also see Acute Pain Service Guidelines for
Anaesthetists)

3. Complications
a) Hypotension from sympathetic blockade / relative hypovolaemia
i) This usually responds to adequate intravascular volume replacement
ii) Occasionally, a low-dose vasopressor infusion is required
iii) If this is considered, occult bleeding must be excluded.
b) Pruritis, nausea & vomiting, or urinary retention (opioid effects)
c) Post-dural puncture headache
d) Infection: epidural abscess
e) Pneumothorax (rarely)

4. NB: Further guidelines for the management of epidural catheters can be obtained
from The Acute Pain Service Guidelines for Anaesthetists. Manuals are stored in
each ICU station.

H. PICCO Catheters

1. Introduction
a) PiCCO uses a combination of thermodilution and pulse waveform analysis to
provide an estimate of cardiovascular status.
b) Trainees should become familiar with the theory of insertion, indications,
interpretation and complications of PiCCO catheters.
c) Indicated in the assessment & response to therapy in shock states.
38
2. Technique
a) A normal CVC line can be used.
b) The peripheral arterial catheter is inserted into a femoral, brachial or axillary
artery using an aseptic Seldinger technique.
c) The pulse waveform analysis of continuous cardiac output is calibrated by
thermodilution according to the device instructions.
d) Calibration should be repeated once per nursing shift and as indicated.
e) Additional measurements of Global End-diastolic Volume Index (GEDI) and
Extravascular Lung Water Index (ELWI) can be made via thermodilution.
3. Below are the normal values and a suggested decision tree from the manufacturer
which should be used as a guide only:

Table: PiCCO Values and Decision Tree
Variable Abbr. Normal Units
Cardiac Index CI 3.0-5.0 l/min/m
2

Global End-diastolic Blood Volume Index GEDI 680-800 ml/m
2

Intrathoracic Blood Volume Index ITBI 850-1000 ml/m
2

Stroke Volume Variation SVV
s 10
%
Extravascular Lung Water Index* ELWI* 3.0-7.0 ml/kg

39
I. Pulmonary Artery Catheters

1. Policy
a) Insertion of PA catheters must be authorised by the duty consultant.
b) Trainees should become familiar with the theory of insertion, indications,
interpretation and complications of PACs.
c) Insertion of a PAC must never delay resuscitation of a shocked patient.
d) Allow sufficient time for nursing staff to set up insertion trays and transducers.
e) Remove catheters once they are not being routinely used. They may be left in
situ for up to 7 days.

2. Indications:
a) Haemodynamic measurements (CO/I, SV/I, SVR/I)
i) Aid to diagnosis and response to therapy of shock states,
e.g. cardiogenic, septic or hypovolaemic
b) Measurement of right heart pressures (RAP, PAP):
i) Acute pulmonary hypertension
ii) Pulmonary embolism
iii) Cardiac tamponade
c) Estimation of preload / left heart filling (PAOP)
i) Intravascular volume status
ii) LVF
iii) Response to fluid loading
d) Measurement of intracardiac shunt: (Acute VSD)
e) Derivation of oxygen delivery & utilization variables (VO
2
, DO
2
)

a) Insertion protocol as per CVC, with the following features:
i) Sheath introducer (8.5 Fr) with side port, haemostatic valve and plastic
contamination shield.
ii) Shared transducer for RAP (proximal) and PAP (distal) lumens
iii) Check competence of balloon and concentric position
iv) Ensure all lumens are flushed with heparinised-saline prior to insertion.
v) Ensure the system is zeroed and an appropriate scale (0-40mmHg) on the
monitor prior to insertion.
vi) Insert the catheter observing changing waveforms (RA RV PA) on the
monitor, with the balloon inflated and locked, until catheter displays
pulmonary artery occlusion tracing
+ Subclavian and left IJ ~ 50cm
+ Right IJ ~ 40cm
vii) Deflate the balloon and ensure an adequate PA trace. Adjust catheter
depth until a PAOP trace appears with 1-1.5ml air in balloon.
viii) Suture introducer and attach the contamination shield to the hub.
ix) Apply a BioPatch

and non-occlusive dressing.
b) Ensure an adequate PA tracing is on the monitor at all times
40
c) Wedged tracings must be corrected as soon as possible:
i) Flush distal lumen with 2ml N.Saline
ii) Withdraw the catheter until a PA trace is visible
d) Measurement of pressures:
i) Reference pressures to the mid-axillary line
ii) Measure at end-expiration of the respiratory cycle
iii) Do not disconnect ventilated patients to measure pressures.
iv) Measurement of PAOP:
+ End expiration: lowest point in ventilated patients, highest point in
spontaneously ventilating patients
+ Use the electronic cursor on monitors after 2-3 respiratory cycles.
+ Do not use the electronic average of the wedge tracing.
e) Haemodynamic measurements
i) These are routinely performed by the nursing staff, however registrars
should become familiar with the procedure.
ii) Record all measurements in the flow chart in the results folder.
iii) Cardiac outputs:
+ Injectate: 10ml 5% dextrose @ room temperature
+ Inject at random times in the respiratory cycle
+ Take > 3 measurements and ignore values > 10% from average.
iv) Derived variables:
+ CO/CI and SVR are routinely charted (8 hrly or as indicated).
+ Other variables including PVR(I), SV(I), L(R)VSWI are recorded in
the haemodynamics flowsheet.
+ Mixed venous oxygen levels should be measured on a sample taken
from the distal (yellow) port. Oxygen saturation should be directly
measured with co-oximetry.
+ Derived haemodynamic variables (see table), should be used in
conjunction with clinical assessment.

4. Complications
a) Related to CVC cannulation (see CVC section)
b) Related to insertion/use of a PAC
i) Cardiac perforation
ii) Thromboembolism
iii) Pulmonary infarction ~ 0-1.4% (2 persistent wedging)
iv) Pulmonary artery rupture ~ 0.06-0.2% (mortality 50%)
v) Catheter related sepsis
vi) Endocarditis
vii) Pulmonary valve insufficiency
viii) Catheter knotting
ix) Balloon fragmentation / embolism
x) Tachyarrhythmias
xi) RBBB

41
Table: Standard Haemodynamic Variables
Variable Formula Normal range
Cardiac index CO/BSA CI = 2.5-5 l/min/m
2

Systemic vascular resistance SVR
MAP RAP
CO
=

79 9 .

750-1500
dyn.sec/cm
5
/m
2

Systemic vascular resistance
index
79.9
CI
RAP MAP
SVRI
=

1400-2400
dyn.sec/cm
5
/m
2

Pulmonary vascular
resistance index
9 . 79
CI
PAOP PAP m
PVRI
=

150-250
dyn.sec/cm
5
/m
2

Stroke volume index
HR
CI
SVI =

33- 47 ml/beat/m
2

LV stroke work index
( ) 0.0136 SVI PAOP MAP LVSWI =

50-120 g/m
2
/ beat
RV stroke work index ( ) 0.0136 SVI PAOP mPAP RVSWI =

25-55 g/m
2
/ beat
Arterial oxygen content ( ) ( ) CaO Hb SaO PaO
2 2 2
134 0 003 = + . .

17-20 ml/100ml
Venous oxygen content
( ) ( )
CvO Hb SvO PvO
2 2 2
134 0 003 = + . .

12-15 ml/100ml
Oxygen delivery index DO I CI CaO
2 2
10 = 550-750 ml/min/m
2

Oxygen consumption index
( )
VO I CI CaO CvO
2 2 2
10 = 115-160 ml/min/m
2

Oxygen extraction ratio
O ER
VO I
DO I
2
2
2
=
0.24-0.4
Shunt equation
0 10
O v C O c C
CaO O c C
Qt
Qs
2 2
2 2
'
'
=

5-15%
End capillary oxygen content
( ) ( ) 0.003 PAO 1.0 1.34 Hb O c C
2 2
+ = '
80-100 ml/100ml
Alveolar gas equation ( ) ( )
PAO FiO PaCO
2 2 2
760 47 125 = .

100-650 mmHg

42
J. Pleural Drainage

1. Indications:
a) Pneumothorax
b) Tension pneumothorax may require urgent needle thoracostomy
c) Haemothorax
d) Large symptomatic pleural effusion

a) Needle thoracostomy (tension pneumothorax):
i) 14 or 16G cannula placed in mid-clavicular line, 2
nd
intercostal space
ii) Always place an UWSD following this procedure
b) Pleurocentesis: (pleural effusion)
i) Prior to commencement, ultrasound the chest to confirm the presence of
fluid and indentify/mark an appropriate insertion site.
ii) Strict aseptic technique at insertion:
+ Handwash with AVAGARD
MEDISPONGE
(chlorhexidine 4%)
+ Sterile barrier: gown, sterile gloves, mask, hat
sterile drape(s)
+ Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol)
iii) Local anaesthesia in conscious patients.
iv) Seldinger technique:
+ Pigtail catheter or ThalQuick
12F kit.
+ Insert guidewire through needle into pleural space
+ Insert catheter into pleural space over wire
+ Aspirate intermittently with closed system or attach to an UWSD.
v) Record volume removed and send for MC&S, cytology & biochemistry.
vi) Check CXR post-procedure.
c) Underwater seal drainage:
i) Local anaesthesia in awake patients.
ii) Aseptic insertion technique - as above.
iii) Site:
+ Mid-axillary line, 3-5
th
intercostal space
+ Mid-clavicular line, 2
nd
intercostal space ( air only)
+ Do not insert drains through old wounds
iv) ICU patients need large drains: 28F catheter or larger
v) Use soft Mallinkrodt tubes in preference to the stiffer Argyle tubes
vi) Remove the trochar from catheter: do not use the trochar for insertion
vii) For the usual lateral ICD, go for the anterior or mid-axillary lines, avoid
the posterior sites as the chest wall is too thick, and there is a danger to
neurovascular structures
viii) Make a 2-3cm skin incision parallel to the ribs (#10 or #15 scalpel)
43
ix) Instruments & technique:
+ Blunt dissect using short artery forceps, avoid long forceps.
+ Do not plunge into the chest with either instrument.
+ Access to the intercostal space is by careful blunt dissection of the
intercostal muscles above the rib below.
+ The chest wall hole must be 2-3 cm wide in order that a finger can be
inserted into the pleural space to identify possible adhesions.
+ The soft tube should be guided by the intrapleural finger so that the
tube goes in between the finger and chest wall
x) Connect to an underwater seal drain apparatus
xi) Insert 2 purse string sutures:
+ 1 to fasten the tube
+ 1 (Z or purse-string) to close the skin incision on drain removal.
xii) Dressing: occlusive dressing (Hypafix)
xiii) Check CXR.
xiv) Maintenance
+ Remove or replace drains inserted in unsterile conditions as soon as
possible.
+ Leave the drain in situ until:
a. Radiological resolution of pleural collection (air/fluid)
b. No ongoing air-leak (no drain bubbling)
c. Minimal drainage (< 150 ml/24 hrs).
+ Additionally, in ventilated patients, consider clamping drain for > 4
hours and removing if the patient remains stable and/or post CXR.
+ Surgically placed drains are the responsibility of the surgeon and
should only be removed in consultation.

3. Complications
a) NB: minimised using the blunt technique
b) Incorrect placement - extrapleural, intrapulmonary, subdiaphragmatic
c) Pulmonary laceration - haemorrhage, fistula
d) Pneumothorax
e) Bleeding
i) local incision, intercostal vessels
ii) lung
iii) IMA (with anterior placement)
iv) Great vessels (rare)
f) Infection
i) Soft tissue
ii) Empyema
g) Mechanical (kinking, luminal obstruction)
44
K. Endotracheal Intubation

1. Policy:
a) Endotracheal intubation in ICU patients is a high risk but vital procedure:
i) Usually an emergency procedure, with limited time.
ii) Usually indicated for acute respiratory failure, or associated with limited
respiratory reserve
iii) Patients may have cardiovascular instability and significant co-morbidities
iv) Patients may have cervical spine or oropharyngeal trauma / surgery
v) Patients are at risk of vomiting and aspirating
vi) Positioning is difficult.
b) Familiarisation with the intubation trolleys, equipment and drugs is essential.
c) Intubation should ideally not be done as a sole operator procedure.
Skilled assistance should always be sought.
d) If you are alone (i.e. after hours): call for help!
i) Expertise in intubation is always available.
ii) Remember emergency anaesthesia staff.
e) The majority of ICU patients mandate rapid sequence induction.

2. Indications
a) Institution of mechanical ventilation
b) To maintain an airway
i) Upper airway obstruction
+ Potential e.g. early burns
+ Real e.g. epiglottitis, trauma
ii) Patient transportation
c) To protect an airway
i) Patients at risk of aspiration
ii) Altered conscious state
iii) Loss of glottic reflexes
d) Tracheal toilet

3. Techniques
a) Orotracheal intubation is the standard method of intubation in this unit.
b) Nasotracheal intubation may be indicated where:
i) Patients require short-term ventilation and are intolerant of oral ET tubes.
ii) Nasal Fibreoptic intubation may be indicated for:
+ Oro-maxillary surgery and pathology
+ Inability to open the mouth:
e.g. intermaxillary fixation, TMJ trauma, rheumatoid arthritis.
+ Upper airway obstruction and nasal route preferred
iii) Contraindicated in base of skull & LeForte facial fractures
c) Methods:
i) Direct laryngoscopy, Airtraq
or Glidescope
after rapid sequence induction

ii) Fibreoptic bronchoscopic awake intubation (oral or nasal)
iii) Intubating laryngeal mask LMA Fastrac

45
4. Endotracheal Tubes
a) Standard tube:
i) Low pressure, high volume cuff.
ii) Males: 8mm secure at 21-23cm to incisors
iii) Females: 7-8 mm secure at 19-21cm to incisors
iv) Do not cut tubes to less than 26 cm length
b) Double lumen tubes: *rarely indicated in ICU:
i) Unilateral lung isolation for bronchopulmonary fistula, abscess or
haemorrhage
ii) These tubes should be inserted as a temporary manoeuvre prior to a definitive
procedure
iii) Allow differential lung ventilation
iv) Males: Left 41F
v) Females: Left 39F
vi) NB: right bronchial tubes harder to site.
vii) Position should be checked with bronchoscope.
c) Intubated patients from theatre may have the following tubes that are not
recommended for prolonged intubation. These tubes must be changed if intubation
is anticipated > 48 hrs and if safe and feasible.
i) Plain PVC tubes - no above cuff suction port
ii) Armoured tubes - risk kinking & obstruction
iii) RAE tubes - difficulty with suction & malposition

5. Protocol for endotracheal intubation in ICU
a) Personnel:
i) Intubation is a 3-4 person procedure - skilled assistance is mandatory
ii) The top end intubator coordinates the procedure
iii) One person to administer drugs
iv) One person to apply cricoid pressure (CP) post-induction:
+ This is routine for all emergency intubations
+ CP is considered safe in the presence of suspected spinal injury.
+ CP must be correctly applied - distortion of the larynx and difficulty in
intubation may occur if poorly applied.
v) One person to provide in-line cervical spine immobilisation (trauma and
spinal patients only).
b) Secure adequate IV access
c) Equipment (kept in difficult airway & intubation trolleys in P4-A,B&C).
Ensure the following equipment is available and functional:
i) Adequate light
ii) Oropharyngeal airways
iii) Working suction with a rigid (Yankauer) sucker
iv) Self-inflating hand ventilating assembly and mask
v) 100% oxygen, i.e. working flowmeter at 15 l/min
vi) 2 working laryngoscopes (standard & long blades)
vii) Magill forceps
viii) Malleable introducer and gum-elastic bougie
46
ix) 2 Endotracheal tubes
+ Normal size + 1 size smaller
+ Check cuff competence
x) Access to difficult intubation equipment.
+ Be aware of the Failed Intubation Drill.
+ Glidescope or Airtraq

+ Intubating Fastrach LMA
+ Cricothyroidotomy equipment
a. Percutaneous kit or
b. #15 scalpel & #6.0 cuffed ETT
d) Monitoring (on all patients) :
i) SpO
2
, ETCO
2
, ECG
ii) Invasive BP *desirable but not essential and must not delay intubation
e) Drugs
i) Induction agent - propofol, fentanyl, ketamine, midazolam
ii) Suxamethonium - 1-2mg/kg is the muscle relaxant of choice.
+ Contraindicated in:
a. Burns > 3 days
b. Chronic spinal injuries (i.e. spastic plegia)
c. Chronic neuromuscular disease (e.g. GBS, motor neurone disease)
d. Hyperkalaemic states. (K
+
> 5.5)
+ Consider Rocuronium (1-2 mg/kg) if Sux. contraindicated
iii) Atropine - 0.6-1.2mg available
iv) Adrenaline - 10ml 1:10000 solution available

f) Procedure: Rapid sequence induction and orotracheal intubation
i) Pre-oxygenate with 100% oxygen for 3-4 minutes.
ii) For patients on mask CPAP/NIV, pre-O
2
with the NIV mask
iii) Preload with 250-500ml IV crystalloid
iv) Inotropes may be necessary after induction/intubation
v) Induction agent + suxamethonium
vi) Cricoid pressure applied
vii) Direct visualisation of vocal cords and tracheal intubation
viii) Inflation of cuff until airway sealed
ix) Confirmation of ETCO
2

x) Chest and gastric auscultation with manual ventilation
xi) Cricoid pressure released
xii) Secure tube at correct length
xiii) Connect patient to ventilator (see default ventilator parameters)
xiv) Ensure adequate sedation muscle relaxant
47
xv) Consider insertion of a naso/oro-gastric tube.
+ Required by the majority of ICU patients.
+ Insertion will avoid repeating the CXR.
xvi) Chest X-ray
xvii) Confirm blood gas analysis and adjust F
I
O
2
accordingly.

g) Sedation post-intubation:
i) None if comatose or haemodynamically unstable
ii) Propofol and fentanyl as clinically indicated.

6. Maintenance of endotracheal tubes
a) Securing to face
i) Secure ETT with white tape after insertion.
ii) Ensure that the loop of tape is snug around back of neck but not too tight to
occlude venous drainage. Should allow 2 fingers under tape.
iii) Re-secure with adhesive tape once CXR check done.
b) Cuff checks
i) Volumetric (sufficient air to obtain a seal + 1ml) tests are done following
insertion and whenever a leak is detected with a manual hyperinflation
once per nursing shift.
ii) Seal is assessed by auscultation over trachea during normal ventilation.
iii) Manometric tests are inaccurate and do not correlate with mucosal
pressure. These are an adjunct only if cuff malfunction is suspected.
c) Persistent cuff leaks
i) Tubes requiring more than 8ml of air to obtain a seal or if there is a
persistent cuff leak must be examined by direct laryngoscopy as soon as
possible even if taped at the correct distance at the teeth.
ii) Ensure that:
+ The cuff has not herniated above the cords
+ Tube has not ballooned inside the oral cavity and pulled the cuff
above the cords.
iii) Patients at high risk for cuff leaks:
+ Nasal RAEs - prone to outward migration
+ Cut tubes - do not cut tubes < 26 cm
+ Facial swelling - burns, facial trauma
+ Patients requiring high airway pressures during ventilation
48
7. Endotracheal tube change protocol
a) Ensure adequate skilled assistance, equipment, drugs and monitoring as for de
novo intubation.
b) Procedure
i) Set the F
I
O
2
= 1.0 and change SV modes to SIMV.
ii) Ensure sufficient anaesthesia and muscle relaxation (fentanyl / propofol +
neuromuscular blockade)
iii) Perform laryngoscopy and carefully identify:
+ Patency of upper airway after suction
+ Anatomy of larynx
+ Degree of laryngeal exposure and swelling.

iv) IF clear view of larynx and no or minimal laryngeal swelling:
+ Application of cricoid pressure by assistant and careful, graded
extubation under direct laryngoscopic vision.
+ Maintain laryngoscopy and replace tube under direct vision.

v) IF impaired visualisation of larynx:
+ Re-evaluate the need to change ETT
+ Use gum elastic or ventilating bougie
+ Place bougie through tube under direct vision and insert to a length
that would be just distal to the end of the ETT (approximately 30cm
from end of tube)
+ Have an assistant control the bougie so that it does not move during
movement of the endotracheal tube
+ Application of cricoid pressure by assistant and careful, graded
extubation
+ Maintain laryngoscopy and ensure bougie is through the cords on
extubation
+ Replace tube over bougie and guide through larynx under available
vision.
+ Inflate cuff, check ETCO
2
, auscultation, expired tidal volume and then
release cricoid pressure.
+ Secure tube with tape.

49
L. Weaning Guidelines

1. Weaning may be initiated by medical or senior nursing staff.
2. Weaning is contraindicated with any of the following:
a) Unstable ICP (abort weaning if ICP increases)
b) Need for heavy sedation (e.g. upper airway obstruction)
c) Haemodynamic instability
d) Significant bronchospasm
e) High work of breathing.
3. Trial pressure support daily if the patient meets both the following criteria:
a) PaO
2
/FiO
2
ratio > 150
b) Patient can take spontaneous breaths if SIMV resp-rate reduced.
4. Weaning protocol:
a) See the flow diagram following page.
b) Set initial pressure support to maintain adequate V
T

i) Start at 10 cmH
2
O and adjust to:
+ V
T
6 ml/kg IBW for patients recovering from ARDS.
+ V
T
8 ml/kg IBW for all others.
+ IBW Males = 0.91 x (height [cm] 152.4) + 50
+ IBW Females = 0.91 x (height [cm] 152.4) + 45.5
ii) Alternatively, use target V
T
= 80-100% of set SIMV V
T

iii) Allowable PS range = 5 - 25 cmH
2
O
+ If V
T
cannot be achieved with 25cmH
2
O, cease trial
c) Assess at 15 and 30 minutes for weaning success criteria
d) Assess each hour for suitability to wean PS
e) Once PS has reached minimum (5 cmH
2
O) then wean PEEP to 5 cmH
2
O
f) If PS & PEEP = 5 cmH
2
O then asses for extubation.
5. Weaning Success Criteria:
i) RR < 30/min
ii) SpO
2
> 90%
+ May be set lower with COPD, e.g. >86-88%
iii) F
I
O
2
0.5
iv) No respiratory distress as shown by 2 or more of the following:
+ HR > 120% baseline
+ Accessory muscle use
+ Diaphoresis
+ Paradoxical abdominal movements
+ Marked dyspnoea

50
Flowchart: Ventilation Weaning Protocol
PaO
2
/FiO
2
> 150
&
PEEP < 10 cmH
2
O
Pass
Fail
NO Weaning Contraindication:
- Unstable ICP
- Need for heavy sedation
- Haemodynamic instability
- Significant bronchospasm.
AND
Start Weaning Settings:
- Reduce patient sedation
- Reduce SIMV-Rate to 8bpm
- Adjust initial PS to target V
T

8ml/kg IBW, or
6ml/kg IBW if ARDS
- Allowed PS range (5-25 cmH
2
O)
- PEEP remains on previous setting.
Check each 15 minutes -
Weaning Success Criteria:
- RR < 30/min
- SpO
2
> 90% (*lower in COPD)
- FIO
2
0.5
- No respiratory distress as shown by
2 or more of the following:
HR > 120% baseline
Accessory muscle use
Diaphoresis
Paradoxical muscle movements
Marked dyspnoea
Assess After Each Hour -
Set Pressure Support Level:
- If weaning successful after 1
st
Hour
cease SIMV
- If successful on subsequent hours
decrease PS, as per
- If no previous weaning failure
decrease PS by 4 cmH
2
O
- If previous episode of failure
decrease PS 1-2 cmH
2
O
- If at minimum PS = 5 cmH
2
O
decrease PEEP by 1-2 cmH
2
O
Weaning Failure:
- IF post PS decrease
return to previous settings
*note change to PS decrease rate
- IF post return to settings
set PS to max = 25 cmH
2
O
- IF on maximum PS
return to SIMV settings

- IF PS
Max
or SIMV, patient should be
reviewed by SR or Consultant
Weaning Complete:
- If PS = 5 & PEEP = 5 cmH
2
O
- Check ABG
- Assess for Extubation see over.
51
M. Extubation

1. The decision to extubate is made by medical staff, in consultation with either the
senior registrar or duty consultant.
2. Extubation is to be performed by medical or senior nursing staff, with airway
competent medical staff immediately available.
3. Criteria to predict successful extubation are helpful, however, ongoing success
should never be assumed:
a) FiO
2
< 0.5 with PEEP 5 cmH
2
O
b) PaO
2
> 70 mmHg ** lower values may be appropriate in
SpO
2
> 90% chronically hypoxaemic patients
c) RR < 30 with PS 5cmH
2
O (Drger)
d) pH > 7.2
e) No respiratory distress (see over)
f) Patient able to obey commands
g) Patient able to protect airway and cough
h) Patient able to cope with amount of secretions
i) Reason for intubation resolved.
*this may include checking for an air leak with the cuff deflated
4. The Tobin Index may additionally be used to predict extubation failure:
a) Place patient on PS = 2 and PEEP = 5 for 30 mins
b) RR/V
T
> 105 predicts extubation failure
5. Early extubation to NIV may be considered for some patients who present with
hypercapnic exacerbation of COPD or pulmonary oedema:
a) Performed with close supervision by senior medical staff.
b) If no improvement after 1-2 hrs, the patient should be considered for
reintubation.
6. Extubation protocol:
a) Ensure equipment, monitoring and adequate assistance is available, as for
intubation
b) Plastic surgical and ENT patients with intermaxillary fixation/wiring require
consultation with the Parent Clinic.
i) A wire cutter must be present in the room at all times.
ii) The parent clinic should be given opportunity to be present during extubation
if the jaws are wired.
c) All patients should receive supplemental oxygen post-extubation.

52
N. Emergency Surgical Airway Access

1. Policy
a) Call for skilled assistance then proceed without delay.
b) Difficult airway & failed intubation trolleys are in areas A, B & C
c) Cricothyroidotomy and jet ventilation are recommended procedures for urgent
surgical airway access and emergency oxygenation.
d) Standard percutaneous tracheostomy is not an emergency procedure.

2. Indications:
a) Refer to the failed intubation drill in the clinical protocols section.
b) Inability to establish an effective airway despite:
i) Basic manoeuvres - jaw thrust / chin lift / oral-nasal airways
ii) Attempted LMA insertion
c) Inability to ventilate.

3. Cricothyroidotomy
a) Surgical technique
i) Equipment
+ Size 15 scalpel + handle
+ Size 6.0 cuffed endotracheal tube
+ Straight forceps
+ Oxygen delivery circuit: Laerdal bag
ii) Procedure
+ Palpate cricothyroid membrane.
+ 2cm horizontal incision through skin and cricothyroid membrane
+ Insert forceps into wound and open to enlarge the wound
+ Consider insertion of long blue ventilating bougie into trachea
+ Insert endotracheal tube, directly into the trachea or over bougie
+ Remove bougie and connect oxygen circuit
+ Confirm placement with ETCO
2
, auscultation and CXR
+ Perform catheter suction ASAP after adequate oxygenation
+ Cricothyroidotomy is a temporary airway - arrange a definitive surgical
airway (ENT surgeons) as soon as possible.
b) Percutaneous technique
i) Equipment
+ Cook Melker
Emergency Cricothyrotomy Catheter kit (cuffed)

ii) Procedure
+ Palpate cricothyroid membrane with neck well extended
+ 1cm horizontal incision through skin
+ Locate tracheal lumen with fluid-filled syringe & needle/cannula
+ Insert wire through cannula, then remove the cannula over the wire.
+ Insert dilator/introducer & tube assembly over wire in single motion
+ Remove wire & introducer leaving the cuffed tube.
+ Inflate cuff & suction prior to ventilation.
+ Confirm endotracheal placement with ETCO
2
& CXR.
53
4. Jet Ventilation
a) Equipment
i) Cook Jet Ventilation Kit
(Enk Oxygen Flow Modulator Set)

ii) Oxygen flow meter:
+ 15 lpm standard meter - set to highest flow rate
+ 50 lpm high-flow meter - set at 20-30 lpm
b) Procedure
i) Palpate cricoid membrane with neck well extended.
ii) Locate tracheal lumen with fluid filled syringe & needle/cannula.
iii) Feed cannula off needle down the trachea.
iv) Attach oxygen delivery tubing from flow-meter to cannula.
v) Occlude lumens in tubing to produce the jet of oxygen
1 sec ON : 4 sec OFF
vi) Jet ventilation is a temporary emergency measure,
arrange a definitive surgical airway as soon as possible.

O. Fibreoptic Bronchoscopy

1. Policy:
a) This is only to be used by skilled personnel and authorised by the duty consultant.
b) Under no circumstances may the bronchoscope be loaned to other clinics.
c) Expertise with bronchoscopy takes time. Registrars are encouraged to approach
the Department of Thoracic Medicine to attend bronchoscopy clinics to become
familiar with the anatomy of the tracheobronchial tree and use of the flexible
fibrescope.

2. Indications:
a) Difficult intubation (trained staff only): not used as aid to failed intubation
b) Persistent lobar collapse that is refractory to physiotherapy
c) Foreign bodies
d) Diagnostic bronchoalveolar lavage (BAL)

3. Protocol for fibreoptic intubation
a) Indication as per endotracheal intubation
b) Procedure
i) All equipment, drugs and monitoring c.f. routine endotracheal intubation
ii) Supplemental oxygen must be given via a mask and may also be given via the
suction channel of the bronchoscope.
iii) Can be via oral (with bite protection mandatory) or via nasal route
iv) Local anaesthesia / preparation of the airway:
+ Nasal mucosa - topical 10% lignocaine or 2% amethocaine spray.
+ Pharynx - viscous lignocaine gargle
+ Larynx - choice according to operator experience
a. Transtracheal injection and/or direct application through the scope
b. Nebulised - 5 mls 4% lignocaine
c. Superior laryngeal nerve blockade (2-3ml 1-2% lignocaine).

54
v) Check tube cuff
vi) Place a warmed appropriately sized ETT (7mm tube for either sex) into
posterior nasal space.
vii) Insert the scope through the tube under direct vision.
viii) Identify the vocal cords and advance the scope into the trachea.
ix) Advance the ETT over scope into trachea, maintaining view of the tracheal
rings or carina, then remove the scope.
x) Confirm ETT placement by ETCO
2
, auscultation and CXR.
xi) NB: Suction at least 500ml water or saline through scope immediately
following use and notify the equipment nurse that the scope has been used
ASAP.

4. Protocol for BAL
a) Diagnosis of nosocomial pneumonia in selected patients
i) Determination of colonization vs. infection in chronically ventilated patients.
ii) These patients should ideally be off antibiotics for 24-48 hours.
iii) Sufficient reserve to tolerate procedure:
+ Ideally PaO
2
> 70 and FiO
2
< 0.7
+ BAL will commonly result in a 10% reduction in PaO
2
for up to 24 hours
after procedure
b) Procedure
i) Ensure sufficient sedation & place patient on 100% oxygen
ii) Select lobe to be lavaged from recent CXR
iii) Local anaesthetic gel is contra-indicated (interferes with culture media)
iv) If possible, do not suction through scope prior to lavage (upper airway
bacterial contamination)
v) Pass the scope directly into the selected lobe
vi) Wedge the scope as far as possible ideally to 3
rd
generation bronchi
vii) Lavage with 4-6 x 20-40 ml aliquots of sterile normal saline
viii) Aspirate between aliquots and label aliquots accordingly
ix) Send aspirates for quantitative culture and atypical pneumonia screen as
directed.

P. Tracheostomy

1. Policy:
a) Percutaneous tracheostomy (PCT) is the preferred procedure in suitable patients.
b) This procedure is only to be performed by experienced consultant staff or
advanced vocational trainees under supervision.
c) Patients must have the option of surgical tracheostomy cleared by the parent
clinic (either medical or surgical). This is a courtesy.
d) The decision to do a PCT is at the discretion of the ICU consultant.
e) PCT is an elective procedure and has no place in urgent airway access.

55
2. Indications :
a) The indications for PCT are the same as surgical tracheostomy:
b) Airway maintenance
i) Prolonged intubation, e.g. > 10 days
ii) Laryngeal pathology this may also be a contraindication to PCT
c) Airway protection
i) Delayed return of glottic reflexes
ii) Tracheal toilet

3. Contraindications to PCT
a) Lack of consent.
b) Coagulopathy
i) Platelets: < 100,000
ii) APTT: > 40
iii) INR: > 1.5
c) Difficult anatomy - e.g. previous neck surgery, short fat neck
d) Unstable cervical spine injury
e) Grade III or IV intubation (relative consider use of Glidescope)
f) F
I
O
2
> 0.6 / PEEP > 10cmH
2
O

4. Procedure:
a) Ensure consent has been obtained and documented.
b) Equipment, monitoring and drugs as per endotracheal intubation
c) Coagulation screen prior to procedure.
d) Bedside procedure light essential.
e) General anaesthesia - the airway operator must be appropriately trained.
f) Ventilate the patient on 100% oxygen.
g) Tracheostomy equipment:
i) Standard technique: modified Cook Ciaglia kit using the Blue Rhino
ii) Tracheostomy tubes
+ EVAC
aspirating tubes are standard for all tracheostomies.

a. Includes patients having surgical tracheostomies
b. Ensure that an EVAC tube goes with the patient to theatre.
+ Patients who have non-aspirating tracheostomy tubes in place (e.g.
from CTSU or other hospitals) must have these tubes changed to an
EVAC tube as soon as safe and feasible. This is usually 4-5 days post-
tracheostomy.
+ Other tubes:
a. Foam cuffed tubes: indicated in patients with tracheomalacia or
persistent air leaks
b. Uncuffed tube (usually size 6.0) as part of weaning of
tracheostomised patients to facilitate secretion clearance
c. Fenestrated tube: these are either cuffed or un-cuffed with a
fenestration to allow patients to talk.
d. XLT extended length tubes: useful for patients with marked
neck or soft tissue swelling.
56

h) Insertion technique:
i) Aseptic technique.
ii) Goggles are essential for both the operator and anaesthetist
iii) Local anaesthetic infiltration (2% lignocaine + 1:200000 adrenaline) over
the pretracheal rings.
iv) Check the tube cuff, lubricate and insert the dilator into the tube.
v) 2cm horizontal incision over 1
st
or 2
nd
tracheal ring
vi) Pretracheal tissue blunt dissection down to fascia
*look for anterior jugular vein and ligate if identified.
vii) Insert a 14G IV cannula mounted on a syringe with saline into trachea and
aspirate through saline/water to confirm intratracheal placement.
viii) Removal the stylet and reconfirm intratracheal placement by aspirating air
via the IV cannula
ix) Insert the guide-wire through the IV cannula and remove the cannula.
x) Insert a small dilator over the wire into the trachea and make a hole large
enough to accommodate the main dilating instrument.
xi) Blue Rhino
graduated 1-step dilator:

+ Lubricate with water, not gel
+ Place the dilator and guide cannula (white) over the wire, noting:
a. The black marker on the guide at the proximal end of the Rhino
b. The silver marker on the wire at the proximal end of the guide
+ Slowly insert to the required ETT size, ensuring that both markers
(wire and guide) remain in alignment at the proximal end.
xii) Remove the dilator leaving the white guide cannula on the wire and insert
the tracheostomy tube & dilator over the wire/guide into the trachea
xiii) Remove the dilator and wire, inflate the cuff and suction the trachea
xiv) Ventilate and confirm ETCO
2
- self-inflating bag or ventilator
xv) Secure tracheostomy tube with tapes.
xvi) Obtain a CXR post procedure.
xvii) Document the procedure in the case notes and complete a separate
operation note.

5. Complications (of tracheostomy)
a) Bleeding
b) False passage
c) Loss of the airway: immediately re-intubate the patient orally
d) Pneumothorax
e) Cricoid cartilage fracture
f) Laryngeal dysfunction
g) Tracheal stenosis
h) Infection

57
6. Prolonged care of tracheostomy
a) Cuff checks
i) Volumetric (sufficient air to obtain a seal) tests are done following
insertion and whenever a leak is detected with a manual hyperinflation
once per nursing shift.
ii) Manometric tests are inaccurate and do not correlate with mucosal
pressure. These are an adjunct only if cuff malfunction is suspected.
b) Tube changes
i) Routine change at 28 days.
c) Aspirate EVAC tube 2 hourly or more frequently if > 10ml supraglottic
secretion per hour.

Q. Pericardiocentesis

1. Policy
a) This procedure must be authorised by the duty ICU consultant and performed
by consultant staff, trainees under supervision, or cardiology.
b) Confirmation of pericardial effusion or tamponade with echocardiography is
required prior to the procedure, except in peri-arrest situations.
c) Liaison with cardiology is essential.

2. Indications
a) Symptomatic pericardial effusion (tamponade).
b) Although advocated in EMST (ATLS), this procedure has limited utility in
traumatic pericardial tamponade.

3. Procedure
a) Strict aseptic technique.
b) Local anaesthetic infiltration in an awake patient.
c) This procedure should be performed under ultrasound guidance.
d) Technique: Seldinger technique and insertion of a pigtail catheter
i) Insert needle on syringe at 45 from the horizontal axis and aim for tip of
left shoulder
ii) Advance slowly and aspirate until confirmation by aspirating blood or serous
fluid
iii) Insert catheter using Seldinger technique over guidewire.
iv) Confirm placement by aspiration and/or echocardiography
v) Check CXR (pneumothorax)
vi) Suture and occlusive dressing if leaving for > 24 hours.

4. Complications
a) Arrhythmias
b) Cardiac tamponade!
c) Myocardial laceration
d) Pneumothorax, pneumopericardium
e) Liver laceration

58
R. Intra-aortic balloon counterpulsation

1. Policy:
a) The ICU consultant should be involved in the decision to insert an IABP
b) Only to be performed by a consultant or advanced vocational trainee under
supervision.
c) Become familiar with the theory of insertion, indications, interpretation and
complications of IABP.

2. Indications :
a) As a mechanical bridge prior to, and/or following myocardial revascularization
or transplantation:
b) Ischaemic heart disease
i) Low cardiac output states following cardiac surgery
ii) Cardiogenic shock: in association with angiography and revascularization
(PTCA, stent or CAVG)
iii) Acute mitral incompetence (papillary muscle rupture) or VSD following
AMI pending operative repair.
c) Myocardial disease
i) Severe myocardial contusion
ii) Severe myocarditis
iii) Cardiomyopathy
iv) Severe | blocker overdose.

3. Contra-indications:
a) Aortic regurgitation
b) Aortic dissection
c) Severe peripheral vascular disease
d) Tachyarrhythmias (relative)
e) Coagulopathy (relative)

4. Procedure protocol
a) Strict aseptic technique
b) Check IABP function prior to insertion:
i) Adequate helium cylinder volume
ii) Arterial pressure manifold: referenced to mid-axillary line and correctly
zeroed
iii) Dedicated 5 lead ECG connected to IABP
iv) Turn on and leave in standby mode
v) Initial settings:
+ ECG sense: 1:3 ratio
+ Augmentation: minimum (pre-insertion only)
+ Inflate and deflate times: zero
59
c) Insertion procedure:
i) Local anaesthesia in awake patients
ii) Scrubbed assistant recommended
iii) Select size (by patients height) < 165cm : 34ml balloon
> 165cm : 40ml balloon
iv) Femoral artery, Seldinger technique, insertion of a 12F introducer.
v) Check the length for balloon catheter insertion, using the angle of Louis
(level of T
4
) as the surface landmark, prior to insertion.
vi) Insert the balloon to the level of T
4
. The double black marker on the
balloon catheter must be visible this indicates that the balloon has fully
exited the sheath.
vii) Connect to pressure transducer and pump.
viii) Press the [IAB fill] button to fill the balloon & wait for completion.
ix) Press the [assist/standby] button to start the pump.
x) Start on minimal augmentation and increase to maximum.
NB: subsequent augmentation should not be set below 50%
xi) Suture in place and cover with an occlusive dressing.
xii) Set timing:
+ Check balloon inflation against pressure wave:
set to peak of dicrotic notch.
+ Check balloon deflation against ECG:
prior to QRS complex and
observe decrease in end diastolic pressure.
+ Check diastolic augmentation on pressure wave.
+ Select augmentation ratio: *standard = 1:1
d) Maintenance
i) Check CXR post insertion:
tip of IABP below T
4
(carina) & origin of the left subclavian artery
ii) Neurovascular obs of insertion site, lower limbs and left arm hourly.
iii) Nurse at < 30 elevation.
iv) Document pump timing (ratio) and adequacy of augmentation.
v) Assess haemodynamic response: CI, MAP, SVR, filling pressures, CXR.
vi) Ensure clear balloon tubing is exposed:
+ Monitor condensation (due to rapid helium shuttling), or
+ Blood in tubing (balloon rupture).
e) Timing during arrhythmias
i) Ectopics: keep on ECG trigger, system will automatically deflate on
ectopic
ii) Tachycardia > 160/min :
+ Reduce augmentation (equal to patient systole)
+ Decrease ratio to 1:2 if reducing augmentation is not adequate
iii) Atrial fibrillation: move deflate slide to extreme right to deflate on R wave
(not required on newer pumps)
iv) VT or VF: defibrillate or cardiovert as required, the IABP is isolated
60
v) Cardiac arrest (no output) start ECM
+ Effective output: set on pressure trigger to synchronise balloon
inflation with ECM
+ No output: set internal mode for a fixed rate of 40 bpm + 20ml
augmentation
f) Weaning:
i) Commence when patients haemodynamics have improved.
ii) Methods:
+ Reducing ratio from 1:1 to 1:2 to 1:3 and / or
+ Reduce augmentation. NB: minimum balloon inflation 50%
g) Removal of catheter
i) Notify cardiac / vascular surgeons
ii) Cease heparin infusion 3 hours prior to removal
iii) Disconnect IABP tubing: do not aspirate the balloon
iv) Withdraw balloon up to (but not into) the introducer sheath. Even empty
the used balloon will not fit into the sheath, and may rupture if attempted.
v) Remove the sheath and balloon as single unit, applying pressure
immediately.
vi) Use Femostop
local pressure during catheter removal:

+ Remove IABP catheter with Femostop at 60-80mmHg
+ Inflate dome to 20mmHg above systolic as catheter is fully withdrawn
+ Reduce pressure by 15mmHg at 10-15 min intervals
+ If bleeding occurs, reinflate the Femostop to the previously effective
pressure and recommence cyclic pressure reduction
+ Remove Femostop and apply a firm dressing
vii) 10-20% may require surgical repair to the artery.

5. Complications:
a) Limb ischaemia thrombotic or embolic
b) Bleeding at the insertion site or systemically
c) Infection
d) Aortic dissection
e) Occlusion of origins of aortic arch vessels if too high
f) Occlusion of renal/splanchnic vessels if too low
g) Thrombocytopaenia
h) Balloon rupture: gas embolism
i) Femoral artery aneurysm

61
S. Cardiac Pacing

1. Policy:
a) ICU consultant should be involved in decision to insert cardiac pacing wire.
b) If inserted by ICU staff, the procedure is only to be performed by consultant
staff or advanced vocational trainees under supervision.
c) Become familiar with the theory of insertion, indications, interpretation and
complications of TVP.

2. Indications:
a) Medical pacing with adrenaline or transthoracic pacing may be adequate to treat
many symptomatic bradycardias. Note: this is particularly relevant for
retrievals and has obviated the need for prophylactic pacing in some high-risk
patients.
b) Any sustained symptomatic bradycardia which does not respond to medical
treatment, or predisposes to a malignant ventricular arrhythmia.
Note: pacing is indicated by the haemodynamic consequences of the rhythm,
not the arrhythmia per se.
c) Ventricular tachycardias (especially polyphasic) may respond to overdrive
suppression pacing.
d) Following cardiac surgery in high-risk patients (epicardial leads):
i) Valve replacement / repair: especially mitral.
ii) VSD repair / papillary muscle rupture.
iii) Acute myocardial infarction.

3. Types:
a) Semi-rigid, bipolar pacing lead (VVI): insert under image intensification
(standard TVP at RAH)
b) Paceport PA catheters - standard at RAH
c) Balloon flotation leads - ECG or pressure guided catheters
d) Epicardial leads
i) Placed during cardiac surgery in high risk patients
ii) Usually unipolar ventricular, but may be bipolar, atrial or ventricular:
check the operative note and liaise with the surgeon.

4. Paceport PA protocol
a) VVI mode only
b) Ensure a ventricular demand pacemaker box is available
c) Insert the Paceport PA catheter using standard technique (see PAC section)
d) A pressure transducer should be attached to the RV as well as the distal port
e) The RV port should be 1 to 2cm distal to the tricuspid valve
i) In some patients the catheter may wedge before the RV port is in the RV in
these cases an alternate technique should be used
f) Attach the adapter to the RV port
g) Insert probe to the reference mark
62
h) Attach ECG monitoring and advance until ST elevation indicates contact with
the epicardium
i) Secure the probe and connect side port to a saline flush
j) Commence pacing
k) Check adequate capture and sensing (see next section)

63
5. Semi-rigid Wire protocol: (VVI lead)
a) Strict aseptic technique
b) Image intensification
c) Local anaesthesia where appropriate
d) Insertion protocol:
i) 6F peel away sheath or PAC introducer
ii) Right IJ vein is the preferred route, then left subclavian.
NB: if permanent pacing is likely then avoid subclavian placement.
iii) Under I-I control, feed the wire until the tip just stops on the RV wall
iv) Connect to the control box (switched off)
v) Set output and sense to their minimum value, and rate 20bpm faster than
the patient's own rate (or 70bpm, whichever is greater).
vi) Turn the generator on and gradually increase the output while watching the
ECG for capture.
vii) If there is no capture or a high output is required:
+ Place on demand mode
+ Turn output right down, advance or reposition the wire slightly
+ Try to capture again. An ideal capture setting is ~ 2 mA
+ Ensure wires are not exposed and tape both sides
viii) Suture the wire and apply an occlusive dressing
ix) Arrange a post-insertion CXR.
x) Always be aware of the risk of tamponade even when pacing has been
unsuccessful.
e) Daily check:
i) Battery strength
ii) Capture: set the output ~ 2x higher than threshold for safety.

6. Flotation Catheter Insertion
a) These may be inserted either blind, under ECG guidance (standard
recommendation), or via pressure guidance for catheters having an infusion
lumen (c.f. PA catheter insertion).
b) Aseptic technique & local anaesthesia where appropriate
c) Insertion protocol:
i) 6F peel away sheath, do not use a PAC introducer as these will leak
ii) Attach V
5
lead of an ECG to the distal electrode of catheter & monitor
iii) Note P then QRS wave-form changes as the catheter advances to the RV
iv) Advance catheter another 2cm, deflate the balloon & advance 1cm
v) Connect to the pulse generator (switched off)
vi) Set output and sense to their minimum value, and rate 20 bpm faster than
the patient's own rate.
vii) Turn the generator on and gradually increase output while watching the
ECG for capture.
viii) If there is no capture or a high output is required - see (5.d.vii) above
ix) Suture the wire and apply an occlusive dressing
x) Arrange a post-insertion CXR.

64
T. Oesophageal Tamponade Tubes

1. Policy:
a) All patients with tamponade tubes should be intubated prior to insertion and
managed in ICU.
b) The ICU consultant should be involved in the decision to insert an oesophageal
tamponade tube.
c) Become familiar with the theory of insertion, indications, and complications.
d) Routine placement in ICU is performed by the GE Unit.

2. Indications :
a) Variceal haemorrhage:
i) Where endoscopy cannot be done due to bleeding
ii) Failure of sclerotherapy, banding and/or octreotide infusion.

3. Types of tubes:
a) Minnesota: oesophageal and gastric balloons and 2x aspirating ports
b) Sengstaken: oesophageal and gastric balloons and gastric aspirating port
c) Linton: gastric balloon and aspirating port

4. Procedure:
a) Preferrably use a bulk & frame bed.
b) Prior to insertion:
i) Check both balloons for leaks
ii) Inflate the gastric balloon with 300ml of air and check pressure reading.
iii) Deflate all balloons completely and lubricate the tube
c) Estimate insertion length =
(bridge of nose to earlobe) + (nose to xiphoid process)
d) Insert under direct vision using a laryngoscope then x-ray to ensure the tube is
not folded up in the oesophagus.
NB: inflating the gastric balloon in the oesophagus is virtually 100% fatal!
e) Inflate the gastric balloon in 50ml increments up to 300ml while monitoring the
balloon pressure. NB: If the balloon pressure exceeds 5mmHg above the pre-
insertion pressure then incorrect (oesophageal) placement is probable and this
mandates deflation of the balloon and reinsertion of the tube.
f) Pull back until resistance is felt as the balloon rests against the gastric fundus.
g) Note the measurement at the lips, and fix securely with gentle traction:
i) Rope and pulley system with 500ml bag of fluid, or
ii) Adhesive tape to face.
h) Inflation of the oesophageal balloon is usually not required. It should only be
inflated in consultation with ICU consultant. If required, connect a pressure
gauge to the oesophageal balloon, and inflate to a pressure of 40 mmHg
i) Recheck position on x-ray.
j) After 12-24 hours, the balloons should be let down and if bleeding does not
recur the tube may be removed.
k) Sclerotherapy is usually performed: ( 50% patients will otherwise re-bleed)

65
U. Extracorporeal Membrane Oxygenation

1. Extra Corporeal Membrane Oxygenation (ECMO) is a method of providing
oxygenation to the blood in cases of overwhelming respiratory failure (veno-venous
ECMO) or temporary circulatory support in reversible cases of refractory
overwhelming cardio-respiratory failure (veno-arterial ECMO).

2. The ECMO service started in 2009 in the RAH ICU, and continues to be developed
further.

3. Any cases of potential ECMO support will be discussed in detail prior to initiation,
and will be supervised closely by ICU consultants.

4. If caring for a patient on ECMO all relevant protocols and contact details will be
made available. Care of the patient on ECMO includes specific requirements.

5. The ECMO circuit and equipment must not be altered without the ICU consultant
and/or perfusionist supervision.

66

PART 3 - DRUGS AND INFUSIONS

A. Policy

1. Patients admitted to the ICU must have a complete drug history documented:
a) Premorbid and current medications.
b) Previous adverse drug reactions and allergies.
c) Note potential drug interactions.
2. Charting of drugs and infusions is to be done by ICU medical staff.
a) Parent clinics must not write on the ICU flowchart.
b) Therapeutic changes suggested by the home team must be communicated to the
appropriate ICU medical staff.
3. All changes or additions to drug and fluid orders must be written and signed for on the
flowchart.
a) Nursing staff must be notified of such changes.
b) Verbal orders alone are neither sufficient nor legal.
4. All drugs, infusions and fluids are reviewed and transcribed at least daily.
5. Printed sticky labels for the commonly used infusions and drugs should be used
where possible.
6. Standardisation of infusion concentrations is essential for the prevention of drug
errors. Infusion concentrations should not be changed (e.g. double strength) from
the protocols outlined below.
7. Vasoactive or hypertonic infusions (e.g. TPN) must be administered through a
dedicated lumen of a CVC or PICC.
8. Vasoactive infusions must not be used in the general wards, other than for patients en
route to ICU and who are being continuously monitored.
9. All antibiotics written on the ICU flowchart must also have an indication of date
started and due date for review and/or completion.
10. Patients cleared for discharge from ICU must have all appropriate drugs, infusions and
fluids prescribed on the standard hospital forms, prior to discharge. Where
appropriate, old drug charts should be re-written.
11. Patients discharged on TPN must have their details entered in the TPN folder (stored
in the Unit A office area).
12. Any changes to acute pain drug regimens in patients under the care of the Acute Pain
Service should be done in consultation with the Acute Pain Service.
13. Any proposed changes to specialty type drugs, e.g. immunosuppressives,
anticoagulants, antiplatelet agents, etc should be discussed with home teams.

67
B. Principles of drug prescription in Intensive Care

1. Ideally, drugs should only be prescribed where proven benefit has been demonstrated.
2. Drugs should be prescribed according to Unit protocols and guidelines.
3. Ensure that the drug doses are correct: seek advice if unsure.
4. The risks and benefits of starting any drug must be carefully considered.
5. Critically ill patients have altered pharmacokinetics and pharmacodynamics, with the
potential for toxicity and drug interactions.
6. Where possible:
a) Use drugs that can be titrated or prescribed to an easily measured endpoint.
b) Use drugs that can be measured to monitor therapeutic drug levels.
c) Avoid drugs with narrow therapeutic indices (e.g. digoxin, theophylline),
particularly in patients with associated hepatic or renal dysfunction.
d) Cease a drug if there is no apparent benefit.
e) If two drugs are of equal efficacy, choose the cheaper drug as the cost of drugs in
ICU is significant.

C. Cardiovascular Drugs

1. Inotropes

Inotropes (specifically catecholamines) are frequently used in ICU. There are varied
prescription practices and preferences for these drugs, mostly based upon the reported
pharmacological effects of the different agents.

a) General principles:
i) Defence of blood pressure in critically ill patients forms the basis of
haemodynamic resuscitation and organ perfusion. This must be interpreted
in the context of the patients pre-morbid BP, particularly for those
patients with renovascular hypertension or cerebrovascular disease.
ii) Hypovolaemia is the most common cause of hypotension and low cardiac
output in ICU and must be assiduously monitored and corrected.
iii) The main indications for the use of inotropes are to increase myocardial
contractility, heart rate and/or vascular tone.
iv) The use of inotropes requires regular haemodynamic monitoring (arterial
line and CVC) and, where indicated, a PA catheter or PiCCO or Edwards
Vigileo cardiac output system.
v) No single inotrope (or mixture of inotropes) has been shown to be superior
to another.
vi) There is marked inter-individual variation in the response to inotropes.
This is partly due to pre-existing chronic illness, genetic variation, co-
administration of other drugs, dynamic qualitative and quantitative changes
in adrenergic receptor kinetics.
vii) Prolonged exposure to catecholamine infusions can produce adrenergic
receptor down-regulation. The clinical implications are:
68
b) Catecholamines
i) Receptor effects may be unpredictable, however, in general:
+ |-adrenergic effects predominate at low doses, and
+ o-adrenergic effects at higher doses.
ii) It is impossible to predict the dose range for an individual patient.
iii) Prescription on a body weight basis (g/kg/min) is of little clinical utility.
iv) Infusions should be started at a low rate (3-5 g/min) and titrated to a set
clinical response, e.g. MAP (not systolic)
v) There is no well established maximal dose
vi) The use of renal protection dose dopamine is no longer indicated
vii) Regular assessment should be made of both global (pH, lactate) and
regional effects (urine output/creatinine clearance, limb perfusion).
c) Phosphodiesterase inhibitors (milrinone)
i) Inhibition of PDE
3
increases intracellular cAMP and calcium, causing:
+ an increase in myocardial contractility
+ systemic and pulmonary vasodilatation, and
+ improved diastolic relaxation (lusitropy)
ii) Any resultant hypotension (due to systemic vasodilatation) is usually
treated with a vasopressor (e.g. noradrenaline).
iii) Phosphodiesterase inhibitors have longer half-lifes than catecholamines,
are less titratable and their half-life is prolonged with renal failure.

Table: Cardiovascular effects of inotropes
Agent
|1 effects |2 effects o1 effects o2 effects
| Chronotropy
| Dromotropy
| Inotropy
| Inotropy
Vasodilatation
Bronchodilatation
| glucose/lactate
| Inotropy

Vasoconstriction

| Inotropy

Vasoconstriction

Adrenaline
Noradrenaline
Dopamine

| effects predominate at low dose

o effects predominate at high dose

Dobutamine + + (+) -
Isoprenaline + (+) - -
+ = strong effect (+) mild effect - = no effect

69
Table: Inotropic Agents Used in ICU
Agent Standard Infusion Uses
Noradrenaline 6 mg / 100 ml 5% dextrose
(ml/hr = g/min)
First line drug in septic shock
Maintenance of cerebral perfusion pressure
Adrenaline 6 mg / 100 ml 5% dextrose
(ml/hr = g/min)

Cardiopulmonary resuscitation
Acute severe asthma
Anaphylaxis
Cardiogenic shock
Second line drug in septic shock after noradrenaline
Medical pacing
Dobutamine 500 mg / 100 ml 5% dextrose
(ml/hr approx g/kg/min)
Primarily a vasodilator, weak inotropic action
Traditionally used in cardiogenic shock or low
output, high afterload states or when filling
pressures high
Often used in combination with noradrenaline
Dopamine 400 mg / 100ml 5% dextrose
(ml/hr approx g/kg/min)
No advantage over adrenaline/noradrenaline
Renal dose dopamine is not used
Endocrine side effects
Isoprenaline 6 mg / 100 ml 5% dextrose
(ml/hr = g/min)
Vasodilator, chronotrope (rarely used)
Medical pacing
Levosimendan 12.5 mg / 250 mL 5% dextrose
Loading dose: 12-24g/kg/10min
Dose rate: 5-15 ml/hr.
NB: Loading dose may cause
marked hypotension, may be
omitted.
Calcium sensitizer
Increases myocardial contractility in an oxygen
efficient manner and dilates coronary and systemic
vessels
Role in Intensive Care not established
Milrinone 10mg / 100 ml 5% dextrose
Loading dose: 50g/kg/20 min
Dose rate: 0.5 g/kg/min*
Cardiogenic shock due to diastolic failure
Pulmonary hypertension following valve
replacement
Catecholamine induced down regulation
*Standard milrinone prescription for 70 kg patient: Loading dose: 3500 g = 35 ml over 20 minutes
Maintenance: 2100 g/hr = 20 ml/hr.

2. Vasopressor agents

a) General principles
i) Vasopressors usually act directly on the peripheral vasculature and are
primarily used to acutely elevate blood pressure
ii) The catecholamines have variable effects on the peripheral vasculature.
iii) The most common cause of hypotension in ICU patients is hypovolaemia.
iv) Pressor agents should not be used as an alternative to fluid resuscitation.
70
b) Indications (in ICU)
i) Tissue infiltration with local anaesthesia
ii) Topically prior to nasal intubation
iii) Hypotension following sympathetic block (e.g. epidural anaesthesia)
iv) Hypotension refractory to large doses of catecholamines (vasoplegia):
+ Consider relative hypoadrenalism
+ Consider use of vasopressin
c) Complications
i) Rebound hypertension
ii) Vagal reflex bradycardia
iii) Tachyphylaxis

Table: Vasopressors
Agent Standard Infusion / Dose Uses
Metaraminol 10mg / 10ml 5% dex: titrate Potent short acting vasoconstrictor
Ephedrine 30mg / 10ml 5% dex: titrate
Synthetic indirect sympathomimetic.
Commonly used in anaesthesia, little
benefit over adrenaline.
Vasopressin
20units/20ml 5%dex:
1.8mls/hrs (0.03u/min)
Noradrenaline resistant hypotension.
May be useful in septic shock
Phenylephrine
Not available in Australia
Methoxamine

3. Antihypertensive agents

i) The most common cause of hypertension in ICU patients is sympathetic
drive due to pain, agitation or delirium. These should be treated with
adequate sedation and analgesia.
ii) Patients in the recovery phase of acute renal failure are often hypertensive.
This usually represents the resetting of endogenous neurohumoral
mechanisms and as such does not routinely require treatment.
iii) Hypertension following an intracranial event (haemorrhagic or ischaemic)
is common and the underlying mechanism dictates therapy. A high BP
may be tolerated in ischaemic stroke, c.f. the setting of SAH with an
unclipped aneurysm, where treatment would be paramount.
iv) Target therapy should be titrated against the patients premorbid BP.
v) In the absence of adverse effects, the maximal therapeutic dose of a
selected agent should be used prior to commencing a second or third agent.

71
b) Indications
i) Acute
+ Acute perioperative control of hypertension post-cardiac, carotid, or
cerebrovascular surgery, or for patients with critical myocardial
ischaemia.
+ Hypertensive crisis (malignant hypertension)
+ Pre-eclampsia / eclampsia
+ Phaeochromocytoma
+ Untreated aneurysm or vascular injury,
e.g. intracranial aneurysm, ruptured/dissected aorta
ii) Other indications for vasodilators
+ Reduction of afterload in cardiac ischaemia and CCF
+ Adjunct to passive warming in hypothermia
iii) Chronic
+ Sustained essential hypertension
+ Ischaemic heart disease
+ Cerebrovascular disease
c) Complications are many, but in relation to ICU patients:
i) First-dose effect / hypotension
+ especially in hypovolaemic patients
ii) Reflex tachycardia
iii) Tachyphylaxis
iv) Pulmonary vasodilatation causing shunt and hypoxaemia
v) Cyanide toxicity (SNP)
vi) Angioedema especially ACEI
vii) Deterioration in renal function
viii) Electrolyte disturbances

Table: Antihypertensive & Vasodilator Agents
Agent Infusion & Dose Uses
Glyceryl
trinitrate (GTN)
30mg / 100ml 5%D
(non PVC bottle and giving set)
Range 2-25 ml/hr
First line drug in RAH ICU
Can be given topically.
Mainly venodilation:
Useful in cardiac ischaemia
Less predictable control of BP than SNP
Tachyphylaxis develops within 24-48hr
will need additional agents for persistent |BP
Sodium
nitroprusside
(SNP)
50mg / 250 ml 5%D
Range 3-40 ml/hr
Rapid control of hypertensive crises.
Tachyphylaxis and metabolic acidosis may imply
cyanide toxicity (total dose > 1.5mg/kg/24 hrs)
Phentolamine 10mg / 10ml 5%D: titrate Pure o-blockade, short acting antihypertensive
Hydralazine 5-10 mg as bolus
20-40 mg 6-8 hourly
Short to medium term IV agent.
Often use with |-blockers to control reflex tachycardia
Useful in renovascular hypertension

72
Amlodipine 5-10mg oral bd Long acting oral Ca
++
antagonist.
Caution in renal impairment
Captopril Start low dose ~ 5-6.25mg
| up to 50mg orally 8 hrly
Syrup: 5mg/ml or tablets
Acute hypertension: 5-25mg
sublingually prn
Treatment of hypertension
Left ventricular dysfunction, esp post-MI
Left ventricular failure
Diabetic nephropathy
Caution in renovascular disease and renal failure
Perindopril Start 2.5mg daily
| up to 10mg daily orally
Phenoxy-benzamine Oral : 10mg/day and increase
until postural hypotension
IV : 1mg/kg/day
dilute to 200-500ml
1/3 dose over 1/24
2/3 dose over 1/24
Long acting o blocker
Preoperative preparation of phaeochromcytoma
Idiosyncratic hypotension may occur
Prazosin Start with 0.5mg, and
increase up to 5mg tds orally
o-blocker
Potent antihypertensive agent
Beware first dose effect, esp if under-filled
Metoprolol Oral: 25-100mg bd
IV: 1-2mg bolus every 2-3
minutes up to 10 mg.
High sympathetic drive states: neurogenic BP
All grades of hypertension, inc renovascular
Cardiac ischaemia
Control of reflex tachycardia with vasodilators
Thyroid crisis
Caution in poor LV function, asthma
Mainly eliminated by hepatic metabolism
Esmolol Loading dose 0.5 mg/kg
Infuse 100mg/10ml and titrate
Ultra-short acting |-blocker
Useful as trial for patients with poor LV function.
Adjunct to vasodilators post cardiac surgery
Clonidine 25g boluses of up to
150g/24hrs
Oral: 75g bd
| up to 150-300g tds.
Acute, centrally mediated hypertension
Useful post cardiac surgery
Withdrawal states
Care with hepatic or renal dysfunction
Rebound hypertension with chronic use
Sedation, especially 1
st
dose
Dexmedetomidine 400 g in 40mls
load 1g/kg over 20min
infuse 1-5ml/hr
Selective alpha-2-agonist
Acute, centrally mediated hypertension
Not a first line drug.
Selected use by senior medical staff only
Sedation
MgS04 5-10 mmol loading
Infuse at 4-12 mmol/hr
Target plasma [Mg] ~ 1.5-2
mmol/L
Pre-eclampsia / eclampsia
Phaeochromocytoma
Sympathetic overdrive in tetanus

73
4. Antiarrhythmics

i) Prior to administration of antiarrhythmic agents, optimise correction of the
following:
+ Hypovolaemia
+ Metabolic abnormalities
a. | K
+
, Mg
++
, HPO
4
=
, alkalosis
b. Hypoxaemia, hypo/hyper-carbia
+ Myocardial ischaemia or cardiac failure (especially post-cardiac
surgery)
+ Sepsis
+ Pain and agitation.
ii) All antiarrhythmic drugs are potentially arrhythmogenic.
iii) Virtually all depress myocardial contractility.
iv) Antiarrhythmics drugs are indicated where:
+ The arrhythmia causes haemodynamic compromise (hypotension or
prolonged tachycardia >120-130/min) or
+ Susceptible patients with myocardial ischaemia.
v) Consider anticoagulation if AF > 48 hours
b) Indications
i) Termination of an acute arrhythmia
ii) Prophylaxis against recurrence
iii) Rate control

74
Table: Antiarrhythmic Agents
Agent Infusion & Dose Uses
Amiodarone Acute use:
900mg / 250ml 5%D:

Load 100ml / 1 hr (5mg/kg)
Infuse 10 ml/h for 24-48 hrs
(15mg/kg/day)

Bolus Dose 150-300mg

Chronic:
200-400 mg IV/oral daily
Rapid AF / flutter or MAT
Monomorphic ventricular tachycardia
Generally does not suppress contractility
Can cause acute hypotension if given too rapidly
Less proarrhythmic than most other drugs
Causes |QTc, but rarely Torsade de pointes
Renal excretion is minimal no need to change dose
in renal failure
Long term side-effects rare in short-term use.
Interference with digoxin kinetics and assay.
Interference with thyroid function tests.
Magnesium 5-10 mmol IV slow bolus
Infuse at 2-5 mmol/hr. 2.4g MgSO4
= 10mmol Mg
++

Acts principally as a calcium blocker
Useful in AF and Torsade de pointes
Verapamil 5-10 mg IV slow bolus Conversion atrial flutter SR
SVT 2
nd
line to Adenosine
Digoxin Loading dose: 0.5-1 mg IV.
Maintenance: 62.5-250 g IV/day

Levels: 0.61.0 mmol/l
Ventricular rate control in rapid AF (usually 2
nd
line to
amiodarone in critically ill)
Narrow therapeutic index esp in renal failure and
metabolic abnormalities (| K
+
, Mg, PO4, alkalosis)
Proarrhythmic potential high in critically ill patients
Minimal inotropic effect in critically ill patients
Hypokalaemia potentiates effects
Metoprolol 1-2mg IV bolus (up to 10 mg)
25-100mg oral bd
Used in high sympathetic drive states : neurogenic
hypertension
Control of reflex tachycardia with vasodilators
Caution in poor LV function, asthma
Mainly hepatic metabolism
Sotolol 10-80 mg IV slow bolus
(10-15 min)
Class III and |-blocking actions
Supraventricular tachyarrhythmias
Conversion AF/flutter SR
Low pro-arrhythmic potential
Adenosine 6-12 mg rapid IV push Diagnosis / conversion of SVT
Lignocaine 0.4% solution = 4mg/ml :
60ml/hr (4mg/min) for 1-2 hrs
45ml/hr for 2-4 hrs
30ml/hr for 2-4 hrs
2
nd
line drug after amiodarone
Sustained, recurrent VT
No longer routinely used for prophylaxis for VT
VF resistant to defibrillation (now questioned)
Potent negative inotrope, pro-convulsant
Phenytoin 15mg/kg loading / 1 hr
300 mg/day
(level 40-80 mmol/l)
Digoxin toxicity
Tricyclic induced malignant arrhythmias
75
5. Thrombolytic Therapy

NB: All patients with acute myocardial infarction should be considered as potential
candidates for primary angioplasty. The Cardiology cover must be notified of all
patients with an acute MI, as early as possible. The duty cardiologist will decide
between primary angioplasty, thrombolysis, and expectant management.

a) Indications
i) Acute myocardial infarction
+ Thrombolytic therapy is standard in the management of AMI,
wherever primary angioplasty is not performed.
+ Administered in consultation with the duty cardiologist.
+ The patient should be advised of the potential risks and benefits.
+ Patient criteria
a. No specific age limit discuss with Cardiology
b. Ischaemic chest pain > 30 min & < 12 hrs
i. Benefit is inversely proportional to delay in thrombolysis,
therapy should be considered a medical emergency
ii. Late therapy may be inappropriate for small infarcts.
c. ECG evidence of acute infarction:
i. | ST segment > 2mm in two (or more) chest leads, or
ii. | ST segment > 1mm in two adjacent limb leads, or
iii. New LBBB
iv. Posterior infarction (|R in V
1
+ |ST in V
2
)
d. No benefit has been demonstrated for patients with ST-depression,
T-wave inversion, or a normal ECG.
ii) Haemodynamically significant pulmonary embolism.
+ An unequivocal diagnosis is necessary prior to thrombolysis (spiral CT
or angiogram).
+ Tenecteplase is preferred in life threatening pulmonary embolism
iii) Ischaemic Cerebrovascular Accident
+ Within 4.5 hrs of onset of symptoms
+ CT head: confirming CVA and excluding intracranial haemorrhage
+ Oedema on initial CT head is associated with a higher incidence of
bleeding
+ In consultation with a neurologist according to RAH protocol.

b) Contraindications:
i) Absolute:
+ Active internal bleeding.
+ Recent head trauma, major trauma or surgery within 3 weeks.
+ CVA within 6 months.
+ Refractory hypertension (> 200/100 mmHg)
76
ii) Relative:
+ Lack of verbal informed consent.
+ Known bleeding diathesis
+ Current use of anticoagulants (warfarin)
+ Active peptic ulceration or other GI bleeding within 6 months.
+ Prolonged CPR (> 10 mins) and/or traumatic resuscitation
+ Pregnancy.
+ Diabetic proliferative retinopathy.
+ Non-compressible vascular puncture/injury.
iii) Each of these relative CIs should be considered in view of the potential
clinical benefit and risk to each patient.
c) Complications
i) Bleeding (incidence of cerebral haemorrhage is ~ 0.5%)
ii) Anaphylaxis/anaphylactoid reactions: hypotension, rash, bronchospasm
iii) Reperfusion arrhythmias
d) Routine follow-up
i) ECG at 1 and 4 hours post TNK
ii) Cardiac enzymes 6, 12 and 24 hours post infusion
iii) If ST-elevation persists 1 hr post-TNK,
contact cardiology regarding rescue angioplasty.

Table: Thrombolytics
Drug Dose Protocol
Tenecteplase
TNK
Single dose:
1. 0.5 mg/kg over 10 sec
2. non-glucose containing line
3. flush line with N.Sal pre & post

Maximum dose = 50mg (=10,000U)
Aspirin 150mg pre-Rx, then daily
Enoxaparin 30mg IV prior to TNK
Enoxaparin 1mg/kg sc bd
(if renal function normal)
If renal impairment consider heparin IV
instead of enoxaparin.
Alteplase

Dose = 0.9 mg/kg.
Give 10% of dose as bolus over 1 minute.
Give remainder of dose over 60 mins via
syringe pump.
Maximum total dose s 90 mg.
Refer to RAH protocol.
Observe vital signs and neurological
observations every 30 minutes for the first
6 hours post infusion then hourly for the
next 16 hours
Repeat BP more frequently if elevated
Keep BP <180/105
Tenecteplase -
PTE
As Above Heparin 5000U IV pre-TNK
Heparin infusion: APTT > 50-80 secs
Bleeding
protocol:

Monitor:
APTT
PT / INR
Fibrinogen level
Euglobulin clot lysis time
Apply local pressure (if possible)
Reverse heparin with protamine
Cryoprecipitate 10 units + FFP 2 units
Defibrination or intracranial bleed:
tranexamic acid 10 mg/kg over 20
minutes then 1mg/kg/hr infusion

77
6. Antiplatelet Agents

Table: Antiplatelet Agents
Agent Usual dose Indications/Comments
Aspirin 75-150 mg Post acute coronary syndrome
Other thrombotic cardiac event
Post TIA / stroke
Clopidogrel 75mg orally daily

300mg oral loading dose pre-PTCA
(then 75mg daily)
Irreversibly modifies platelet ADP receptor,
inhibiting aggregation
Uses: prevention of vascular ischaemic events
e.g. MI, CVA, PTCA
ReoPro
(abciximab)
Bolus: 0.25mg/kg IV over 1 min,
10mins before PTCA

Infusion:
0.125g/kg/min IV for 12hrs.
(max rate = 10g/min)

Only to be ordered by Cardiology
Binds to platelet glycoprotein IIb/IIIa receptor,
inhibiting platelet aggregation and thrombus
formation
Primarily used with PTCA
Used with aspirin and heparin
(target ACT >200sec)
Increased risk of major bleeding and
thrombocytopaenia
Tirofiban
(aggrastat)
Bolus:
0.4 g/kg/min
for 30 mins

Maintenance:
0.1 g /kg/min
for at least 48hrs

NB: reduce doses by 50% with
severe renal insuff. (e.g. creat
clearance <30ml/min)
Only to be ordered by Cardiology
Blocks glycoprotein IIb/IIIa receptor
Short half-life (1.4-1.8 hrs)
Uses: unstable angina, non-Q wave MI
Use with heparin and aspirin
Continue through angiography, and for 12-24hrs
post-PTCA
Check platelet count 6hrs post-bolus, then at
least daily. If <90,000 cease and contact
cardiology
SEs: bleeding (major 1.4%), thrombocytopenia,
fever

78
D. Respiratory Drugs

1. Inhaled bronchodilators

a) General Principles:
i) Treatment of bronchospasm in ICU (including acute severe asthma).
ii) They are not routinely used in all ventilated patients.
iii) Once commenced, they must be reviewed frequently regarding efficacy:
+ Audible wheeze, respiratory rate
+ Subjective and objective work of breathing
+ Lung compliance
+ Blood gases.
b) Indications:
i) Pre-existing asthma / chronic obstructive pulmonary disease (COPD)
ii) Acute severe asthma or exacerbation of COPD
iii) Bronchospasm 2 to infection, aspiration or during mechanical ventilation,
not primarily due to airway secretions
iv) For the treatment of hyperkalaemia (nebulised salbutamol only)
c) Metered dose inhalers:
i) MDIs are the default therapy for ICU patients
ii) Indications for nebulisers are:
+ Inadequate response to 10 puffs of MDI
+ Status Asthmaticus

2. Parenteral therapy

a) Indications:
i) Adjunctive therapy for patients with acute severe asthma or COPD not
responding to nebulised agents
ii) Selected patients who are difficult to wean from ventilation
(usually due to COPD)
iii) Maintenance therapy in patients with COPD
b) Complications
i) Hypokalaemia, metabolic alkalosis
ii) Arrhythmias - |
2
-agonists, theophylline
iii) Intercurrent infection - steroids
iv) Polyneuropathy - steroids
v) Increased lactate - |
2
-agonists
vi) Metabolic acidosis - |
2
-agonists

79
Table: Bronchodilators
Drug Infusion/ dose Clinical uses
Salbutamol MDI 4 puffs every 4 to 6 hrs
Max 10 puffs 4 hrly if needed
First line bronchodilator
Default method of administration
Salbutamol (nebulised) Nebulised in N.Saline (1ml:1ml)
continuously, 2 or 4 hrly
Bronchospasm refractory to MDI
Severe hyperkalaemia
Ipratropium MDI 4 puffs every 6 hrs
Max 10 puffs 6 hrly if needed
Chronic obstructive pulmonary disease
Bronchorrhoea
Ipratroprium bromide Nebulised in addition to salbutamol
(1ml:1ml)
Budesonide (nebulised
steroid)
Nebulised 1 mg b.d. Steroid dependent COPD
Acute exacerbation of COPD
Beclomethasone MDI 2-4 puffs b.d. Use 4 puffs with a wet circuit
Fluticasone MDI 2-4 puffs twice daily Use 4 puffs for a wet circuit
For patients on Seretide
Inhaler
(Salmeterol & Fluticasone)
use Fluticasone MDI
For patients on Symbicort
Turbuhaler
(Eformoterol & Budesonide)
use Fluticasone or Beclomethasone MDI
Adrenaline (IV) 6 mg / 100 ml 5%D
(ml/hr = g/min)
Acute severe asthma
Rapid onset and offset of action
Titrate until clinical pressor response
(may require up to 100 g/min)
Salbutamol (IV) 6 mg / 100 ml 5%D
(ml/hr = g/min)
Acute severe asthma
Longer duration of action
Hydrocortisone 100 mg IV 4-8 hourly All patients with acute severe asthma
Wean over 48-72 hrs once asthma begins to
resolve
Acute exacerbation of COPD
Theophylline 1000mg / 100ml 5%D
Loading 5-7mg/kg,
Infuse 2-4ml/hr (1gm/day)
Levels: 55-110 umol/l
Second line, adjuvant drug.
May improve respiratory drive in COPD
Narrow therapeutic index: proarrhythmic
Prostacyclin
(inhaled)
500g + 10ml diluent (50g/ml)
Add to 40ml NSal, infuse with
syringe driver into nebuliser (set at
8l/min flow rate) at 2-4 ml/hr.
Selected patients with ARDS with pulmonary
HT and severe hypoxia.
Consultant authorisation mandatory.
80
E. Sedation, Analgesia and Muscle Relaxants

1. Sedatives and analgesics
a) Adequate analgesia and anxiolysis are primary goals in the management of the
critically ill patient.
b) Pain and anxiety are associated with significant adverse effects:
i) Hypertension, tachycardia
ii) Increased myocardial and cerebral oxygen consumption
iii) Gastric erosions
iv) Intracranial hypertension
v) Persistent catabolism
c) Sedatives and analgesics are also associated with adverse effects:
i) Respiratory depression
ii) Prolonged ventilation and associated complications (e.g. nosocomial
infections)
iii) Emergence delirium and sympathetic overdrive.
iv) Hypotension due to unmasked hypovolaemia.
v) Gastroparesis, ileus and resultant feed intolerance
vi) Increased cost, ventilator days
d) Sedation protocol for ICU patients:
i) It is important, although often difficult, to obtain a reasonable balance
between the awake, distressed patient and the patient that is over-sedated.
ii) Sedation should be given by infusion to maintain constant levels, with
boluses as required for discrete interventions.
iii) Titrate infusions to clinical effect: there is marked inter-individual variability
and absolute doses are meaningless
iv) Patients with renal, hepatic or associated encephalopathy may require lower
doses (or no sedation at all)
v) Prescribe the desired sedation level by circling the box on the flow chart:

Table: Sedation Levels
Light:
default
eyes open to speech, easily roused
purposeful responses
usually spontaneous or partial support ventilation
nocturnal sedation
Moderate: eyes closed
rouses to tactile or painful stimuli,
usually partially or fully ventilated
Heavy: no motor response to stimulus
weak cough on suction
fully ventilated paralysis

81
vii) Nurse controlled sedation protocol
+ Titrate sedation to prescribed level (as above)
+ If the patient becomes over-sedated
a. Hold the infusion until the patient becomes responsive
b. If ongoing sedation is required, recommence the infusion at half the
previous rate.
+ If the patient is under-sedated
a. Use a bolus of sedation/analgesia and increase rate according to
dose range prescribed.
b. If insufficient repeat until a satisfactory sedation level is attained.
+ Sequential increases in infusion rate, without the use of a bolus dose,
increases the risk of over-sedation as the infusion approaches steady-
state (5 half-lives)
+ Remember, the half-life for fentanyl increases with the duration of
infusion, so time to steady-state may be greatly prolonged see context
sensitive graph below.
+ Grimacing alone is not a reliable sign and may only indicate awareness
or reflex activity.
+ Infusions should not be titrated to responses during high-intensity
stimuli, e.g. suction. In this situation, bolus sedation may be required.
viii) NB: In the absence of a specific contraindication, sedation should be held
daily from 0800 for all patients, except those prescribed deep sedation.
ix) PCA or epidurals are considered when the patients are awake. Notify the
Acute Pain Service of these patients (see next section)

2
50
100
150
200
250
300
4 6 8 10 12 14
Fentanyl
Propofol
Infusion Duration (Hrs)
C
o
n
t
e
x
t
-
S
e
n
s
i
t
i
v
e

H
a
l
f
-
T
i
m
e

(
m
i
n
s
)
82
Table: Sedatives / Analgesics
Drug Infusion/dose Clinical uses
Propofol 10mg/ml (neat solution),

Start at 3ml/hr and titrate
against effect

Maximum 20ml/hr
Short term sedation where extubation is
expected within 24-48 hrs
Do not use where prolonged ventilation is
anticipated, except where repeated
neurological assessment is required (e.g. CHI),
or in the presence of hepatic or renal failure.
Anaesthesia for minor procedures where
prompt return of consciousness is required
(e.g. tracheostomy, CVC)
Potent myocardial depressant/vasodilator
No analgesic effect.
Fentanyl 100-200 g IV bolus
Infusion: 50-200 g/hr
(neat solution)
Haemodynamic stability
Potent medium acting narcotic
Useful for ICU procedures.
Morphine and
Midazolam
morphine 60mg +
midazolam 30mg
per 50ml 5% dextrose
Rate: 1-30 ml/hr
Review rate/sedation at least daily
Effects prolonged in renal failure
Morphine 1-5 mg IV, sc prn, or
PCA per protocol
First line analgesic
Caution in renal failure
Diazepam IV: 2-10 mg prn
Orally: 5-10mg bd-qid*
First line anticonvulsant (IV)
First line anxiolytic esp in delirium
Larger doses may be required in acute alcohol
withdrawal*
Epidural cocktail
(APS protocol)
Fentanyl 5g/ml and
Bupivacaine 0.1% or
Ropivacaine

Standard epidural analgesic regimen
Plain bupivacaine may be used (0.25%)
Maximal duration 4 days unless indicated
Rate: age related doses (per APS)
Dexmedetomidine 400 g in 40mls
load 1g/kg over 20min
infuse 1-5ml/hr
Selective alpha-2-agonist
Short term sedation / weaning from ventilation /
withdrawal states
Not a first line drug.
Selected use by senior medical staff only
Haloperidol 0.5-2 mg IV prn First line major tranquilliser
Delirium, agitation
Esp. in opioid / benzodiazepine withdrawal.
o blocker : may cause hypotension
Chlorpromazine 2.5-5 mg IV prn As for haloperidol; 2
nd
line tranquilliser
More sedating, unpredictable & longer acting
Vasodilator

83

2. Analgesia in Awake Patients See APS Intranet Guidelines

ACUTE PAIN SERVICE 2010
SC AND ORAL OPIOIDS INITIAL DOSES
Age
(yrs)
SC morphine/oxycodone
(mg)
Oral oxycodone*
(mg)
15 39 7.5 12.5 15.0 25.0
40 59 5.0 10.0 10.0 20.0
60 69 2.5 7.5 5.0 15.0
70 85 2.5 5.0 5.0 10.0
> 85 2.0 3.0 2.5 5.0
Recommended dose interval: 2 hourly prn * if pain not severe

Acute Pain Service (APS) contact numbers
Mon-Fri: 0830-1730 pager 22556
After 1730 hrs SD 1175
W/E & Pub Hol via Switch
Notes:
Suggest start in middle of dose range; upper limit of dose range can be
increased if analgesia is inadequate, sedation score is less than 2 and resp rate
> 8 /min (first check that doses are correct/ have been given as ordered)
Sedation score 2 = constantly drowsy, still easy to rouse but unable to stay
awake once woken

Simple analgesia:
Unless contraindicated, paracetamol is best ordered for all patients and on a
regular rather than prn basis
Dose equiv. SC (mg) Oral (mg)
Morphine 10 30
Oxycodone 10 20
Fentanyl 150 microgram -
Buprenorphine 400 microgram (patch) 800 microgram (SL)

84
3. Muscle relaxants
i) These agents have a limited role in ICU and must not be used unless the
patient is adequately sedated (heavy sedation).
ii) Non-depolarising agents (except rocuronium) should not be used for
emergency (rapid sequence induction) endotracheal intubation.
b) Indications
i) Depolarising: suxamethonium
+ First line relaxant for emergency endotracheal intubation (see section on
intubation)
ii) Non-depolarising: rocuronium, vecuronium, atracurium
+ Acute control of ventilation post-intubation
+ Patient transport / retrieval on Oxylog ventilator who cannot be
managed by other means
+ Selected patients with poor lung compliance who are difficult to
ventilate following heavy sedation
+ With anaesthesia for procedures: tracheostomy, bronchoscopy
c) Complications
i) Hyperkalaemia, bradycardia (suxamethonium)
ii) Sympathetic overdrive, particularly in under-sedated patients
iii) Adverse outcome in head injury when used as a measure to control ICP
iv) Use of non-depolarising relaxants may be associated with increased risk of
critical illness polyneuropathy, especially with concomitant use of steroids.

Table: Muscle Relaxants
Relaxant Dose Comment
Suxamethonium 100-200 mg or
1-2 mg/kg
1
st
line agent in Rapid Sequence Induction (RSI)
Consider pre-treatment with atropine (0.6-1.2mg) if
potential bradycardia
Contraindicated in burns (>3 days), chronic spinal and
neuromuscular disease, hyperkalaemic states (K
+
> 5.5)
Caution in any patient with any central or peripheral
muscle weakness including critical illness related
weakness
Rocuronium 0.6 mg/kg

1.0 mg/kg
for RSI
First line non-depolarising agent in ICU
Rapid onset (60secs)
2
nd
line agent in RSI = alternative to suxamethonium
Duration of action : 30-40 minutes
Vecuronium 6-10mg IV prn 2
nd
line non-depolarising agent in ICU
Duration similar to rocuronium

85
F. Anticoagulation

6. General principles
a) All patients on systemic anticoagulation must have an APTT, INR and CBP
performed daily.

7. Indications
a) Acute systemic anticoagulation:
i) As a general rule, heparin infusions titrated to a therapeutic APTT are used
in critically ill patients. This allows monitoring and the provision for
reversal if indicated (e.g. procedures, bleeding complications).
ii) Therapeutic enoxaparin is effective but potentially more difficult to use in
critically ill patients, due to inability to easily monitor activity, dose
variation in renal disease and inability to reverse effect.
iii) Indications:
+ Proven venous or arterial thromboembolism
+ Acute coronary syndromes: as sole therapy or following TNK
+ Prosthetic heart valves:
a. Prior to commencement of oral anticoagulants
b. During an acute illness, where oral anticoagulation is relatively
contraindicated.
+ AF in patients complicated by emboli < 70 years.
+ AF for more than 48 hours, in which cardioversion is being considered
+ Extracorporeal circuits e.g. CVVHDF, ECMO
+ IABP
iv) RAH Heparin Protocol see below
b) Partial anticoagulation (low dose IV heparin (500 u/hr), IV prostacyclin)
c) Oral anticoagulants (warfarin)
i) The kinetics of warfarin are highly variable in the critically ill.
ii) Normally only used in stable long term patients
iii) Prosthetic valves (mitral > aortic valves)
iv) Previous thromboembolism
v) Maintenance of thromboprophylaxis in high risk patients (# pelvis)

8. Protocol for DVT/VTE prophylaxis
a) All patients must have a documented plan for DVT prophylaxis
b) TED stockings
i) All patients except those with:
+ Significant PVD
+ Significant lower limb trauma, cellulitis, dermatitis or oedema
+ Peripheral venous or arterial access on lower limb(s)
+ For most of the above patients, a single TED should be used on the
unaffected limb
ii) TED stockings can be used in patients with proven DVT to decrease the
incidence of post DVT thrombophlebitis
iii) Continue until the patient can mobilise effectively
86
c) Prophylaxis with sequential calf compression devices (SCCDs)
i) SCCDs have an additive preventative effect to other forms of DVT
prophylaxis
ii) There are a limited number of devices available and priority is given to
patients who are unable to use chemoprophylaxis or are at high risk
iii) If a patient has had a prolonged period of time (greater than 24 hours)
without DVT prophylaxis consideration should be given to a lower limb
ultrasound to exclude DVT prior to application of SCCDs
d) Enoxaparin 40 mg s/c daily
i) LMWH of choice, all patients unless contraindicated
ii) Start on day 1 or as early as possible especially in high risk patients,
including those with:
+ Previous/family history of DVT or PE
+ Significant trauma involving pelvis and lower limb fractures
+ Vasopressor therapy
+ Post hip or knee replacement surgery
+ Prolonged femoral venous catheters
+ Prolonged immobility, neuromuscular wasting
e.g. Guillain Barr, polyneuropathy, spinal injury
+ End stage renal disease (consider UF heparin)
e) Enoxaparin 60 mg s/c daily (20mg mane + 40mg nocte)
i) Should be considered for high risk patients:
+ Pelvic or long bone fractures
+ Significant spinal injury or paralysis
+ Previous PTE/DVT
ii) Routine monitoring is not necessary. If required, measure anti-Xa activity
iii) Continue enoxaparin throughout ICU stay
f) Cease enoxaparin for:
i) Significant bleeding
ii) Suspected HITS - see below
iii) Active and mobile patients who have a short ICU stay and no risk factors
for DVT as outlined above
g) Absolute and relative contraindications for enoxaparin:
i) Significant active haemorrhage
ii) High risk of bleeding
+ Coagulopathy - DIC, thrombocytopenia, liver failure, etc.
+ Post-surgical - neuro, spinal, eyes
+ Major trauma - TBI with parenchymal lesions, liver/spleen injury
iii) Known or suspected adverse reaction to heparin
+ Documented or suspected HITS, known heparin allergy
iv) Patients already on therapeutic anticoagulation
v) Renal failure
h) Unfractionated (UF) Heparin
i) Second line agent for DVT prophylaxis
ii) 5000
U
s/c b.d.-t.d.s. generally has lower efficacy and similar risk of
bleeding in high risk patients compared to enoxaparin
87
iii) Considered in patients with a high risk of bleeding or renal failure, due to
its relatively shorter duration of action and ease of reversal.
i) For patients with a high risk of bleeding, communication with the relevant
surgical teams (neurosurgery, spinal, ophthalmology, etc) is essential.
j) NB: No other DVT prophylaxis protocols are to be used
i) Except for patients post - pelvic surgery
ii) The adjusted dose heparin protocol may be used,
see VTE Prophylaxis in Orthopaedics on the RAH Intranet

9. High risk trauma patients - must have an active plan for VTE prophylaxis

10. Perioperative anticoagulation in patients on Warfarin
a) Heparin infusion remains the first choice in ICU, as the effect is more readily
monitored and reversed.
b) Where heparin is contraindicated, consider danaparoid or consult haematology.

11. Protocol for Heparin Induced Thrombocytopaenia Syndrome (HITS)
i) HITS is a prothrombotic drug reaction caused by platelet-activating
antibodies
ii) It is an intense hypercoagulable state that is often complicated by venous
and arterial thrombosis
iii) Risk factors
+ Duration of therapy *see 4T table
+ Type of Heparin UFH > LMWH
+ Type of patient postsurgical > medical > pregnancy
b) Diagnosis
i) The 4T Score pre-test probability of HITS
+ Points - 0, 1, or 2 for each of 4 categories (see table)
+ Maximum possible score = 8
a. High risk 6-8 points
b. Intermediate risk 4-5 points
c. Low risk 0-3 points
+ If probability is intermediate or high do a HIT screen for antibodies.
+ If high probability cease heparin immediately pending test results
ii) HIT Screen
+ ELISA detects antibodies against heparin and PF4.
+ Also detects other non-HIT heparin-Ab, therefore lower specificity
+ If ELISA positive then test further with a "functional assay",
serotonin release assay (SRA)
iii) Lower limb doppler U/S

88
Table: HITS Probability Score 4T Score
Risk Factor 2 Points 1 Point 0 Points
Thrombocytopenia Platelet fall > 50%
Nadir > 20
Platelet fall 30-50%
or >50% fall due to surgery
or nadir 10-19
Platelet fall < 30%
Nadir < 10
Timing of onset of
platelet fall (or other
sequelae of HITS)
Day 5-10
or
Day 1 with heparin
in last 30 days
> Day 10 or timing unclear
or
< Day 1 with heparin
in last 31-100 days
< Day 4
No recent heparin
Thrombosis or
other sequelae
Proven new thrombosis,
skin necrosis
or
Anaphylactoid reaction
after IV heparin bolus
Progressive or recurrent
thrombosis,
erythematous skin lesions,
suspected thrombosis,
asymptomatic upper limb DVT
None
OTher cause
of platelet fall
None Possible Definite
Pretest probability score: High (6-8) | Intermediate (4-5) | Low (0-3)

d) Treatment principles
i) Two Dos
+ Do stop all heparin (including flushes, LMWH, etc )
+ Do start an alternative non-heparin anticoagulant in therapeutic doses.
a. Lepirudin - difficult to use, or
b. Danaproid - may cross react
c. Discuss with haematology
ii) Two Donts
+ Dont administer warfarin acutely and if warfarin has already been
administered, give vitamin K
+ Dont give prophylactic platelet transfusions
iii) Two Diagnostics
+ Test for HIT antibodies
+ Investigate for lower limb DVT
89
7. Anticoagulants

Table: Anticoagulants
Drug Infusion / Dose
Warfarin
Variable dose INR
See age-adjusted Warfarin loading protocol below
Daily INR
Heparin (infusion)
25000u/50ml = 500u/ml
See below: titrate against APTT:
Cease 4-6 hours prior to surgical procedures
Heparin (subcut)
5000 u subcut bd <70 kg
5000 u subcut 8 hrly >70 kg or high risk DVT
Enoxaparin (Clexane
)
Prophylaxis:
40mg subcut daily
20mg subcut daily if Creat clearance < 30ml/min
High risk 20mg mane 40mg nocte
Treatment:
1mg/kg subcut bd - lean body mass
1mg/kg subcut once daily if Creat clearance <30ml/min
Prostacyclin (infusion)
Dose: 0.2-0.6 g/kg/hr
500g (+10ml diluent): add to 40ml NSal = 10g/ml solution
Start at 2ml/hr and monitor platelet count
May cause hypotension
Danaparoid sodium
(Orgaran
)
Infusion
IV loading dose:
< 60kg 1500 U
60-75 kg 2250 U
75-90 kg 3000 U
> 90 kg 3750 U
Infusion: 2250
U
of danaparoid in 250ml 5% dextrose:
44 ml/hr (400 U/hr) x 4 hours
33 ml/hr (300 U/hr) x 4 hours
22 ml/hr (200 U/hr)
Adjust dose to anti-Xa levels (target 0.5-0.8 anti-Xa U/ml)
Long half life (25 hrs): cease early if changing to oral anticoagulants
Danaparoid (subcut) 750 U 8-12 hourly
Lepirudin Complex see below

90
Table: Heparin Infusion Protocol
Weight (kg) 45-55 56-65 66-75 76-85 86-95 >95
Bolus (U) 3,500 4,200 4,900 5,600 6,300 7,000
Infusion (U/hr) 900 1,100 1,250 1,400 1,600 1,800
Infusion adjustment
APTT IV bolus Stop Infusion Rate Change Repeat APTT
< 37 5,000 units | 400u/hr 6 hrs
38-64 | 200u/hr 6 hrs
65-110 No change Daily
111-130 | 50u/hr 6 hrs
131-140 30 min | 100u/hr 6 hrs
141-150 60 min | 150u/hr 6 hrs
>150
120 min or
APTT < 150
| 200u/hr 2 hrs
Note: Infusion: 25,000 units in 50ml syringe = 500U/ml
Check first APTT 6 hrs after bolus dose

8. Lepirudin
a) Recombinant direct thrombin inhibitor
b) Dose range varies by a factor of 20x
i) Care must be used in determining the precise dose
ii) Renally excreted and must be carefully monitored in the critically ill
c) NB: bolus is only used if patient has life threatening thrombus

Table: Lepirudin Infusion Protocol
CrCl (ml/min) Bolus Dose
Maintenance Infusion
mg/kg/hr % original dose
> 60
0.4 mg/kg
(max 44mg)
0.1 (max 11mg/hr) 100%
45-60 0.2 mg/kg 0.05 50%
30-44
None
0.025 25%
15-29 0.01 10%
< 15 0.005 5%
CVVHDF 0.01 10%

91

Table: Age Adjusted Warfarin Loading Protocol*
Day INR
Dose (mg) according to age (yrs)
s 50 yrs 5165 yrs 6680 yrs > 80 yrs
1 < 1.4 10 9 7.5 6
2 (16hrs after 1
st
dose)
s 1.5 10 9 7.5 6
> 1.6 0.5 0.5 0.5 0.5
3 (16hrs after 2
nd
dose)
s 1.7 10 9 7.5 6
1.82.3 5 4.5 4 3
2.42.7 4 3.5 3 2
2.83.1 3 2.5 2 1
3.23.3 2 2 1.5 1
3.4 1.5 1.5 1 1
3.5 1 1 1 0.5
3.64.0 0.5 0.5 0.5 0.5
> 4 0 0 0 0
4 (16hrs after 3
rd
dose)
s 1.5 1015 914 7.511 69
1.6 8 7 6 5
1.71.8 7 6 5 4
1.9 6 5 4.5 3.5
2.02.6 5 4.5 4 3
2.73.0 4 3.5 3 2.5
3.13.5 3.5 3 2.5 2
3.64.0 3 2.5 2 1.5
4.14.5 Omit next dose, then
12 0.51.5 0.51.5 0.51
> 4.5 Nil. Hold dose.
*Roberts GW, Gallus AS, Druskeit T et al. Comparison of an age adjusted warfarin loading protocol
with empirical dosing and Fennertys protocol. Aust NZ J Med. 1999; 29: 731-6.

NB. This table is meant only as a guide, and was developed for non-critically ill
patients, whose pharmacodynamics may differ significantly from the intensive care
population. INR must be checked daily.

92
G. Endocrine Drugs

1. Insulin
a) Indications:
i) Diabetic emergencies DKA and hyperosmolar coma
ii) Treatment of hyperkalaemia
+ 50% dextrose 50ml, plus Actrapid 10
U

iii) Perioperative diabetic patients (both insulin and non-insulin dependent)
iv) General ICU patients
+ Hyperglycaemia > 10 mmol/l or glycosuria in acute illness:
a. Maintaining BGL 10mmol/l using an insulin infusion is
recommended for all critically ill patients.
b. Majority of ICU patients will require insulin using this protocol.
c. NB: This protocol is not designed for patients with diabetic
ketoacidosis and is a guideline only.
d. Some patients will require individual manipulation of dose.
+ Subcutaneous sliding scale insulin:
a. No longer recommended by the RAH Endocrine Unit.
b. May be used in a small number of less critically ill patients with a
limited need for insulin and for recovering patients in whom IV
access is not available
c. A regular dose of subcutaneous insulin, adjusted according to BGL
is also suitable in ICU patients.

b) ICU Insulin Protocol see following page.
i) Target BGL = 5-10mmol/l
ii) Take BGL from arterial line, substituted every 4hrs by finger prick for
patients on insulin infusions
iii) Protocol Precautions:
+ If insulin rate 8 U/hr and the BGL remains high, measurement may
be erroneous take a sample from another site and send it to the lab
for BGL check.
+ Consider holding the infusion if feed or glucose infusions are stopped.
+ Potassium level
a. Administration of insulin reduces K
+
levels.
b. Check K
+
on ABG specimen at least twice daily and more often if
the insulin infusion rate is high or changing acutely.
c. If [K
+
] < 3.5 mmol/l
KCl ~ 30 mmol over 1h via a pump.

93
Flowchart: Blood Glucose Management in ICU

Table: Insulin Infusion Protocol
BGL Bolus
Starting
infusion
Subsequent infusion Repeat BGL
mmol/l Units IV Units/hr Units/hour Hours
>15 2 2 Increase by 1 1
10.1-14.9 1 1 Increase by 1 1
8-10 0 0
If BGL dropping continue current rate.
If static or rising increase by 0.5
1
5-7.9 0 0
Continue current rate
If BGL dropping for 2 consecutive hrs
decrease rate by 0.5.
1 (2hrly if
BGL stable
for 6 hrs)
3.5-4.9 0 0 Cease
1 (4hrly if off
insulin>6hrs)
<3.5 Call MO 0 Cease 1

c) Discharge Management:
i) See Insulin Protocol for Patients Discharged from ICU below.
ii) Pre-discharge, cease insulin infusion for at least 4 hours and check BGL
iii) Order BGL to be checked 8 hourly on the ward
iv) See Diabetes Management Guidelines on the RAH intranet.

Target BGL = 5-10mmol/l
Perform BGL on Admission
BGL = 5-10mmol/l
BGL > 10 mmol/l
Commence Protocol
Perform BGL 4hrly
94
Flowchart: Insulin Protocol for Patients Discharged from ICU

*See Diabetes Management Guidelines on the RAH Intranet
95
2. Diabetes insipidus: protocol for DDAVP
a) Diabetes insipidus may occur in the following situations:
i) Post ablative pituitary surgery
ii) Severe head injury, esp. anterior cranial fossa #, trauma
iii) Evolving brain death
iv) Lithium administration
b) Indications for DDAVP
i) Acute perioperative management (24-48hrs) of DI following pituitary
surgery is usually fluid based. Use of DDAVP is rarely indicated.
ii) In the above situations:
+ Persistent polyuria in the absence of diuretics
a. > 300ml/hr for > 3-4hrs
b. Ensure you document/inform the nurse that you want to be
notified if this occurs, as can quickly get behind
+ Altered conscious state, inability to detect thirst or take oral fluids
+ Low urine osmolality in the presence of high plasma osmolality
+ Pre-existing hyperosmolar state or predisposition to pre-renal failure
where persistent polyuria may exacerbate this.
c) Maintenance fluids should be prescribed in the usual manner, according to
volume status, renal function and osmolality.
d) DDAVP Prescription
i) Dose 1-2 g s.c. bd as required. (4g is excessive)
ii) Adjust maintenance fluids according to the response
e) In patients with brain death, DI should be treated promptly as a delay can result
in significant electrolyte abnormalities.

3. Steroids
a) Indications
i) Pre-existing steroid therapy:
+ Wide variety of indications, doses and durations of therapy.
+ The need to continue steroids, with or without dose adjustment, should
be assessed.
ii) A number of conditions present within the ICU where steroid therapy may
be beneficial. In the majority of these supporting data is variable and the
decision to administer steroids should be made on a case-by-case basis:
+ Adult meningitis - esp. pneumococcal & prior to antibiotics
+ Septic shock - non-responders to a SST
+ ARDS - fibro-proliferative phase + negative cultures
+ Anaphylaxis
+ Post-extubation laryngeal oedema / stridor
b) Contra-indications / non-indications
i) Active infection
ii) ARDS except as above
iii) Acute head injury
iv) Guillain-Barr syndrome
v) Fat embolism syndrome
96
c) Relative drug potencies

Table: Steroid Doses / Relative Potencies
Drug
Equivalent
dose (mg)
Glucocorticoid
activity
Mineralocorticoid
activity
Hydrocortisone 100 1 1
Prednisone 25 4 0.3
Methylprednisolone 20 4 0
Dexamethasone 4 30 0
Cortisone acetate 125 0.8 0.8
Fludrocortisone 1 10 250

d) Short synacthen test (SST)
i) Indication:
+ Suspicion of hypoadrenalism
+ Hyperkalaemia, hyponatraemia, hypoglycaemia, refractory acidosis
+ May be in association with septic shock (incidence is 75%):
a. Refractory hypotension despite aggressive inotropes/IVT
b. Relative hypothermia
ii) Test:
+ Semi-quantitative adrenal response to extrinsic ACTH
+ Baseline serum cortisol
+ Synacthen 250 g IV
+ Serum cortisol level at 30 and 60 minutes
iii) Interpretation:
+ Normal (septic): baseline > 250 nmol/l, increment > 250 nmol/l
+ Hypoadrenalism: baseline < 200 nmol/l, no response to ACTH
+ Intermediate: baseline 200-1000 nmol/l
may or may not increment > 250 nmol/l
+ Note:
a. Hydrocortisone will interfere if given pre-test (false neg).
b. Dexamethasone wont but has less mineralocorticoid (thus
haemodynamic) benefit
c. Aim to perform the test and use hydrocortisone ASAP
iv) Increment < 250 nmol/l may warrant steroid replacement therapy:
+ Hydrocortisone 50 mg qid iv
+ Can be started post-SST and stopped if SST normal
+ Fludrocortisone 50 g daily NG can also be given.
97
H. Renal Drugs - Diuretics

a) Oliguria in acutely ill patients is frequently a manifestation of:
i) Hypovolaemia relative or absolute
ii) Decreased cardiac output
iii) Direct renal toxicity, or
iv) A combination of these factors.
b) Therapy should be directed toward causative factors and not maintenance of urine
output by the administration of a diuretic agent.
c) Urine output, in the absence of diuretic use, represents one of the best markers of
end-organ perfusion and is a useful guide to clinical management.
d) Diuretics should never be used to treat oligo/anuria, they are only a treatment for
fluid overload

2. Indications
a) Symptomatic fluid overload
i) Pulmonary oedema
ii) Congestive cardiac failure: cor pulmonale
b) Hyperaldosterone states: ascites
c) Clinical fluid overload
d) Chronic renal failure (maintenance)

3. Contraindications
a) Hypovolaemic and/or Na
+
-depleted states
b) Known drug hypersensitivity (esp. sulphonamide group)

4. Complications
a) Hypovolaemia
b) Hyperosmolal states due to inappropriate diuresis in hypovolaemia
c) Potentiation of renal failure - 2 to hypovolaemia
d) Electrolyte disturbance especially | K
+
, Mg, PO
4
, metabolic alkalosis
e) Natriuresis and kaliuresis will alter urine electrolytes and osmolality for 24-48
hrs post dose.

98
Table: Diuretics
Drug Infusion/dose Clinical uses
Frusemide 40-250 mg/day
IV / oral
First line, potent loop diuretic
Doses may be increased in diuretic dependence
| K
+
, Mg, PO4, metabolic alkalosis common
Acetazolamide 250-500 mg IV tds Carbonic anhydrase inhibitor
Alkaline diuresis with HCO3
-
excretion
Used for severe metabolic alkalosis after
correction of hypovolaemia: | K
+
, Mg, PO4
May be useful in weaning COPD from ventilation
with post hypercapnic alkalosis
Spironolactone 25-100 mg oral bd Potassium sparring diuretic
Often given with loop and thiazide diuretics
Indicated as part of diuretic treatment regime for
left ventricular failure
Use in ascites especially if secondary
hyperaldosteronism
Mannitol 20% solution /
200 mg/ml

Dose 100 ml prn
(20g)

(0.5g/kg is
too much!!)
Potent osmotic diuretic
May cause initial hypervolaemia, then late
hypovolaemia and hyperosmolal states.
Causes an osmolal gap
(measured-calculated osmolality).
Maintain measured osmolality < 300 mosmol/l
Limited role in suspected acute life-threatening
intracranial hypertension as a bridge to definitive
surgical therapy.
Limited (unproven) roles in rhabdomyolysis,
transfusion reactions, myoglobinuria for renal
protection

99
I. Gastrointestinal Drugs

1. Stress ulcer prophylaxis
a) Routine stress ulcer prophylaxis is not indicated.
i) Low prevalence of clinically significant bleeding due to stress ulceration
ii) No evidence of survival benefit
iii) Possible increased incidence of VAP
b) High risk stress-ulcer patients
i) Prophylaxis - ranitidine 50mg iv tds
ii) Reduce dose in renal compromise
c) Patients on pre-existing therapy (with PPIs or H
2
-blockers) should be continued
d) Patients with known or clinically suspected GI bleeding should commence on a
PPI
e) Enteral feeding should be commenced as soon as possible

2. Acute GI bleeding
a) Definition
i) Overt bleeding
+ Blood in the NGT
+ Haematemesis or malaena
ii) Plus either:
+ | MAP > 20 mmHg
+ | Hb > 20 g/L in 24 hours
+ Required 2
+
units blood transfusion in 24 hrs
iii) Blood in the NG tube is frequently due to local erosion and by itself does not
constitute clinically significant GI bleeding.
b) Management
i) Resuscitation - ABC
ii) Correct coagulopathy
iii) Cease heparin / anticoagulants
iv) Commence PPI - pantoprazole 40 mg bd/tds.
v) Endoscopy sclerotherapy
vi) If the source is not identified and with ongoing bleeding, consider:
+ Labelled red cell scan
+ Angiography (+/-embolisation) or
+ Colonoscopy.

100
3. GI drugs

Table: GI Drugs
Drug Dose Clinical uses
Metoclopromide 10 mg IV 6 hrly, prn Persistent vomiting, nausea
Large gastric aspirates
(in combination with erythromycin)
Erythromycin 100 mg IV bd Large gastric aspirates
(in combination with metoclopramide)
Droperidol 0.625 mg IV prn Potent, effective antiemetic
Minimal side effects
Tropisetron 2 mg IV / oral daily Third line antiemetic after metoclopramide and
droperidol
Use if anticholinergic side effects are to be
avoided.
Ondansetron 4 mg IV prn / 12 hrly Second line, antiemetic
(not available at RAH)
Ranitidine 50 mg 8hrly IV
150-300 mg daily po
Peptic ulcer disease
First-line stress ulcer prophylaxis
Does not prevent acute rebleeding
Reduce dose in renal failure.
Pantoprazole Acute RX:
40 mg IV bd/tds
Maint. RX:
40 mg daily
Refractory peptic ulcer, ulcerative oesophagitis
First line RX for peptic ulceration
Z-E syndrome
Upper GI bleeding
Octreotide Bolus: 50 ug IV
Varices: 50 ug / hr
Fistulae: 100-200
IV / sc 8-hrly
Variceal bleeding
(as effective as sclerotherapy)
Enteric, pancreatic fistulae
Sulphonylurea overdose
Severe secretory diarrhoea, e.g. post-chemo

101
J. Antibiotics

1. Policy
a) Prescription of antibiotics must conform to RAH guidelines.
b) The over-prescription and irrational use of antibiotics is associated with the
development of bacterial resistance, nosocomial infection and drug related
morbidity
c) All antibiotics must be reviewed daily and where appropriate, discussed with
Infectious Diseases or Clinical Microbiology.
d) Record the day and expected course of antibiotics in the left-hand margin of the
drug chart, e.g. D4/7 = day 4 of a 7 day course.
e) Record date, test and results (including sensitivities) in the results folder.

2. Principles of antibiotic prescription
a) The treatment of infection consists of (in order of priority)
i) Adequate resuscitation
ii) Surgical drainage of infected collections where indicated
iii) Relevant samples for microbiological and/or histological analysis
iv) Standard cultures:
+ Blood - 2 sets at different times from venous stabs
+ Urine
+ Sputum
+ Any other suspicious site
v) Rational prescription of empiric antibiotics
vi) Prompt administration of culture-directed antibiotics
vii) NB: time to effective ABx treatment affects outcome.

b) General indications for antibiotics:
i) Prophylaxis for invasive procedures and operations
+ Proven indications
a. Abdominal surgery which involves a breach of the colonic mucosa
(traumatic or elective), or draining an infected cavity
b. Selected obstetrical and gynaecological procedures:
i. Caesarean section with ruptured foetal membranes
ii. Vaginal hysterectomy
c. Insertion of a prosthetic device
d. Compound fractures
e. Amputation of gangrenous limb
+ Unproven but recommended
a. Lacerations penetrating into periosteum or into joint cavities
b. Crush injuries
c. Insertion of a neurosurgical shunt
d. Cardiac valve replacement
e. Arterial prosthesis

102
ii) Empirical antibiotics where infection is likely prior to definitive
bacteriological diagnosis:
+ Obtain as many cultures as possible before antibiotics commenced.
+ In sick patients "best guess" antibiotics should be commenced prior to
results
+ When gram stain or culture results return, antibiotic cover should be
rationalised to specific treatment for isolated organisms.
iii) Specific infections where the organisms is known

c) Complications of antibiotics
i) Antibiotic effect related
+ Bacterial resistance
+ Nosocomial infection
+ Pseudomembranous colitis
ii) Systemic reactions
+ Skin rashes
+ Anaphylactoid / anaphylactic reactions
iii) Specific organ toxicities, e.g.
+ Interstitial nephritis, ATN
+ Seizures
+ Marrow suppression, thrombocytopaenia
+ QT prolongation
iv) Cost

d) Gentamicin
i) Pharmacodynamic properties
+ Concentration-dependent killing peak:MIC ~ 10:1
+ Significant post-antibiotic effect
ii) Toxicity
+ Nephrotoxicity - non-oliguric renal failure
+ Ototoxicity - permanent, vestibular or auditory
iii) Dosing
+ All dosing for gentamicin is by Lean Body Weight (LBW)
+ Estimate lean body mass:
a. Male: 50kg + 0.9kg/cm height > 150cm
b. Female: 45kg + 0.9kg/cm height > 150cm
+ Initial Dose: 5-7 mg/kg *irrespective of renal function
+ Measure level 6-10 hrs post-dose:
a. See target levels on following graph, or
b. Liaise with ICU Pharmacist (Pg: 22916) or
Drug Information (Ext: 25546) re further dose requirements.
+ Synergistic gentamicin, e.g. tds dosing in endocarditis
a. Measure pre-dose trough levels
b. Aim for < 1.0 mg/L to avoid toxicity.

103

e) Vancomycin
i) Pharmacodynamic properties
+ Time-dependent killing max 24h-AUC:MIC ratio
+ Moderate post-antibiotic effect
ii) Toxicity
+ Ototoxicity < 2%
+ Nephrotoxicity
a. Very rare (20 case reports 1956-84)
b. Probably non-existent with current preparations
+ Red-man syndrome rate of IV administration.
iii) Preference in ICU is for continuous infusion, c.f. interval dosing.
+ Moderately irritant to veins
+ If given via a peripheral line,
infusion volume should be 250ml solution @ 10ml/hr
iv) Renally cleared. Plasma t
|
= 4-6 hrs
v) NB: assessment of renal function by serum creatinine is sub-optimal.
Elderly patients and those with low muscle mass may have a significantly
impaired GFR in the setting of a high-normal creatinine

Do NOT use if
CrCl < 60 ml/min
104
Table: Vancomycin Dosing Schedule
Renal Function
CrCl
> 50 ml/min
CrCl
10-50ml/min
CrCl < 10 ml/min
CRRT
I
n
i
t
i
a
l

D
o
s
i
n
g

Loading dose IV
1.0g or
15 mg/kg if wt >80kg, or
25 mg/kg if critically unwell
slow infusion (1/24) in All Patients
Infusion Rate 2.0g / 24 hrs 1.0g / 24 hrs Not indicated
Subsequent Dosing 1.0g IV 12 hrly 500mg IV 12 hrly Per levels

Level Monitoring
1hr pre-dose #6
(usually day 3)
Daily

I
n
f
u
s
i
o
n

D
o
s
e

A
d
j
u
s
t
m
e
n
t

Target Level Infusion: 20-25 mg/L
[Vanc] < 15mg/L
| Dose 1g/day
max = 4g/day
| Dose 0.5g/day
Not indicated [Vanc] = 20-25mg/L Cont. Cont.
[Vanc] > 30mg/L
Hold 24 hrs
Recheck Level
Hold 24 hrs
Recheck Level

I
n
t
e
r
v
a
l

D
o
s
e

A
d
j
u
s
t
m
e
n
t

Target Level - Interval [Trough]: 15-20 mg/L
[Vanc] < 10mg/L
| Dose 1g/day
max = 4g/day
| Dose 0.5g/day
Dose & Interval
Per
Daily Levels
[Vanc] = 10-15mg/L | Dose 0.5g/day | Dose 0.25g/day
[Vanc] = 20-25mg/L | Dose 0.5g/day | Dose 0.5g/day
[Vanc] > 25mg/L
Hold 24 hrs
Recheck Level
Hold 24 hrs
Recheck Level

105
Table: Antibiotic Infusion Schedules
Antibiotic
IV Loading
All Patients
Max Hrs
Stability
1
Standard Infusion Dose (per 24 hrs) Renal Function
CrCl > 50 ml/min CrCl ~ 10-50ml/min CrCl < 10 ml/min CRRT
Vancomycin
2

1.0-2.0g 24 2.0-4.0g 1.0g Not indicated
Penicillin G 1.2-1.8g 12 4.8-14.4g 4.8-9.6g 2.4g 4.8-9.6g
Amoxycillin 1.0-2.0g 6 4.0-12.0g 4.0-6.0g 2.0g 4.0-12.0g
Flucloxacillin 1.0-2.0g 24 4.0-12.0g 4.0g 4.0-12.0g
Piperacillin 4.0g 24 12.0-16.0g 8.0g 12.0-16.0g
Tazocin 4.5g 24 13.5g 9.0g 13.5g
Ceftriaxone 1.0g 24 1.0-4.0g
Ceftazidime 1.0-2.0g 24 3.0-6.0g 2.0-4.0g 1.0-2.0g 2.0-4.0g
Meropenem 1.0-2.0g 8 3.0-6.0g 1.0-2.0g 0.5g 2.0g
1
Standard Infusion Orders: 24 Hrs Dose in 100ml {N.Saline | 5%Dext.} @ 4ml/hr
(per Max Hrs Stability) 12 Hrs (Dose / 2) in 100ml {N.Saline | 5%Dext.} @ 8ml/hr
8 Hrs (Dose / 3) in 100ml {N.Saline | 5%Dext.} @ 12ml/hr
6 Hrs (Dose / 4) in 100ml {N.Saline | 5%Dext.} @ 16ml/hr
2
Vancomycin should be diluted into 250mls if given via a peripheral line. Loading dose over at least 60 mins, or 10mg/min.
*NB: Add the reconstituted solutions to a 100mL bag of compatible fluid, having first removed an equivalent volume of solution,
i.e. so the final total volume of the bag remains 100ml, then administer over the required interval.
106
3. Ventilator associated pneumonia (VAP)
a) Significant cause of mortality and morbidity in ICU
b) Clinical diagnosis based on combination of some of the following
i) New CXR infiltrates (hard to see in patients with ARDS)
ii) New clinical chest signs
iii) Increasing oxygen requirement
iv) Increased purulent sputum
v) Indications of systemic sepsis
+ Increased WCC
+ Fever
+ Hypotension
c) Treatment
i) Sputum culture
ii) Commence antibiotics immediately
+ Tazocin 13.5g/24hrs (or 3 divided doses) &
Gentamicin 5mg/kg on day 1, then as per levels
+ If gentamicin contraindicated, ciprofloxacin 200-400mg b.d.
+ In patients with known MRSA or ICU stay > 5days
a. Add vancomycin
b. Stop if no gram positive organisms seen on micro
iii) Review sputum culture
+ If no organism and not on ABx consider another diagnosis
+ De-escalate to narrow spectrum therapy ASAP
+ Normal treatment 5-7 days except pseudomonas sp. then 10-14 days

4. Antibiotic prophylaxis
a) Peri-operative (Table)
i) Ongoing prophylactic therapy is required for selected post-operative
patients in ICU.
ii) Refer to individual protocols for recommendations on pre-operative
antibiotic prophylaxis.

107
Table: Peri-operative Antibiotic Prophylaxis
Specialty Procedure Antibiotics
Orthopaedics Elective cases Cefazolin 1g IV 8h x 3 doses
Traumatic wounds
Involving bone or joint
compound fractures
Cefazolin 1g IV 8h x 2 days
+ severe tissue damage
+ myonecrosis
+ vascular injury
Cefazolin 1g IV 8h x 2 days
+ Gentamicin 5 mg/kg IV daily x 2 days
+ Benzyl pen. 3 g IV stat, 1.2 g IV 6h x 2 days
Abdominal Surgery Colorectal Cefazolin 1 gm gentamicin 3 mg/kg
+ Metronidazole 500mg IV single doses
Biliary surgery Gentamicin 3 mg/kg x 1 dose, or
cefazolin 1g x 1 dose
Vascular surgery Elective cases
+ severe bowel injury
+ myonecrosis or
vascular injury

Amputation
Cefazolin 1g IV 8h x 3 doses
+ Gentamicin 5 mg/kg LBW IV daily x 2 days
+ Metronidazole 500 mg IV bd x 2 days
+ Benzyl pen. 3 g IV stat, 1.2 g IV 6h x 2 days

+ Metronidazole 500 mg IV bd x 2 doses
Neurosurgery CSF leak / # Skull base None: treat only if signs of meningitis
Craniotomy / ICP insertion Cefazolin 1g IV at induction
Head & neck,
thoracic
Craniofacial with breach of
nasal or oral mucosa
+ Metronidazole 500 mg IV bd x 2 doses
Cardiac Surgery CABG
CABG + Penicillin allergy

Vancomycin 1g (over 1 hr)
+ Gentamicin 240mg at induction
Cardiac valve surgery Vancomycin 1g + 500mg 12 hrs later
+ Gentamicin 240mg at induction

108
Table: Perioperative Endocarditis Prophylaxis

109
Table: Empirical Antibiotics
Infection Type / Comment Antibiotics
Pneumonia
Community acquired
Immunocompetent
Admitted to ICU / HDU
(i.e. respiratory failure)
Azithromycin 500mg IV daily, plus
*Ceftriaxone 1 IV daily
For treatment failure, consider Moxifloxacin
400mg IV daily Flucloxacillin 1g 6h
(if high suspicion of S.aureus)
*Default ICU therapy differs from the RAH standard protocol (penicillin + gentamicin) due to
the wide variability in renal function in ICU patients and the inability to use baseline creatinine
as a marker of renal function.
Ventilator associated
Hospital acquired
Tazocin 4.5g IV 8 hrly or 13.5g/day
+ Gentamicin 5 mg/kg IV daily
Consider Vancomycin 1g b.d. IV
See above
Immunocompromised host Contact ID
Aspiration
No antibiotics without evidence of proven infection.
With proven infection
Benzyl penicillin 1.2g IV 6 hrly, plus
metronidazole 500 mg IV 12 hrly
Exacerbation of
COPD
No clinical signs of pneumonia Treat as community acquired pneumonia
Epiglottitis Usually H. influenzae Ceftriaxone 1 g IV daily
Meningitis/
encephalitis
Suspected bacterial
Usually: meningococcus
pneumococcus, or
H. influenzae
Ceftriaxone 2g IV 12 hrly, plus
Penicillin 1.8g to 2.4g IV 4 hrly
Dexamethazone 10mg IV
before or with the first dose of antibiotic
then 6hrly for 4 days
Not definitely bacterial Consider Acyclovir 10mg/kg IV 8hrly
Urinary tract
infection

Without systemic sepsis in patients
with a urinary catheter
No treatment.
Remove / change catheter
With systemic sepsis Amoxycillin 2g IV 6 hrly, plus
gentamicin 5mg/kg IV daily, or
Ceftriaxone 1gm IV daily
if unable to tolerate gentamicin
Intra-abdominal
sepsis
Faecal peritonitis
Perforated viscus
Amoxycillin 2 gm IV 6 hrly
Recurring intra-abdominal sepsis or
failed Rx with above
Consult ID/Clinical Microbiology
Pancreatitis
No CT evidence of necrosis No antibiotics
Significant CT necrosis Tazocin 4.5g IV 8 hrly
Biliary sepsis

Acute cholecystitis

Ascending cholangitis
Amoxycillin 1 g IV 6 h
+ Gentamicin 5 mg/kg/d IV x 7 days
Amoxycillin 2 gm IV 6 h
+ Gentamicin 5 mg/kg/d IV
Previous biliary tract surgery or
known biliary obstruction
add Metronidazole 500mg IV BD x 7 days

110
Gynae sepsis
Septicaemia secondary to PID Amoxycillin 2g IV 6 h
+ Gentamicin 5 mg/kg IV dly
Suspected S. aureus infection Lincomycin 1.2g IV bd
+ Gentamicin 5 mg/kg IV dly x 7 days
Suspected Bacterial
Endocarditis
Community acquired Benzyl penicillin 1.8 g IV 4 h
+ Gentamicin 1 mg/kg IV tds
Flucloxacillin 2g IV qid
Hospital acquired
Prosthetic valve, or
Penicillin allergic
Vancomycin 1g IV bd
+ Gentamicin 1 mg/kg IV tds
3 sets of blood cultures, and review at 48 hrs
Manage pre-dose trough levels for gentamicin <1 mg/L to avoid toxicity
Fungal
Septicaemia
Suspected candidiasis Amphotericin 0.5-1 mg/kg/day, or
Fluconazole 400 mg IV daily
(in non-neutropaenic patients)
Suspected aspergillosis Voriconazole IV/oral 6mg/kg BD loading for 24
hours, then 4mg/kg BD
or
Caspofungin 70mg IV daily loading for 24
hours, then 50mg daily
1. Consult ID for all proven fungaemias
2. Remove all potential sources of infection (lines, catheters, etc)
3. Monitor renal / hepatic function during the course of antifungal therapy.
4. Adjust the amphotericin dose in renal insufficiency, or consider the use of fluconazole if
appropriate
5. Voriconazole levels can be monitored for toxicity and clinical responses.
6. IV voriconazole is contraindicated in patients with CrCl < 30mL/min due to accumulation
of the excipient
Burns No antibiotics without evidence of bacterial infection
Cutaneous
infections
Wound infection
+ signs of systemic sepsis
Benzylpenicillin 1.8 g IV 4 h
+ Flucloxacillin 1-2 g IV 6 h or
Cefazolin 1g IV 8h
Synergistic gangrene
Necrotising fasciitis

In addition to surgery
hyperbaric oxygen
Meropenem
plus
Lincomycin 600 mg IV 8 hrly, or
Clindamycin 600 mg IV 8 hrly
Consider IV-Ig 2.0g/kg total dose (3 days)
Severe oral infections Penicillin 1.2 g IV 4-6 hourly
+ Metronidazole 500 mg IV bd
Line sepsis
Patient not overtly septic Remove unnecessary, old or clinically suspect
lines & send for culture.
Blood cultures by venipuncture
No antibiotics
Patient overtly septic
Prosthetic valve / arterial graft
High risk patient
Vancomycin 1 g IV BD until blood culture
results available

111
Table: Antibiotics for Specific Organisms
Organism 1
st
choice 2
nd
choice
Pneumococcus Benzyl penicillin 1.2g IV 4-6 h Ceftriaxone 1 IV dly
Staphylococcus aureus Flucloxacillin 2 gm IV 6 h
Vancomycin 1gm IV bd or
Cefazolin 1-2g IV 8h
Meningococcus Benzyl penicillin 1.2g IV 4-6 h Ceftriaxone 1g IV dly
Meningococcus contacts Ciprofloxacin 500mg po x 1dose Rifampicin 600mg po bd x 2 days
MRSA Vancomycin 1g IV bd Consult ID
Enterococcus
Amoxycillin 1-2 g IV 6 h
(+ Gentamicin 5 mg/kg if SBE)
Vancomycin 1g IV dly
(+ Gentamicin 5mg/kg if SBE)
Gp A Strep.
With Shock
Benzylpenicillin 1.8g 4 hrly IV
+ Lincomycin 1.2g IV bd
+ Intragam 2.0g/kg total dose (3 days)
Consult ID

Cease IG when pt. improves
Haemophilus influenzae Ceftriaxone 1g IV daily
Amoxycillin 1-2 g IV 6 h
(if sensitive)
H. influenzae contacts
(meningitis)
Rifampicin 600 mg oral bd x 4 days Ceftriaxone 1g IM dly x 2 doses
E. Coli Gentamicin 5 mg/kg IV dly Ceftriaxone 1g IV dly
Enterobacter Gentamicin 5 mg/kg IV dly Meropenem 500mg IV 8h
Klebsiella Gentamicin 5 mg/kg IV dly Ceftriaxone 1g IV dly
Pseudomonas aeruginosa Piperacillin 4 g IV 8 hrly
+ Gentamicin 5-7 mg/kg IV dly

Choice based on sensitivity results:
Ceftazidime 2g IV 8hrly or
Tazocin 4.5g IV 8hrly
PLUS
Gentamicin 5-7 mg/kg IV daily or
Ciprofloxacin 400mg IV bd
Legionella spp. Moxifloxacin 400mg IV daily Azithromycin 500mg IV daily
Mycoplasma pneumoniae Erythromycin 1g IV 6h
Pneumocystis jurovecii Co-trimoxazole 15-20 ml IV 6 h
+ methylpred 40mg bd x 5d,
methylpred 40mg die x 5d,
methylpred 20mg die x 11d,
Pentamidine isethionate
4 mg/kg/day IV
+ methylprednisolone
40mg 6 hrly x 7days
Clostridium difficile:
1. Mild / moderate

2. Severe, or relapse post RX
Cease antibiotics
1. Metronidazole 400 mg o tds
(or 500mg IV if npo)
x 7-10 days
2. Repeat above
Consult ID or Clinical Micro.
Treatment options are:
Bacitracin 25,000
U
6hrly 7-10d
or
Vancomycin 125mg po 6hrly 7-10d
Clostridial infection

(Polymicrobial Infection)

Benzylpenicillin 1.8g IV 4 hrly
+ Gentamicin 5 mg/kg IV dly
+ Metronidazole 500 mg IV bd
+ surgical debridement
hyperbaric oxygen
Lincomycin 600 mg IV 8 hrly

NB: Dose for Ceftriaxone is 1.0g IV daily, except where the site of infection
is meningitis or endocarditis, or the infection is life-threatening
112
PART 4 - FLUIDS AND ELECTROLYTES

A. Principles of Fluid Management in Intensive Care

1. All fluids, infusions are reviewed daily and
a) Rewritten on the ICU flowchart (Units A & B), or
b) In the IV Fluid chart in the ward folder (Unit C).
2. Assessment of volume status and fluid balance involves all of the following:
a) Clinical markers
i) Skin turgor, mucous membranes, capillary refill, peripheral perfusion
ii) HR, BP, Urine output
iii) CVP, PAOP
iv) PiCCO catheter - GEDI, ELWI, stroke volume variability.
v) CXR, interstitial oedema
vi) Echo IVC distensibility index, LVOT- VTI variability
b) Biochemical markers
i) Serum Na
+
, Cl
-
, osmolality
ii) Urea / creatinine ( ratio)
iii) Bicarbonate
iv) Haematocrit
c) Charted fluid balance (notoriously inaccurate!)
i) Total intake including drug/infusion volumes
ii) Total output including urine output, drains, NG losses, blood loss
iii) Insensible losses due to pyrexia, transcellular shifts, etc.
(NB: usually impossible to quantify accurately)
3. Fluids should be considered in two components:
a) Maintenance fluids
i) Usually crystalloids:
+ 4% dextrose + 1/5 N.Saline
+ 5% dextrose / N.Saline
+ Hartmanns
ii) Usual volumes: 25-30 ml/kg/day 80-120 ml/hr
iii) TPN (refer to guidelines)
b) Replacement / resuscitation fluids
i) N.saline should be used for most fluid resuscitation.
+ Equivalent to 4% albumin for resuscitation
+ Better for patients with head trauma.
ii) Colloid (4% albumin, gelofusine) may be considered for fluid resuscitation
in selected patients. Greater cost, no demonstrable advantage.
iii) Blood and blood component therapy as indicated and according to
NH&MRC guidelines.
iv) Crystalloid replacement is usually used for excessive renal, enteric and
burns losses (see below).
v) Hyperchloraemia may be harmful so consider the use of fluids with other
anions, e.g. Hartmanns.
113
4. Composition of commonly used fluids (1000ml solution):

Solution Na
+
K
+
Cl
-
Ca
++
Lact. Gluc. Osm. Prot.
N Saline 150 150 300
N/2 Saline 75 75 150
N/5 Sal. + 4% Dex. 30 30 40 g 282
5% Dextrose 50 g 278
Hartmanns 131 5.0 111 2 29 280
Gelofusine (500ml) 77 60 274 20g
Albuminex 4% (500ml) 70 62.5 25g

5. Fluid management in burns patients

a) The RAH Burns Unit uses the modified Parkland regimen.
b) This is a guide - other clinical markers such as urine output, heart rate, blood
pressure, CVP, serum sodium and osmolality, and haematocrit must be taken
into account.
c) As a result, both solution composition and administration rate may have to be
modified in order to maintain the above parameters within normal ranges.
d) Protocol:
i) Assess the patients % burn surface area (%BSA) using an accurate chart.
ii) Assess patient weight (kg).
iii) Formula:
+ First 24 hours = total fluid (as Hartmanns solution):
Wt. x %BSA burn x 4.0 ml
a. give the total fluid during first 8 hours post-burn
b. give the total during the subsequent 16 hours
+ Second 24 hours fluid is given as Albuminex 4%
Wt x %BSA burn x 0.5 ml
+ Other maintenance fluid is given according to the above physiological
parameters
+ The primary endpoint of fluid resuscitation is generally accepted to be
urine output ~ 0.5-1 ml/kg/hr
+ Catecholamines:
a. Should be commenced only when adequate volume replacement is
unable to maintain a satisfactory urine output, or there is
associated myocardial failure.
b. The duty consultant or SR should be consulted prior to use.
iv) Commence enteral feeding as soon as possible, per protocol.

114
B. Nutrition

1. Enteral nutrition

a) Enteric feeding is the preferred mode of nutritional support and must be considered
in all patients as soon as possible after admission to ICU.
b) Advantages
i) Early EN in trauma patients has been associated with improved outcome.
ii) Use of the gut decreases mucosal atrophy, which may reduce bacterial
translocation thereby reducing the incidence and duration of sepsis.
iii) The incidence and severity of gastric erosions and stress ulceration may be
reduced.
iv) Cheaper than TPN
v) Complications of central vascular access (especially infection) are reduced
or avoided.
c) Disadvantages
i) Regurgitation / aspiration
ii) Nosocomial pneumonia
iii) Diarrhoea (other causes are more likely than enteral feed)
d) Indications
i) As soon as possible in all intubated / tracheostomised patients, where
admission and duration of intubation is expected to be > 24-48 hours.
ii) Patients with an operative jejunostomy may commence feeding within 6
hours of placement.
e) Contraindications
i) Gastrointestinal (including oesophageal) perforation, gastrointestinal
fistulae, bowel obstruction, ileus.
ii) Recent bowel anastomosis is not a contraindication however, discussion
with the surgical team is essential.
iii) Absent bowel sounds is not a contraindication.
f) Protocol (see feeding protocol at bedside)
i) Liaise with the dietician (who will order feeds) during the fluid round.
ii) Outline any problems: e.g. hyperkalaemia, renal failure, osmolality
iii) Place a 12F or larger nasogastric tube (to allow reliable aspiration)
iv) Use orogastric tubes in patients with anterior and middle cranial fossa #
v) Check the position of the feeding tube with x-ray prior to use.
vi) Nurse the patient at 30-45 head up.
vii) Commence feed at 80 ml/hr continuously according to the protocol.
viii) Aspirate the tube 6 hrly
+ Including all NG tubes and PEGs.
+ Do not aspirate jejunostomies, naso-duodenal/jejunal tubes or PEJs

115
ix) Flush jejunostomy/gastrostomy tubes with 20ml N.saline 6hrly.
+ Aspirate < 250 ml:
a. Return aspirate to stomach
b. If rate < max, then increase rate by 20 ml/hr
c. Repeat aspiration at 6hrs and
if < 250 ml then | to max rate (usually 80-100 ml/hr)
+ Aspirate > 250 ml:
a. Return 250ml
b. Halve the feed rate (not less than 20 ml/hr)
c. Continue to aspirate 6 hrly
d. Consider prokinetics:
i. Metoclopramide 10 mg IV 6 hrly, plus
Erythromycin 100 mg IV bd
ii. Continue until tolerating feed for > 72hrs,
then cease and observe
iii. Recommence as needed
e. Reduce narcotic administration if possible.
+ If aspirates > 250 ml while receiving prokinetics consider:
a. Post-pyloric feeding tube
(either using Cortrak
device or endoscopically by the GI Unit)

b. Feeding jejunostomy
c. Nasogastric naloxone 4-8mg tds
d. TPN.
x) Consider a PEG, PEJ or feeding jejunostomy in long term patients
e.g. Guillain Barr or severe head injury
xi) Cease feeds 4 hrs prior to extubation, tracheostomy, ET tube change.
xii) There is no requirement to cease feeds until immediately prior to going to
theatre, unless:
+ Surgical procedure on the GIT
+ Planned for tracheostomy or ETT change.
xiii) Remember to modify insulin dose when feeds are reduced or ceased.

2. Enteral Protocol

a) See over page.

116
Flowchart: Nutritional Therapy Protocol

117

3. Post-pyloric feeding protocol:

a) Commence feed at 1ml/kg/hr, up to a maximum 80 ml/h.
b) No need to cease feed for any procedures.
c) Consider placement of a NG tube to aspirate and ensure an empty stomach.

4. Parenteral Nutrition

i) TPN may be harmful in critically ill patients.
ii) Enteral nutrition is preferred and TPN should only be considered for patients
in whom this is not possible.
iii) Supplementing EN with TPN is not beneficial and should be avoided.
iv) Refer to Clinical Duties Outside ICU, regarding the responsibilities and
management of ward patients receiving TPN.
v) TPN is usually ordered by the Unit A Senior Registrar, under the supervision
of the Unit A consultant.
vi) IV access may be via a CVC or PICC line, with the latter being preferred.
vii) TPN for ICU patients is prescribed during the midday fluid round.
viii) Patient being discharged from ICU on TPN must be entered into the TPN
folder in Unit A.

b) Indications for TPN in the patient who cannot be fed enterally are:
i) GIT Failure > 7-10 days and expected duration of support > 5-7 days.
+ Prolonged post operative ileus
+ Enteric fistulae
ii) Short GIT syndrome following major intestinal resection.

c) Complications of TPN:
i) Depression of immune function, esp. in cancer patients
ii) Gut villous atrophy
iii) Metabolic imbalance
+ Electrolyte disturbances (| K
+
, HPO
4
=
, Mg
++
)
+ Glucose intolerance: hyperglycaemia and glycosuria
+ Hyperosmolar dehydration syndrome
+ Rebound hypoglycaemia on cessation of TPN
+ Hyperbilirubinaemia
+ CO
2
production, esp. in COPD patients
iv) Fluid imbalance
v) Trace element and vitamin deficiencies
vi) Central venous access complications

118
d) Protocol
i) On commencement:
+ Add the following orders to the patient's drug folder:
a. Cernevit MV 1 ampoule IV daily.
b. Trace elements 1 ampoule daily
c. Vitamin K 10 mg IV weekly
d. Commence insulin:
i. Initial dose = 5
U
s.c. qid *hold if BGL < 10
ii. Check BGL qid
iii. Adjust the dose on subsequent days guided by BGLs
iv. Sliding Scale regimens are no longer used.
+ Commence TPN solution at a lower rate (40ml/hr) in starved patients
a. Potential movement of K
+
/ HPO
4
=
into cells with refeeding
b. May cause acute severe hypokalemia and hypophosphataemia.
+ Slowly increase to desired rate, usually 60-80 ml/hr.
+ Dietician will provide a calculated energy requirement as a guide
ii) Daily:
+ Review the patient, CVC site, biochem, BGL chart and fluid balance.
+ Prescribe TPN selecting the most appropriate option from the
following table.
+ These bags are pre-prepared and must not be altered, i.e. no further
additives. Patients requiring K
+
, PO
4
and fluids etc. above the quantities
provided must receive these in a separate line/infusion.
iii) Intralipid
+ Commence TPN with lipid-free solutions (#3, #4)
+ Lipid is indicated if the period of malnutrition > 4 weeks or if the patient
is hyperglycaemic.

Table: Average daily requirements
Water 30-40 ml/kg/day
Calories 30-40 kcal/kg/day
1. Glucose: 2g/kg/day @ 4.1 kcal/g
2. Fat: 2g/kg/day @ 9 kcal/gram
Protein 0.5-1.0 g/kg/day
1. 2:5 essential:total amino acids
2. 150:1 kcal:g N2 (non-nitrogen kcal)
Sodium 1.0 mmol/kg/day
Potassium 1.0 mmol/kg/day Dependent on renal function
Phosphate 0.2 mmol/kg/day Dependent on renal function
Vitamins
B groups daily
B12, Folate, A, D, E, K weekly
Trace elements as required.
Replacement
solutions
1. Urine
2. Nasogastric/ileostomy
3. Pancreatic/biliary fistulae
1. Normal saline KCl 10 ml/L
2. Normal saline KCl 10 ml/L
3. Hartmanns solution

119
Table: Baxter TPN Solution Options
Composition
Baxter Option 1
With Lipid
With Potassium
Baxter Option 2
With Lipid
No Potassium
Baxter Option 3
No lipid
With Potassium
Baxter Option 4
No Lipid
No Potassium
Total Volume (ml) 2000 2100 2000 2100
Glucose (gm) 250 250 500 500
Lipids (gm) 100 100 0 0
Energy (kcal) 2270 2270 2300 2300
Protein (gm) 100 100 100 100
Nitrogen (gm) 16.5 16.5 16.5 16.5
Na
+
(mmol) 73 73 73 73
K
+
(mmol) 60 0 60 0
Mg
++
(mmol) 5 5 5 5
HPO4
=
(mmol) 37.5 7.5 30 0
Cl
-
(mmol) 70 110 70 110
Acetate (mmol) 150 82 150 82
Solution shelf life 12 mths room T 6 mths room T 12 mths room T 6 mths room T
1. Lipid source is Clinoleic 20% which comprises olive oil 80% and soya oil 20%.
2. Multivitamin and trace elements to be given separately from TPN.
3. Nothing may be added to TPN bags.
4. All solutions come in triple phase bag and have light protection cover.
NB: Specialised prescription TPN can be ordered via pharmacy, e.g. when large daily potassium requirements are not feasibly
administered by 10mmol/100ml bags and the standard 60mmol/2L TPN.
120
C. Blood Component Therapy

1. Indications
a) Blood component therapy should only be given if benefit outweighs the risk
b) Potential risks including
i) Mis-identification / acute transfusion reaction
ii) Transfusion associated acute lung injury
iii) Bacterial / viral infection
iv) Immune modulation
c) The best way to reduce the risk of blood component therapy is to reduce
requirements
i) Minimise unnecessary blood sampling
ii) Minimise blood loss during procedures
iii) Consider nutritional and iron stores state

2. Red Blood Cells
a) Elective *as per NHMRC / ASBT guidelines.
i) Haemoglobin < 70g/L
ii) Haemoglobin 70-100g/L, plus any of the following:
+ Ongoing bleeding.
+ Dyspnoea, tiredness/weakness, angina, syncope.
+ Cardiac ischaemia or cardiac failure due to anaemia.
iii) Blood sent for type & screen is held for 10 days for compatibility
testing. However, if the patient requires transfusion, a new specimen is
needed for cross-match every 72 hours.
b) Resuscitation
i) Abnormal bleeding is usually surgical and requires urgent surgical and/or
radiological intervention.
ii) A full cross-match takes 30 minutes if marked urgent (not including the
time for transfer of blood); this should be performed if possible while
volume is replaced with crystalloid or colloid.
iii) If blood is required faster than this the request Time Required box
should be marked:
+ Desperate group O Rh(D)-ve blood is issued immediately (see
massive transfusion protocol)
+ 10 minutes group-specific (ABO/Rh-D) but without full
compatibility testing
+ 30 minutes urgently processed, fully crossmatched blood
iv) NB: The requesting MO accepts full responsibility for (a) or (b)
v) Blood replacement should start immediately with:
+ Rapid blood loss leading to hypovolaemia and shock.
+ Blood loss is estimated or anticipated to exceed 20-25% of blood
volume, i.e. 1000-1500 ml in a normal adult.

121

Procedure Comments
Laboratory
investigations
CBE, INR, APTT, fibrinogen; Samples to
Blood Bank for T&S; Biochemical profile,
blood gases etc.
Repeat CBE, INR, APTT, fibrinogen after
blood component infusion, or every 4 hr
until stable.
Take samples at earliest opportunity as
results may be affected by colloid
infusion.
Mis-identification is commonest
transfusion risk.
May need to give components before
results available.
Use Massive TransfusionPriority
Processing labels with Red bag to alert
lab for speedy processing.
Suitable red cells Un-crossmatched group O Rh(D)
negative in extreme emergency until
blood group known, then group-specific.
Then fully crossmatched blood when
time permits.
To prevent hypothermia by the use of
blood warmer and/or rapid infusion
device.
Employ intra-op blood salvage if
available and appropriate.
Rh(D) positive is acceptable if patient is
male or post-menopausal female.
Laboratory will complete compatibility
testing after issue.
Further compatibility test not required
after replacement of 1 blood volume (8
10 units).
Blood-warmer indicated if flow rate >50
ml/kg/hr in adult.
Salvage contraindicated if wound heavily
contaminated.
Platelets Anticipate platelet count <50x10
9
/L after
2 x blood volume replacement.
Target platelet count: >100x10
9
/L for
multiple/CNS trauma or if platelet
function abnormal.
Target >50x10
9
/L for other situations.
FFP (1015 ml/kg 1
litre or 4 units for an
adult)
Aim for INR <1.5 and APTT <40 secs.
Allow for 30 min thawing time.
INR >1.5 and APTT >40 secs correlates
with increased surgical bleeding.
Keep Ca
++
>1.13mmol/L
Cryoprecipitate
(2-4 units)
Replace fibrinogen. Aim for fibrinogen
>1.0 g/L. Allow for 30 min thawing time.
Fibrinogen <0.5 strongly associated with
microvascular bleeding.
Fresh whole blood Request hospital Blood Bank to contact
ARCBS on-call MO.
Anticipated major blood loss in elective
patients with platelet or coagulation
abnormalities. Continued significant
bleeding even after use of conventional
component therapy. Role in haemostasis
controversial.
Recombinant FVIIa
(Novoseven)
~90 g/Kg
Obtain approval from consultation with
senior Surgeons / Anaesthetists /
Intensivists and Haematologists /
ARCBS on-call MO.
May be considered when the patients
condition continues to deteriorate to
likely haemorrhagic death, usually as a
desperate effort after all other measures
fail.

122
3. Massive transfusion Protocol
a) Definition:
i) Loss of one blood volume within a 24 hr period.
ii) Alternative, more practical definitions:
+ 50% blood volume loss within 3 hr, or
+ 150 ml/min rate of loss.
b) The RAH has a massive transfusion protocol which should be activated as soon
as the need is identified
c) Correction of critical bleeding requires simultaneous approach to:
i) Control the source of bleeding
ii) Contact key personnel required for haemorrhage control
iii) Maintain blood volume
iv) Prevent hypothermia and acidosis
d) Principles
i) Trauma patients with critical bleeding are coagulopathic on presentation
ii) Prevention of further coagulopathy with aggressive management is much
more effective than delayed treatment
iii) Acidosis worsens coagulopathy
iv) Hypothermia worsens coagulopathy
e) On identification
i) Take blood for:
+ Group and match
+ CBE
+ Extended coags and place in red bags
ii) Notify transfusion medicine on 47*
iii) Dispatch blood samples ASAP
iv) Transfusion will provide products in Massive Transfusion Packs
v) Notify transfusion when bleeding controlled

123

124

125
4. Platelets
a) Prophylactic transfusion before surgery or other at risk procedures:
i) Platelet count < 50 10
9
/L
ii) Platelet count > 50 10
9
/L
with evidence of (inherited or drug-induced) platelet dysfunction.
b) Prophylactic transfusion in marrow failure:
9
/L, or
ii) Higher levels with clinical evidence of bleeding
c) Therapeutic transfusion for uncontrolled haemorrhage:
9
/L
and/or evidence of platelet dysfunction.
d) ITP: Only if life-threatening bleeding is present.
e) Platelet dysfunction can contribute to bleeding with a normal platelet count

5. Fresh Frozen Plasma (FFP)
a) Prophylactic transfusion before surgery or other invasive procedure that could
result in significant bleeding:
i) Urgent correction of prolonged INR or APTT in warfarin overdose or
vitamin K deficiency (see below)
ii) Correction of prolonged INR or APTT in liver disease
iii) Correction of inherited coagulation factor deficiencies where specific
coagulation factor concentrates are not available
b) Therapeutic transfusion for uncontrolled haemorrhage in:
i) Warfarin overdose
ii) Liver disease
iii) Vitamin K deficiency
iv) Inherited coagulation factor deficiencies where specific coagulation factor
concentrates are not available
v) DIC
c) Plasma exchange in TTP & related syndromes
d) Post massive transfusion with coagulopathy:
i) Indicated if the INR (prothrombin time) > 1.5, or
ii) APTT (activated partial thromboplastin time) > 40 seconds

6. Extended Life Plasma
a) Recent regulatory changes allow transfusion laboratories to used thawed FFP
for up to 5 days.
b) By using thawed FFP the product can now be provided immediately, c.f. the
standard 20-30 minute delay normally involved in thawing.
c) Five day thawed FFP will be labelled Extended Life Plasma

126
Table: Guidelines for the management of an elevated INR
Clinical setting Action
INR < 5.0
Bleeding absent
Lower the dose or omit the next dose of warfarin.
Resume therapy at a lower dose when the INR approaches therapeutic range.
If the INR is only minimally above therapeutic range (up to 10%), dose reduction
may not be necessary.
INR ~ 5.09.0*
Bleeding absent
Cease warfarin; consider reasons for | INR and patient-specific factors.
If bleeding risk is high, give vitamin K1 (1.02.0mg orally or 0.51.0mg IV) .
Measure INR within 24 hrs, resume warfarin at a reduced dose once INR is in
therapeutic range.
INR > 9.0
Bleeding absent
Where there is a low risk of bleeding
Cease warfarin, give 2.55.0mg vitamin K1 orally or 1.0mg IV
Measure INR in 6-12 hrs & resume warfarin at a reduced dose once INR < 5.0.
Where there is high risk of bleeding
Cease warfarin, give 1.0mg vitamin K1 IV.
Consider Prothrombinex-HT (2550 IU/kg) and FFP (150300mL)
Measure INR in 6-12 hrs, resume warfarin at a reduced dose once INR < 5.0.
Any clinically significant
bleeding where warfarin
induced coagulopathy is
considered a
contributing factor
Cease warfarin therapy, give 5.010.0mg vitamin K1 intravenously, as well as
Prothrombinex-HT (2550 IU/kg) and fresh frozen plasma (150300mL), assess
patient continuously until INR < 5.0, and bleeding stops.
or
If fresh frozen plasma is unavailable, cease warfarin therapy, give 5.010.0mg
vitamin K1 intravenously, and Prothrombinex-HT (2550 IU/kg), assess patient
continuously until INR < 5.0, and bleeding stops.
or
If Prothrombinex-HT is unavailable, cease warfarin therapy, give 5.010.0mg
vitamin K1 intravenously, and 1015mL/kg of fresh frozen plasma, assess
patient continuously until INR < 5.0, and bleeding stops.
* Bleeding risk increases exponentially from INR 5 to 9, INR 6 should be monitored closely.
Vitamin K effect on INR can be expected within 6-12 hours.
Examples of patients with a high bleeding risk:
active gastrointestinal disorders (such as peptic ulcer or inflammatory bowel disease)
those receiving concomitant antiplatelet therapy
those who underwent a major surgical procedure within the preceding two weeks, and
those with a low platelet count.
In all situations carefully reassess the need for ongoing warfarin therapy.
From consensus guidelines Australian Society of Thrombosis and Haemostasis 2004

127
6. Cryoprecipitate
a) Bleeding and fibrinogen < 1.0 g/L in:
i) DIC.
ii) Massive transfusion.
iii) Hereditary hypofibrinogenaemia.
b) 10
U
of cryoprecipitate will | plasma fibrinogen by ~ 1.0g/l
c) Standard dose = 8
U
for hypofibrinogenaemia.

7. DDAVP
a) Standard dose = 0.3-0.4g/kg intravenously over 30 mins
b) Increases factors VIII:C, VIII:vWF and platelet adhesion.
c) Indications: actual, or significant risk of bleeding with,
i) Haemophilia A
ii) type I von Willebrand's disease
iii) Post cardio-pulmonary bypass
iv) Clinical scenarios where platelet dysfunction is likely
+ Uraemia
+ Drugs - aspirin, clopidogrel

8. Recombinant activated factor VII (rFVIIa, NovoSeven)
a) TGA approved indications
i) Haemophilia patients with antibodies to factor VIII
ii) Glanzmann's thrombasthenia with antibodies to GPIIb-IIIa and/or HLA,
and who have past or present refractoriness to platelet transfusions
iii) Patients with congenital factor VII deficiency
b) Effective in improving coagulopathies associated with trauma, major surgery,
and organ transplantation = off-label indications.
c) No risk of virus transmission and contains no human protein
d) Binds to tissue factor (TF) activating both factors IX and X.
i) High doses activate factor X on the surface of activated platelets
ii) Has both TF-dependent and TF-independent effects
e) Recommended dose for the treatment of a severe coagulopathy is 50g/kg
f) Acts within a few minutes and has a half-life of about 2.5 hours.
g) Requires consultant approval because of high cost and absence of current TGA
approval for these indications.

9. Disseminated intravascular coagulation (DIC)
a) Definition
i) DIC occurs when the balance of the haemostatic and fibrinolytic systems
becomes disordered. It occurs in response to severe pathophysiological
stimuli and is a part of multisystem organ dysfunction (often associated
with ARDS and acute renal failure). It is characterised by:
+ Microthrombi formation causing microvascular obstruction
+ Consumption of platelets and clotting factors
+ Abnormal fibrinolysis
128
b) DIC screen:
i) Complete blood picture
+ microangiopathic haemolytic anaemia with red cell fragmentation
+ haemolysis
+ thrombocytopenia
ii) Extended coagulation screen:
+ prolongation of TCT, APTT, PT
+ hypofibrinogenaemia
+ low factor VIII
+ excess fibrinolysis with elevated FDPs
iii) Liver and renal function tests
c) Treatment
i) Treatment of the underlying cause
ii) Replacement of blood components in the bleeding patient
+ FFP - based on INR/APTT
+ cryoprecipitate - for marked fibrinogen deficiency
iii) Controversial therapies (following consultant approval only)
+ heparin, fibrinolytics (tPA)
+ anti-fibrinolytics (EACA)

10. Activated Protein C - Drotrecogin alfa (activated)
a) The role of Activate Protein C (APC) in ICU practice is unclear:
i) Not currently used in routine practice in the RAH.
ii) RAH is involved in an ongoing trial with APC at the time of writing this
manual
b) Xigris
is a recombinant form of human Activated Protein C

c) Pharmacological effects
i) Antithrombotic effect by inhibiting Factors Va and VIIIa.
ii) Indirect profibrinolytic activity by:
+ inhibiting plasminogen activator inhibitor-1 (PAI-1), and
+ limiting activation of thrombin-activatable-fibrinolysis-inhibitor.
iii) APC may exert an anti-inflammatory effects:
+ inhibiting TNF production by monocytes
+ blocking leukocyte adhesion to selectins, and
+ limiting thrombin-induced inflammatory responses within the
microvascular endothelium.
d) Indications are severe sepsis and at least 2 organ failures which could include:
i) Cardiovascular - inotropes despite adequate filling
ii) Respiratory - PaO
2
/FiO
2
< 250
iii) Renal - poor urine output < 0.5ml/kg/h
iv) Haematology - platelets < 80,000
v) Metabolic - lactic acidosis, pH < 7.3 & lactate > 5.
e) APC infusions should be ceased 1-2 hours before and restarted 12 hours after
major surgical procedures, or sooner after minor procedures.
129
f) Full anticoagulation should not be given in addition to APC but DVT
prophylaxis can be administered. APC cannot be monitored but may affect
APTT slightly
g) Increased bleeding risk with a low platelet counts (<30,000) even if platelets are
administered.
h) Administration of APC for severe sepsis requires approval of the Duty
Consultant and hospital administration due to the high cost of the drug.
i) Prescribed by a RAH ICU consultant after:
i) Completing the patient assessment criteria with a second ICU consultant
ii) Completed and signed RAH Checklist is faxed to pharmacy - ext 25891
j) Dose: 24 g/kg/hr given as a continuous infusion for 96 hours
i) Dose is based on actual body weight
ii) No dose adjustment for hepatic or renal impairment, or sepsis severity
iii) Calculate the dose & infusion rate from the table below
iv) Diluted to 50mls with normal saline & administered via a syringe pump
v) The resulting infusion solution must be used within 12 hours

Table: Xigris Dosing Schedule
Patient wt
(kg)
Dose of Xigris

diluted to 50ml NS
Final concn
(g/mL)
Infusion rate
(mL/hr)
40 10 mg 200 4.8
45 10 mg 200 5.4
50 10 mg 200 6.0
55 15 mg 300 4.4
60 15 mg 300 4.8
65 15 mg 300 5.2
70 20 mg 400 4.2
75 20 mg 400 4.5
80 20 mg 400 4.8
85 20 mg 400 5.1
90 25 mg 500 4.3
95 25 mg 500 4.6
100 25 mg 500 4.8
105 30 mg 600 4.2
110 30 mg 600 4.4
115 30 mg 600 4.6
120 30 mg 600 4.8
125 35 mg 700 4.3
130 35 mg 700 4.5
135 35 mg 700 4.6
140 40 mg 800 4.2

130
11. Blood transfusion reaction protocol
a) Plasma can cause reactions ranging from mild pruritus, erythema and urticaria
through to severe flushing, hypotension, fever, angioedema, bronchospasm and
fulminant anaphylaxis.
b) Suspected Reaction Protocol
i) Stop the transfusion immediately do not disconnect the IV line.
ii) Recheck the patient identification on the blood product pack label against
the patients wristband and verbally with the patient if possible.
iii) If there is an unexplained discrepancy, discontinue the transfusion and
treat as per (iv, v below)
iv) Mild Reactions
+ | Temp. < 1.5 C
+ Mild or no hives or rash.
+ Action - slow the rate and continue transfusing the same unit of blood.
v) Severe Reactions
+ Severe hives and/or a rash.
+ | Temp. > 1.5C and is the only clinical sign or symptom
+ Action
a. Consider an antihistamine and antipyretic
b. Cease and then restart transfusing the same unit of blood after
approximately 20 minutes.
+ If there are further signs & symptoms of a reaction
discontinue & order a transfusion reaction investigation
+ If there is a sudden and acute change in the patients condition, e.g.
cyanosis, bad headache, backache, or significant change in pulse or
blood pressure for no apparent clinical reason
discontinue & order a transfusion reaction investigation
vi) Investigation of a transfusion reaction:
+ A transfusion reaction investigation form (IMVS 224) should be
completed and sent to Transfusion Medical Unit (TMU) with:
a. A description of the relevant clinical findings and vital signs
b. A post-reaction 10ml EDTA blood specimen, preferably from a
vein other than that used for transfusion
c. Any used or unused blood packs and the attached IV set(s).
+ If there is a major reaction, it is also recommended that the first urine
specimen voided after reaction is saved, and patients urine output
over the next few hours is recorded.
+ Further blood samples for biochemical assays, coagulation tests, and
cultures will be needed.
+ Administration of incompatible blood constitutes a sentinel event.
vii) Haemovigilance
+ The IMVS and RAH are participating in the Blood Safe
haemovigilance scheme, an adverse incident reporting system aimed at
the quality and safety improvement of transfusion practices.
+ Contact the Transfusion Safety RN (Pager: 1575, Tel: 22975)
131

Table: Blood Transfusion Reactions
Type Signs & Symptoms Treatment Prevention
Febrile non-haemolytic
transfusion reaction

(FNHTR)
Pyrexia (> 1C rise)
Rigors/chills
Anxiety

Withhold transfusion.
Mild fever without other
symptoms may be treated
by slowing infusion.
An antipyretic may be
helpful.
Investigate as for
suspected HTR if the
reaction is significant.
Consider use of
leucodepleted red cells or
platelets if a recurrent
problem.
Circulatory Overload Distended cervical veins.
Pulmonary oedema
Dyspnoea. Headache.
Heaviness in limbs.

Discontinue.
Institute treatment for fluid
overload,
e.g. diuretic
Give all fluids slowly to
patients with compromised
cardiac or renal status.
Use red cell concentrates.
If anticipated, give diuretic.
Allergic Flushing
Urticaria, itchy hives
Facial oedema
Slow rate of flow.
Consider anti-histamine.
Watch for laryngeal
oedema and development
of anaphylaxis.
When anticipated,
use prophylactic
antihistamines.
Anaphylaxis Dyspnoea from laryngeal
oedema or bronchospasm,
sometimes cyanosis and
collapse
Discontinue transfusion
immediately.
Institute treatment for
anaphylaxis,
e.g. Adrenalin, steroids
Use of Medi-Alert
wristband in proven
IgA deficient patients.
Acute Haemolytic
Transfusion Reaction

(HTR)

Pyrexia
Rigors/chills
Lumbar pain
Pain along vein
Jaundice
Haemoglobinuria
Oliguria later uraemia

immediately.
Get expert advice
immediately.
Save all used packs, blood
samples.
Save all urine.
Collect fresh blood
samples.
Extreme care in
collecting the correct
blood sample for T&S.
Careful compatibility
testing by laboratory.
Careful method for storing
& labelling blood.
Careful identification
of the correct recipient.
Infected blood Bacterial sepsis with
hyperpyrexia
Pain in limb & chest
Headache
Pallor
Burning pain along vein
Low blood pressure
Rapid pulse
Profound collapse & shock
immediately.
Acute medical emergency
get advice immediately.
Save used packs, all blood
samples, with labels.
Save all urine.
Anti-shock treatment and
antibiotics.
Storage at correct temp.
Do not remove from
refrigerator until
immediately before
transfusion
Non-cardiogenic
pulmonary oedema.
Transfusion related acute
lung injury (TRALI): rare
Dyspnoea
ARDS picture within 6
hours after transfusion.
Maintain blood pressure &
cardiac output with fluid
support. May require
ventilatory support.
Difficult, usually in the
setting of multiparous blood
donor with anti-recipient-
WBC antibodies.
NB: See RAH Intranet, Transfusion Medicine (http://rahadm05v.had.sa.gov.au/)

132
D. Guidelines for the Management of Electrolytes


a) Total body water (60% total body weight):
i) intracellular fluid : predominant ions : K
+
, PO
4
2-

ii) extracellular fluid:
+ 75% interstitial fluid: predominant ions : Na
+
, Cl
-

+ 25% plasma volume (PV)

b) Osmotic equilibrium is maintained by Na
+
/K
+
pump
i) ECF ions therefore reflect total osmolality:
Calculated osmolality = 2xNa
+
+ urea + glucose
ii) Magnesium is a cofactor for this pump

c) Most electrolyte disturbances in critically ill patients relate to changes in the
distribution and concentrations of the predominant ECF and ICF ions.
d) As a general rule, changes in one ion will be reflected in the associated cation or
anion.
e) Electrolyte disturbances should be considered in terms of the following groups:
i) Erroneous results
+ Lab error
+ Bloods taken from a drip arm
+ Haemolysed specimen - traumatic (old IA lines), delayed samples
+ Osmolar agents
ii) Decreased or increased losses: usually
+ Renal
+ Extra renal: GIT, skin losses
iii) Transcellular shifts.
iv) Decreased or increased intake
Plasma - Interstitium
ECF ICF
ATP
Mg
++
Na
+
K
+
HPO
Protein
Mg
4
=
=
++
Cl
HCO
-
-
3
133
f) Treatment should be directed at the underlying cause.
g) Rapid correction of electrolyte disturbances may be deleterious.
h) One electrolyte disturbance may be predictive of another electrolyte disturbance
e.g. |K
+
often associated with |Mg
+

i) The following paragraphs outline the common electrolyte disturbances.

2. Hyponatraemia: Na
+
< 130 mmol/l

a) Aetiology / classification
i) Misleading result
+ Isotonic - Hyperlipidaemia
- Hyperproteinaemia
+ Hypertonic - Hyperglcaemia
- Mannitol, glycerol, glycine or sorbitol excess
ii) Water Retention
+ Renal Failure
+ Hepatic Failure
+ Cardiac Failure
+ SIADH
+ Drugs
+ Psychogenic polydipsia
iii) Water retention and salt depletion
+ Post-operative, post-trauma
+ Patients with excess fluid losses given inappropriate replacement
+ Adrenocortical failure
+ Diuretic excess

b) Diagnosis & Management:
i) Factitious: ignore and manage underlying condition then recheck Na
+

ii) Misleading:
+ Hyperglycaemia: | BGL 10 mmol/l | [Na
+
] 3 mmol/l
a. Hyponatraemia per se is real, but treatment is directed at the
underlying cause, where correction of the hyperglycaemia will
correct the plasma [Na
+
]
b. NB: Total body Na
+
deficit may co-exist with diuresis in DKA
+ Mannitol:
a. |[Na
+
] early, then diuresis & late |[Na
+
] are more problematic
b. Maintain adequate plasma volume with N.saline initially
+ Alcohols: permeate solutes, o[Na
+
] less problematic
iii) Hypovolaemic states:
+ Restore volume with colloid or normal saline according to clinical
markers: urine output, plasma [Na
+
], RAP
+ Aim for slow Na
+
correction: s 2 mmol/l/hr, unless seizures.
+ Urine Na
+
is uninterpretable after diuretics or catecholamines for 24hrs
134
iv) Hypervolaemic states: *most common clinically
+ Fluid restriction < 15 ml/kg/day
a. Water Excess ~ (140 - Na
+
)/140 x (Wt x 0.6)
e.g., 70kg patient with plasma [Na
+
] = 120 mmol/l:
= (140 - 120)/140 x (70kg x 0.6)
= 6 litres
b. Will slowly correct excess - ADH group & reset osmostat
c. Treat the underlying cause - CCF, nephrotic synd., ascites
v) SIADH
+ Causes
a. Ectopic ADH production by tumours
e.g. small cell bronchogenic tumour
b. CNS disorders
e.g. tumour, abscess, trauma, SAH etc
c. Pulmonary diseases
e.g. TB, pneumonia, abscess etc
+ Diagnosis
a. Hypo-osmolar hyponatraemia
b. Urine osmo > plasma osmo
c. Urine Na
+
> 40 mosm/l
d. Normal endocrine, renal, hepatic, cardiac function
e. No diuretics or drugs affecting ADH secretion
f. Corrected by water restriction alone
+ Management: fluid restriction
vi) Severe Symptomatic Hyponatraemia : fitting, or decreased consciousness
+ Resuscitation / ABC
+ Consider anticonvulsants - phenytoin benzodiazepines
+ Hypertonic saline (3%) may be indicated
a. Always discuss use with the Duty Consultant
b. Correct [Na
+
] rapidly only to ~ 120mmol/l
+ Thereafter, slow correction with N.saline over 24-36hrs (s 2 mmol/l/hr)
+ Treat the underlying cause.

3. Hypernatraemia: Na
+
> 145 mmol/l

a) Hypernatraemia is always a hyperosmolar state
b) Most body fluids have a [Na
+
] < plasma net water loss
c) Aetiology / classification:
i) Water depletion / inadequate replacement
+ Renal
a. Diuretics, glycosuria
b. ARF/CRF, partial obstruction
c. Central diabetes insipidus
i. Post traumatic head injury or surgery
ii. CNS infection, tumour, granulomatous disease, GBS
135
d. Nephrogenic diabetes insipidus:
i. 1 : congenital renal resistance to ADH
ii. 2 : hypokalaemia, hypercalcaemia, lithium, multiple
myeloma, sickle cell anaemia, nephrocalcinosis, amyloid
+ GIT losses - diarrhoea, vomiting, fistulae, SBO
+ Respiratory - IPPV with dry gases
+ Skin losses
a. Fever, high ambient temperature
b. Vasodilatory states
c. Exfoliative skin disorders, burns
d. Thyrotoxicosis
+ Unconsciousness
+ Reset osmostat
ii) Salt gain - Na
+
gain > H
2
O gain
+ Iatrogenic
a. Most common cause
b. Excess normal saline ~ 150 mmol/l [Na
+
]
c. NaHCO
3
, feeding formulae, TPN
+ Mineralocorticoid excess:
a. Conn's, Cushing's syndromes
b. Steroid excess
d) Management
i) Hypovolaemic states
+ Restore volume according to clinical markers:
BP, HR, urine output, RAP
a. Hartmanns solution - slightly hypo-osmolar
b. Colloid: initial resuscitation, severe hypovolaemic states
ii) Slow Na
+
correction: s 2 mmol/l/hr
+ Water deficit: ~ (Na
+
- 140)/140 x (B.Wt x 0.6)
e.g. 70 kg patient, with plasma [Na
+
] = 160 mmol/l
~ (160-140)/140 x (70 x 0.6)
~ 6.0 litres
1 litre water replacement will reduce [Na
+
] ~ 3-4 mmol/l
+ In addition to basal fluid requirements & ongoing losses
+ Replace over a 24-48 hr period with 5% dextrose
+ Monitor [Na
+
] regularly
+ Manage aetiological causes
+ Cease causal drugs and inappropriate IVT
+ DDAVP for central DI only ~ 1-2 g s.c.

136
4. Hypokalaemia: K
+
< 3.0 mmol/l plasma
K
+
< 3.5 mmol/l serum

a) Aetiology / classification:
i) Compartmental / transcellular shift
+ Alkalaemia | pH ~ 0.1 | [K
+
]
pl
~ 0.5 mmol/l
+ Catecholamines / salbutamol
+ Insulin / anabolism - refeeding effect
+ Hypomagnesaemia - ICF K
+
depletion
+ Toxic / poisoning - barium, toluene
+ Familial periodic paralysis
+ Hypothermia
ii) Reduced intake - urine [K
+
] < 20 mmol/L
+ Starvation
+ TPN
iii) Increased clearance/losses
+ Renal - urine [K
+
] > 20 mmol/L
a. Diuretics | distal tubular flow
i. Loop agents - frusemide, bumetanide
ii. PT agents - acetazolamide, mannitol
iii. Early DT - thiazides
b. Steroids / Mineralocorticoid excess
i. Conns, Cushings, Bartters syndrome
ii. Ectopic ACTH - Small cell Ca lung
- Pancreatic, thymus carcinoma
iii. Exogenous steroids
c. Drugs
i. Anionic drugs - antibiotics (penicillins, amphotericin)
ii. High dose gentamicin
iii. Lithium
d. Hypomagnesaemia, Hypocalcaemia
e. RTA I, II
+ GIT losses
a. Villous adenoma
b. Ureterosigmoidostomy
c. Fistulae, malabsorption syndromes
d. Diarrhoea, Laxatives
+ Skin losses

b) Management:
i) Treat underlying cause
ii) Correct hypovolaemia: volume contraction will potentiate both alkalosis
and hypokalaemia
iii) Always add Mg
++

+ normomagnesaemia is essential for correction of hypokalaemia
iv) Look for and treat concurrent hypophosphataemia
137
v) Potassium preparations
+ KCl: 10 ml = 10 mmol/l
+ KH
2
PO
4
: 10 ml = 10 mmol/l
+ K-acetate: 5 ml at 5 mmol/ml
25 mmol K
+
+ 25 mmol acetate (bicarbonate)

5. Hyperkalaemia: K
+
> 5.0 mmol/l serum
K
+
> 4.5 mmol/l plasma

a) Aetiology / classification:
i) Artefactual
+ Drip arm specimen
+ Tourniquet / Haemolysed specimen (extravascular)
+ Thrombocytosis > 750,000
Leukocytosis > 50,000
ii) Compartmental / transcellular shift
+ Acidosis | pH ~ 0.1 |[K
+
] ~ 0.5 mmol/l
+ Insulin deficiency: DKA
NB: normo- or hypo-kalaemia in the presence of severe DKA is
associated with a marked total body K
+
deficit, which must be
addressed prior to correction of the acidaemia.
+ Familial periodic paralysis
+ Suxamethonium
+ Digoxin, |-blocker overdose
+ Fluoride poisoning
+ | ECF tonicity
a. Water moves from cells |[K
+
]
ICF
and passive diffusion
b. Seen with large doses of mannitol given rapidly (1.5-2.0 g/kg)
c. Hyperkalaemia of DKA is due to this in addition to the acidaemia
& insulin deficiency
iii) Cellular disruption / death
+ Tissue breakdown
+ Rhabdomyolysis, haemolysis (intravascular), ischaemia / reperfusion
+ Severe burns
+ Tumour lysis syndrome, leukaemia
iv) Increased intake - rarely a problem unless impaired renal function
+ Massive transfusion
+ Direct IV/oral
+ Drugs (penicillins)
138
v) Reduced clearance
+ Acute renal failure
a. Any cause for | distal tubular flow, or | distal NaCl delivery
b. Hypoaldosteronism
i. Mineralocorticoid deficiency, Addisons
ii. |K
+
is multifactorial - K
+
ICF
K
+
ECF

- |distal tubular flow
- |DT aldosterone effect
+ Type IV RTA
+ ACE Inhibitors
+ Potassium sparing diuretics
a. aldosterone antagonists - spironolactone
b. distal Na
+
channel inhibitors - amiloride, triamterene

b) Management:
i) The clinical scenario will dictate treatment
ii) Acute K
+
> 6.0 mmol/l is a medical emergency
iii) Associated with acute ECG changes, or haemodynamic compromise:
In following order (not mixed together),
+ CaCl
2
10 ml IV stat
+ NaHCO
3
50-100 ml IV stat
+ Glucose 50% 50g + Insulin 20 units
+ Salbutamol nebs continuously
iv) Refractory or persistent:
+ CVVHDF
+ intermittent dialysis
v) Chronic | K
+
or slow rate of rise or no ECG changes:
Resonium 30g oral / PR 8 hourly
vi) Address aetiological factors
vii) Normalise renal function / volume status

6. Acid base disturbances
a) Acid base disturbances in ICU are frequently mixed disorders
b) Correction of these should be directed at the underlying cause and maintenance
of cardiopulmonary homeostasis.
c) Primary correction of an acid base disturbance with acid or alkali is seldom
required.

139
7. Rules of thumb *these are approximations only
a) Primary metabolic disturbances: last 2 digits of pH will reflect PaCO
2

i) Met Acid to min 7.10 e.g. pH 7.25 PaCO
2
25 mmHg
ii) Met alkalosis to max 7.60 e.g. pH 7.57 PaCO
2
57 mmHg
b) Primary respiratory acidosis:
i) |HCO
3
~ 1mmol/l per 10mmHg |PaCO
2
above 40 to max 30
c) Primary respiratory alkalosis
i) |HCO
3
~ 2.5mmol/l per 10mmHg |PaCO
2
below 40 to min 18
d) Chronic respiratory acidosis |HCO
3
~ 4mmol/l per 10mmHg |PaCO
2
above 40 to
max 36

8. Metabolic acidosis
a) Assessment of metabolic acidosis must include the anion gap:

Anion Gap = [Na
+
+ K
+
] - [Cl
-
+ HCO
3
-
] ~ 12-17 mmol/l

Unmeasured cations Unmeasured anions
Mg
++
~ 1.2 mmol/l Albumin ~ 15 mEq/l
Ca
++
~ 2.2 mmol/l H2PO4
-
~ 2 mmol/l
IgG Small HSO4
-
~ 1 mmol/l
Organic ~ 5 mEq/l

~ 7.0 mEq/l ~ 23 mEq/l

b) This allows sub-classification of metabolic acidosis into raised or normal anion
gap acidoses.
i) Beware a low [Alb] in critically ill lowering the measured AG
ii) Measurement of chloride in the lab is highly variable
iii) Assessment of the AG must be viewed within the clinical context.
c) Aetiology of raised anion gap:
i) Renal failure - H
2
PO
4
-
, HSO
4
-
(rarely AG > 23)
ii) Lactic acidosis - types A&B
* normal AG does not exclude a lactic acidosis
iii) Ketoacids - |-OH-butyrate, acetoacetate
- diabetes mellitus, starvation, alcohol
iv) Rhabdomyolysis - organic acids
v) Drugs / poisons:
+ Aspirin - salicylate, lactate, ketones
+ Paracetamol - lactate, pyroglutamate
+ Ethanol - acetoacetate, lactate
+ Methanol - formate (formaldehyde), lactate
+ Paraldehyde - formate, acetate, lactate, pyruvate
+ Ethylene glycol - oxalate
+ Xylitol, Sorbitol - lactate
+ Fructose - lactate
140

Table: Classification of Lactic Acidosis
Type A Type B Drug induced Hereditary
Severe exercise
Seizures
Cardiac arrest
Shock
Hypoxia
Anaemia

Thiamine deficiency
Diabetes
Hepatic failure
Renal failure
Infection
Leukaemia, lymphoma
Pancreatitis
Short bowel syndrome
Phenformin
Metformin
Ethanol
Methanol
Salicylates
IV fructose
Xylitol
Sorbitol

G6PD deficiency
Fructose-1,6-DP-
deficiency

d) Aetiology of low or normal anion gap:
i) Hyperchloraemic metabolic acidosis
+ Resolving renal failure
+ Resolving DKA
+ Renal tubular acidosis / carbonic anhydrase inhibitors
+ Mineralocorticoid deficiency
+ Pancreatic, enteric fistulae
+ Ureterosigmoidostomy
+ IV HCl, NH
4
Cl, Arginine
ii) Metabolic alkalosis due to HCO
3
-
gain
iii) Hypoalbuminaemia
iv) Myeloma - IgG has positive charge, |'s AG
v) Increased Mg
++
or Ca
++
(rarely)
vi) Artefactually elevated Cl
-

vii) ? Hyperlipidaemia
e) Management
i) High anion gap
+ Treat the underlying cause
+ No indication for NaHCO
3

ii) Normal anion gap
+ Treat the underlying cause.
+ Replace HCO
3
serum level and losses
a. Approx. deficit = (24 - [HCO
3
]) x (Wt. x 0.6) mmol/l
e.g. for a 70kg patient with a [HCO
3
] = 4 mmol/l
deficit = (24 - 4) x (70 x 0.6)
= 840 mmol (= ml of standard bicarb solution)
b. Replace 1/3-1/2 of this amount then remeasure blood gases.

141
9. Metabolic alkalosis
a) Aetiology / classification
i) Common causes:
+ Diuretics
+ Vomiting
+ Post-hypercapnia > 48 hours
+ Commonly associated with hypovolaemia and/or hypokalaemia
however, actual causation by these is debated
ii) Increased proton losses: acid loss is either renal or GIT
+ Renal
a. | Na
+
reabsorption (hypovolaemia, dehydration, etc.)
b. Cushing's syndrome, exogenous steroids
c. Hyperaldosteronism 1 / 2
d. Bartter's syndrome (JGA hyperplasia)
e. Liddle's syndrome
f. Hypercalcaemia / hypomagnesaemia nephrogenic DI
g. Drugs: steroids, diuretics, carbenoxolone
+ GIT
a. N/G suctioning, protracted vomiting
b. Diarrhoea
iii) Increased bases
+ Administration of NaHCO
3

+ Metabolism of exogenous acid anions - citrate, lactate, acetate
+ Milk/alkali syndrome
+ Renal conservation of HCO
3
-
- acidosis, hypercarbia
iv) Factors tending to maintain an alkalosis
+ Any fluid loss replaced with insufficient Na
+
H
+
excretion
(contraction alkalosis)
+ Hypovolaemia
+ Hypokalaemia, hypochloraemia, hypomagnesaemia
+ Chronic hypercapnia
+ Mild chronic renal failure
b) Management
i) Correct hypovolaemia
*normal ECF volume is essential for the correction of alkalosis
ii) Inotropic support of cardiac output and GFR
iii) Correct | K
+
, Mg
++
, HPO
4
=

iv) Consider acetazolamide if the alkalosis is persistent - provided the above
are corrected.

142
10. Respiratory acidosis
a) Aetiology
i) Any cause of hypoventilation respiratory failure (see diag.)
+ A. Respiratory centre / CNS
+ B. Upper motor neuron / spinal cord
+ C. Anterior horn cell
+ D. Lower motor neuron
+ E. Neuro-muscular junction
+ F. Respiratory muscles
+ G. Elasticity/compliance of lungs/chest wall
+ H. Structural integrity of chest wall & pleural cavity
+ I. Increased airways resistance intra/extrathoracic
ii) May be acute or chronic

b) Management
i) Restore ventilation / manage underlying cause(s)
ii) No indication for HCO
3

2. Respiratory alkalosis
b) Aetiology
i) Early hypoxia, shock or hypotension
ii) Anxiety, hysteria, neurogenic hyperventilation
iii) PTE
iv) Hepatic failure
v) Prescribed hyperventilation (rarely indicated)
c) Management
i) Treat underlying cause
ii) Neurogenic hyperventilation is a marker of severity of head injury

143
PART 5 - CLINICAL MANAGEMENT

The following clinical protocols are designed to facilitate clinical management of
patients in the Intensive Care.

These protocols may vary from other ICUs and do not represent the sole means of
patient management. However, they do represent the standardised approach that this
ICU has evolved over the years.

Each clinical scenario is managed according to the particular situation and individual
patient - it is neither practical nor appropriate to apply rigid policies to clinical
situations. However, as clinical medicine is more of an art than a science, these
protocols are designed to assist in areas that are unfamiliar and to standardise
approaches by all staff members of the Unit.

The following protocols are outlined.

A. Cardiopulmonary resuscitation
B. Failed intubation drill
C. Respiratory therapy
D. Management of cardiothoracic patients
E. Renal failure
F. Neurosurgical protocols
G. Microbiology protocols
H. Drug overdose
I. Withdrawal of therapy
J. Organ donation and brain death

144
A. Cardiopulmonary Resuscitation

Flowchart: Basic Life Support

145
Flowchart: Advanced Life Support

146
Flowchart: Paediatric Cardiorespiratory Arrest

147
B. Induced Hypothermia Post Cardiac Arrest

1. Aim: To improve CNS outcome by actively cooling T
Core
to ~ 33C
2. Inclusion Criteria
a) Non-traumatic cardiac arrest with return of spontaneous circulation
a) Unconscious, intubated and ventilated
b) Absence of an immediately correctable cause for coma
c) T
Core
> 34.5C
4. Exclusion Criteria
a) Cardiac arrest related to trauma or intracranial injury
b) Ongoing CPR and/or persistent cardiovascular instability
c) Cardiology consultation need for intervention
d) Criteria that preclude 40mls/kg of cold Hartmanns solution,
e.g. acute pulmonary oedema, T < 34.5C
e) Time from cardiac arrest to ED > 12 hrs
f) Pregnancy relative C/I
5. Procedure - Initial Treatment Protocol
a) ECG and routine blood tests as indicated
b) Record core temperature: rectal, oesophageal or bladder catheter
c) Ensure adequate IV access (1x 16G)
d) Document neurological function, specifically:
i) Pupillary responses to light
ii) Response to painful stimuli (all limbs), vocalization
iii) Reflexes gag, conjunctival, lash, tendon & plantar
e) Hartmanns (at 4C): Bolus = 40mls/kg @ 100mls/min
f) Maintain MAP ~ 80-100mmHg (note premorbid BP)
g) Maintain K
+
~ 4-5mmol/L and Mg
++
between 0.8-1.2mmol/L
h) If temp > 35C after 1 hour, add surface cooling (cooling blanket / packs)
i) If patient is shivering and/or temp > 33C:
i) Midazolam (0.05mg/kg bolus, repeat 5min as required)
ii) Midazolam infusion of 1-5mg/hr
iii) If sedation ineffective, consider a non-depolarizing muscle relaxant
j) Aim for core temp. ~ 32-33C
6. Observations
a) Maintain temp ~ 32-34C for 24 hrs from the time of first temp 33C
b) To increase temp (T < 31.5C), use heated air blanket until 33C
c) To decrease temp (T > 34.5C), use cold packs, cooling blanket, sedation and
then consider using non-depolarizing muscle relaxants
7. Complications
a) Arrythmia
b) Reduced cardiac index / increased systemic vascular resistance
c) Hyperglycaemia
8. Aftercare
a) At 24 hrs cease all active cooling and allow passive rewarming.
b) If temp increases < 1C per 4 hours then rewarm actively to temp > 36C
c) Once temp > 35C, cease sedation and no further muscle relaxants
148
C. Failed Intubation Drill

Oxygenate/ventilate
Committed to
Intubation
Best Attempt
Laryngoscopy
ILMA +/-
Bronchoscope
Failure to
Ventilate
Crico-
Thyroidotomy
FURTHER
ATTEMPTS USING
ADVANCED DEVICE
- McCoy / Flextip
- Glidescope
- Airtraq
- Bronchoscope
Intubate
Intubate
Call for help
No
CALL
EMERGENCY
Failure
or SpO
2

< 88%
Yes
149
Failed Intubation Drill - Notes:

1. Good anaesthetic algorithms for managing the difficult airway (ASA, DAS) have
limited application in ICU patients where our hand is usually forced. Allowing
the patient to wake-up in the event of a failed intubation is rarely practical.

2. Risk of failed intubation in ICU is unquantified but certainly higher than the 0.5-
1% incidence of the general anaesthetic population.

3. Following rapid sequence induction we are generally committed to securing the
airway somehow.

4. Time is of the essence. ICU patients have limited O
2
reserves and desaturate
quickly. If an intubation technique fails, move on quickly to an alternative.

5. If intubation attempts fail, or the patient desaturates significantly:
a) Refocus efforts toward oxygenating the patient.
b) Failure to achieve manual ventilation is an absolute emergency
(incidence in anaesthesia 0.001-0.002%).

6. The intubating laryngeal mask (ILMA or Fastrach)
a) Shown in many studies to be easy to insert (~ 100% success after 3 attempts)
b) Provides an adequate airway for ventilation in 96% of surgical patients.
c) Default airway device for the cant intubate/cant ventilate scenario.

7. All of the equipment in the algorithm is available on the RAH ICU difficult
intubation trolley. Become familiar with it, and practice using examples kept in the
registrar teaching room.

8. Before intubating, ensure you have a contingency plan for a difficult airway/failed
intubation tailored to suit your skill mix and experience.

9. Always have the difficult intubation trolley at hand during intubations.
150
D. Respiratory Therapy

1. Respiratory failure

a) Definition: failure of efficient gaseous exchange and/or effective ventilation:
i) Hypoxaemia: PaO
2
/FiO
2
ratio < 300 mmHg
ii) Hypercarbia: PaCO
2
> 50 mmHg, with a pH < 7.35

2. Oxygen delivery capacities of available oxygen circuits.

Table: Oxygen Delivery Devices
Apparatus/Device Oxygen flow (l/min)
Approximate
FIO2 (%)
Nasal catheters
2
4
6
28
35
45

Semi - rigid masks
(e.g. Hudson, CIG)
5
6
8
10
12
35
50
55
60
65
Venturi type mask
(e.g. Ventimask, Accurox)
2 - 8
24 - 50
(per manufacturer)
Nasal High Flow
(humidified circuit)
30-50 l/min 21 - 95
Reservoir plastic masks
(Non-rebreathing mask)
6 - 15 FiO2 = 21% + 4% per l/min
Non Invasive or Invasive
positive pressure
mechanical respiratory
support
Variable 21 - 100
Oxylog 1000 and 2000

Oxylog 3000
Variable

Variable
Airmix : 60
No airmix : 100
40 - 100

151
3. Humidification

a) All intubated patients must have adequate humidification of inspired gases for
optimal mucociliary function and conservation of temperature.
b) Optimal humidification requires the following
i) Delivery of gas to the trachea at a constant temperature (32-36C)
ii) Relative humidity 75-100% saturation
iii) No increase in circuit resistance
iv) No increase in circuit dead space
v) Applicable to spontaneous and controlled ventilation
vi) Sterile inspired gas
c) Types of humidifiers available
i) Heat/moisture exchangers (HME)
+ Effective for most patients: first line humidification
+ Incorporates a bacterial and viral filter
+ Cannot be used with nebulised drugs
+ Change to wet circuit (FP) in patients with bronchorrhoea or mucous
inspissation. Secretions increase resistance and reduce HME efficacy.
+ Single use & change every 48 hrs, or as required
ii) Fisher Paykel (FP) evaporative humidifier (wet circuit)
+ Indications
a. Bronchorrhoea or mucous inspissation
b. Hypothermic or heat-loss susceptible patients (e.g. burns)
c. Hypernatraemic patients
+ Set chamber to 40C
+ Set chamber control to Auto / Mask/Tube
iii) Inspiron (aerosolised T-piece)
+ Relatively inefficient humidification
+ Allows variable FiO
2
: 0.21-0.7

4. MDI bronchodilators

a) MDI + Spacer = preferred method of administration.
b) Can be used in ventilated patients, but requires dose adjustment.
c) Each patient has their own canister.
d) MDI adapter must be present in circuit:
i) Inspiratory limb of Fisher Paykel wet vent circuit
ii) Dry circuits need a separate adapter between HME and stress reliever.
e) Shake MDI well
f) Should be puffed with single puff dose during inspiration.
g) Standard MDI Doses:
i) Salbutamol: 4 puffs 4-6 hrly max = 10 puffs 4 hrly.
ii) Ipratropium: 4 puffs 6 hrly max = 10 puffs 6 hrly.
iii) Steroids: 2-4 puffs BD (beclomethasone or fluticasone)

152
5. Nebulised bronchodilators

a) See section on respiratory drugs.
b) These agents are the mainstay of treatment of bronchospasm in Intensive Care
(including acute severe asthma).
c) They are not to be routinely used in all ventilated patients.
d) Once commenced, they must be reviewed daily regarding efficacy. This is
assessed by improvements in audible wheeze, lung compliance, respiratory rate
and blood gases.
e) Indications:
i) Pre-existing asthma / chronic obstruction pulmonary disease (COPD)
ii) Acute severe asthma
iii) Acute bronchospasm 2 to infection, aspiration or during IPPV
iv) Acute exacerbation of COPD
v) Acute hyperkalaemia
f) All patients admitted to ICU for acute severe asthma:
i) Continue routine prophylactic/preventative agents
ii) Additional bronchodilators for episodes of bronchospasm
iii) Should not be routinely started on empiric antibiotics, unless there is clinical
evidence of infection (also applies to exacerbation of COPD).
+ Clinical evidence of infection may be
a. New onset fever, WCC
b. Change in quantity/quality of sputum
c. New radiological infiltrate
d. Bacteria, positive viral PCR or WCC in a sterile fluid
iv) Should be reviewed by the Thoracic Medicine Unit.

6. Mechanical ventilation

a) Mechanical ventilation is one of the mainstays of intensive care medicine.
b) An understanding of the indications, complications, practical aspects of mechanical
ventilators and respiratory failure is essential.
c) Standardisation of default ventilation modes and settings is essential for patient
safety, particularly in a large unit with large numbers of staff.
d) Registrars should familiarise themselves with the ventilators, understand the
default settings and common modes of ventilation.
e) The nurse educators and senior CCRNs are useful resource people to aid in
troubleshooting and assistance with the ICU ventilators.
f) All changes to ventilation orders must be recorded on the flowchart.
g) Also, notify the bedside nurse of any prescribed ventilation changes.
h) All ventilator alarms must be addressed as soon as possible: patient disconnection
or barotrauma are potentially lethal.
i) Upon initiation of ventilation, the default FiO
2
= 1.0 (100%). This should be
titrated down as soon as possible based upon SpO
2
and PaO
2
.
153
j) Indications for mechanical ventilation
i) Respiratory Failure
ii) Maintenance of cardiopulmonary homeostasis
+ Following cardiac arrest
+ Post operative support in high risk surgical patients
+ Control of intracranial pressure.
iii) Relaxant anaesthesia
iv) Need for tracheal intubation, other than for respiratory failure
k) Parameters for institution of ventilation
i) Clinical assessment is the most sensitive assessment of respiratory failure.
ii) Do not delay the initiation of ventilatory support pending results, blood gases
or mechanical measurements where clinically indicated, e.g.
+ Threatened airway
+ Fatigue / exhaustion
+ Failure of secretion clearance
+ Overt respiratory failure
+ Speech impairment due to dyspnoea
+ Reduced GCS in the absence of other causes
iii) Objective measurements are adjuncts to clinical assessment and must be used
in the clinical context, e.g.
+ Respiratory Rate: RR > 35 bpm
+ Vital capacity: VC < 15 ml/kg
+ Oxygenation: PaO
2
/FiO
2
< 300
+ Ventilation: PaCO
2
> 60 mmHg *with a pH < 7.2
l) Principles in optimising ventilation in ICU patients
i) Optimise oxygenation:
+ Use the lowest FiO
2
to achieve an adequate SpO
2
/ PaO
2

a. Default: SpO
2
> 95% and/or PaO
2
> 80 mmHg
b. Lower values may be appropriate with chronic lung disease
+ PEEP = 5-15 cmH
2
O
ii) Optimise PaCO
2
:
+ Adjust relative to premorbid PaCO
2

+ Permissive hypercapnia in patients with poor lung compliance
iii) Optimise patient-ventilator interface:
+ Reduce work of breathing through the ETT and ventilator circuit
a. Pressure support (10-20 cmH
2
O) in all patients
b. Automatic Tube Compensation (ATC), if available
+ Prevent gas trapping: measurement and manipulation of auto-PEEP
+ Patient positioning
iv) Optimise sedation and analgesia
+ Review the need for sedation daily and cease where appropriate.
154
v) Minimise volutrauma (barotrauma)
+ A modified ARDSNet Ventilation Protocol is used at the RAH (see
following section #6).
+ This protocol is not the default setting for ventilation of patients on
arrival in the ICU, rather this protocol should be prescribed for patients at
risk of barotrauma and acute lung injury, where no contraindication exists
(e.g. acute CHI, severe asthma).

m) Modes of mechanical ventilation used in ICU
i) Synchronised intermittent mandatory ventilation (SIMV)
+ PEEP + Pressure Support + Pressure limited to 40 cmH
2
O:
+ Default ventilation setting at RAH
+ Features:
a. Prescribed tidal volume / variable airway pressure
b. Baseline / intermediate ventilation mode to begin weaning
c. Mean airway pressure < 25-30 cmH
2
O
+ Complications
a. Patient ventilator dyssynchrony, gas trapping
b. Barotrauma / volutrauma
ii) Pressure control ventilation (PCV) + PEEP:
+ Features
a. Requirement for full ventilation: i.e. not a weaning mode
b. Mean airway pressure > 25-30 cmH
2
O
c. Prescribed peak pressure, variable tidal volume
+ Complications
a. High sedation requirements, occasional use of muscle relaxants
b. Patient ventilator dyssynchrony, gas trapping
iii) Pressure Support Ventilation (PSV) + PEEP
+ Indications
a. Stand alone mode of ventilation in patients with adequate respiratory
drive and mechanics
b. Weaning from ventilation
c. Patients with gas trapping, high auto-PEEP and high work of
breathing (e.g. COPD)
+ Complications
a. Increased patient respiratory effort compared with other mandatory
modes of ventilation
b. May precipitate incipient or overt cardio-respiratory failure or fatigue
during weaning

155
n) Complications of mechanical ventilation
i) Haemodynamic
+ Reduced preload
+ Increased RV afterload unmasked hypovolaemia
ii) Respiratory
+ Altered V/Q ratios
+ Nosocomial and/or aspiration pneumonia
+ Volutrauma / Barotrauma
+ Ventilator associated lung injury
+ Patient ventilator dyssynchrony
iii) Metabolic
+ Post-hypercapnoeic metabolic alkalosis
+ SIADH
iv) Raised intracranial and intraocular pressure
v) Global
+ Need for sedation
+ Reduced patient mobility (DVT, pressure sores, muscle deconditioning,
reduced joint movement.)
+ Critical illness weakness
vi) Local
+ Pressure effects from intubation, tracheostomy or face masks

o) ICU ventilators:
i) Drger EVITA 2 Dura ventilator
+ The Evita 2 are the default ventilator at the RAH.
a. Modes: - SIMV, PCV, Pressure Support, CPAP, APRV.
b. Non-invasive ventilation modes are also available.
+ Specific features:
a. Auto flow: automated adjusted inspiratory flow according to lung
mechanics during controlled ventilation
b. Rise time: manual adjustment in all modes
c. Automated estimation of auto-PEEP and occlusion pressure (P
0.1
)
d. 100% O
2
suction button: delivers 100% oxygen for 3 minutes
e. Programmable default parameters
f. Flow and Pressure - Volume loops
g. Preset emergency and apnoea ventilation parameters
h. Automatic tube compensation to assist weaning
i. Automated respiratory mechanics module:
i. static and dynamic compliance
ii. inspiratory airway resistance
iii. negative inspiratory pressure
iv. vital capacity
j. Nitric oxide delivery system
156
+ Default settings:
SIMV: 600 x 12 | PS = 5 | PEEP = 5 | FiO
2
= 1.0
a. Press Mode setting button
b. Select the desired parameter via the respective button. Adjust the
displayed value via the rotating knob, then press to select the desired
value.
c. Select mode: SIMV
i. FiO
2
: 1.0
ii. Select tidal volume: 0.6 l
iii. Select respiratory rate: 12 bpm
iv. Pressure support: 5 cmH
2
O
v. PEEP: 5 cmH
2
O
vi. Rise time: 0.2 secs
vii. Adjust T
Insp.
so that I:E ratio is 1:2 (default 1.7 secs)
d. Extra settings mode:
i. Flow trigger: 5 l/min
ii. Backup ventilation (CMV) : off
+ PC (Pressure control) + PEEP PSV
a. The actual settings that are set on the ventilator must be
prescribed.
b. Default settings:
P
Insp
= 30 x 12 | PEEP = 5 | Fi
O2
= 1.0 | I:E=1:2
c. Select mode: PCV+
d. Settings:
i. Select total inspired level of pressure (Pinsp) which includes
PEEP: Default: 30 cmH
2
O
ii. Select desired rate: 12
iii. Adjust T
Insp.
so that I:E ratio is 1:2 (default 1.7 secs)
iv. Rise time: 0.2 secs
v. Pressure support: 5 cmH
2
O
vi. Select PEEP: 5 cmH
2
O
vii. FiO
2
: 1.0
e. Alarms / limits unchanged from default
f. Do not exceed total inspired pressure > 40 cmH
2
O
g. Tidal volume is determined by the patients compliance
h. I:E ratio = 1:2
*alteration of the I:E ratio is potentially hazardous and should only
be done following discussion with the duty consultant.
+ Measurement of auto-PEEP
a. Measurement of intrinsic PEEP at end expiration + closed airway
b. Not accurate in SV modes or with patient effort, patients should be
well sedated.
c. If I:E ratio or RR are altered:
i. Expiratory time is reduced
ii. Auto-PEEP may be affected and should be measured
d. Press the [Special Procedure] button & select [PEEPi]
157
i. Press [Start] to begin the automatic 7sec manoeuvre
ii. Read off the PEEPi and trapped gas volume (Vtrap)
iii. The value displayed includes applied PEEP, so:
auto-PEEP = PEEPi - applied PEEP
+ Measurement of occlusion pressure (P
0.1
)
a. Measurement of the negative airway pressure generated in the first
100msec of inspiration against an occluded airway.
b. Reflects diaphragmatic effort and neuromuscular drive
c. Normal value = 3-4 mbar
d. Higher values > 6 mbar reflect fatigue
e. Press [Special Procedure] button
i. Select P
0.1
and press start to begin
ii. Read off P
0.1

+ Always examine the flow, pressure and volume vs time graphs, e.g.
a. Flow does not return to baseline prior to next breath may indicate
dynamic hyperinflation.
b. Pressure that does not return to set PEEP may also indicate dynamic
hyperinflation.
c. Sudden reversal of flow pressure which does not trigger a breath may
indicate wasted patient effort.
d. Inspiratory hold and observing the peak-plateau pressure gradient
can give an indication of airflow resistance.
+ Examine P-V loops for clinical patterns of:
a. Upper/lower airway obstruction
b. Recruitable lung
c. Dynamic hyperinflation.
+ PS (pressure support) + PEEP
a. Settings described above for use with SIMV, PCV
b. Note total inspiratory pressure, when using PS on the Evita, is the
dialed value plus dialed PEEP value
c. Stand alone settings:
i. Select mode: CPAP
ii. Rise time: 0.2 secs
iii. Pressure support: 10 cmH
2
O
iv. PEEP: 5 cmH
2
O
v. FiO
2
: 1.0
+ CPAP
a. As above for PS but with PS = 0 / PEEP = 5cmH
2
O.

158
7. RAH - ARDSNet Ventilation Protocol

a) Initial Ventilator Set-up and Adjustments (Drger)
i) Mode: SIMV + PS = 5 cmH
2
O
ii) Resp. Rate: 18 bpm
iii) Inspiratory Flow Rate: Autoflow
iv) Tidal Volume: 6 ml/kg IBW

b) Tidal Volume Settings are determined by calculated Ideal Body Weight
i) Males = 0.91 x (height [cm] 152.4) + 50
ii) Females = 0.91 x (height [cm] 152.4) + 45.5
iii) Calculate IBW and Vt = 6 x IBW

c) Maintenance / Management
i) Adjust RR to achieve the pH goals according to ABGs. (see below).
ii) Adjust Vt according to plateau pressure goals.
NB: Observe spontaneous tidal volumes and adjust PS downwards if
volumes generated are higher than the calculated goal Vt.
iii) Adjust FIO
2
according to SpO
2
and PaO
2

iv) Check and adjust I:E ratio.

d) Goal pH pH = 7.20 7.45
i) Acidosis management: pH < 7.20
+ | RR until pH > 7.20 or PaCO
2
< 25mmHg
a. max RR = 35bpm
+ If pH < 7.20 and RR = 35, then
a. | Vt by 1 ml/kg IBW steps until pH > 7.20
b. Pplat. goal may be exceeded
ii) Alkalosis management: pH > 7.45
+ Decrease RR if possible

e) Goal Plateau Pressure: Pplat < 30 cmH
2
O
i) Check inspiratory plateau pressure with a 0.5sec inspiratory pause every 4
hrs and after each change in PEEP or Vt.
ii) Method (Drger): go into measurements + press inspiratory hold for
0.5sec Pplat will appear on the screen next to Pplateau for 1 second.
iii) Pplat > 30 cmH
2
O
+ | Vt by 1 ml/kg IBW steps
+ min Vt = 4ml/kg IBW
iv) Pplat < 25 cmH
2
O and Vt < 6ml/kg IBW
+ | Vt by 1ml/kg IBW
until Pplat >25 cmH
2
O or Vt = 6ml/kg IBW.

159
FiO2 PEEP
0.3 5
0.4 5
0.4 8
0.5 8
0.5 10
0.6 10
0.7 10
0.7 12
0.7 14
0.8 14
0.9 14
0.9 16
0.9 16
1 16
f) Goal Arterial Oxygenation:
PaO
2
= 55-80 mmHg or SpO
2
88-95%
i) If SpO
2
or PaO
2
are outside goal range, use the table
(right) to adjust FiO
2
/ PEEP combinations for the PaO
2

range required.
ii) Take ABGs only as clinically indicated, changes can
be made according to SpO
2
.
iii) Examples:
+ If a patient is on FiO
2
0.4 and a PEEP of 5 and the
PaO
2
= 54 mmHg the next step would be to
increase the PEEP to 8 cmH
2
O.
+ If a patient was on FiO
2
= 0.9 / PEEP = 14 and the
SpO
2
= 99% the next step would be to decrease the
FiO
2
to 0.8.

g) Goal I:E Ratio = 1:1.0 1:3.0
i) After any RR change, check the I:E ratio and modify
the T
Insp

ii) Do not inverse the I:E ratio with this protocol
risk of breath stacking and hypotension.

8. Extra-Corporeal Membrane Oxygenation (ECMO)

a) ECMO can be used to provide either:
i) Oxygenation in cases of overwhelming respiratory failure (veno-venous
ECMO) or,
ii) Circulatory support in reversible cases of refractory overwhelming cardio-
respiratory failure (veno-arterial ECMO).
b) ECMO services commenced at the RAH in 2009, and continue to evolve.
c) Any cases for potential ECMO support will be discussed in detail prior to
initiation, and will be supervised closely by duty ICU-ECMO consultant.
d) If caring for a patient on ECMO all relevant protocols and contact details will
be made available.
e) Care of the patient on ECMO includes specific requirements.
f) The ECMO circuit and equipment must not be altered without the ICU
consultant and/or perfusionist supervision.
g) NB: The policies, protocols and procedures for ECMO are contained in a
stand-alone manual which is attached to the ECMO machine.

160
9. Non-invasive ventilation

a) Definition: Mechanical positive pressure respiratory support in the absence of
tracheal intubation (e.g. via a face mask, nasal mask, head piece/box)

b) Modes
i) Continuous positive airway pressure (CPAP)
ii) Bi-level positive airway pressure (BiPAP).

c) Indications
i) As an adjunct to weaning from ventilation, e.g. extubation to NIV
ii) Incipient respiratory failure with high work of breathing in selected diseases:
+ Acute exacerbations of COPD
+ Cardiogenic pulmonary oedema
+ Obstructive sleep apnoea
+ Acute quadriplegia
+ Post-extubation hypoxia due to pulmonary oedema or atelectasis
+ Cystic fibrosis
+ Febrile neutropaenia with pulmonary infiltrates
+ Pneumonia
+ As a bridge where:
a. Appropriate airway assistance is sought or resuscitation is
undertaken, prior to induction and safe intubation, or
b. Appropriateness of invasive ventilatory support is being considered.

d) Prerequisites
i) Adequate glottic reflexes should be present to protect from aspiration:
moribund patients require intubation where appropriate
ii) Patients receiving CPAP or BiPAP are generally managed in Units A&B.
iii) Unit C patients requiring NIV should be considered for transfer.
iv) Selected patients may be managed in Unit C:
+ Tracheostomised patients with isolated PEEP dependency - i.e. slow
weaning
+ Rapidly resolving respiratory failure with face mask CPAP/BiPAP
a. Diuresing pulmonary oedema
b. Resolving stridor
c. Stable COPD during hospitalisation for exacerbation
d. Patients with OSA, with and without their own machines

e) Complications
i) Aerophagia, gastric distension, aspiration
ii) Claustrophobia and mask intolerance
iii) Pressure necrosis of nasal bridge
iv) Dry secretions
v) Barotrauma
vi) Reduced preload and hypotension
vii) Raised intracranial and intraocular pressure
161

f) Ventilators
i) Drger CPAP circuit.
+ Adjust flow rate to maintain desired CPAP level (typically > 40 l/min)
+ Select CPAP (cmH
2
O) on external PEEP valve
+ Select FiO
2
(air / oxygen mix with two rotameters)
+ Always use with wet humidified circuits (Fisher-Paykel)
ii) BiPAP
Vision / Harmony ventilators

spontaneously ventilating, non-intubated patients
+ Select IPAP = Inspiratory positive airway pressure
+ Select EPAP = Expiratory positive airway pressure (PEEP)
+ Pressure support = IPAP - EPAP
iii) CPAP via Drger EVITA

+ Select non-invasive mode
+ Select CPAP in [OtherModes]
+ Set CPAP/PEEP and FiO
2

+ Adjusting Press Support and Press Rise Time will add assisted breaths to
CPAP. See ASV.

g) Assisted Spontaneous Ventilation
i) The Drger Evita is best configured to achieve ASV by Pressure Support.
+ The same settings as CPAP on Evita
+ Select non-invasive mode
+ Adjust Press Support and Rise Time to provide the assisted breaths
+ Default settings:
a. Pressure support 10 cmH
2
O (above PEEP)
b. PEEP 5 cmH
2
O
c. Inspiratory time 4 sec
d. Trigger 5 l/min
ii) Vision
BiPAP
+ Microprocessor controlled spontaneous breathing assist ventilator in
either CPAP or spontaneous/timed breathing mode (S/T).
+ Mixes pipeline oxygen with ambient air via an internal pump
+ Monitors machine pressure against proximal airway (mask pressure) to
ensure effective delivery of pressure despite circuit leaks.
+ Uses internal algorithm for respiratory cycling and leak adjustment.
+ Nasal, face & full head masks can be used.
+ Liquid crystal displays
a. IPAP, EPAP, rate, oxygen
b. Vt, Vmin, PIP, insp. time/total cycle time.
c. Leak (patient & total), % patient triggered breaths
d. Graphical display of pressure, volume & flow.

162
+ Need to calibrate for tubing and mask.
+ Operation machine starts up in mode previously used.
a. Press [Mode] hard key to display CPAP or S/T mode
b. Select soft key parameters displayed & turn adjustment knob
accordingly
c. Press [Activate New Mode] soft key to select the new mode.
d. The ventilator will continue in the old mode until activated
+ CPAP Mode
a. Default setting: CPAP 5cmH
2
O, FiO
2
1.0
b. Only CPAP setting & FiO
2
soft keys are active.
+ S/T Mode
a. Default setting: IPAP 15cmH
2
O, EPAP 5cmH
2
O, Rate 12, Timed
insp 1 sec, FiO
2
1.0, IPAP rise time 0.1 sec
b. Adjust settings accordingly
+ Setting modification
a. Press [Parameter] hard key
b. Select soft key & turn adjustment knob.
c. Press [Monitoring] hard key to return to monitoring screen
+ Alarm limits
a. High Pressure 30 cmH
2
0
b. Low Pressure 5 cmH
2
0
c. Low Min Vol 0 l/min
d. High resp rate 30 b/min
e. Low resp rate 6 b/min
f. Low press delay 20 sec

10. Weaning from ventilation

i) No mode of weaning has been demonstrated to be superior to another
ii) Short-term patients with acute resolution of respiratory failure (e.g. post-
operative, drug overdose, trauma) may be rapidly weaned to extubated.
iii) Long-term patients with multiple intercurrent problems take longer and
effectively go at their own pace.
iv) It is important to balance over-sedation and prolonged ventilation against
rapid weaning, patient exhaustion and failed weaning or extubation.
v) See Flowchart: Ventilation Weaning Protocol, p50.

163
b) Clinically important determinants for weaning from ventilation:
i) Resolution of the process requiring ventilation
ii) No new CXR abnormality
iii) Completion of therapeutic options that require ventilation
(e.g. debridements, operations)
iv) Appropriate conscious state; cooperative patient
v) Appropriate peripheral motor function
vi) Adequate analgesia
vii) Haemodynamic stability
viii) Metabolic, acid-base stability

c) Methods
i) Spontaneous effort is required for the patient to be weaned
ii) SIMV with reducing rate and tidal volume in conjunction with PSV and
PEEP is standard
iii) Use PSV + PEEP alone once the patients spontaneous rate is sufficient to
prevent a respiratory acidosis at pH < 7.3
iv) Intubated CPAP
v) T-piece weaning: intermittent T-piece and positive pressure (PSV / CPAP /
SIMV).
vi) Non-invasive bi-level ventilation

d) Objective measurements
i) Adjuncts to the assessment of weaning success.
ii) These are not specific and must be interpreted in the clinical context.
iii) Respiratory rate and tidal volume are the most sensitive:
+ Rate (f): < 30/min
+ Tidal volume: > 5 ml/kg
+ f/V
T
: < 100 (rapid shallow breathing index)
+ PaO
2
/FiO
2
:

> 200 and PEEP < 10 cmH
2
O
+ PaCO
2
< 60 mmHg

11. Extubation protocol

a) Ensure equipment, monitoring and adequate assistance, in case of re-intubation.
b) Extubation is preferentially done during daylight hours and is a medical
responsibility.
164
c) Extubation criteria:
i) Return of adequate conscious state to maintain adequate protective laryngeal
reflexes and secretion clearance.
ii) Adequate pulmonary reserve (see objective measures above)
iii) In patients with upper airway surgery or swelling the demonstration of an
adequate air leak around the deflated endotracheal tube cuff and assessment
with pre-extubation laryngoscopy.
iv) Plastic surgery and ENT patients require consultation with the Parent Clinic.
Those patients with intermaxillary fixation and wiring must have a person
from the Parent Clinic familiar with the placement of the wires and a wire
cutter present during extubation.
d) All patients must receive supplemental oxygen post extubation.

12. Protocol for ventilation in the prone position

i) This technique may improve oxygenation in up to 60% of patients with
severe ARDS. This may buy time, however no mortality benefit has
been demonstrated to date.
ii) Prone ventilation in critically ill patients is potentially hazardous:
+ Difficult airway and patient access
+ Increased risk of endotracheal tube dislodgment or malpositioning
+ Difficulty in tracheal suction
+ Pressure necrosis particularly involving the face and eyes.
+ High incidence of facial oedema
+ Labour intensity
+ Difficulty in performing CPR
iii) The decision to ventilate a patient prone is made by the Duty Consultant.
iv) Patients must only be turned if adequate numbers of staff are available,
ideally during working hours, in discussion with senior nursing staff.

b) Indications
i) Local or anatomical factors, e.g. posterior burns
ii) Severe ARDS
+ Rationale of improved oxygenation in prone ventilation in ARDS:
a. Improvement in FRC by alveolar recruitment
b. Preferential redistribution of pulmonary blood flow
improved V/Q ratios
c. Uniform distribution of lung water and exudate
d. Reduction in intrapleural pressures
e. Non-restriction of abdominal contents
f. Reduction of diaphragmatic splinting and improved movement of
the posterior diaphragm.
165
+ Timing
a. Severe ARDS with PaO
2
:FiO
2
ratio < 100
b. Pulmonary hypertension : MPAP > 35 mmHg
c. Non-response to standard supportive care
i. Optimisation of fluid balance
ii. Treatment of infection
iii. Circulatory support

c) Contraindications
i) Absolute
+ Inadequate staff or insufficient staff familiarity
+ Spinal injury
+ Pelvic fracture unstable
+ Orthopaedic traction
+ Open abdomen
ii) Relative
+ Anterior UWSD
+ Patients on CVVHDF or with an IABP
+ Morbid obesity
+ Patients unable to lie flat
+ Closed head injury

d) Procedure
i) Staff required
+ More than one intensive care doctor
+ Minimum of four nurses
ii) Essential monitoring / equipment
+ Electrocardiograph (ECG) electrodes placed on the back
+ Arterial line
+ Pulse-oximetry
+ End-tidal carbon dioxide monitor
+ Intubation /resuscitation trolleys
+ Closed suction device in situ
+ 2 secure IV accesses.
iii) Safety check before turn
+ Check ETT position on CXR prior to turn
+ ETT should be secured with cotton tape and adhesive tape
+ Check security of tracheostomy tapes
+ Secure all invasive lines and drains.
+ Ensure patency, accessibility and sufficient slack for the turn
+ Recirculate/hold dialysis if in progress
+ Deflate air mattress
+ Ensure the patient is heavily sedated
+ Consider the use of neuromuscular blocking drugs
+ Apply lubricant to the eyes and close with tape or plastic film
166
+ Replace head pillow with a small foam gel pad.
+ Ensure sufficient padding
iv) Procedure
+ Explanation to patient and relatives where appropriate
+ Ensure adequate sedation and or analgesia
+ The doctor must take control of the head and airway and coordinate
the turn
+ Place the patient flat on their back with arms by the side
+ Lift the patient (on a draw sheet) to side of the bed away from the
ventilator, i.e. turn towards the ventilator.
+ Place a firm pillow or foam support under the hips and shoulders
+ Tuck lower hand under hip
+ Slowly roll the patient onto the pillows/foam taking care of lower the
arm & shoulder
+ Place the head to one side, check the eyes are shut
+ Check the airway, oxygen saturation, ventilation, invasive lines
(position and access to them) and haemodynamic response
+ Place the arms in an anatomical position: check a/c and elbow joints
+ Check all potential skin pressure points
+ Re-inflate the air mattress
+ Take an arterial blood for gas analysis.
v) Maintenance
+ Routine ICU observations
+ Hourly face pressure care and head repositioning
+ Monitor plantar flexion, neck hyperextension and facial oedema
+ Continuous ETCO
2
monitoring whilst prone
+ ABG as soon as the patient is stabilised.
+ CXR can be conducted whilst patient is prone (ensure that CXR
request clearly states patient is prone)
vi) Duration
+ If there is a major deterioration in the arterial oxygenation, the patient
must be turned supine as soon as possible.
+ If the oxygenation is unchanged or improved, leave prone for up to 12
hrs. Some patients may show gradual improvement over this period.
+ Repeat rotations once per shift according to clinical progress /
response.
+ In general, patients should not be turned at night.
+ Ensure all safety issues are followed in reverse when return patient to
supine position.

167
E. Management of Cardiothoracic Patients

1. General Principles
a) The following guidelines apply to elective post-cardiac surgical patients.

2. Respiratory
a) Following surgery commence all patients on default ventilator settings:
SIMV + PS 20cmH
2
O + PEEP 5cmH
2
O + F
I
O
2
= 1.0
b) After the first ABG, adjust the F
I
O
2
to maintain a PaO
2
> 80mmHg
c) Wean from ventilation according to past history, surgery performed and current
clinical status
d) Extubation criteria:
i) Temperature > 36C
ii) Awake, able to obey commands
iii) Adequate analgesia
iv) Cardiovascular stability on minimal inotropes
(< 10g/min noradrenaline or adrenaline)
v) Adequate gaseous exchange: PaO
2
> 80 mmHg on F
I
O
2
s 0.5, PEEP 5cm
vi) Bleeding: drain losses < 100 ml/hr
e) Respiratory failure post-op secondary to collapse / consolidation is common.
i) Ensure good analgesia and frequent, effective physiotherapy
ii) CPAP may be required in the first 48 hours.
f) Patients with poor LV function / recurrent acute pulmonary oedema are prone to
extubation failure and may benefit from the use of ACE inhibitors, inodilators
or a trial of spontaneous ventilation prior to extubation.

3. Management of bleeding
a) Notify the surgical team.
b) Perform appropriate investigations: ACT, APTT/INR, Hb, Plts, fibrinogen.
c) Treat abnormalities of above:
i) Protamine 50mg slow IV if ACT > 125 sec or APTT > 60 sec
ii) FFP if INR > 1.5
iii) Give platelets if count below 80,000 or as below.
d) If bleeding continues or is brisk or > 1500mls in first 12 hours.
i) Platelet transfusion of one adult pack, irrespective of platelet count.
ii) Perform CXR and/or echocardiogram to exclude tamponade
iii) Initiate review by cardiothoracic surgeons
e) Consider re-opening if:
i) Bleeding > 200 ml/hr for 3-4 hrs, or
ii) Total loss > 1500-2000 ml.
iii) If no evidence of tamponade re-open in OT.
If evidence of tamponade consider re-opening in ICU

168
4. Hypotension
a) Hypovolaemia
i) Return any remaining pump blood as soon as possible
ii) Correct fluid/blood losses as appropriate
maintain Hb > 80 g/L and CVP ~ 6-10 mmHg
iii) Check ECG
b) Myocardial failure
i) Noradrenaline, often with low dose dobutamine (to improve regional blood
flow to splanchnic/renal vascular beds), is the first choice inotrope
combination. Adrenaline is used for severely impaired ventricles.
ii) If required inotropes > 10g/min and the patient is euvolaemic, consider:
+ PA catheter insertion
+ Pulse contour CO measurement e.g. PiCCO or Edwards Vigileo.
+ Echo to exclude tamponade, AMI, papillary muscle rupture, or VSD.
iii) Consider pacing (either epicardial or transvenous) if hypotension is rate
related (HR < 60). A-V sequential pacing is the ideal mode (DDD)
iv) Consider IABP if hypotension persists despite inotropes.
v) Consider milrinone for patients with predominantly diastolic cardiac
failure or pulmonary hypertension.
vi) Levosimendan may have a role in patients with poor LV function, both
prophylactically during surgery and post-operatively
c) Vasodilatation
i) Noradrenaline is the 1
st
line agent for persistent vasodilatation and
hypotension.
ii) Consider vasopressin ~ 0.02-0.04 g/min
iii) Consider insertion of a PA catheter or PiCCO/Vigileo system to determine
CO, SVR and SV to aid in management.
d) Tamponade
i) This is a medical emergency. If suspected, the cardiothoracic surgeon and
duty consultant must be notified immediately.
ii) Diagnosis:
+ Refractory hypotension despite adequate volume replacement and
inotropic support
+ Cessation / reduction of blood coming from drains
+ Globular heart shadow on CXR and muffled heart sounds may be
present but are unreliable signs
+ Diastolic equalisation of right-sided pressures on PA catheter insertion
+ Echocardiographic evidence of tamponade.
iii) Treatment
+ Support MAP with aggressive volume and inotropic support.
+ Ensure sufficient blood is cross-matched (> 6 units)
+ If stable, reopening in theatre is the definitive treatment
+ In emergent situations the chest may need to be opened in ICU.

169
5. Hypertension
a) MAP should be kept at approximately 70 mmHg for the first 24-36 hrs.
b) This may vary according to the patients pre-morbid BP.
c) Management:
i) Ensure adequate analgesia
ii) Nitroprusside 50 mg in 250 ml 5% dextrose:
titrate to maintain MAP ~ 70 mmHg.
iii) If nitroprusside infusion > 40-50 ml/hr (2 g/kg/min), consider:
+ |-blocker: metoprolol 1-2 mg IV, (if no contraindication)
+ Clonidine: 25-50 g IV (up to 300g/24 hrs)
+ Hydralazine: 10-20 mg IV
+ Captopril: 6.25-12.5mg 2 hourly PRN (up to 150mg/24 hrs)

6. Sedation/Analgesia
a) Generally as per general ICU sedation protocols
b) In patients difficult to sedate and expected to be extubated within 24 hrs,
consider dexmedetomidine (Precedex):
i) o
2
:o
1
-agonist activity ~ 1600:1, providing both sedation and analgesia
ii) Loading dose: 0.5-1.0 g/kg/min over 10 mins
iii) Infusion: 0.2-0.7 g/kg/hr
iv) Patients coming from theatre should not require a loading dose
v) Complications: hypotension, bradycardia.
c) Morphine IV 1-2mg boluses PRN while on ventilator
d) Morphine subcutaneously post-extubation
e) Paracetamol IV or po 4/24 PRN for first day then 6/24 if no contraindication
f) Oxycodone po 4/24 PRN in appropriate dose from second postoperative day

7. Anticoagulation
a) All patients receive subcutaneous heparin
i) < 70 kg 5000
U
12 hrly
ii) > 70 kg 7500
U
12 hrly
b) All patients with coronary artery graft should receive aspirin 300mg po daily
post-extubation, or via a NGT if extubation is delayed.
c) Commence patients with mechanical valve replacements on warfarin (5mg
nocte) from the second post-operative day if extubated.
d) Patients with a mitral valve replacement ventilated > 48hrs may require
heparinisation as will patients in AF for > 48hrs.
e) For antiplatelet drugs see drugs and infusions subsection thrombolysis

8. Antibiotic prophylaxis
a) See guidelines in antibiotic section in Drugs.

170
9. Other Drugs
a) Calcium Channel Blockers
i) Patients receiving radial artery grafts generally receive diltiazem 30mg po
tds from first postoperative day
b) Stress ulcer prophylaxis is not routinely indicated unless the patient has pre-
existing peptic ulcer disease.
c) Insulin is managed as per the general ICU protocol.

10. Management of Minimally Invasive Mitral Valve Repairs
a) These are performed through a right sided mini-thoracotomy with the patient on
femoro-femoral bypass
b) Patients generally have a pain buster placed perioperatively for analgesia
c) Management as for other cardiothoracic patients.
d) Clarify with surgeon whether warfarinisation is required postop. This may vary
with exact type of repair, use of annuloplasty ring, heart rhythm etc.

171
F. Renal Failure

1. Background

a) The mortality from acute renal failure remains high: from 8% in isolation to
70% when associated with other organ or system failures.
b) Patients who die with acute renal failure, usually die from the underlying cause
rather than ARF itself.
c) There is a spectrum of renal dysfunction with variable definitions of what
constitutes Renal Failure.
d) Bellomo has proposed the following definitions:

Creat ACreat Urea AUrea UO
Normal 15-70 2-6 >800
Acute Renal Impairment > 120 > +60 > 8 > +4 <800
Acute Renal Failure > 240 > +120 > 12 > +8 <400

e) Approx. 30% of ICU patients have pre-existing renal impairment.
f) Patients at high risk of developing ARF are those with:
i) Pre-existing renal impairment (creatinine > 120).
ii) Severe sepsis
iii) Hypertension
iv) Diabetes
v) Arteriovascular disease
vi) Heart failure
vii) Large contrast media loads
g) The minimum urine output required to excrete the obligatory solute load is ~
0.5 ml/kg/hr.
h) ARF can be oliguric or non-oliguric. Non-oliguric renal failure has a better
prognosis.
i) Duration of ARF is variable and depends upon resolution of the underlying
injury, severity of the injury and pre-morbid renal function.
j) Consequences of ARF:
i) Fluid overload.
ii) Uraemia encephalopathy, platelet dysfunction, pericardial effusions.
iii) Acidaemia.
iv) Electrolyte derangements K
+
, PO
4
=
, HCO
3
-

v) Accumulation of pro-inflammatory cytokines (theoretical)

172
2. Pathogenesis ARF in critically ill patients is usually multifactorial.

a) Pre-Renal
i) The most common cause of renal failure in ICU.
ii) Aetiologies:
+ Low cardiac output states
+ Hypovolaemia.
+ Vasodilation - sepsis, vasodilators
+ Renal vasoconstriction - NSAIDs
+ Renal artery obstruction - stenosis, embolus, post-surgical
iii) Reduced renal blood flow
+ | GFR and renal function
+ | angiotensin-II and glomerular efferent arteriolar constriction
+ || blood flow to the renal medulla
+ If maintained, then ischaemic renal injury occurs (e.g. ATN).
b) Renal
i) Acute Tubular Necrosis.
+ Ischaemic - see above
+ Nephrotoxic - drugs, contrast, myoglobin, sepsis
ii) Interstitial Nephritis - infections, drugs
iii) Vascular disease - renal vein occlusion, HUS, vasculitis
iv) Glomerulonephritis
c) Post-Renal
i) Obstruction of the renal collecting system leads to |GFR.
ii) Must be considered in unexplained renal failure.
iii) Cannot be reliably ruled out clinically and hence requires imaging.
iv) Ensure a bladder catheter is inserted and draining freely.
v) Aetiologies:
+ Drugs - opiates, anticholinergics
+ Pelvic neoplasms.
+ Retroperitoneal collections (e.g. blood, pus, fibrosis).
+ Pregnancy.
+ Prostatic Obstruction
+ Renal calculi
d) Specific Renal Failure Syndromes
i) Increased intra-abdominal pressure (IAP)
+ Effects at all levels - pre-renal, renal and post-renal
+ May consider decompression when IAP > 20 mmHg with ARF.
ii) Hepato-Renal Syndrome - predominantly a pre-renal
+ | albumin, vasodilatation, splanchnic shunting
+ diuretics for oedema, lactulose, diarrhoea, |intra-abdo pressure
iii) Rhabdomyolysis - pre-renal, renal and post-renal
iv) Ineffective plasma volume
+ e.g. nephrotic syndrome, liver failure, cardiac failure.

173
3. Renal Investigations

a) Blood tests
i) Creatinine
+ Logarithmic (inverse) relationship with GFR.
+ Can lose up to 60% renal function and still maintain a normal
creatinine. Conversely in severe renal failure, a small decrease in renal
function can cause large rises in serum creatinine.
+ Lags behind the evolution of renal injury.
+ Insensitive where muscle mass is low elderly, wasting diseases
ii) Creatinine clearance (Cl
Cr
)
+ Cl
Cr
slightly overestimates GFR due to tubular secretion
+ Estimated on IMVS biochemistry (eGFR) from single specimen
creatinine, thus has same inaccuracies as creatinine
+ Measured Cl
Cr
requires min 8 hour urine collection
iii) Urea
+ Less accurate indicator of GFR than creatinine
+ Modified by diet, catabolic state, GIT blood, liver disease
iv) Electrolytes - Na
+
, K
+
, HPO
4
2-
, ABGs.
v) GN screen - ESR, C
3
, C
4
, ANA, RhF, ANCA, anti-GBM.
vi) Haemolysis screen - RBC frags, |LDH, |haptoglobins, bilirubinaemia.
b) Urine
i) M,C& S - infection must always be excluded
ii) Myoglobin
iii) Urinary electrolytes - impossible to interpret in the presence of diuretics or
natriuretic agents (e.g. catecholamines).
iv) Urinary sediment
+ Epithelial cell casts - ATN
+ RBC / WBC casts - GN
+ Eosinophils - interstitial nephritis
+ Crystals - oxalate (e.g. ethylene glycol)
- urate (e.g. tumour lysis)
c) Imaging
i) Ultrasound
+ Exclude urinary tract obstruction.
+ Doppler studies can assess renal artery and venous flows
ii) CT Renal Tract (non-contrast) highlights renal stones and masses.
iii) IVP - rarely required given availability of U/S and CT.
iv) DMSA scan - a static radionuclide scan to reveal kidney structure.
v) MAG3 scan - a dynamic radionuclide scan
- renal function, collecting system obstruction, ATN.
d) Biopsy
i) Glomerulonephritis
ii) Interstitial nephritis
iii) Infiltration

174
4. Renal protection

a) Established renal protection strategies
i) Fluid resuscitation to maintain circulating blood volume.
ii) Haemodynamic support of blood pressure and cardiac output using inotropes
(adrenaline, noradrenaline, dobutamine).
iii) Exclusion of post-renal obstruction (check IDUC, renal tract U/S,
nephrostomy).
iv) Avoidance / close monitoring of nephrotoxic drugs
+ aminoglycosides, amphotericin
+ contrast agents
+ ACE inhibitors
+ NSAIDs
v) Prompt detection & treatment of urinary infection.
b) Unproven strategies for renal protection
i) Frusemide infusion / high dose
ii) Mannitol infusion / intermittent
iii) Aminophylline infusion
iv) N-acetyl cysteine
v) Calcium channel blockers
vi) Clonidine
vii) HCO
3
-
for rhabdomyolysis.
c) Contrast Prophylaxis
i) Best evidence is to use HCO
3
-

ii) Add 150ml 8.4% NaHCO
3
to 850ml 5% Dextrose.
iii) Run at 3ml/kg the hour prior to contrast administration,
then continue at 1ml/kg/hr for 6 hours
d) Low Dose Dopamine
i) May temporarily increase urine output
ii) Does not reduce the incidence of dialysis dependent renal failure or
mortality. (ANZICS CTG).

175
5. Indications for renal replacement therapy

a) Symptomatic or refractory:
i) Acidosis
ii) Hyperkalaemia
iii) Fluid overload - e.g. pulmonary oedema
iv) Uraemia - urea > 35 mmol/l or symptomatic
b) Severe sepsis
i) Developing oliguric renal failure
ii) Removal of cytokines / inflammatory mediators (unclear benefit)
+ High ultrafiltration rates increase clearance
+ The clinical significance is currently being studied.
c) Diuretic resistant pulmonary oedema.
d) Drug removal.
i) Salicylate
ii) Methanol
iii) Theophylline
iv) Ethylene glycol
v) Lithium
vi) Other drugs (water-soluble drugs that are not highly protein bound).
e) The decision to commence RRT should be discussed with the duty consultant.
f) Generally, RRT is initiated early in the course of ARF, before serious
complications develop.
g) The choice of RRT modality depends on patients type and severity of illness,
equipment availability and local expertise.
h) The renal unit should be notified early of patients who are potential long-term
dialysis candidates.

6. Renal Replacement Therapy Principles

a) Haemofiltration.
i) Convective solute and fluid removal down a hydrostatic pressure gradient
to form an ultrafiltrate (UF).
ii) Clears middle molecules (>500 D) and fluid.
iii) UF formation is dependent on the pressure gradient and membrane
characteristics (effective pore size & surface area).
iv) Predilution replacement of ultrafiltrate with balanced salt solution
increases the availability of urea for convective transfer by favouring its
movement from red cells.

176
b) Haemodialysis.
i) Diffusion of solute down a concentration gradient across a semi-permeable
membrane, running dialysate fluid counter-current to blood flow
ii) Clears urea, creatinine, electrolytes (i.e. small molecules).
iii) Solute clearance is adjusted by changing the dialysate fluid solute
concentration, blood and dialysate flow rates.
iv) Intermittent HD (IHD)
+ Utilised if the patient is stable and requires longer-term dialysis.
+ Takes 3-5 hours using higher blood flows of 300 ml/min
+ Fluid removal occurs quickly, not tolerated in unstable patients.
+ Performed by the Renal Unit.
v) Sustained Low Efficiency Dialysis (SLED)
+ Similar to standard IHD but occurs over 8-12 hours
+ Lower blood and dialysate flow rates.
+ Well tolerated by the critically ill.
+ Used in some ICUs (not the RAH) for nursing and cost reasons.
+ Although better tolerated than IHD in the critically ill, there is little
evidence to confirm equipoise with CVVHD/F in terms of outcomes.

c) Continuous veno-venous haemodiafiltration (CVVHDF).
i) Standard form of continuous renal replacement therapy in this Unit.
ii) The combination of ultrafiltration and dialysis improves solute clearance.
iii) Advantages of CVVHDF over conventional intermittent haemodialysis:
d) Effective and more flexible control over fluid balance.
e) Greater cardiovascular stability.
f) Does not require attendance of Renal Unit staff.
g) May have a role in modification of the septic response.
h) Some trials suggest improved patient mortality (not proven).
i) Allows patients to receive continuous protein rich diet.

7. Complications of CVVHDF
a) Hypothermia.
b) Prolonged exposure to heparin: | incidence of HITS, bleeding
c) Prolonged venous access: infection, thrombosis.
d) Air embolism.
e) Increased nursing workload.
f) Catheter flow disruption (high access pressures).
177
Diagram: CVVHDF Circuit
Heparin
Ultrafiltrate
Replacement
To Patient
Dialysate
Solution
Effluent
Deaeration
Chamber

178
8. CVVHDF Equipment

a) Dialysis catheters
i) Priority of site placement and optimal catheter length:

Femoral R.IJ L.IJ R.SC L.SC
25cm 15cm 20cm 15cm 20cm

ii) Use Dolphin Protect
high flow catheter guided as above

iii) Heparin lock all catheter lumens 8 hourly when not in use
+ 5000
U
in 3 mls, divided equally into both lumens.
b) Filters
i) Older filters were made from cellulose and would often initiate an
inflammatory response (i.e. membrane reaction).
ii) Membranes are now synthetic (polycarbonate, polyacrylonitrile)
iii) These are more permeable and biocompatible
iv) We use Prisma
AN69 filters:
+ Membrane = acrylonitrile
+ Membrane thickness = 50um.
+ Surface area = 1m
2

(larger filters 1.22m
2
allow |blood flow and clearance)
+ Blood volume in set = 150ml
c) Dialysis machine settings
i) The PrismaFlex
is the standard dialysis machine at the RAH

ii) Older Prisma machines are still in use but are being phased out.
d) For patients on ECMO, CVVHDF can be performed via the ECMO circuit
without additional Vas-Cath placement.
i) Must be discussed with ICU consultant supervising ECMO

9. Prescribing CVVHDF
a) Orders for the PrismaFlex or Prisma
should be written on a standard sticker.

b) The following variables require assessment/prescription for CVVHDF.
c) Haemofiltration solution (replacement)
i) Gambro
Hemosol B-zero solution - bicarbonate buffered, 5L bag

ii) Flow rate = 1000-2000 ml/hr (higher rates in catabolic patients)
iii) Ultrafiltration rates of 35 ml/kg/hr may improve survival.
iv) Standard is to deliver replacement post-filter, but may be given pre-filter if
required (e.g. short filter life problem, or for intracellular urea clearance)
v) If given pre-filter on the PrismaFlex
, still require at least 100ml/hr

replacement post-filter for the deaeration chamber to function properly.
d) Dialysis solution
i) Gambro
Hemosol B-zero solution - bicarbonate buffered, 5L bag

ii) Rate = 500-2000 ml/hr (higher rates if marked electrolyte abnormalities)
e) Blood flow rate
i) When commencing CVVHDF, gradually increase blood flow as tolerated
by patient haemodynamics
ii) Target rate = 250ml/min - limited by machine/access pressures.
179
f) Anticoagulation
i) Blood passing through the filter activates the clotting cascade.
Anticoagulation is often required to prolong filter life
ii) Circuit is primed with heparin 5,000
U

iii) No ongoing anticoagulation is required for patients with coagulopathy
iv) Systemic anticoagulation (if no contra-indications to anticoagulation)
+ Heparin 5000 units stat, then continue at 1,000 units/hr
+ Heparin is infused into the circuit pre-filter
+ Check APTT after 6 hrs and then daily if stable
+ End-point is filter life rather than a therapeutic APTT (i.e. if filter is
working and APTT < 45sec, there is no need to increase heparin dose)
v) Regional anticoagulation
+ Utilised when:
a. Maintenance of filter life is problematic.
b. There is a contra-indication to systemic anticoagulation
c. No contraindication to heparin administration.
+ The circuit still needs to be primed with heparin
+ Heparin is administered pre-filter as above
+ Protamine 5-10 mg/hr post-filter
vi) Check APTT 6 hourly after any dose changes.
vii) For patients with heparin induced thrombocytopenia (HIT) consider
+ Citrate (see citrate protocol)
+ Prostacyclin 5 ng/kg/min (see protocol)
+ Danaparoid (given systemically, not into circuit see protocol)
g) Fluid removal
i) Determine how much fluid should be removed from the patient. Consider
its effects on patient haemodynamics
ii) The amount of fluid removed is the difference between the effluent and the
dialysate plus replacement fluid volumes
h) Potassium
i) Gambro
Haemosol B-zero solution contains no potassium.

ii) Supplementary K
+
:
+ Required for all patients, except in the initial management phase of
marked hyperkalaemia
+ Should to be added to both the replacement & dialysate bags
iii) Target [K
+
] = 3-4mmol/L, dose = KCl 15-20 mmol per 5L bag
iv) K-Acetate can be used in severe acidosis:
+ Acetate is effectively metabolised to HCO
3
-
via the liver
+ Vial = 25mmol/5ml, dose = 3-4mls per 5L bag
i) Drug prescription
i) Consult Antibiotic Guidelines / Pharmacy regarding antibiotic dosing
+ e.g. meropenem, ciprofloxacin, fluconazole
ii) Monitor drugs that are renally cleared and potentially toxic
+ e.g. gentamicin, vancomycin, digoxin

180

G. Neurosurgical protocols

1. Neurotrauma in ICU

a) Close liaison and communication with the neurosurgeons is essential for the
coordinated management of acute head injuries.
b) ICU management of the neurotrauma patient includes:
i) Acute trauma resuscitation
ii) Liaison and coordination with other clinics in the multi-trauma patient.
iii) Cardiopulmonary / renal / metabolic homeostasis.
iv) Maintenance of cerebral homeostasis
NB: refer to cerebral perfusion pressure (CPP) algorithm
v) Transport for imaging

c) Principles of ICU management:
i) Ventilation
+ Maintain normoxia: PaO
2
> 80 mmHg
+ Ventilation to normocapnia: PaCO
2
= 35-40 mmHg
ii) Haemodynamics:
+ Fluid maintenance
a. Maintain euvolaemia
b. Crystalloid depending upon Na
+
and measured osmolality
c. Avoid dehydration if patients become polyuric (DI / mannitol)
+ Maintain cerebral perfusion pressure:
a. CPP ~ 6070 mmHg
i. A lower threshold may be tolerable in some patients
ii. Must be discussed with the ICU Consultant
b. MAP ~ 80 mmHg in the absence of ICP measurement
c. NB: use inotropes if required once euvolaemic
+ Avoid interference with cerebral venous return
a. Nurse patients at 30 head-up elevation
b. Neutral head position
c. Avoid circumferential ETT ties, etc.
+ ICP control Mannitol (osmotherapy):
a. Patient must be euvolaemic and normotensive (relative to pre-
morbid BP) before the administration of mannitol
b. The indications for mannitol prior to ICP monitoring are:
i. Unequivocal signs of intracranial hypertension prior to
imaging or evacuation of an intracranial mass lesion
ii. Threatened transtentorial/brainstem herniation, or
iii. Progressive neurological deterioration not due to systemic
pathology.
c. Measured osmolality should not exceed 320mosmol/l
i. Mannitol and alcohol cause an osmolal gap
ii. calculated = measured osmolality
181
d. Standard dose = 0.25g/kg
i. 1.25ml/kg of 20% mannitol
ii. Duration of action is variable (90min 6hrs)
e. A urinary catheter is essential.
+ Hypertonic saline is a reasonable alternative to mannitol.
a. Standard dose is 20ml of 20%NaCl
b. Slow IV push through a CVC
+ Hyperosmolar infusions are to be discussed with the ICU Consultant
iii) Seizure prophylaxis - indications:
+ Closed head injury with structural damage
(intracerebral or paraxial haematomas)
+ Penetrating head injuries
+ Depressed skull fracture
+ Pre-existing epilepsy
+ Phenytoin prescription:
a. 15 mg/kg loading over 30 minutes
b. 300 mg iv daily or 400mg NG x 7 days only
c. Monitor levels: therapeutic 40-80umol/l
iv) Antibiotics - indications:
+ Insertion of ICP monitoring catheters: cefazolin 1g stat
+ Base of skull fractures: antibiotics are not indicated in the absence of
signs of meningitis
+ Nosocomial infections: as per infectious diseases guidelines.
v) Sedation:
+ Consider the use of propofol in patients where regular review of CNS
status is required (majority of patients)
+ Control large sympathetic swings with morphine / midazolam,
fentanyl boluses (100-200g IV)
+ Many opioids have been demonstrated to increase ICP and should not
be used as sole therapy to control intracranial hypertension.
+ The use of muscle relaxants is relatively contraindicated. Infusions of
muscle relaxant must be discussed with the ICU Consultant.
+ Consider |-blockade or clonidine in labile neurogenic hypertension.
vi) Nutrition:
+ Establish enteral feeding as soon as feasible
+ Maintain BGL in the normal range: hyperglycaemia is common in the
acute phase and may precipitate a hyperosmolar state with resultant
polyuria. Use insulin infusions if necessary.
vii) Stress ulcer prophylaxis is not routinely indicated (see protocol)
viii) Thromboprophylaxis:
+ All patients should have TED stockings and sequential calf
compression devices applied within 8hrs of admission unless contra-
indicated.
+ Pharmacological thromboprophylaxis is relatively contraindicated in
the first 72 hrs after injury or surgery or if there is ongoing bleeding.
182
+ Thromboprophylaxis may be commenced when indicated following
discussion with Neurosurgery
+ In patients at high risk of VTE or with contra-indications to
mechanical prophylaxis, consideration should be given to early
insertion of a caval filter
ix) Avoid hyperthermia.

d) Monitoring of head injured patients:
i) Cardiorespiratory:
+ In addition to routine ICU monitoring ETCO
2
is recommended
a. Interpret with caution & calibrate with PaCO
2
when,
i. Change in ventilation
ii. Sudden rise in ICP
b. Adjust ETCO
2
to PaCO
2
= 35-40 mmHg
ii) Neurological:
+ ICP monitoring
a. At the RAH ICP monitors are inserted by neurosurgeons
b. Indications:
i. Severe CHI (GCS < 8) and an abnormal CT scan, or
ii. GCS < 8 and two of
- Age > 40 yrs
- Focal motor signs
- Hypotension after volume resuscitation
iii. Brain swelling following evacuation of intracranial
haematoma
iv. Intracerebral haematomas where the decision to operate will
depend on ICP
v. Polytrauma patients in whom cerebral status cannot be
adequately assessed (e.g. patients requiring ventilation)
vi. Rarely in non-traumatic raised ICP
- Meningitis / encephalitis
- Hepatic failure.
+ Ventricular drain and external pressure monitor:
a. Closed system
b. CSF for M,C&S as clinically indicated
c. Set height for drainage according to neurosurgical consultation.
d. Preferred for ICP monitoring in CHI

183
Flowchart: Cerebral Perfusion Pressure Algorithm

THERAPY FAILURE:
ICP > 20 mmHg for > 10min or CPP < 60 mmHg
1. Ensure accurate MAP, ICP and where relevant, SjO
2
readings
2. Immediately correct hypovolaemia and hypoxia
3. Check PaCO
2
and ensure normocarbia PaCO
2
35-40 mmHg
4. Ensure adequate sedation
5. Consider drainage 2-5ml CSF if intraventricular catheter in situ
6. Exclude contributing factors
- Neck position / venous obstruction
- 30 head-up position
- Fever, Seizures
7. Commence osmotherapy with Hypertonic saline or mannitol and
notify ICU Consultant
8. Consider short-term hyperventilation whilst arranging urgent CT
9. Consider neuromuscular blockade
10. Notify neurosurgeon on-call
Non-Surgical Lesion
1. Attempt to maintain CPP > 60 mmHg with fluids / inotropes
2. Consider additional therapies after discussion with Duty ICU
Consultant:
- Propofol / barbiturate coma
- Hypothermia
Initial Therapy to Optimise CPP
1. Maintain euvolaemia with IV fluids
2. Ensure appropriate sedation
3. Commence inotropes to maintain CPP 60 - 70 mmHg (MAP ICP)
4. Maintain normocarbia, PaCO
2
35-40 mmHg

URGENT
CT Head Scan
Surgical Lesion
Immediate
Neurosurgical
Consultation
184
2. Aneurysmal Subarachnoid Haemorrhage

a) Principles of ICU management:
i) Admission to ICU/HDU:
+ Acutely prior to angiography or surgery
+ Post-operatively
ii) Priorities:
+ Monitoring of airway and adequacy of ventilation
+ Maintenance of adequate cerebral perfusion
maintain appropriate MAP (relative to premorbid BP)
+ Monitoring of conscious state (GCS)
+ Early diagnosis and treatment of causes of reduced GCS
a. Rebleed from aneurysm (notify neurosurgeon)
b. Hydrocephalus (notify neurosurgeon)
c. Vasospasm
d. Seizure
iii) Monitoring:
+ ECG, SpO
2
, Invasive BP
+ ICP in patients with a ventricular drain in situ:
a. May be set at a level (usually 10 cm) above head and/or
b. Connected to monitor transducer
c. CSF culture as clinically indicated

b) Prevention and treatment of vasospasm
i) Specific drug therapy:
+ Nimodipine:
a. Indications
i. CT proven SAH
ii. IV preferably through central line (2 mg/hr)
*may be given through a peripheral IV
iii. Change to oral as soon as possible (60mg 4hrly)
b. Complications: hypotension (may require cessation of nimodipine)
+ Statins:
a. Statins may reduce the incidence of radiological vasospasm and
improve outcomes following SAH.
World Federation of Neurosurgeons Classification
Grade GCS Motor Deficit
I 15 Absent
II 13-14 Absent
III 13-14 Present
IV 7-12 Present or absent
V 3-6 Present or absent
185
b. In the absence of a contra-indication patients should be
commenced on simvastatin 80mg daily.
ii) Triple H therapy (hypertension / hypervolaemia / haemodilution):
+ Has no role in the prevention of vasospasm
prophylactic HHH therapy may be harmful
+ It is imperative to avoid hypotension and hypovolaemia.
+ Patients should have fluid therapy targeted at maintaining euvolaemia.
iii) Euvolaemic hypertension
+ May be indicated in selected patients with proven vasospasm post-
aneurysmal clipping / coiling.
+ Induced hypertension must be titrated to a mean arterial pressure:
systolic BP is not an accurate indicator of cerebral perfusion pressure.
+ Principles:
a. Discuss with ICU consultant prior to initiating therapy
b. Intra-arterial pressure monitoring is mandatory
c. Maintain IV volume
i. Continue IV filling until clinically euvolaemic
ii. Avoid volume overload (pulmonary congestion/oedema)
iii. Monitor electrolytes 8 hrly normal osmolality and [K
+
].
d. Commence noradrenaline titrated to:
i. MAP > 90mmHg, or
ii. MAP > 10mmHg above premorbid baseline
(for known hypertensive patients)
iii. Reset target MAP if high doses (> 10ug/min) are required, or
if polyuria, arrhythmias or other complications ensue.
+ Complications:
a. Pulmonary oedema, hypoxia
b. Cardiac arrhythmias, myocardial ischaemia
c. Polyuria, electrolyte disturbances
iv) Chemical (papaverine / verapamil) or balloon angioplasty
+ Limited role in angiographically proven vasospasm
+ Requires transport for angiography and may be performed on
consecutive days.
v) Operative therapy:
+ Early (within 48 hrs): currently recommended at RAH
a. Advantages (proposed): prevention of rebleeding, reduction of
vasospasm, prevention of ischaemia
b. Disadvantages: high intraoperative risk of rupture, difficult
dissection
+ Late (after 11 days)
a. Advantages: easier procedure, opportunity to monitor.
b. Disadvantages: re-rupture, prolonged risk of vasospasm
vi) Anticonvulsants: as clinically indicated
vii) Steroids not indicated
186
2. Status epilepticus
a) Definition:
i) More than 30 minutes of:
+ Continuous seizure activity
+ Two or more sequential seizures without full recovery of
consciousness between seizures
b) Principles of ICU management
i) Assessment of airway and adequacy of ventilation
+ Intubate and ventilate if appropriate
+ Avoid muscle relaxants after intubation
ii) IV access
iii) Control of seizures:
+ Midazolam: 1-10 mg/hr via infusion, or
Diazepam: 10-20 mg IV prn
+ Phenytoin: 18 mg/kg load, then 300 mg daily
check for previous administration
therapeutic 40-80umol/l
+ If refractory: (liaise with neurologists)
a. Clonazepam 1-2 mg IV prn or by infusion 0.5-2 mg/hr
b. Consider Valproate 200-500mg po/IV 8 hrly
c. Nasogastric Levetiracetam
d. Thiopentone infusion
i. Loading dose: 5mg/kg of 25mg/ml solution
(2500mg / 100ml N.sal)
ii. Infusion: 1-3 mg/kg/hr
(~ 150 mg/hr or 6 ml/hr)
e. Obtain EEG and consider EEG monitoring
iv) Look for a cause and treat appropriately: CT scan with contrast if unclear
+ Previous epilepsy / poor compliance
+ Intracranial pathology:
a. Vascular (haemorrhage, thrombosis), spasm
b. Infection (consider LP if no evidence of raised ICP on CT)
c. Tumour
+ Extracranial pathology:
a. Metabolic: exclude hypoglycaemia, thiamine deficiency
b. Check electrolytes: especially Na
+
, Ca
++
, Mg
++
, K
+
, PO
4
=

+ Infection
+ Severe hypertension
c) Maintenance of homeostasis / seek and treat complications
i) Ensure adequate hydration: maintenance fluids according to
creatinine/urea, Na
+
and osmolality
ii) Ensure adequate urine output: prolonged seizures may be associated with
rhabdomyolysis
iii) Evaluate for joint dislocations and occult fractures

187
4. Exclusion of acute cervical spinal injury following trauma
a) Safe practices are vital to prevent secondary damage to the cord
b) Spinal immobilisation should be practiced in all patients with;
i) significant distracting injury or injury above the clavicles
ii) altered conscious state for any reason (head injury, alcohol, drugs etc)
iii) neck pain or tenderness
iv) abnormal neurological signs or symptoms
v) NB:
+ Hard collars allow up to 73% of normal flexion and extension and so
still need appropriate spinal care even if in place.
+ Soft collars do not provide effective C-spine immobilisation.
c) Clinically clearing the C-spine requires all of the following criteria to be
fulfilled;
i) normal conscious state, with no drugs or alcohol onboard
ii) no neck pain or tenderness
iii) no abnormal neurological signs or symptoms
iv) no significant distracting injury, or significant injury above the clavicles
and then,
v) normal head control (unassisted)
vi) pain-free movement
d) If all of these are confirmed, the hard-collar can be removed, and the C-spine
cleared.
e) If the C-spine cannot be clinically cleared for any reason, radiology needs to be
performed (the majority of patients seen in Trauma Resus)
f) Virtually all patients presenting to Trauma Resus require a trauma series of
adequate AP, lateral, and odontoid C-spine plain views
g) A complete series of 3 plain views will still miss up to 7% of C-spine injuries
hence the importance of clinically clearing (if possible) the C-spine even if the
Xrays appear normal.
h) If the C-spine cannot be clinically cleared following normal plain films,
maintain spinal precautions and liaise with the Trauma Registrar.
i) Clearing the C-spine in the patient with altered conscious state:
i) If drugs, alcohol or minor closed head injury are the problem, they are
often resolved within 12 hours maintain spinal precautions until that
stage, and then assess clinically
ii) If the patient is unlikely to become clinically assessable and clearable
within 12-24 hours (most intubated patients):
+ Perform a complete plain Xray series in ED, and:
+ Perform a limited CT;
a. C
0-2
in all, during first visit to scanner
b. CT any suspicious areas on the plain films
c. CT may be required to visualise cervicothoracic junction
or
d. CT entire cervical spine with 3-D reconstructions (the current
recommendation)
188
+ If these films are all documented normal, the collar may be removed
and the C-spine cleared as per RAH protocol.
+ Any ongoing concerns are referred to the Trauma and/or Spinal
Registrar
j) Flexion-extension views of the C-spine must not be performed, unless ordered
by the Spinal Unit, with the Spinal Fellow in attendance
k) As with the C-spine, the thoracolumbar spine should be imaged in all patients in
whom it can not be clinically assessed. This should be done prior to arriving in
ICU. If CT chest and abdomen have been performed, these images can be used
to assess and clear the thoracic and lumbar spines.
l) 25% with a spinal injury at one level will have a second non-contiguous injury.
Therefore, if a fracture is found anywhere in the spine, the entire spine should
be Xrayed
m) Spinal Xrays should ideally be performed in an Xray area (Trauma Resus Room
or Xray Dept) prior to ICU admission. Quality of spinal Xrays performed in
ICU is usually very poor
n) The Trauma Registrar must document the status of spinal clearance on the
Trauma Form
o) Steroid use in acute spinal cord injury is not currently recommended by the
Spinal Injuries Unit.
p) The RAH Trauma Service Procedures, Practices and Guidelines (TSPPG) on
Acute Spinal Injury Management is available on the RAH Intranet and
contains more detail.
189
H. Microbiology Protocols

1. Policy
a) The prompt diagnosis and treatment of infection in critically ill patients is both
important and difficult.
b) Sepsis is the most common cause of death in critically ill patients. It must be
aggressively sought and promptly treated with surgical drainage (where
indicated) and appropriate antibiotics.
c) Simple preventative measures are the most important factors in the containment
of nosocomial infection and minimisation of bacterial resistance:
i) Compulsory hand washing and/or use of alcohol hand-gel by all staff
ii) Attention to aseptic technique for invasive procedures
iii) Attention to invasive procedure protocols as outlined in this manual
iv) Avoidance of over-prescription of antibiotics
d) Regular routine microbiological examination in critical care patients is not cost
effective. Investigations should only be ordered on specific indications.
e) Septic screens must follow the guidelines below.

2. Definitions
a) Systemic Inflammatory Response Syndrome (SIRS)
i) Describes the inflammatory process that occurs in response to a variety of
clinical insults resulting in a clinical picture suggestive of sepsis
ii) The syndrome includes at least 2 of the following:
+ temperature > 38 or < 36

C
+ heart rate > 90 bpm
+ respiratory rate > 20 bpm, or
PaCO
2
< 32 mmHg
+ WCC > 12,000/mm
3
, or
< 4,000/mm
3
, or
> 10% immature (banded) neutrophils
iii) SIRS is non-specific and may be due to non-infectious causes:
+ Trauma, Post-operatively after major surgery
+ Haemorrhagic shock, post blood transfusion
+ Pancreatitis
+ Burns
+ Drug reactions
+ Intracranial pathology, esp. intraventricular or thalamic blood
b) Sepsis: the presence of SIRS 2 to infection
c) Septic shock: decreased vital organ perfusion/function 2 to sepsis
d) Nosocomial infection is defined as infection that occurs during hospitalisation
that was neither present, nor incubating on admission.
e) Colonisation is defined as the presence of microorganisms that do not elicit an
inflammatory response.

190
3. Septic screen
a) Routine, performed only on the clinical suspicion of sepsis:
i) New pyrexia
ii) | WCC, ||WCC, or | Platelets
iii) Deterioration in gaseous exchange or pH
iv) Cardiovascular instability
+ Hypotension / relative hypovolaemia
+ Increased or new inotrope requirement
v) Oliguria or increased creatinine
b) Screen:
i) Urine - C&S
ii) Tracheal aspirate - urgent gram stain, C&S
iii) Blood culture x2
iv) Any other drainage fluid as indicated, e.g. wound, pleural etc.
c) Other
i) Fungal cultures
ii) Pleural fluid, CSF
iii) Sinus x-rays
iv) Bronchoscopy specimens (BAL)
d) Urine:
i) UTI in a catheterised patient is defined as:
+ > 10
5
bacteria + positive culture of organisms, plus
+ > 500 WBC/HPF.
ii) Bacteria and white cells are a normal finding in a catheterised patient
iii) Treatment with antibiotics will not result in clearance of colonisation and
is only indicated for systemic involvement.
iv) The only effective treatment is catheter removal.
v) Bladder wash-out may reduce bacterial load / infective risk.
e) Tracheal aspirate:
i) Cultures often grow mixed colonising oral flora:
+ Gram positive cocci - S. aureus and S. pnuemoniae
+ Gram negative bacilli - H. influenzae
+ Yeast - Candida sp.
ii) Antibiotics will not result in a clearance of colonisation and are only
indicated for invasive (local or systemic) infection.
f) Blood cultures:
i) May be contaminated by skin organisms: requires careful technique:
+ Clean the skin with an alcohol or betadine swab
+ Clean the top of culture medium bottle with an alcohol swab:
allow to completely dry before injecting.
+ Use a sterile needle and aseptic technique during venipuncture
+ Inject blood immediately into bottle with same needle - do not touch
the needle.
ii) Blood cultures are best taken by clean venipuncture.
iii) Skin organisms grown from a single bottle are usually considered a
contaminant but must be interpreted in the context of the patient.
191

4. Investigation of pneumonia
a) Community acquired pneumonia:
i) Usual organisms: S. pneumoniae, H. influenzae
ii) Less commonly:
+ Bacterial: Legionella sp., Gram neg bacilli, S. aureus
+ Viral: Influenza A, B, Parainfluenza, Adenovirus, RSV
+ Other : Mycoplasma pneumoniae,
Chlamydia psittaci (birds),
Coxiella burnetti (sheep or cattle),
TB, Chlamydia pneumoniae
iii) Investigations
+ Haematology - High (> 15000) or Low (< 3000) WCC
- coagulopathy
+ Biochemistry - note renal function and LFTs
+ CXR
+ ABGs
+ Microbiology: * prior to antibiotic Rx where possible
a. Blood cultures x 2
b. Endotracheal aspirate
i. M,C&S + urgent gram stain
ii. Legionella culture
iii. Respiratory viral Ag (PCR) & culture
NB: If not intubated, then collect a nasopharyngeal aspirate
for respiratory viruses
c. Urine - L. pneumoniae 1 Ag
* only where high index of suspicion or outbreak
d. Pleural fluid - M,C&S
b) Community acquired pneumonia Immunosuppressed Host:
i) Possible organisms
+ As above plus
a. Bacterial: Nocardia
b. Viral: CMV, HSV, varicella zoster
c. Fungal: candida, cryptococcus, aspergillus
d. Protozoal: pneumocystis jirovecii (PCP)
+ Consider non-infective causes of a similar picture e.g. ARDS
ii) Investigations: * As per above, plus
+ Sputum or tracheal aspirate - limited value, need BAL!
a. Pneumocystis stain
HIV patients only all others require BAL
b. Acid fast bacilli
+ Viral studies, request CMV, HSV.
+ Consider BAL if initial cultures negative
a. PCP staining on BAL only for HIV(-) patients
+ HIV serology

192
iii) Treatment prior to microbiological diagnosis: refer to antibiotic guidelines
& discuss with ID.

c) Nosocomial pneumonia in ICU
i) Principles:
+ Accurate diagnosis and treatment are important but difficult.
+ Incidence: 20% of all ICU patients
70% of patients with ARDS
major cause of death in patients with ARDS
+ Clinically indistinguishable from pulmonary fibrosis, alveolar
haemorrhage, atelectasis and other causes of lung infiltrates
+ Clinical diagnosis, including use of tracheal aspirate, has poor
sensitivity and specificity
+ Appropriate antibiotics do improve outcome
+ Empiric broad-spectrum antibiotics are potentially harmful.
ii) Consider nosocomial pneumonia when:
+ New and persistent CXR changes
+ Tachycardia, tachypnoea
+ Fever or hypothermia - temperature >37.5 or <35.5
+ Leucocytosis or leucopaenia - WCC: >10 or < 4 x 10
9
/l
+ Purulent sputum
+ Deterioration in lung function
iii) Confirmation of pulmonary infection:
+ Tracheal aspirate MC&S
+ Preliminary results to direct therapy may be obtained on gram stain
+ Consideration should be given to obtaining pulmonary samples by
bronchoalveolar lavage (or open lung biopsy) for patients with:
a. Persistent signs of pneumonia
b. Inadequate response to antibiotics
c. Inabililty to obtain adequate tracheal aspirates, or
d. To exclude non-infectious causes of respiratory failure
e.g. interstitial fibrosis or alveolar haemorrhage
+ Septic screen including blood cultures should also be performed.

193
5. Vascular catheter sepsis
a) Refer to the invasive procedures section
b) Suspect line sepsis when:
i) Evidence of systemic infection
+ New, unexplained fever
+ Unexplained | or | in WCC
+ Deterioration in organ function
+ Positive blood culture by venipuncture with likely organisms
(coagulase negative staph, candida), and/or
ii) Evidence of local infection - inflammation or pus at the insertion site
iii) The following patients are more susceptible to line infections:
+ Prolonged vascular access (> 7-10 days)
exponential increase in line infection after 4 days.
+ Endovascular infection (SBE, prosthetic graft infection)
+ Cutaneous infection
+ Burns
+ Severe intra-abdominal infection (pancreatitis)
+ Deep-seated infections (empyema / abscess)
iv) The incidence of line sepsis with the antibiotic impregnated lines is around
1% and most of these are due to Candida spp.
c) Protocol
i) Take blood cultures from a peripheral vein
ii) Positive blood cultures from the line may only indicate colonisation so
blood culture bottles must be carefully labelled as to site of sampling
+ Common organisms in line sepsis are normal skin flora
e.g. Staph spp., C. albicans
+ In ICU gram negative organisms can also be involved
iii) On suspicion of line sepsis the line should be removed
iv) The tip of the catheter should be sent for culture
+ Avoid contamination of the catheter tip with skin organisms
+ Skin should be cleaned thoroughly with alcohol, allowing at least one
minute drying time, before removing the catheter
v) Catheter related bloodstream infection is defined as infection where the
same organism is grown from the blood and from the catheter tip
d) Treatment
i) Removal of the line will usually clear low-virulence organism
bacteraemias, e.g. S. epidermidis
ii) Antibiotics are indicated if:
+ The patient is high risk - e.g. joint or endovascular prosthesis
+ Infection with a virulent organism, e.g. S. aureus
+ Signs of sepsis continue after catheter removal
iii) If ongoing sepsis occurs, additional blood cultures should be taken prior to
starting antibiotics
iv) Refer to antibiotic guidelines.
194
e) Further venous access:
i) Reassess the need for ongoing central access, consider PICC line
ii) Whenever possible:
+ Wait 24 hours before reinsertion
+ Select a different insertion site
iii) Guidewire exchanges are not performed unless:
+ Mechanical problems in a new catheter (leaks/kink & < 4 days old)
+ Difficult or limited central access (e.g. burns)

6. Bacterial Meningitis
a) Steroids should be started before antibiotics in all patients with a high
probability of bacterial meningitis.
i) No demonstrated benefit given post-antibiotics.
ii) Should occur in A&E / pre-retrieval - check on admission
b) Dose: dexamethasone 10mg 6 hrly for 4 days
c) Antibiotics are as per ID guidelines

7. Fungal infections
i) The incidence of systemic fungal infections in ICU patients has increased:
+ Increased numbers of immunosuppressed patients admitted to ICU
+ The use of broad-spectrum antibiotics, and
+ Prolonged use of intravascular catheters
ii) Fungaemia is an indication to commence antifungal therapy.
iii) Whilst candidaemia is associated with significant mortality, systemic
infections can occur with negative blood cultures.
b) Risk factors for candidaemia and disseminated candidiasis:
i) Neutopaenia
ii) Long term CVC use
iii) Candida colonization
iv) Broad spectrum antibiotics
v) Haemodialysis
vi) Immunosuppressants
c) Antifungal prophylaxis
i) Systemic prophylaxis is not recommended for general ICU patients
ii) Solid organ transplant patients do not require prophylaxis
iii) Posaconazole prophylaxis is effective and tolerated in bone marrow
transplant and neutropaenic cancer patients
d) Indications for antifungal therapy
i) Candiduria in high risk patients with deteriorating clinical status
ii) Single positive blood culture in a high-risk patient
iii) Isolation of candida from any sterile body site (except urine)
iv) Positive microscopy for yeast from a sterile specimen
v) Histological evidence of yeast or mycelial forms in tissue from high-risk
patients
195
e) Specific antifungal therapy *always seek ID opinion
i) Fluconazole
+ Proven candidaemia
+ Dose: 400 mg IV daily
ii) Voriconazole
+ Suspected or confirmed aspergillosis, or resistant candida
+ Loading Dose: 6 mg/kg IV bd x1 day, then
4 mg/kg IV bd x3 days
*do not continue IV past 24 hrs if CrCl < 30 ml/min
+ Maintenance: 200-300mg po bd
iii) Caspofungin
+ Second line agent to voriconazole or in presence of renal failure
+ Loading Dose: 70 mg/day
+ Maintenance: 50 mg/day
iv) Amphotericin B / Ambisome
+ Rarely indicated due to potential nephrotoxicity.

8. Protocol for patients with necrotising soft tissue infections
i) This is a generic group of patients with life threatening infections
involving combinations of mucocutaneous, fascial and myofascial planes
ii) These infections represent a medical emergency: patients may present with
severe septic shock and rapidly developing multiple organ failure
iii) In rapidly progressive infections, local signs of inflammation may
underestimate the degree of underlying tissue necrosis
iv) Usually due to one or more of the following organisms:
+ Anaerobes - clostridium spp, bacteroides
+ Gram positives - group A streptococcus, staphylococcus
+ Gram negatives - enteric organisms
b) Management protocol:
i) Appropriately trained personnel, familiar with the severity of the patient's
condition and with appropriate resuscitative equipment, must accompany
these patients during all phases of their management
ii) The hallmarks of management involve a detailed multidisciplinary
approach coordinated by the duty Intensive Care consultant and involving
the following:
+ The duty ID consultant must be notified as soon as possible.
+ Prompt and effective resuscitation, restoration of vital organ perfusion
and control of metabolic emergencies (e.g. hyperkalaemia,
hypoglycaemia, coagulopathy). This is coordinated by the Intensive
Care team and must not significantly delay surgery.
+ Early, aggressive and repeated surgical debridement.
a. Patients with necrotising soft tissue infections must be reviewed
by a plastic surgical consultant (not trainee) ASAP.
b. The Duty Anaesthetist must be notified as soon as surgery is
planned.
196
+ Prompt identification of organisms with early prescription of
appropriate empirical, then specific antibiotics as required (refer
empirical and specific antibiotics section).
+ Immune Globulin (IVIg)
a. Clearest evidence in Gp A Strep infections.
b. Should be used in conjunction with clindamycin
c. Liaise with ID in all cases & confirm if to be used
d. Standard regimen over 3 days:
i. 1.0g/kg Day1
ii. 0.5g/kg Days 2&3
e. Rescue Therapy
i. May be considered in cases where surgery would prove
devastating, or where surgery is unduly delayed
ii. Dose: 2.0g/kg as single bolus over 3-6hrs.
NB: This may be > 3000ml IVIg
+ Hyperbaric oxygen is an adjunctive therapy in selected patients:
a. HBO must not delay debridement and resuscitation must be
maintained during treatments.
b. Indications for hyperbaric oxygen:
i. Progressive bacterial (clostridial) gas gangrene.
ii. Selected patients with severe multisystemic disease not
responding to resuscitation, antibiotics and surgery.
c. The number of HBO treatments on a given day will depend on the
stability of the patient, availability of staff and timing of surgery.
d. As a general rule, patients undergoing surgical debridement will
return to ICU following surgery for stabilisation and assessment
prior to subsequent transfers for HBO. This will be co-ordinated
by the duty Intensive Care and hyperbaric medicine consultants.

197
I. Drug overdose

These guidelines have been influenced by and modeled on an excellent text: Murray L,
Daly F, Little M, Cadogan M. Toxicology Handbook. Elsevier 2007.


a) The majority of drug overdoses are poly-pharmaceutical and respond to general
supportive measures.
b) Overall, early mortality is low and usually relates to cardiorespiratory arrest.
c) Following admission, morbidity relates primarily to aspiration pneumonitis, or a
delay in definitive respiratory care.
d) There is a poor correlation between depth of coma and preservation of glottic
reflexes. Accordingly, if there is any doubt the patient should be intubated.
e) Antidotes such as naloxone or flumazenil:
i) Should generally not be used as alternatives to supportive measures
ii) Are not to be used to facilitate gastric lavage or charcoal administration
iii) The main utility is in aiding diagnosis of the underlying cause of coma
- small doses only are required
iv) Usefulness in treatment is limited by their short half-lives
v) Continuous infusion is required where ongoing therapy is contemplated
vi) Both agents may initiate a withdrawal syndrome or unmask to the toxicity
of co-ingestants. In the case of flumazenil these effects may be life
threatening.
f) ICU/HDU admission criteria following an overdose:
i) Intubated patients
ii) Reduced GCS with potential airway compromise
iii) Uncontrolled seizures
iv) Persistent hypotension
v) ECG criteria:
+ Ventricular or supraventricular tachyarrhythmias
+ Sinus tachycardia > 140/min with tricyclics or thyroxine
+ AV block 2
nd
or 3
rd
degree
+ QT
C
interval > 0.5s
+ QRS interval > 0.12s
+ Acute RBBB
vi) Metabolic disturbance requiring HDU-level of care
vii) Requirement for extracorporeal elimination

198
2. Gastrointestinal Decontamination

a) A variety of approaches have been used historically in an attempt to reduce the
dose absorbed following an oral ingestion.
b) There is minimal evidence for improved survival or shortened duration of
toxicity, particularly when applied to unselected patients.
c) The decision to use decontamination requires individual patient risk-benefit
analysis. Appropriate patients and modalities should be selected, and
gastrointestinal decontamination should never proceed to the detriment of
resuscitative and supportive care.
d) Gastric lavage
i) Largely historical
ii) Formal lavage (large bore tube placement, water instillation and aspiration)
should not be performed.
iii) For intubated patients, an orogastric or nasogastric tube of appropriate
(standard) size should be inserted, and any gastric content aspirated
iv) No additional fluid should be instilled via the tube.
e) Charcoal
i) Charcoal aspiration has a high morbidity and mortality:
+ Adequate airway reflexes must be present, or
+ If there is any doubt the patient should be intubated
ii) For appropriate ingestions administer:
+ 1g/kg body weight (to a maximum of 100g) stat
+ 25g 4 hourly x 3 doses - slow release medications
- drugs with enterohepatic circulation
+ Cease administration should an ileus develop.
iii) Indications:
+ Presentation < 1hr from ingestion
a. Compound bound by charcoal
b. Ingestion expected to cause significant morbidity or mortality.
+ Presentation > 1hr, consider administration for:
a. Salicylates
b. Slow release or enteric coated preparations
c. Agents which delay gastric emptying, and
d. Drugs with enterohepatic circulation.
iv) Charcoal ineffective for:
+ Elemental metals and their salts
+ Hydrocarbons and alcohols
+ Acids or alkalis
v) With multiple dose charcoal administration, constipation is likely and the
addition of sorbitol may be considered.
199
f) Whole bowel irrigation
i) Use of polyethylene glycol solution to decontaminate the bowel.
ii) Use restricted to life threatening overdoses where:
+ The agent is a slow release or enteric coated preparation
+ The agent is not expected to be bound by charcoal.
+ A good outcome is not expected with supportive care and antidote
administration alone.
+ The patient presents before the advent of severe toxicity
iii) May be potentially useful following:
+ Iron overdose > 60mg/kg
+ Slow release potassium chloride > 2.5mmol/kg
+ Major slow release verapamil or diltiazem ingestion
+ Symptomatic arsenic trioxide ingestion
+ Lead ingestion
+ Body packers (heroine)
iv) Contraindications
+ Good outcome expected with standard care
+ Uncooperative patient
+ Uncontrollable vomiting
+ Reduced GCS or seizures expected in subsequent 4 hours
+ Ileus or bowel obstruction
+ Intubated patients (relative)
v) Technique
+ Polyethylene glycol solution (standard endoscopy bowel prep.)
+ Administer via correctly placed nasogastric tube at 2L/hour
(25ml/kg/hr in children)
+ To minimize vomiting start at a slower rate & titrate up as tolerated
+ Administer metoclopramide to enhance gastric emptying
+ Be prepared for explosive diarrhoea
- sit on commode or place effluent tube for example
+ Continue until rectal effluent is clear or an ileus/abdominal distension
occurs.

3. Osmolal Gap

a) OG = Measured calculated osmolality
b) Calculated Osmo = 2 x (Na + K) + Gluc + Urea + ethanol
c) Baseline osmolar gaps are highly variable in the normal population.
d) Evaluation of potential toxic alcohol ingestion requires serial assessments over
time looking for a characteristic pattern with worsening acidaemia, increasing
anion gap and decreasing osmolar gap.
e) Single measurements may confirm an ingestion but are not reliable in excluding
it.

200
Flowchart: Approach to the unconscious, undetermined overdose

RESUSCITATION (ABCDEFG)
1. Airway
2. Breathing
3. Circulation
4. Dont Ever Forget Glucose
Consider:
1. Glucose 50%
2. Naloxone
3. Thiamine
History:
1. Patient
2. Relatives
3. SAAS Crew
Examination:
1. Clinical toxidromes
2. Trauma
3. Nerve palsies
4. Pressure areas
5. Preganacy?
Investigation:
Blood Urine
Biochem:
Electrolytes
Glucose
Renal
LFTs
Coags

Urine drug
screens rarely
influence
management and
should be used
sparingly
Drug levels:
Paracetamol
routinely
Others as
indicated
only

Other
ECG
ABG
Measured
osmolality

NO Metabolic Acidosis
1. Sedatives
2. Hypnotics
3. Paracetamol
4. Theoplylline

5. Anticholinergics
6. Antihistamines
7. Antipsychotics
8. Antidepressants
9. Anticonvulsants
10. Lithium
11. Organophosphates
Metabolic Acidosis
Normal Anion Gap
1. Acid ingestion
2. Toluene sniffing
3. Bicarbonate loss
Raised Anion Gap
+
Osmolal Gap

OG < 10
Salicylates
Cyanide
Carbon monoxide
Lactic acidosis
OG > 10
Methanol
Other alcohols
201
4. Specific therapies / protocols

a) Paracetamol: Acute overdose
i) Defined as a single ingestion, or staggered ingestion occurring over 8
hours or less.
ii) If the time of ingestion can be defined risk assessment and the decision to
treat may be based upon the Rumack-Matthew nomogram (use the initial
ingestion time as the assumed total ingestion time when plotting staggered
ingestions occurring over < 8hrs).
iii) Where the nomogram cannot be used (repeated supratherapeutic
ingestions, sustained release preparations) the decision to treat is based
upon the dose/kg ingested, a serum level, and aminotransferase levels
iv) Potentially hepatotoxic dose in a fit adult is > 200 mg/kg (or > 10g)
v) Markedly less in high risk individuals:
+ Chronic alcoholics and the malnourished
+ Pre-existing liver disease
+ Those taking cytochrome P450 inducing medications
vi) The risk of hepatic injury without NAC (N-acetylcysteine) is predicted by
plotting a level taken 4-15 post ingestion on the Rumack-Matthew
nomogram.
vii) The probability, with a 4hr drug level, is:
+ 1-2% < 1320 mol/L (200mg/L)
+ 30% ~ 1320-1980 mol/L (200-300mg/L)
+ 90% > 1980 mol/L (> 300mg/L)
viii) The risk of hepatic impairment with NAC is determined primarily by the
time from overdose to commencement of NAC:
+ Survival is 100% where NAC is commenced within 8 hours
+ Benefit is reduced if NAC commenced at 8-24 hours
+ Benefit is not confirmed if commenced beyond 24 hours, except in the
setting of hepatic failure.
ix) The administration of NAC is indicated in the following settings:
+ Patients who present within 8 hours of ingestion and have a 4-8 hour
level falling above the treatment line
+ All patients presenting 8-24 hours post-ingestion
*may be ceased if the subsequent level is non-toxic and transaminases
are normal
+ Patients presenting beyond 24 hours post-ingestion with detectable
paracetamol and elevated transaminases
+ Unknown time of ingestion with detectable paracetamol
*may be ceased if subsequent history allows for plotting of a
demonstrably non-toxic level on the nomogram
+ Late presenters with clinical or biochemical evidence of hepatic injury
202
x) NAC may be ceased in the following settings:
+ Patients in whom NAC was commenced < 8 hours post-ingestion who
are clinically well and without hepatic tenderness at the completion of
the 20 hour infusion (no further investigation required)
+ Patients in whom NAC was commenced > 8 hours post-ingestion who
are clinically well and have normal transaminases at the completion of
the 20 hour infusion. Those whose transaminases are abnormal at this
time should continue an infusion at 100mg/kg/16 hrs until
transaminases and INR (tested 12-24 hourly) are falling.
xi) Consultation with liver transplant services (FMC) for consideration of
transplant should commence with any of the following high risk criteria:
+ INR > 3.0 at 48 hours or > 4.5 at any time
+ Oliguria or creatinine > 200 mol/L
+ Acidosis with pH < 7.3 after resuscitation
+ Ongoing hypotension with systolic BP < 80mmHg
+ Hypoglycaemia
+ Severe thrombocytopenia
+ Encephalopathy (any degree)
xii) The above guidelines do not apply to:
+ Sustained release paracetamol preparations
+ Repeated supra-therapeutic ingestions
+ Toxicological advice should be sought in these settings.
+ The default position, if in doubt, should be to treat with NAC.

Graph: Modified Rumack-Matthew Nomogram

203
Table: N-Acetylcysteine Administration
NAC 150mg/kg in 200mls of 5% dextrose over 30 minutes
NAC 50 mg/kg in 500mls of 5% dextrose over 4 hours
NAC 100mg/kg in 100mls of 5% dextrose over 16 hours

b) Lithium - Acute overdose
i) Generally produces significant GIT symptoms with nausea, vomiting,
abdominal pain and diarrhoea.
ii) Ingestion < 25g in the setting of normal renal function is benign
iii) Ingestion > 25g may cause more significant GIT toxicity
iv) Neurotoxicity is rare with good supportive care and hydration
v) Renal impairment, dehydration and sodium depletion cause a reduction in
renal lithium excretion and increase the risk of delayed neurotoxicity
vi) Patients presenting late with established neurotoxicity should be managed
as for chronic toxicity, and have similar long term morbidity
vii) Lithium levels > 5mmol/L 4-8 hrs post ingestion are not uncommon
viii) Treatment
+ Normal saline rehydration
+ Maintenance of urine output > 1ml/kg/hr
ix) Haemodialysis is reserved for:
+ Those with established or worsening renal failure, and
+ Those presenting late with established neurotoxicity

c) Lithium - Chronic poisoning:
i) The clinical features of chronic toxicity are primarily neurological
ii) Develops when renal lithium excretion is impaired for any reason
iii) Serum lithium levels correlate poorly with clinical toxicity
iv) Neurotoxicity may persist well after lithium levels return to normal.
v) The Hansen-Amdisen classification may be used to grade severity:
+ Grade 1 (mild): tremor, weakness, ataxia, hyperreflexia
+ Grade 2 (moderate): stupor, rigidity, hypertonia, hypotension
+ Grade 3 (severe): myoclonus, convulsions, coma
vi) Lithium levels
+ Confirm a diagnosis but should not be used to grade severity
+ Are useful serially to monitor response to therapy
vii) Principles of therapy
+ Careful correction of fluid and sodium balance
+ Cease lithium and any medications that may impair excretion
+ Monitor urine output, renal function, electrolytes and lithium levels
204
viii) Indications for haemodialysis
+ Neurotoxicity and a serum level > 2.5 mmol/L
+ Grade 3 neurotoxicity regardless of level
+ Pre-existing renal or cardiac disease preventing the achievement of an
adequate urine output with hydration alone
+ Repeated haemodialysis treatments may be required

d) Opioids
i) Produce CNS and respiratory depression, frequently at just above analgesic
doses
ii) Death is due to respiratory failure, either primary effect or compounded by
aspiration, and good supportive care ensures survival
iii) Some opioids may possess additional cardiac and neurologic toxicity
- e.g. dextropropoxyphene, tramadol, pethidine
iv) Controlled release preparations may cause delayed and prolonged toxicity
v) Treatment is generally supportive
vi) Naloxone (50 to 100g IV repeated as needed)
+ Useful for diagnostic purposes
+ Can assist in the management of airway and breathing
+ May result in a withdrawal syndrome
vii) If repeated naloxone boluses are required to ensure a protected airway,
intubation is the preferred method of ongoing management
viii) If a naloxone infusion is established:
+ Initial hourly requirement is generally half the effective dose used over
the preceding hour, i.e. that required to achieve airway protection and
adequate tidal volumes
+ Infusions require constant observation/assessment
+ Hospital deaths have occurred due to inadequate observation

e) Carbon monoxide
i) CO is a common cause of poisoning death and most occur pre-hospital.
ii) Those that arrive at hospital alive should survive, and in-hospital
management involves supportive care and identification of those at risk of
long term neuropsychiatric sequelae
iii) Acute effects are due to tissue hypoxia
iv) Delayed neurological effects are secondary to unrelated and incompletely
understood mechanisms
v) HbF binds CO more avidly than HbA, and the foetus is at particular risk
vi) Deliberate self poisonings involve high concentration, short term
exposures, and are associated with fewer long-term sequelae than
industrial and domestic exposures (low concentration, prolonged
exposures)
205
vii) High risk features for delayed neurological sequelae:
+ Loss of consciousness or coma
+ Persisting neurological deficit (e.g. confusion)
+ Cerebellar signs
+ Metabolic acidosis
+ Myocardial ischaemia
+ Age > 55yrs
viii) Treatment options
+ Normobaric oxygen at high flow via non rebreather mask
a. Continue until all symptoms resolve
b. Pregnant women to continue for 24 hours with concomitant foetal
assessment
+ Hyperbaric oxygen
a. May be indicated in patients with 1 or more high risk factors
b. Indications and effectiveness are controversial

f) Cyanide
i) Acute cyanide poisoning is rare, dramatic and lethal
ii) Removal from the source of exposure, good resuscitative care and selective
antidote use provide the best chances of survival
iii) Most deaths will occur pre-hospital, and those who arrive alive in hospital
post-inhalational exposure are likely to survive with supportive care.
iv) Risks to those involved in care delivery are negligible.
v) Decontamination should involve removal of clothes and washing of skin
with soap and water.
vi) Cyanide levels are not available in a timely manner and do not aid
management
vii) Serum lactate levels parallel cyanide levels and may be used as a proxy
marker of exposure
viii) A lactate level > 10 mmol/L correlates with a toxic cyanide level
(in the absence of an alternative cause for elevation)
ix) Management should proceed along normal resuscitative lines with the
delivery of 100% oxygen
x) Consider using an antidote in the following settings:
+ Altered mental state
+ Seizures
+ Hypotension
+ Significant and persisting metabolic acidosis (lactic)
xi) Antidote choice and administration
+ 100% oxygen in all cases
+ Hydroxocobalamin (1
st
line)
a. 5g in 200mls of 5% dextrose over 30 minutes
b. Repeat in 15 minutes if no improvement
+ Sodium thiosulphate (adjunct to Hydroxocobalamin, or 2
nd
line)
a. 12.5g IV
b. Repeat dose at 30 minutes if acidosis persists
206
+ Sodium nitrite
a. 300mg IV over 3 minutes
b. Follow immediately with sodium thiosulphate
c. Half dose may be repeated in 30 minutes if required
d. Monitor methaemoglobin (must not exceed 40%)

g) Toxic alcohols
i) A variety of alcohols (methanol, ethylene and diethylene glycol etc) are
used as industrial solvents, cleaning agents and reactants.
ii) Accidental ingestions are rarely of sufficient volume to cause toxicity
iii) Deliberate ingestion is associated with severe metabolic acidosis,
multiorgan dysfunction and potentially death.
iv) Cause an initial ethanol like intoxication followed by a progressive
metabolic acidosis and compound specific end organ toxicities which may
include:
+ Retinal toxicity/blindness (methanol)
+ Acute renal failure (multiple agents)
+ Seizures (multiple agents)
+ Refractory hypotension (multiple agents)
+ Delayed neurological sequelae (diethylene glycol)
v) Diagnosis is based upon a history of suggestive ingestion and a
characteristic evolution of metabolic acidosis
+ Initially: | osmolar gap (OG) + normal pH and anion gap (AG)
+ Evolution of acidosis with | pH, | OG and | AG
+ Variability in osmolar gap amongst the normal population is such that
a single assessment of acid-base, AG and OG is insufficient to
exclude significant exposure (although it may confirm it)
vi) Specific treatment
+ Ethanol
a. Commence ASAP, regardless of symptomatology, in all with:
i. Acidosis, or
ii. An elevated OG (with or without acidosis),
b. Check baseline BAL, if > 0.1g/dl a loading dose is not required
c. Titrate to BAL to 0.1g/dl to 0.2g/dL while on dialysis
d. May be given orally (via NGT) or by IV infusion
e. Oral protocol *not used in ICU
i. Loading dose of 1.8ml/kg of 43% ethanol
(4 x 30ml vodka shots for a 70 kg adult)
ii. Maintenance infusion of 0.2-0.4 ml/kg/hr
(1 x 40ml vodka shot per hour)
f. Intravenous protocol
i. Loading dose: 8ml/kg of 10% ethanol
ii. Maintenance: 1-2ml/kg/hr of 10% ethanol
g. Actual requirements vary widely between individuals, and serial
blood alcohol assessments are required to ensure a level within the
target range
207
h. If on CVVHDF, then safer to dialyse against desired [ETOH]
i. 0.1g/dl = 5ml ETOH / 5l Bag (inc. replacement)
ii. first bag may be run at 0.2g/dl = 10ml ETOH / 5l bag
+ Haemodialysis (HD)
a. Significantly more efficient at clearing alcohols than CVVHD
b. Indications
i. Serum pH < 7.3
ii. Serum bicarb < 20 mEq/L
iii. Worsening acidosis or vital signs despite supportive care and
ethanol infusion
+ Folate 50mg IV QID
+ Thiamine 300mg IV daily

h) Organophosphorous agents
i) Includes the organophosphates (OP) and carbamates (CM)
ii) Similar initial presentation
iii) Most deaths occur as a consequence of respiratory failure
iv) OPs as a group have greater lethality
+ Form a covalent bond with serine esterase enzymes
+ In contrast to the competitive bond formed by CM.
v) There is great variability amongst the OPs in terms of enzyme aging,
toxicity profiles, and pralidoxime responsiveness
vi) High quality supportive care and aggressive use of antidotes is necessary to
ensure survival.
vii) The diagnosis is essentially clinical:
+ Muscarinic features - diarrhoea, emesis, urination
- miosis, lacrimation, salivation
- bronchorrhoea, bronchospasm
- bradycardia, hypotension
+ Nicotinic features - fasciculation, tremor, weakness
- respiratory muscle paralysis
- tachycardia, hypertension
+ CNS features - agitation, seizures, coma
- delayed neuropsychiatric effects
viii) Cholinesterase levels:
+ Plasma cholinesterase levels fall more rapidly and recover more
quickly than RBC cholinesterase levels, they are useful in confirming
exposure but do not correlate with toxicity.
+ RBC cholinesterase levels correlate better with toxicity and response
to therapy, but take longer to perform (limiting their clinical utility)
ix) Decontamination
+ These agents do not vapourise at atmospheric pressure
+ There is no risk to care providers from inhalational exposure
+ The characteristic odour is due to a hydrocarbon solvent, which may
cause headaches & eye irritation, but is otherwise harmless
+ Staff should wear impermeable gowns, gloves, glasses and facemasks
208
+ Care should be delivered in a well ventilated setting
+ The patients clothing should be removed and the skin washed with
soap and water
x) Treatment
+ Ventilatory and CVS support as indicated
+ Atropine
a. Reverses muscarinic effects only will not reverse paralysis!
b. Titrate 0.6-2.4 mg at 3-5 min intervals until signs of successful
atropinisation are noted
i. Drying of secretions
ii. Breathing less laboured
iii. Reduction of ventilatory resistance
c. Over 10-20 mg, or infusions of up to 5 mg/hr may be required in
severe poisoning
d. NB: HR and pupil size are not useful for clinical monitoring after
nerve agent exposure
+ Diazepam IV
a. Treatment of seizures
b. Reduces the incidence of neuropsychiatric sequelae
c. Regular dosing is recommended.
+ Pralidoxime Iodide
a. Efficacy is unclear and is likely to be compound specific
b. Default is to give ASAP
c. Not required for documented carbamate ingestion (although not
contraindicated)
i. 1g IV over 30 minutes
ii. 500 mg/hr for 24 hours
iii. May be ceased at 24 hours in the absence of nicotinic or
muscarinic features. The benefit of continuing beyond 24
hours is unclear and warrants specialist consultation.

i) Calcium Channel Blockers
i) Of the common slow release formulations, verapamil and diltiazem
frequently cause profound CVS collapse 4-16 hrs post-ingestion.
ii) Other agents within the class rarely cause major toxicity
iii) Onset of toxicity may be delayed:
+ Up to 2 hours post-ingestion of the standard preparation, and
+ Up to 16 hours after ingestion of the SR formulation
iv) Ingestion of > 10 tablets of verapamil SR or diltiazem SR may cause
serious toxicity
v) The key issues in management are:
+ Identification of patients at risk
+ Judicious use of the pre-toxicity window of stability
+ Consideration of GIT decontamination options
(including whole bowel irrigation), and
+ A graduated approach to developing or established toxicity
209
vi) Risk of serious toxicity is significantly increased by:
+ Co-ingestion of other cardiac medications, and
+ Underlying cardiac disease or advancing age
vii) Graduated response to hypotension: failure to achieve stability at each step
should prompt immediate initiation of the next
+ Fluid load with 10-20 ml/kg isotonic crystalloid (avoid overload)
+ Calcium load
a. Calcium gluconate - 60ml of 10% solution, or
b. Calcium chloride - 20ml of 10% solution
c. Commence an infusion to keep calcium levels > 2.0mEq/L
+ Atropine to a total of 1.8mg
+ Catecholamine infusion effects are variable in terms of:
a. Central - negative inotropic & chrontropic effects
- Adrenaline is an appropriate 1
st
line agent
b. Peripheral - reduced vascular tone
-Noradrenaline 1
st
line agent
+ High dose insulin & dextrose / euglycaemia
a. Most effective when used early
b. Do not persist with escalating inotrope doses in the setting of
continued instability
c. Seek guidance from Clinical Toxicologist (via switchboard or
Poisons Information Centre) or ICU consultant staff regarding
protocol
+ Cardiopulmonary bypass, ECMO and intra-aortic balloon pumps have
been used successfully as extraordinary manoeuvres

j) Beta Blockers
i) Overdoses generally result in minimal toxicity and require only simple
supportive care.
ii) By contrast overdoses of sotalol or propranolol may be life threatening
iii) In addition to class |
1
and |
2
effects (bradycardia, conduction blocks and
hypotension)
+ Propranolol
a. Na
+
channel blocking effects wide complex arrhythmias
b. Highly lipid soluble enters the CNS (causing coma and
seizures)
+ Sotalol
a. Blocks cardiac K
+
-channels
b. Causing QT prolongation and Torsades
iv) The clinical response to overdose is highly variable, but the threshold for
severe toxicity from propranolol may be as low as 1g
v) With the exception of sotalol and slow release preparations, toxicity is
usually apparent within a few hours post-ingestion
vi) PR prolongation in the absence of bradycardia is an early marker of
toxicity
210
vii) Approach to immediate life threatening symptoms:
+ Bradycardia and hypotension
a. Atropine
b. Adrenaline
c. Noradrenaline
d. Glucagon 5-10mg bolus & 1-5mg/hr infusion, or
e. High dose insulin dextrose euglycaemia
(targeting impaired contractility)
+ Wide QRS
a. Sodium bicarbonate bolus 1-2 mEq/kg
b. Repeat as required
c. Intubate and hyperventilate targeting serum pH = 7.5 to 7.55
+ Torsades de pointes
a. Isoprenaline
b. Magnesium
c. Overdrive pacing

k) Tricyclic Antidepressants (TCAs)
i) Tricyclic antidepressant use has escalated after an initial reduction
secondary to SSRI introduction
ii) TCAs remain a significant cause of toxicological morbidity and mortality
iii) Self poisoning is associated with rapid onset CNS and CVS toxicity that is
expected to peak between 4 and 6 hours post ingestion:
+ Dose > 10mg/kg is potentially life threatening
+ Dose > 30mg/kg is expected to cause severe cardiotoxicity and coma.
+ Prompt intubation, hyperventilation and sodium bicarb administration
at the onset of major toxicity is life saving.
iv) The investigation of choice is the 12 lead ECG, with diagnostic and
prognostic features including:
+ Prolongation of the PR and QRS intervals
+ Terminal R wave in aVR
+ Increased R/S ratio (>0.7) in aVR
+ QRS > 100 ms is predictive of seizures
+ QRS > 160 ms is predictive of ventricular tachycardia
v) The approach to resuscitative management includes the following:
+ Prompt intubation and hyperventilation (to serum pH 7.5-7.55) at the
onset of CNS depression
+ Ventricular arrhythmias are unlikely to respond to defibrillation:
a. NaHCO
3
~ 2 mmol/kg IV every 2 minutes until perfusing rhythm
restored
b. Lignocaine is a 2
nd
line agent if arrhythmias persist despite |pH.
+ Hypotension is managed with crystalloid and alkalinisation followed
by noradrenaline
+ Seizures are managed with benzodiazepines (*avoid phenytoin)

211
K. Bites and Envenomation

1. Up to date and detailed information on envenomation may be found at the
toxinology website http://www.toxinology.com/ managed by the Womens &
Childrens Hospital
2. Medical advice for doctors can be sought by contacting the clinical toxinologist,
A/Prof Julian White via the WCH switchboard (Ph: 81617000)
3. Emergency cases are seen through the Emergency Departments of major hospitals,
while less urgent cases are seen after discussion with the treating doctor.

K. Limitation of Therapy

a) Limitation may involve either withholding and/or withdrawal of life supporting
therapies. There is no ethical or legal distinction between these processes.
b) Limitation of therapy involves potentially challenging ethical and legal issues;
however, in patients with no realistic chance of survival or meaningful recovery,
decisions to limit life-sustaining therapies are both clinically and ethically
indicated.
c) Assisted suicide and euthanasia are medically and ethically distinct from limitation
of therapy, are illegal in SA and should never occur.
d) The administration of medication to relieve the suffering of a dying patient is
imperative, even though a side-effect may be to hasten the onset of the patients
death. Such therapy is legally distinct from euthanasia.
e) At the RAH, approximately 70% of all ICU deaths involve some limitation of
therapy.
f) Absolute requirements for limitation of therapy are:
i) Medical consensus, including the treating ICU and admitting clinical teams
ii) Clear and open discussion with the patient, family, or next of kin, regarding
this consensus medical opinion; and, an absence of objection to this
proposed management direction.
iii) Clear documentation in the patients case-notes, along with a description of
the process by which the decision was made.
g) Counselling patients and families in limitation of therapy requires clarity and
sensitivity to ensure that all parties understand and accept the plan of management.
The concerns and wishes of the patient and family are important considerations.
h) The overriding goal is to provide the best care possible for the patient. This may be
to concentrate on palliation, rather than life sustaining therapies.
i) The decision to limit treatment is a consultant responsibility.

212
L. Brain Death and Organ Donation

1. Reference: ANZICS Statement on Death and Organ Donation - Third Edition 2008

2. For further information, trainees should liaise with the Organ Donation Hospital
Medical Directors:
a) Dr David Evans
b) Dr Stewart Moodie
c) Dr Peter Sharley
d) Dr Alex Wurm

3. Declaration of brain death
a) This is an absolute requirement prior to beating-heart organ donation
b) Declaration must be made by two members of the ICU staff:
i) The Duty ICU consultant, and
ii) Another ICU doctor (more than 5yrs qualified with appropriate experience).
c) The declaration of brain death may be by either clinical or imaging certification.

4. Clinical certification of brain death
a) The procedure is completed on a Certification of Brain Death form (MR150.0) and
documented in the case notes.
b) Record the time of onset of coma
i) Last time the patient showed response such as breathing, pupil reaction or
coughed on suction.
ii) This can be determined from the nursing observations
c) Pre-conditions:
i) A recognised irreversible cause of coma must be identified.
ii) Potentially reversible causes of unresponsiveness and coma have to be
excluded, including the effects of:
+ Hypotension
+ Hypothermia *core temp must be > 35C
+ Drugs or poisons.
+ Neuromuscular blocking drugs
+ Metabolic or endocrine disturbance including:
a. Deranged renal or hepatic function
b. Hyperglycaemia, hypoglycaemia, thyroid function
c. Electrolyte disturbances
iii) Ability to perform examination of
+ Cranial nerves
+ Apnoea testing (e.g. not severely hypoxaemia or high cervical injury)
d) Clinical confirmation of absent brain stem function:
This procedure is performed separately by 2 doctors, with the first test at least 4
hours after the onset of coma (longer in the case of hypoxaemic/ischaemic
injuries).

213
i) Absent pupillary responses to light, both direct and consensual
ii) Absent corneal reflexes
iii) Absent vestibulo-ocular reflex
+ No nystagmus on injection of 20ml iced water into the ear
+ Check tympanic membranes prior to this procedure
+ Occulo-cephalic reflexes are often tested, but are not formally required
iv) Absent gag / cough reflex
v) Absent response to pain in the cranial nerve distribution.
vi) Apnoea following disconnection from the ventilator:
+ Pre-oxygenate patient with 100% oxygen
+ Disconnect ventilator and connect to bag with 100% oxygen insufflation
at low flow (1-2 l/min)
+ Wait until PaCO
2
> 60 mmHg and pH < 7.30
a. Confirm this by blood-gas analysis
b. Ensure PaO
2
> 60mmHg
+ Continuously look for apnoea clinically
e) The following are compatible with Brain Death
i) Spinal reflexes
ii) Sweating, blushing and tachycardia
iii) Normal BP without pharmacological support
iv) Absence of Diabetes Insipidus
f) The 2 practitioners may choose to be present at each examination, however,
each must perform and be responsible for one of the 2 examinations
g) From the onset of coma until the second set of testing, there should be a
continuous period of observation by nursing staff
h) Families may benefit from witnessing the clinical testing for brain death
i) The time of death is the time when certification of brain death is completed i.e.
on completion of the second examination and documentation in the case notes.
j) There is no legal requirement for certification of persons not considered for
organ donation, however this is encouraged as it can assist in counselling
relatives and the subsequent cessation of inappropriate medical intervention.

5. Imaging (Non-clinical) certification of brain death
a) Clinical examination is consistent with brain death, however, the preconditions
(2c) for clinical certification cannot be met.
b) Demonstrated absence of cerebral blood flow is therefore required.
c) Ideally there should be a period of observation of 4 hours to increase the likelihood
that no flow will be demonstrated.
d) Absence of cerebral blood flow may be established by either:
i) Radionuclide cerebral perfusion scan (Tc99 HMPAO).
ii) 4 vessel cerebral angiography (rarely performed at the RAH)
e) Certification of brain death is by 2 clinicians, (not including the doctor who
performed the imaging investigation) who have considered the onset and cause of
coma, the clinical examination and the results of the investigation performed.

214
6. Organ donation
i) Any patient who is, or may become brain dead is a potential donor. There are
no automatic exclusion criteria.
ii) Identifying potential organ donors involves all Intensive Care staff.
iii) All potential donors should be offered the opportunity to donate
iv) Notify the Donor Coordinator from the South Australian Organ Donation
Agency (Ph: 82077117) when a potential donor is identified.
b) Criteria for brain dead organ donation
i) The patient has been declared brain dead (for donation after cardiac death see
below)
ii) All brain dead patients should be discussed with the Donor Coordinator,
regardless of these listed relative contraindications.
iii) Usually, no patient history of:
+ HIV
+ IV drug abuse
+ Untreated bacterial, fungal or viral infection.
+ Malignancies other than primary brain tumours and minor skin lesions.
+ Treatment with hormones of human pituitary origin.
+ Dementia (or family history of dementia).
+ Disease of the donor organ
c) Procedure:
i) Organ donation should not be discussed with the family until brain death has
been certified and the family informed.
ii) Counselling families with regard to brain death and organ donation requires
considerable compassion, knowledge, skill and time. While this is primarily a
consultant responsibility, advanced trainees are encouraged to participate in
the process.
iii) Family approaches regarding donation prior to death should be referred to the
consultant
iv) The wishes of the patient and family are paramount.
v) A donor kit is kept in the cupboard in P4A which contains a check-list, plus
all the forms and specimen bottles required.
vi) Following consent for organ donation, blood should be sent for:
+ HTLV-1, HIV 1 + 2
+ HBsAg, HBsAb, HBcAb, HCV
+ CMV-IgG, EBV, RPR
+ Group and X-match
+ Tissue typing volume of blood varies according to blood group
+ Mark the request forms: Urgent Organ Donor, Copy to: SAODA
vii) Coronial approval will be sought by the Donor Coordinator where required.
viii) The RAH Designated Officer may give permission for donation if all efforts
to find relatives have failed.
ix) Notification of the recipient and procuring teams (which may come from
interstate) and coordination of operating theatre time, collation of results and
investigations are dealt with by the Donor Coordinator(s)
215
x) Donor coordinators may seek assistance from ICU staff with ordering
investigations.
xi) The following investigations are normally required:
+ Recent ECG
+ Recent CXR
+ Echocardiography
+ ABG
d) Management of the organ donor:
i) The situation is time critical as it is not possible to stabilise a brain dead
patient indefinitely.
ii) Aim to ensure perfusion and protection of all organs for donation to achieve
the optimal outcome for all recipients
iii) Avoid focused management strategies aimed at single organ systems
iv) Ventilation:
+ Adequate oxygenation (PaO
2
> 60 mmHg ; F
I
O
2
< 0.5 is preferred)
+ PaCO
2
~ 35-45 mmHg
v) Cardiovascular instability:
+ Common around the time of cerebral herniation (coning).
+ Hypertensive episodes should be treated with short acting agents.
+ Maintain MAP > 70 mmHg with fluid or inotropes.
+ Ensure adequate volume loading before using high doses of inotropes
+ High dose inotropic support may reduce organ viability.
vi) Aim for a urine output > 0.5ml/kg/hr
vii) Maintain normothermia:
+ Established hypothermia can be difficult to manage.
+ Prevention is preferred, using active warming devices if necessary.
viii) Check biochemistry and maintain normal electrolytes.
ix) Diabetes insipidus is a common problem and treatment should commence on
clinical suspicion and not be delayed for confirmatory results. Immediate
treatment with fluid replacement and DDAVP (1-2 g IV bd)
x) Hypernatraemia in the donor adversely affects liver transplant outcomes.
xi) Evidence for hormonal resuscitation is conflicting. Steroids and vasopressin
may be considered.
xii) Consider non-depolarising muscle relaxants if spinal reflexes persist, as these
may be disconcerting for relatives and attending carers.

7. Tissue Donation
a) Patients who die in the ICU may also become tissue donors
b) Tissues donated include
i) Corneas
ii) Heart valves
iii) Bones

216
8. Donation after Cardiac Death (DCD) (Draft protocol)

a) The National DCD protocol is still under development and local protocols may
change. (Refer to the national guidelines)
b) DCD may be an option in patient where:
i) There is a clear decision to withdraw therapy
ii) The period between withdrawal and death is likely to be short
iii) There is a desire for organ donation
c) Organ donation should not be discussed with family before discussion about
withdrawal of therapy (unless raised by the family)
d) Brain death organ donation is preferable to DCD
e) If treatment is futile and the patient is likely to progress to brain death, consider
discussion with the family about allowing this to occur.
f) Kidneys, liver and lungs may be donated
g) Patient eligibility
i) Family supportive of DCD organ donation
ii) Age < 65
iii) Adequate organ function
iv) Withdrawal of therapy is planned due to futility of ongoing treatment
v) Patient expected to die within 60 minutes of therapy withdrawal.
h) Process
i) Identify any potential DCD donor & refer to the duty ICU consultant.
ii) Discuss futility of treatment/withdrawal of therapy with the family. In certain
circumstances a 2
nd
ICU consultant may become involved to avoid any
perceived conflict of interest.
iii) Discuss the subject of organ donation with the family. The Australian Organ
Donation Register records may assist with family discussions.
iv) The Organ Donation Hospital Medical Director(s) should be involved.
v) Enlist the help of the Organ Donation Coordinator early.
vi) Withdrawal is best done as planned event in working hours and the ODC will
normally organize a team meeting of all those involved
vii) Coordination is required between ICU theatre and retrieval teams
viii) The organ retrieval teams should not be involved in patient care before death
ix) The role and validity of ante-mortem interventions, such as heparin, are still
under debate and senior advice should be sought.
x) Withdrawal may occur either in the ICU or the theatre viewing room.
xi) Certification of death needs to be done by an ICU consultant or a Senior
Registrar of more than 5 years experience. If an arterial line is present this is
the preferred method looking for absent cardiac output
xii) A following the loss of cardiac output the patient is observed for a period of
time (currently 2 minutes) to ensure auto-resuscitation does not occur
xiii) The time interval from death to the operating theatre should be minimized.
i) Other considerations
i) DCD is difficult therefore the family must be strongly supportive of organ
donation and have an understanding that progression to actual donation will
rely on time to death post withdrawal of therapy.
ii) Theatre and ICU resource issues may impact on this process
217

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1

Royal Adelaide Hospital

(chlorhexidine 4%) + gloves

(chlorhexidine 4%) + sterile gloves

radial or femoral kits (Seldinger technique).

) saline flush at 3ml/hr.

catheters are used for CVVHDF and plasmapheresis

after rapid sequence induction

Emergency Cricothyrotomy Catheter kit (cuffed)

(Enk Oxygen Flow Modulator Set)

aspirating tubes are standard for all tracheostomies.

graduated 1-step dilator:

local pressure during catheter removal:

device or endoscopically by the GI Unit)

is a recombinant form of human Activated Protein C

Vision / Harmony ventilators

high flow catheter guided as above

is the standard dialysis machine at the RAH

should be written on a standard sticker.

Hemosol B-zero solution - bicarbonate buffered, 5L bag

, still require at least 100ml/hr

Hemosol B-zero solution - bicarbonate buffered, 5L bag

Haemosol B-zero solution contains no potassium.

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