“10 FASTHUG SSS”

Intensive Care Daily

Checklist
Dr R P von Rahden

R P von Rahden
January 2014 v3.0
 ...

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 1 of 34

Introduction and Disclaimer

Critical Care is the term given to the multidisciplinary care of patients who are critically ill.

Critically Ill patients are those who have a profound physiological compromise, which is so severe
that the patients are at imminent risk of death, but which can potentially be reversed with
appropriate management.

Patients become critically ill as a result of the combined effect of several factors:
1. A severe initiating insult (trauma, surgery, major infection, haemorrhage…)
2. A dysregulated immune response
a. An excessive inappropriately generatlized innate immune response, which can
damage the body and add to the injury caused by the initiating insult
b. A suppressed adaptive immune response, which leaves patients
immunosuppressed and thus vulnerable to infection
3. The influence of comorbidities and genetic factors.

The result of these is critically ill patients develop dysfunction of multiple organ systems
simultaneously, and lose their ability to maintain basic homeostasis.

Critical Care is the discipline of multimodal physiological support. It is a discipline of detail

management. The same Critical Care mindset should apply to both the early stabilization phase
(“Emergency Medicine”) and in the later more prolonged phase of Intensive Care. In both phases
of management, Critical Care practitioners must simultaneously symptomatically support a wide
number of organ failures.

When there are so many things going wrong simultaneously, it is easy to forget something.
And in Critical Care medicine, this can be lethal. Even if we have done a brilliant job of managing a
patients’ airway and circulation, if the patient dies anyway due to a complication of an electrolyte
disorder that we have forgotten to treat, all the effort is wasted.

In an attempt to reduce the chances of forgetting something vital, I have created a mnemonic-
based checklist which I try to use after seeing each patient on the daily ICU round. The mnemonic
that I have developed is an extension of Prof Jean-Louis Vincent’s groundbreaking “FASTHUG”
checklist. The intention of this checklist is to be exactly that: a list for me to check that I haven’t
forgotten something in the overall patient plan.

This checklist is NOT in order of priority, and so should not be used to guide initial stabilization (I
am developing another mnemonic for this purpose). It is therefore intended primarily for use in the
Intensive Care Unit, rather than in the Emergency Department. Nor is this checklist intended to
guide HOW a patient is assessed, or to act as a framework for clinical presentation at wardrounds.
It is only intended to be a tool to increase safety by reducing the chances of errors of omission,
and its use is not obligatory.

In the pages that follow, I describe the mnemonic, and, in order to make the document reasonably
self-contained, have included some suggestions for management of common items. These
“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 2 of 34
suggestions are brief, and fuller guidelines and protocols should be consulted where these are
available. I have attempted to make the suggestions for management as consistent with
international literature as possible, with modifications for some South African realities (such as
local drug availability), but in some areas where controversy still reigns I have advocated
management plans that reflect my own beliefs and practices. These guidelines have not been
peer-reviewed, and thus are printed without Departmental affiliation.

These suggestions are also focused on adult patients (though the majority of the broad concepts
discussed would apply to paediatrics as well, there are some differences).

I have attempted to ensure that any drug dosages given are correct, but errors do occur, and I
cannot take responsibility for these. It is the duty of the prescriber of any drug to check that the
prescribed doses are correct and compatible with the package insert or SAMF or published
guidelines.

These suggestions for management apply to the general supportive care of MOST critically ill
patients, irrespective of what the initiating event was, but the specific management of the initiating
event must generally take precedence over the “general management” suggestions contained
here.

Finally, directed instruction from the Consultant at the bedside of the specific patient must always
take precedence over any “general” guideline like this.

Please bring errors or suggestions for improvement to my attention.

Richard von Rahden

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 3 of 34

A Mnemonic-Based Checklist of Daily Decisions Required in Adult Critically Ill Patients.

“10 FASTHUGSSS”

A = Airway
B = Breathing & respiratory function
C = Circulation
D = DO2 assessment
E = Electrolytes
F = Fluid
G = Glomerular Filtration Rate & renal function
H = Haemoglobin
I = INFECTIONS?
J = imiJovo / inJections / adJuncts

F = Feed
A = Analgesia
S = Sedation & delirium management
T = Thrombosis management
H = Head up & positioning
U = Ulcer prophylaxis
G = Glucose control
S = Steroids
S = Statins
S = Seizures

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 4 of 34

ABCDEFGHIJ FASTHUGSSS

A : Airway

 Adequate? Fix urgently if not!

o Is enough air moving freely to lungs?
 Self-maintained by patient?
o Yes : is it stable? Is patient at risk of losing their airway?
 Changes in consciousness
 Anatomical changes eg facial injuries, local sepsis, inhalational burns
o No : airway device required!
 Guedel airway : short-term : tolerance implies need for definitive airway
 Difficult intubation expected / inexperienced intubator : Supraglottic Airway OK
 Endotracheal tube is the gold standard, followed in some by tracheostomy
 Intubation
o  Drug Assisted Intubation : Anaesthetic Induction Agent + Muscle Relaxant
o Induction Agents:
 Ketamine 2mg / kg ivi default (2 minute onset)
 Etomidate 0.1 – 0.3mg / kg ivi if haemodynamically unstable (1 minute onset)
 Propofol ONLY if skilled doctor, and ONLY in VERY stable patients
o Muscle Relaxants:
 Succinylcholine (=suxamethonium)
 Default due to 1 minute onset and 5-minute offset
 Contraindicated if K+ > 5.0mmol/l, burns >24 hours old, paraplegia,
hemiplegia, severe chronic abdominal sepsis…
 Rocuronium 1 – 1.5mg/kg
 1 minute onset, but up to 1 hour duration; caution in renal failure
 Cisatracurium 0.15mg/kg or vecuronium 0.1mg/kg also okay
 3 minute onset, 30 minute duration
 Endotracheal tube
o Position of end of tube?
 On CXR : 1 Vertebral Body Height above carina
o Pressure ?
 Cuff pressure < 25cmH2O
o Problems ?
 leaks, occlusions, inspissated secretions…
o Perpetuate ?
 ongoing need?
 replace with tracheostomy?
 Tracheostomy
o Consider if :
 Expected long endotracheal intubation (> 7 days)
 Head injury with poor recovery potential
 Weak patients with poor secretion clearance
 Anatomical upper airway abnormalities
o Placement
 Percutaneous tracheostomy is default choice
 Contraindicated if : poor anatomy, coagulopathy (INR > 1.5, Platelets < 75, or
renal failure-induced thrombocytopathy), poor oxygenation with likely poor
tolerance of ZEEP – these patients need operative tracheostomy
“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 5 of 34
  Percutaneous tracheostomy must always be done as a full sterile procedure,
full draping, 2 doctors (1 for procedure, 1 for airway), on fully anaesthetized
and neuromuscularly blocked patients.
o Placed
 Position ?
 in trachea
 Pressure ?
 Problems ?
 Perpetuate ?

 Consider extubation / extracheation only if all “ROMSHA” points of the Extubation Feasibility
Review below are passed :
o Reason?
 Has the original reason for intubation and ventilation been resolved?
 (most relevant for patients intubated for relief of work of breathing due to
metabolic acidosis)
o Oxygenation adequate?
 Oxygenation Index should be <5 (preferably less than 4.5) unless there is a
STRONG history of chronic lung disease AND a consultant decision is made that as
a result further improvement in OI is unlikely.
o Mechanics adequate? – All of the below
 Respiratory rate ≥ 10
 Respiratory rate ≤ 25
 Tidal volume ≥ 6ml / kg (preferably much larger) on (Inspired Pressure Above PEEP)
≤ 6 cmH2O
 Regular breathing
 No evident use of accessory muscles, no nasal flaring
 If in doubt a T-piece test of no more than 30 minutes can be done.
o Secretions manageable by patient without assistance?
 Minimal secretions
 Moderate THIN secretions in patient with a GOOD cough
 Ask the advice of senior nursing staff as to whether they think patient will cope.
o Heart failure unlikely? (or is optimally managed)
 (positive pressure ventilation aids the failing left ventricle; withdrawal can lead to
acute left heart failure with pulmonary oedema and hence extubation failure)
 If in doubt a T-piece test of no more than 30 minutes can be done.
o Airway capable of being maintained by patient?
 Alert, patient follows commands
 No anatomical airway abnormality that is being “splinted” by the endotracheal tube.
 Post extubation : nebulized adrenaline (1mg (1ml of 1:1000) plus 2ml Normal Saline) may be given
if there is a concern regarding airway oedema, but is of no proven benefit.

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 6 of 34

ABCDEFGHIJ FASTHUGSSS

B: Breathing & respiratory function

 General goals :
o SpO2 ≥ 90% : avoid hypoxaemia
 Accept lower SpO2 only in patients with known chronic hypoxaemic lung disease and
known reasonable function with SpO2 < 90%.
o Avoid hyperoxia
 Reduce FiO2 if SpO2 > 95% (down to FiO2 0.21 if necessary)
o No excessive work of breathing
 Breath Rate << 30 breaths per minute
 No excessive muscle usage : patient appears to be breathing comfortably
o Appropriate respiratory excursions
 Reasonably-sized clinical chest movement and appropriate tidal volumes, at a
regular rate
o Relatively normal PaCO2
 PaCO2 up to 8kPa routinely acceptable in patients with severe lung injury undergoing
lung-protective ventilation if no raised intracranial pressure or known severe
pulmonary hypertension
 PaCO2 4.8 – 5.2 kPa for patients with raised Intracranial Pressure (eg head injury
with diminished GCS)
 Administer oxygen via face mask or nasal cannula
o Use lowest FiO2 that gives SpO2 90-95%
o Use of High Flow Humidified Oxygen (“Optiflow”) via proprietary nasal cannulae may
improve oxygenation, reduce upper airway obstruction, assist some patients with borderline
respiratory muscle strength, and allows titration of FiO2 , and allows humidification which
reduces upper airway damage.
o The need to use FiO2 > 80% (eg reservoir face mask with one-way valves) to achieve SpO2
> 90% generally implies need for positive pressure ventilation (IPPV)
 (possible exception : Pneumocystis jirovecii pneumonia, chronic bronchitis)
 Positive pressure ventilation best given invasively (via endotracheal tube) to almost all patients
o Primary use of non-invasive ventilation (via face mask) is only recommended for patients
with isolated acute left ventricular failure and for those with exacerbations of COPD.
o Non-invasive ventilation via facemask is most appropriately used as a planned step to
facilitate earlier extubation.
 Review frequently which initial pattern(s) of respiratory failure led to initiation of respiratory support
(have they resolved?) and which current pattern(s) of respiratory failure apply now:
o No respiratory disease : intubated for airway protection only
o Reduced breathing movement (Type II respiratory failure – hypoxaemia and hypercarbia) eg
drug overdose, head injury
o Excessive breathing movement and hence need for IPPV to relieve work of breathing eg
patients with severe metabolic acidosis, especially lactic acidosis
o Bronchospasm / intrapulmonary airway obstruction with inability to move air
o Alveolar lung disease (shunt / dead space)
 Review current ventilatory strategy  What is the currently-appropriate ventilatory strategy?
o Routine lung protective?
 (normal lungs or mild alveolar lung disease)
o Open lung: lung protective + recruitment ?
 (severe alveolar lung disease with prominent atelectasis)
“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 7 of 34
 o Neuroprotective?
 (PaCO2 control)
o Bronchospasm?
 Initial ventilator settings : Lung Protective Strategy : DEFAULT FOR MOST PATIENTS
o Mode : Pressure Assist-Control
 (most efficient alveolar air delivery, most physiological waveform, allowing easiest
transition to spontaneous breathing)
o Preset : FiO2 100%, PEEP 10, Rate 15 br/min, Inspiratory Time 1.2s, Flow Trigger 1 L/min
o Initially adjust : Inspiratory Pressure Above PEEP to achieve Expired Tidal Volume of 6ml /
kg of Predicted Mass for Height (with maximum allowance of 50ml extra if catheter mount or
filter used)
o Review every 10 minutes for the first hour, and hourly thereafter
 SpO2 90 – 95% (adjust FiO2)
 VTe 6ml / kg PMfH for mandatory (non-patient triggered breaths) : adjust IPAP
appropriately
o Encourage transition to patient-triggered breaths (and ultimately to Pressure Support mode)
 Initial ventilator settings: Open Lung Strategy (usually for ARDS)
o As for Lung Protective, but preceded by a Recruitment Manoeuvre as directed by a
consultant.
o Occasionally Volume Assist-Control mode may be preferred by the consultant
o Avoid disconnections – arrange for inline suction
o May require ongoing neuromuscular blockade to avoid patient effort and thus reduce
transpulmonary pressure – follow consultant direction
 Initial ventilator settings : Neuroprotective Strategy
o As for Lung Protective except preset Rate 20 br/min, Inspiratory Time 1.0s
o PEEP 10 cmH2O has not been shown to raise ICP, and thus is still an acceptable baseline.
o After 30 minutes : check PaCO2 : desirable range 4.8 – 5.2 kPa
 If PaCO2 < 4.8 kPa : reduce Rate
 If PaCO2 > 5.2 kPa : increase IPAP to increase VTe to 7 to 8 ml/kg PMfH
 Neuroprotection takes priority over lung protection and avoidance of
volutrauma
 Initial ventilator settings : Bronchospasm Strategy
o Mode : Volume (Assist)-Control
o Preset : FiO2 100%, PEEP ZERO, Rate 10 breaths / minute, Inspiratory Time 1.0s (for Avea,
via adjusting flow rate), Flow Trigger 2 L/min
o Adjust set tidal volume to 6ml/kg PMfH
o Set High Pressure Alarm to 50cmH2O
o Ventilate to get chest rise; consider occasional disconnection to relieve gas-trapping
o Wean FiO2 as for Lung-Protective
o Adjust Breath Rate and Inspiratory Time to get full exhalation (return to baseline before next
inhalation) on Flow-Time curve.
o Use of set extrinsic PEEP more than Zero should only be done at Consultant direction after
measurement of Intrinsic PEEP : PEEPe must be kept below PEEPi, and gas trapping must
be looked for.
o DO NOT ALLOW SPONTANEOUS RESPIRATION: DEEPLY SEDATE, CONSIDER NDMR
UNTIL DEEP SEDATION ESTABLISHED.
 Review indicators of ventilation efficiency
o Can the patient be progressively weaned from the ventilator?
 For most patients on the default Lung Protective Strategy, it is appropriate to
encourage spontaneous breath initiation early (decrease the set rate on the Assist-
Control mode so that the patient sets the rate) and then move them to Pressure
“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 8 of 34
 Support mode (where the patient controls their own inspiratory time) as soon as it is
obvious that the patient has a reasonable respiratory pattern; a progressive reduction
in Pressure Support is then done until the patient is receiving minimal Pressure
Support (6cm H2O or below) to maintain a VTe of 6ml/kg PMfH; PEEP is weaned last
(usually kept ≥ 8cmH2O).
 For patients on Open Lung, Neuroprotective or Bronchospasm strategies active
weaning should only occur with Consultant direction, as ongoing Control of
ventilation may be more appropriate in these pathologies
o Review patient synchrony – does the patient look comfortable on the ventilator?
 High breath rates (>25) – consider re-escalating ventilator support (increase
Pressure Support, or return to Pressure Assist-Control mode)
 Tachypnoeic patients on Pressure Support may shorten their Inspiratory Time
inappropriately (<0.75s) and should be returned to Pressure Assist-Control
mode until respiratory drive is more appropriate.
 Excessively high breath rates are wasteful of patient energy and may
precipitate cardiac failure : consider pharmacological control (eg morphine) if
ventilator adjustment does not improve tachypnoea relatively quickly.
 Trigger synchrony : machine gives breaths appropriately when patient makes an
effort – ensure Pressure or Flow Trigger is kept low and thus most sensitive (-
2cmH2O or 1L/min respectively); elevation of threshold should only be done if “auto-
triggering” suspected
 Cycle synchrony : only relevant on Pressure Support mode : ventilator should allow
patient to exhale when patient has finished inspiring : if inappropriate exhalation,
review Flow Cycle Percentage with consultant or consider return to Pressure Assist-
Control
o Oxygenation Index
 OI = (Pmean * FiO2%) / (PaO2 * 7.5) : Pmean in cmH2O or mbar, PaO2 in kPa
 OI > 10 : not readily weanable – improve alveolar lung disease first
 OI 5 – 10 : not ready for extubation, but oxygenation stable enough to allow some
“forced weaning”
 OI < 5 : oxygenation good enough to consider removal from positive pressure
ventilation, but do full Extubation Feasibility Review (see under “Airway” above)
o Rapid Shallow Breathing Index (only useful if on Pressure Support, ΔP < 10cmH2O)
 RSBI = Respiratory Rate / VTe in LITRES
 RSBI > 100 : mechanically inefficient, likely to fail removal from positive pressure
ventilation
 RSBI < 80 : mechanically probably efficient enough to cope with removal from
positive pressure ventilation.

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 9 of 34

ABCDEFGHIJ FASTHUGSSS

C : Circulation

 Correct shock urgently! Correct inadequate Cardiac Output and Mean Arterial Pressure
o Shock = inadequate oxygen delivery to organs relative their need resulting in organ damage
 DO2 to the entire body = Cardiac Output * Oxygen Content of blood
 Need adequate cardiac output to get blood flow to organs :
 Cardiac Index of >2L/min/m2 is recommended
o (CI = body surface area-standardized Cardiac Output)
 Organs such as brain and kidneys need blood at reasonable pressure
 Usual target Mean Arterial Pressure is 65mmHg
 If intra-compartment pressure elevated, elevate target MAP to achieve
Perfusion Pressure of 50-60mmHg
o MAPtarget = IntraCompartment Pressure + Perfusion Pressure
o Eg : head injury with ICP assumed to be 15-20 mmHg, and Cerebral
Perfusion Pressure of 60mmHg desired: MAP target = 75-80mmHg
 Identify MECHANISMS of shock : several typically exist in ICU patients with sepsis or after
injury/surgery
 Try to define in your mind which of these mechanisms currently exist, and tailor the
package of cardiovascular resuscitation to try to address these mechanisms in the
most balanced way possible
o Fluid deficit? Is there an absolute intravascular fluid deficit due to loss of fluid from the
vessels?
 “Hypovolaemic shock”
 Will require rapid fluid administration to replenish intravascular volume
o Pump failure? Is there inadequate cardiac function due to myocardial damage or due to
circulating inflammation-induced myocardial depressant factors?
 “Cardiogenic shock “
 May require reduction of excessive afterload or preload
 May require an INOTROPE
o Pipes failure? Is there abnormal arteriodilation and/or venodilation due to altered
sympathetic tone or due to inflammation-induced vasodilator substances?
 “Distributive shock”
 Maldistribution of blood into abnormally dilated venous beds leads to a
relative intravascular fluid deficit
 Appropriate therapy may be a VASOPRESSOR to limit pooling of blood in venous
system (venoconstriction),
 A VASOPRESSOR may also be necessary to achieve appropriate arterioconstriction
to ensure Mean Arterial Pressure is adequate for pressure-sensitive organs such as
the brain and kidneys (MAP = Cardiac Output * Systemic Vascular Resistance), but
excess arterioconstriction must be avoided as this will lead to excess cardiac
afterload which may significantly reduce Cardiac Output… use a cardiac output
monitor to guide this balance.
o Obstruction to blood flow?
 “Obstructive shock”
 From within vessels : pulmonary thromboembolism…
 Elevate cardiac output and blood pressure multimodally in an attempt to get
flow past the obstruction, anticoagulate, investigate options to lyse clot

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 10 of 34

 From outside of vessels : cardiac tamponade, tension pneumothorax, overdistension
of lungs (eg in bronchospasm)…
 Relieve the obstruction urgently using appropriate technique
 STRONGLY CONSIDER CARDIAC OUTPUT MONITORING IF ≥2 MECHANISMS ARE THOUGHT
TO CO-EXIST
 Define the interim goals for this shift:
o MAP target range
 Default 65-70mmHg
 Neuroprotection (with likelihood of raised ICP) 75-80mmHg
 Higher target range due to possible previous hypertension?
 Lower target range ?
 Ischaemic heart disease
 Uncontrolled bleeder
o Systolic Pressure Upper Limit
 For patients with hypertensive disorders : define the systolic pressure above which
blood pressure reduction will be instituted (160mmHg? 180mmHg) - relate this to
recent levels of blood pressure (avoid an excessive drop to avoid organ
hypoperfusion) and to cardiac reserve (high blood pressures increase cardiac
workload enormously)
o Cardiac Index : REQUIRES CARDIAC OUTPUT MONITOR
 Usually > 2.5 L/min/m2
 Lower (2 L/min/m2) can be accepted in patients recovering from myocardial
ischaemia if organ flow appears adequate (see “D”)
 Note: Patients with predominantly distributive shock may have significantly higher CI
(hyperdynamic circulation) as an adaptive response, but despite this may still have
poor myocardial efficiency, will be dependent on a high heart rate and moderate
ventricular dilation, may cope poorly with increases in afterload, and may thus still
need inotropic support as part of their resuscitative package
o Are there constraints, or need to accept compromises? Ensure that the entire team is aware
of these
 Reason to minimize fluid administration? (eg lung pathology, gut oedema, anuric
intrinsic renal failure)
 Will a degree of ongoing intravascular volume depletion be accepted to avoid
“overspill” damage to other organs?
 Reason to minimize vasopressor-inotropes (eg active ischaemic heart disease)
 Always review patients for signs of intravascular volume deficit even if MAP goals are being met
o Identified by:
 Prominent arterial pulse pressure ventilation (> 12%) on ventilated patient
 (for sign to be valid, patient must be on Controlled ventilation, no
spontaneous patient effort, Inspired Pressure Above PEEP 10-20cmH2O, VTe
≥ 7ml/kg/breath)
 Stroke Volume Variation > 15% on ventilated patient (same constraints as above)
 CVP << 5cmH2O
 Increase in MAP by more than 15%, or increase in CI or SVI of > 10% with straight
leg raise
 Increase in CI or SVI > 10% with 3ml/kg bolus of intravenous fluids
 Collapsing inferior vena cava on ultrasound examination
o Supportively suggested by
 tachycardia
 concentrated urine
 signs of tissue dehydration
“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 11 of 34
  dry mucosae
 shrunken tongue
o Consider whether identified intravascular volume deficit is
 ABSOLUTE
 Fluid has been lost from the circulation
 RELATIVE
 Vessel capacity has increased due to distributive shock mechanism
 Both will require some fluid administration, but one might expect to resolve absolute
hypovolaemia exclusively by fluid administration, whereas with relative hypovolaemia
a vasopressor will be required to limit the excessive vascular capacity and avoid the
need to administer litres of fluid.
o Manage by RAPIDLY-INFUSED intravenous fluid boluses, 3ml/kg per bolus
 evaluate magnitude of improvement after each bolus and decide on further boluses
 type of fluid for boluses (isotonic crystalloid, colloid, blood product) must be decided
together with consultant, considering electrolyte needs, likelihood of endothelial-
glycocalyx damage causing “leaky capillaries”, and specific toxicities of each fluid.
 Decide on pharmacological support appropriate for mechanisms of shock identified above
o Pure cardiac failure with no likely vasodilation
 dobutamine : range 5 – 25 mcg/kg/min, start at 5-10mcg/kg/min, titrate q10min
o Pure vasoplegia – rare, but may occur with epidural infusions and spinal cord injury
 phenylephrine titration range : 0.5 – 5 mcg/kg/min, start at 0.5mcg/kg/min, titrate
q7.5min
 USE OF A CARDIAC OUTPUT MONITOR STRONGLY ADVISED IF DOSE
EXCEEDS 1.5 mcg / kg / min
o Mixed vasoplegia & cardiac dysfunction ...
 Adrenaline titration : typical range 0.05 – 1 mcg/kg/min, start at 0.1mcg/kg/min,
titrate q5min, dose above 1mcg/kg/min usually futile except in young very fit patients
with increased receptor density
 = “fixed combination” vasopressor-inotrope, vasopressor effects dominate at
higher doses, can cause excessive tachycardia, usually adequate as
monotherapy, for most patients MAP monitoring alone is adequate
 Can combine with dobutamine if greater inotropy needed, or with
phenylephrine if greater vasoconstriction with no further inotropy needed, but
o Always use cardiac output monitor to gauge effect of combinations
o NO POINT adding dobutamine or phenylephrine if on adrenaline >
0.8mcg/kg/min (no adrenoreceptors available)
 Only non-adrenoceptor-stimulating vasopressor available in Pietermaritzburg
is ornipressin : off-label use, only to be done with senior consultant input
o AGGRESSIVELY TITRATE TO ACHIEVE THE TARGET RANGES DECIDED ABOVE.
 Reduce doses if dose range is exceeded!
o RE-EVALUATE INTRAVASCULAR VOLUME STATUS AND REVIEW NEED FOR FLUIDS
REGULARLY.
 Ensure that all team members are aware of haemodynamic goals and strategies to be followed.

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 12 of 34

ABCDEFGHIJ FASTHUGSSS

D : Delivery of Oxygen adequate?

 DO2 = Cardiac Output * Oxygen Content of Blood

o = (Heart Rate * Stroke Volume) * (1.34 * Hb * SaO2 + dissolved oxygen)
o Inadequate DO2 may result from global low cardiac output, inadequate perfusion pressure to
pressure-sensitive organs, inadequate Hb, inadequate SaO2
 Simply meeting the default target ranges for A,B,C may be inadequate in certain patients
o Ask: “Is enough oxygen actually reaching the tissues in this patient at the moment?”
 This is a quality-control evaluation step.
 Evaluate markers of successful tissue perfusion
o Brain : level of consciousness improving
o Kidneys : urine output present and improving
 NB: not independently reliable, especially if renal injury has already occurred
o Peripheral tissues warm, short capillary refill time
o Tissues:
 Lactate level :
 assume Type A acidosis unless good reason (metformin, ARVs, known dead
tissue present) to suspect Type B
 with adequate resuscitation should progressively decline, ideally to < 2mmol/L
 Do repeated arterial lactates q4 hr during early resuscitation period
 May show initial rise in 1st 4hours of successful resuscitation (toxin washout
during reperfusion)
 Failure to decline after > 8-12 hours despite best possible resuscitation may
imply organ failure / mitochondrial death, and in absence of identifiable local
ischaemic tissue (eg mesenteric ischaemia) may imply mortality inevitable.
 SSVCO2 – only valid in first 6 hours ( before mitochondrial death likely)
 Improvement from low levels to 70% - 75% suggests adequate perfusion of
tissues
 Levels above 80% suggest mitochondrial dysfunction
 SmixedvenousO2 always more reliable if available (less sampling error)
 Metabolic acidosis progressively resolving
 Initial rise possible as per lactate discussion above
 Be aware of non-hypoperfusion causes of metabolic acidosis that confound
assessment
o Common: hyperchloraemia, azotaemia
 Failure to improve tissue perfusion markers initially mandates more aggressive
resuscitation, re-evaluation of assessment of shock mechanisms, re-evaluation of target
ranges
 Failure of tissue perfusion markers to improve after 12 hours of best-possible resuscitation warrants
consultant decision on utility of ongoing resuscitation.

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 13 of 34

ABCDEFGHIJ FASTHUGSSS

E: Electrolyte abnormalities

 Identify immediately life-threatening electrolyte abnormalities

o Consider causes and ongoing causative factors needing management
o Replace potentially significant deficits of critical ions
 K+ < 3.5mmol/l ... arrhythmia risk
2+
 Mg < 0.8mmol/l ... arrhythmia risk
3-
 PO4 < 0.7mmol/l ... re-feeding syndrome risk
 Na+ < 125mmol/l ... cerebral dysfunction risk
2+
 Ca (ionized) < 0.8mmol / l ... hypotension risk
o Manage potentially significant elevations of critical ions
 K+ > 5.5mmol /l WITH ECG CHANGES
 Na+ > 160mmol/l
 Cl- > 130mmol/l
 PO43- > 2.5mmol/l
 Mg2+ > 4.0mmol/L
 Consider fluid-conservative methods of intravenous replacement for deficits
o Pure K+ replacement :
 80 meq (40ml) 15% KCl in total volume of 200ml (mix with 160ml of either 0.9% NaCl
or D5W) over 4 hours (50ml/hr) : ONLY THROUGH CENTRAL LINE VIA INFUSION
PUMP
 Maximum rate of replacement = 20meq K+ per hour
o Pure Mg2+ replacement :
 4g MgSO4 in 50ml total volume (mix with 42ml 0.9%NaCL or D5W in buretrol) over
15 minutes
o K+ & Mg2+ replacement
 80 meq (40ml) 15% KCl , plus 4g MgSO4 , in total volume of 200ml (mix with 152ml
of either 0.9% NaCl or D5W) over 4 hours (50ml/hr) : ONLY THROUGH CENTRAL
LINE VIA INFUSION PUMP
o Pure PO43+ replacement
 40 meq (20ml) KPO4 in total volume of 200ml (mix with 180ml of either 0.9% NaCl or
D5W) over 4 hours (50ml/hr) : ONLY THROUGH CENTRAL LINE VIA INFUSION
PUMP
 Never give more than 10meq KPO4 per hour – risk of hypocalcaemia
o K+ & PO43- replacement
 40 meq (20ml) KPO4 , plus 40 meq (20ml) 15% KCl, in total volume of 200ml (mix
with 160ml of either 0.9% NaCl or D5W) over 4 hours (50ml/hr) : ONLY THROUGH
CENTRAL LINE VIA INFUSION PUMP
 Infusion rate limitations of both K+ and PO43- apply
o DO NOT MIX MgSO4 with KPO4 in the same bag.
o Non-emergent Ca2+ replacement for low ionized calcium without emergent symptoms
 10ml 10% Calcium gluconate in 50ml total volume (mix with 40ml 0.9% NaCl or D5W
in buretrol) over 10 minutes, re-evaluate ionized Ca2+ 10 minutes after infusion
stopped, watch for arrhythmias during infusion.
o Hyponatraemia is defined as Na+ < 135mmol/L, but urgent specific correction is only
required for Na+ < 120mmol/L with neurological symptoms

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 14 of 34

 
correct at no more than 1mmol/L/hr to 120mmol/L, using 0.9%NaCl if patient is
intravascularly volume depleted and hypertonic saline if patient is intravascularly
replete or overloaded – consult specific guidelines for dosage calculation
 Hypernatraemia
o How severe is it?
 Probably only requires active management when >155mmol/L
o Decide on patient’s fluid volume status as this will influence choice of corrective
management
 Fluid overload plus hypernatraemia suggests total body sodium overload (eg
iatrogenic administration)
 Fluid underload plus hypernatraemia suggests dehydration and hence concentration
of sodium
 Hyperkalaemia
o Define factors influencing urgency of treatment
 Acute (less than 2 days), or chronic?
 Associated with ECG changes?
 Acute hyperkalaemia with ECG changes warrants urgent therapy
o Define likely cause
 Increased intake? (often iatrogenic)
 Decreased elimination from body (renal failure commonly)
 Normal total body potassium but intracellular  extracellular shift (eg acute acidosis)
o Decide on most appropriate management(s) required
 Elimination of excess K+ from the body
 Dialysis [fast] / Diuresis / “Kexalate” [slow]
 Shifting K+ extracellularly  intracellularly
 Dextrose + Insulin
 Beta2 agonists
o Inhaled
o Intravenous
 Antagonizing K+ effect on myocardium
 Broad QRS : controlled Calcium gluconate infusion
 Hyperkalaemic cardiac arrest : CaCl2 1000mg IVI stat
 Hyperchloraemia
o Often iatrogenic, may contribute to metabolic acidosis.

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 15 of 34

ABCDEFGHIJ FASTHUGSSS

F : Fluids

 Consider appropriate post-resuscitation fluid strategy…

 Excessive fluids may be as lethal as inadequate fluids (just on a longer timescale)
 Is the patient haemodynamically unstable?
o Ensure that intravascular volume deficit is identified and corrected aggressively as
described in “Circulation” above!
 Diabetic Emergency?
o  manage according to diabetic emergencies protocols
 Once stabilized, plan the magnitude of ongoing fluid infusion based on:
o Maintenance requirements
 Fluids
 Electrolytes and nutrition
o The overall Phase of the Fluid Requirement Profile that the patient is currently in
 “Resuscitation”
 Still unstable, with chance of ongoing absolute / relative intravascular
hypovolaemia, or need for active fluid replacement
o Expect need to augment Total Body Water
o A positive fluid balance is expected
 “Plateau”
 Inflammatory response has settled, and no more additional fluids appear
needed; fluid administration should match baseline maintenance
o Keep Total Body Water at current level
o A daily neutral fluid balance is desired
 “De-resuscitation”
 Patient is recuperating, but Total Body Water is greater-than-healthy-baseline
and needs to be eliminated from the body to return patient to pre-illness levels
o A daily negative fluid balance is desired.
 For those patients in the “Resuscitation phase”:
o Is there a need to rehydrate dehydrated tissues?
o Are there quantifiable ongoing losses?
 Blood losses?
 Plasma losses (eg open abdomen suction, open wounds seeping into dressings)
 Abnormal nasogastric losses
 Other abnormal GIT losses
 Inappropriate urine losses (eg polyuric renal failure with tubule dysfunction)
o Are there unquantifiable ongoing losses?
 “Capillary leak” (endothelial and glycocalyx malfunction) seen in inflammatory stares
with sequestration into tissues
o What mechanisms are in place to detect having “fallen behind” and hence the need to
administer bolus fluids to replenish depleted intravascular volume? Conversely, what
mechanisms are in place to detect that fluid overload is occurring?
 Especially important in the setting of unquantifiable ongoing losses when estimations
have to be made!
 Remember that in inflammatory states a “best balance” of vasopressors and fluids is
required. How do we identify this balance in this patient?
 For those in the “Plateau” phase
o What markers can we use to remain confident that we are still in this phase?
“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 16 of 34
 o What are the limits of allowable positivity or negativity of fluid balance before active
management is required?
o What to do if fluid administered in order to meet nutritional goals exceeds the overall target
fluid limit?
 For those patients in the “De-resuscitation” phase
o Are they spontaneously de-resuscitating?
o Is there a need for assisted de-resuscitation?
 Tissue oedema? Lung compliance issues? Oxygenation issues? Gut oedema? …
o If assisted de-resuscitation is required, what is the best route?
 Dialysis?
 Diuresis?
 Furosemide boluses?
o Regular?
o P.R.N?
 Furosemide infusion?
 Furosemide infusion + acetazolamide to control contraction alkalosis
o What is the desired practically achievable negative fluid balance?
 Is it being achieved? Does the de-resuscitation plan have to be augmented?

 Default baseline fluid volume for adults = 1ml / kg (actual mass) / hour
o This should include all medications, infusions, feeds etc
 Remember to make allowance for bolus medications
 Eg 200ml of antibiotics given 8 hourly should be regarded as 25ml/hr
o Only if the total volume of medications + infusions + feeds summates to less than 1ml/kg/hr
should the fluids below be administered to “make up the difference”
o [For children <40kg use 2/3 of the fluid predicted by the “4-2-1 rule”]

 Default choice of intravenous fluids post-admission: various forms of crystalloid

o Colloid fluids of whatever type should only be used for bolus replacement of acute identified
intravascular volume deficit, and should NEVER be given by infusion; their specific toxicities
should be actively considered and clear risk-benefit assessments made prior to their
infusion.
o Resuscitation phase while haemodynamically unstable (still needing fluid boluses or
vasopressor-inotropes)
 Head Injury Moderate / Severe
 Normal Saline (0.9% NaCl)
 No head injury
 Ringer’s Lactate / equivalent
o Resuscitation phase, no longer haemodynamically unstable, but requiring to replace
abnormal losses or rehydrate tissues
 Head Injury Moderate / Severe
 Normal Saline (0.9% NaCl) UNLESS Na+ >145mmol/L or Cl- > 115 mmol/L
 Plasma-like losses
 Ringer’s Lactate / equivalent
 Rehydration of tissues / polyuria losses / some NG losses
 0.45% NaCl BUT CHECK U&E FREQUENTLY AND ADAPT
o Plateau Phase, in non-Head Injury, either
 0.45% NaCl + 5% Dextrose (“Rehydration Solution”)
 NB: has no K+
 5% Maintelyte

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 17 of 34

  NOT if plasma [Na+] < 125 mmol / l or [K+] > 5.0 mmol/l
 NB : Do not exceed 1.5ml/kg/hr with these fluids
 If more than this is needed, they aren’t in Plateau phase!
 Giving more than 1.5ml/kg/hr of these fluids which contain 5% dextrose
may result in uncontrolled hyperglycaemia.
 NB : while raised Intracranial Pressure may exist, do not routinely use hypotonic
fluids – discuss in detail with Consultant with joint reference to U&E
o NB: This “initial default” choice must frequently be re-evaluated and adjusted after
consideration of:
 Trends in U&E
 Clinical evaluation
 Reduce baseline fluid volume reciprocally as feed volume increases regardless of Phase of Fluid
o By the time the patient is in the De-Resuscitation phase, the only fluids the patient should be
requiring are those for nutrition and the volumes of fluid used to dissolve drugs.
 Elevated (above 1ml/kg/hr) baseline infusion of crystalloid is a convenient way to deal with tissue
rehydration or with ongoing losses
o especially post-colloid resuscitation
o Set formal target for total fluids in terms of ml/kg/hour (eg 1.5 / 2 / 3 ml/kg/hr) according to
clinical judgement
 As above, subtract volumes of fluid given as medication, infusions, and feeds, and
administer appropriate colloid as described above to “make up the difference”
 Do not use glucose-containing fluids for elevated rate infusions.
o Review elevated baseline fluid infusion order at least every 4 hours to avoid overload
 When replacing quantifiable ongoing losses, remember that loss rates can change
o It is generally safer to “aim low” when setting replacement fluid rates (eg give replacement
fluid at 2/3 the loss rate), and accept the need to give occasional “top-up boluses”
o Regular review of replacement rates (4-hourly) is advised.
 When large volumes of fluid are being infused, be aware of haematological effects:
o Is dilutional anaemia developing?
o Is dilutional coagulopathy a possibility?
o In some cases of abnormal fluid losses due to impaired endothelial-glycocalyx function and
hence sequestration of fluid from the intravascular space into the tissues, could the infusion
of “non-leakable” packed red blood cells be justifiable?

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 18 of 34

ABCDEFGHIJ FASTHUGS

G : Glomerular Filtration Rate & renal function

 Acute Kidney Injury (AKI) should be avoided!

o Established renal failure increases mortality significantly
 Actively look for and manage usual causes of pre-renal dysfunction as per Circulation and Fluids
above
o Inadequate hydration
 look for evidence of fluid depletion
 aggressively correct fluid depletion and evaluate Fluids as above
o Inadequate perfusion pressure
 Ensure Mean Arterial Pressure ≥ 65mmHg
 Consider higher MAP in previously hypertensive patients
 Eliminate / control use of nephrotoxins
o Aminoglycosides, Non-Steroidal Anti-Inflammatories, Intravenous Contrast media...
 Assess urea, creatinine, PO43- : NB ... changes are late
o Cockroft-Gault and MDRD formula unreliable in acute situation
o If available, consider NGAL as a marker of renal tubular injury
 Score according to RIFLE or KDIGO
o RIFLE R, I / KDIGO 1,2
 address pre-renal issues and nephrotoxins aggressively
 Consider likely scenarios that will likely result in renal injury even before biochemical
changes are obvious and manage as for renal injury
 eg septic shock from Gram negative infection / inflammatory shock state with
hypotension
o RIFLE-F / KDIGO 3
 Change strategy from that for RIFLE I,R / KDIGO 1,2
 ensure no ongoing pre-renal deficits still exist, but stop any attempts at supra-
normalization!
 restrict fluids to match actual output
 Plan for Renal Replacement Therapy
 Peritoneal dialysis ... default option if intact abdomen
 IHD ... Grey’s Nephrology investigations, liaise with nephrology
 CVVH
 While awaiting RRT, manage complications:
 Hyperkalaemia: Kexalate, Insulin-Dextrose, Salbutamol
 Oliguria : Furosemide to prevent fluid overload
o usually requires large boluses
o abandon Furosemide if kidneys unresponsive to 1 + 2 + 4 mg/kg
challenges
o Urine output with Furosemide ≠ good kidney function!
 Consider renal replacement therapy for “non-renal” reasons eg toxin elimination, rapid fluid control

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 19 of 34

ABCDEFGHIJ FASTHUGSSS

H : Haemoglobin

 Ensure adequate [haemoglobin] to allow adequate DO2

 Decide on an appropriate Hb target according to patient condition:
o Hb = 10 g/dl for:
 acutely shocked, especially septic shock with evidence of tissue hypoperfusion
 Acute Coronary Syndromes
 strong history of ischaemic heart disease
 post free flap
 with other identified ischaemic tissue
o Hb = 8.5 g/dl (NOT LITERATURE SUPPORTED)
 not shocked, but ongoing significant blood loss likely
 ongoing fluid or inotrope / vasopressor infusions required to maintain haemodynamic
stabilization
 elderly / frail / malnourished patients with ongoing organ dysfunction
 patient symptomatically anaemic at Hb 7.0 g/dl
o Hb = 7.0 g/dl
 haemodynamically stable : no inotrope / vasopressor requirements
 no ongoing blood loss / expected blood loss
 includes controlled Upper GIT bleed!
 not symptomatically anaemic, no evidence of organ dysfunction
 NB: transfused blood may not be fully functional for oxygen carriage for up to 24hours post
administration.
 Transfused blood may not leak from vessels in severe endothelial-glycocalyx dysfunction and may
(by increasing blood viscosity and hence causing greater endothelial stimulation with resultant
increase in vasoconstrictive endothelin production) increase vascular tone in vasodilated patients
who are also anaemic, but these indications for transfusion are NOT LITERATURE SUPPORTED.

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 20 of 34

ABCDEFGHIJ FASTHUGSSS

I : Infections
 Is there a current infection? | Is the current infection being adequately managed?
 Review inflammatory markers associated with sepsis
o Temperature trends
o White Cell Count, Differential
o Platelet Count
o C-Reactive Protein trends as a marker of inflammatory state
o ProCalcitonin as a marker of bacterial infection-driven inflammation
 NB: is a marker of inflammation, no longer considered totally specific for identifying
bacterial infection, is of most use in deciding when to end antibiotics
o Haemodynamics
o Glucose control
 Review all culture results | Consider need for new cultures
 Review markers of micro-organisms
o Beta – D – Glucan
 component of fungal and Pneumocystis cell walls
o Clostridium difficile toxin
 Review potential for infection sites requiring surgical management
o NB pressure points
 Consider infectious agents
o bacteria : antibiotics
o fungi : antifungals
o viruses : antivirals
o remember TB, Pneumocystis and CMV!
 For all antimicrobials : Review
o Agents used
 Are they in line with current local antibiotic guidelines and known recent institutional
flora?
 Are the correct Therapeutic Drug Monitoring levels being achieved
o Initial indication for use
 Empiric Are cultures now available to direct therapy?
 Directed Are antibiotics appropriate for sensitivities?
o Clinical response
 If poor response by 24 hours, review
 Correct antibiotic?
 Source penetration problem?
 Source control problem
 Correct dosing regime?
 Are antibiotics actually being given as prescribed?
o Review this especially if TDM shows incorrect plasma levels being
achieved.
 If good response, review
 elapsed duration of therapy vs planned duration of therapy
 potential for de-escalation
 Default antibiotic course : 7 days (terminate on Day 7) (day of initiation = Day 0)
o Bacterial pneumonia with good response : 5 days
o 14-day course for directed antifungals and for Vancomycin for MRSA
“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 21 of 34
  AntiRetroVirals
o Attempt to continue ARVs in all patients who have previously been on them as soon as
enteral tolerance re-established
 If no enteral tolerance, omit all ARV’s
 Give entire regimen, or give nothing
o New initiation of ARV’s while in ICU may be considered, but only with active involvement and
support of Infectious Diseases Unit.
o Be aware of effects of drug interactions
 ARVs may alter pharmacokinetics of other drugs
o Be aware of acute ARV-related complications
 Eg Type B Lactic Acidosis from NRTI’s – mandates discontinuation in ICU patients
 Immunizations
o Review if tetanus toxoid has been administered to any patient with traumatic injuries.
o Pneumococcal vaccine to be administered to all patients post-splenectomy
 Ideally > 7days post splenectomy to ensure adequate immune response, but if it is
not possible to ensure this, then the vaccine should be given at the latest possible
time while the patient is in the ICU system.

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 22 of 34

ABCDEFGHIJ FASTHUGSSS

J : imiJovo (inJections, adJuncts)

 Review all invasive devices, especially vascular catheters, drains, urine catheters EVERY DAY
 Remove non-functional drains, including non-swinging non-flushable intercostal drains
 Inspect all insertion sites every day for cleanliness
o Remove all invasive devices with obvious local sepsis
o Remove lines that look contaminated eg missing caps, fixed blood setback
 Remove all dysfunctional invasive devices eg overdamped arterial line, central lines with occluded
lumens etc
 Urinary catheter management in presence of infection
o Can it be removed, even if only temporarily?
o Bladder washout with non-absorbable antibiotic eg aminoglycoside ?
o antimicrobial-impregnated catheter?
 Remove vascular catheters that are no longer strictly required:
 if complications occur from a line that is no longer strictly needed, it is medicolegally
indefensible
o Indications for arterial catheterization
 need for beat-to-beat blood pressure monitoring
 poor anatomy for BP cuff
 need for >3 arterial blood gases every day
o Indications for central venous catheterization
 no / inadequate peripheral access
 infusion of sclerosant fluids, including: TPN, vasoactive agents, chemotherapeutics
 actual use of central venous pressures to guide therapy
 need for repeated venous sampling
 Default change dates for vascular catheters (day of placement = Day 0)
o Peripheral Day 2
o arterial Day 7
o central venous Day 7
o renal dialysis lines Day 10 but consider morbidity and availability of alternate site first
o Changes earlier are mandatory if catheters dysfunctional or sepsis is present
o Later changes permissible with consultant consent if poor vascular access / risk
 Minimum requirements for placement of long-duration catheters
o Arterial line to be done as a sterile procedure with 500mm draping all around insertion site,
full clean of site with chlorhexidine-in-alcohol, allowed to dry before needle insertion
o Central line, renal dialysis line to be done as a sterile procedure with > 1000mm draping all
around insertion site, full clean of site with chlorhexidine-in-alcohol, allowed to dry before
needle insertion, operator fully gowned, gloved, masked
o Peritoneal dialysis catheter insertion: patient to be cleaned and draped as for a laparotomy,
with operator fully gowned, gloved, masked and capped.

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 23 of 34

ABCDEFGHIJ FASTHUGSSS

F : Feeding

 Default target: patient’s full daily caloric and protein requirements must be being delivered by 72
hours post admission.
o Major burns: 24 hours goal for full feeds, with initiation of feed attempts within 6 hours
o longer time to full feed by consultant decision in patients who are previously well-nourished
and not in significant catabolic state
 Initiation of feeding attempts by 24 hours:
o Many patients do not require / benefit from / tolerate feeds in first 24 hours (eg stress
gastroparesis) especially if major trauma / major surgery / shocked
 acceptable to defer initial feeding attempts for up to 24 hours
 active attempts at feeding must, however, be made after 24 hours
 Use of most physiological route that is logistically feasible
o eating > NG tube feed > NJ tube feed > TPN
 If not logistically feasible to meet full requirements on enteral feed only by 72 hours, addition of TPN
is expected
o this differs from current ESPEN guidelines, but we believe our population has a higher
incidence of baseline malnutrition than first-world populations on which those guidelines
were based – THIS IS THEREFORE NOT STRICTLY LITERATURE-SUPPORTED
 Chronically malnourished patients: review PO43- before and during feed initiation
o appropriate to limit calories if PO43- < 0.7mmol/l until PO43- is actively replaced
 hypophosphataemia + calorie load  refeeding syndrome risk
 If unsuccessful enteral feeding attempts, review:
o simple gastroparesis
 consider prokinetic agent if differential diagnoses below eliminated
o small bowel ileus : exclude causative pathology pathology
 electrolyte abnormalities
 intra-abdominal sepsis
 consider acalculous cholecystitis
 consider occult leak
o obstruction
o gut atrophy
 Enteral feeding strategy:
o Gastric : use Aspiration Regime as per Department of Dietetics
o Post-pyloric : escalate to 100% over 12 hours watching for abdominal distension
 (25% - 4 hours - 50% - 4 hours – 75% - 4 hours – 100%)
 For choice of enteral feeds: use protocols as per Department of Dietetics
o Gastric feeding, no concern about gut atrophy
 Standard enteral feed, with or without fibre
o Post pyloric feeding, or gastric feeding with concern about mild gut atrophy
 Semi-elemental feed
o Significant concern about gut atrophy
 near-elemental feed at low volume for 48 hours
 For choice of TPN: Consult with Department of Dietetics
o “Renal” for patient with renal disease or need to limit fluid volumes.
 Consider whether IV or enteral glutamine required – discuss with Department of Dietetics
 Passage of stool expected within 48 hours of full enteral feeding is expected
o Active constipation management required if not occurring
“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 24 of 34
  lactulose
 enemas
 decompaction
 Diarrhoea: consider
o infection
 especially Clostridium difficile
o malabsorption (gut atrophy requiring enterocyte re-feeding strategy)
o overflow past partial obstruction
o osmotic effect from feed
o Constipating agents (codeine) may be considered only if
 diarrhoea physiologically disabling
 infection and partial obstruction excluded
 Discuss patient daily with Registered Dietician.

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 25 of 34

ABCDEFGHIJ FASTHUGS

A : Analgesia
 ALL patients should receive some form of analgesia!
o Omission of analgesia in any patient must be actively decided upon, and repeatedly
reviewed
o “P.R.N” analgesia UNACCEPTABLE except in convalescent patients preparing for
discharge.
 Multimodal analgesia to cover various specific pain types.
o Severe pain of all types / visceral pain of any magnitude: Opioid base
 Static analgesia
 Morphine load + infusion / regular timed bolus = default for static analgesia
 Sufentanil load + infusion for static analgesia in patients with significant renal
dysfunction (morphine 6 glucuronide accumulation would lead to prolonged
sedation), or where morphine causes excessive bradypnoea.
 Tramadol = alternative for moderate pain in patients having excessive
respiratory depression from Morphine / Fentanyl, and who have enteral
tolerance
 Dynamic analgesia
 Fentanyl boluses for breakthrough pain / procedures / mobilization (“dynamic
analgesia)
o All types of pain : Paracetomol
 Intravenous route if no enteral access and will facilitate opioid reduction with direct
immediate benefit eg avoidance of ventilation
 Enteral route for almost all patients as soon as enteral feeds established : this may
result in significant morphine sparing
 exception : liver failure : omit paracetomol if significant liver dysfunction
suspected
o Ketamine :
 consider as adjunct in low dose for patients receiving opioids for more than 12 hours
 limitation of hyperalgesia
 significantly useful in some types of somatic pain eg craniotomy, fractures where
NSAIDs contra-indicated
o Non-steroidal anti-inflammatories for somatic pain
 FRACTURE PAIN responds best to NSAIDs
 Concerns of late bone healing impairment debatable and irrelevant in ICU
 NO NSAIDS if:
 haemodynamically unstable
 dehydrated / not fully resuscitated
 significant renal dysfunction
 high risk of bleeding from wounds
 significant thrombocytopaenia / thrombocytopathia
 recent significant history of peptic ulceration
o Clonidine
 useful as adjunctive analgesic in many types of pain, especially neuropathic
o Secondary analgesics
 eg amitryptiline, gabapentin, pregabalin, carbamazepine
 neuropathic pain : review with chronic pain specialist

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 26 of 34

ABCDEFGHIJ FASTHUGSSS

S : Sedation

 NOT every patient should receive sedation!

o Agitated patients should first be evaluated for, and have pain and delirium managed.
o It is DESIRABLE to have patients well-enough analgesed and psychologically supported so
that no sedation necessary
o Excessive sedation lengthens ICU stay and INCREASES PTSD.
 Evaluate for delirium
o Acute confusional state, due to reversible neurochemical disturbance, but significantly
increases distress, may contribute to worse outcomes, thus warrants active management
o To be expected in elderly, but onset must prompt search for sites of pain and occult sepsis
o Lack of attention, disordered thinking, hallucinations possible, may be expressive or
withdrawn
o Formal evaluation via CAM-ICU if feasible
o Management: antipsychotics : haloperidol is the best agent currently available
 NB: benzodiazepines may be needed for acute agitation control but usually
aggravate delirium long-term and should be reduced in delirium states
 Evaluate sedation according to Richmond Agitation-Sedation Score (RASS)
o Set directed goals in terms of target RASS score
 Most patients : RASS 0 to -2 appropriate
 Post-op / during intense stabilization : RASS -3 to -4
 Head injury / severe agitation : RASS -5 : should be less than 10% of patients
o Neuromuscular blockade acceptable as temporary measure only whilst establishing
appropriate sedation in patients requiring RASS -5 for management
o Re-evaluate RASS score every 2 hours and adjust sedation to meet target
o Re-evaluate RASS target every 8 hours
o If RASS -4 or -5 achieved, once-daily complete stop of sedation to allow waking for
neurological assessment is MANDATORY
o ALWAYS CONSIDER POSSIBLE NEED FOR INCREASED ANALGESIA BEFORE
INCREASING SEDATIVE DOSES.
 Agents available:
o Midazolam : P R N bolus dosing appropriate for sedation, infusion if multiple boluses needed
 First-line sedative agent, but is highly implicated in causing PTSD, thus minimize
dose and attempt to wean as soon as possible
o Diazepam : anxiolysis only, or for patients that have received >24 hours of midazolam
 For use also in withdrawal states (benzodiazepine or alcohol withdrawal)
o Lorazepam : useful for night-time sedation, intravenous formulation for patients with severe
renal dysfunction
o Propofol infusion : for intense sedation when rapid waking is required (eg head injury)
 for short-term use (<24 hours) only
o Clonidine : when enteral tolerance present : useful sedative / anxiolytic / analgesic
 useful in withdrawal states
 introduce in most patients requiring sedation for >48 hours

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 27 of 34

ABCDEFGHIJ FASTHUGSSS

T : Thrombosis management

 STOP BLEEDING!
o Get core temperature above 36.5°C in all patients at risk of bleeding
 Exceptions : head injury or recovery from cardiac arrest : target 36.0°C for24 hours
 Assure even warming by targeting warming to 37.5°C (except in head injury)
o If massive transfusion  Massive Transfusion Protocol else targeted therapy
o Significant bleeding history: cyklokapron 1g stat + 1g infused over next 6 hours
o Bleeding + INR > 1.5 : FDP 15ml/kg
o Bleeding + platelets < 75 : 1 “Megapool” platelets
o Bleeding + low fibrinogen : cryoprecipitate
 Replace fibrinogen to over 2
o Bleeding from uraemic thrombopathia : DDAVP, Renal Replacement Therapy
o anaemia will aggravate bleeding : RBC form part of clot

 PREVENT THROMBOSIS when patient no longer at risk of bleeding

o More than 6 hours postoperatively + no intracranial bleeds + warm + no evidence of
bleeding
o All critically ill patients at risk of deep venous thrombosis
o Multimodal prophylaxis
 Mechanical devices – pneumatic leg compression
 Low Molecular Weight Heparin
 enoxaparin 40mg daily subcutaneously
 enoxaparin 80mg daily subcutaneously if mass > 100kg
o Epidural catheter : 12-hour gap between any epidural catheter manipulation and enoxaparin
dosing
 Manage symptomatic thrombosis
o Identified DVT / Pulmonary thromboembolism / acute coronary syndrome
 enoxaparin 80mg q12hr
o consider thrombolytic agents in unoperated STEMI, pulmonary thromboembolism
 Platelet thrombosis:
o Aspirin 150-300mg daily for
 acute coronary syndromes
 after arterial repair
 thrombophilia with platelet count above 1000

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 28 of 34

ABCDEFGHIJ FASTHUGSSS

H : Head-up and positioning

 Default position for all patients in bed semi-sitting (head-up): patients should not lie flat
o Head injury / raised intracranial pressure : 30° head up
o All other patients : 45° head up
 reduces VAP from aspiration of gastric contents
 improves respiratory mechanics and increases functional residual capacity
 improves psychology
 Regular turning to prevent pressure sores
 Early mobilization as much as possible as far as possible

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 29 of 34

ABCDEFGHIJ FASTHUGSSS

U : Ulcer prophylaxis / treatment

 Critically ill patients : gastric hyperacidity + reduced mucosal perfusion may cause stress ulceration
o stress ulceration bleeding occasionally fatal
o increased risk of VAP from bacterial overgrowth
 Prevention:
o Ranitidine 50mg q8hr
 reduce frequency in renal dysfunction
 to daily if RIFLE-F
 q12h if intermediate clinical renal impairment
 continue until on full feeds into stomach with no evidence of bleeding
o PPIs can be used instead, but ranitidine preferred for cost reasons
 Post gastric / duodenal ulcer perforation admitted to ICU
o Pantoprazole 80mg stat, thereafter 40mg daily
 Management of established upper GIT bleeding:
o Endoscopy to diagnose source of bleeding and manage site locally
o Pantoprazole 80mg stat + 200mg/24 hr infusion

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 30 of 34

ABCDEFGHIJ FASTHUGSSS

G : Glucose control
 Diabetic emergency :  Diabetic Emergencies Management Guideline
o Concept:
 Rehydrate aggressively using crystalloids (tissue dehydration usually significant)
 Give regular / continuous insulin until ketosis resolved
 BE > -3
 preferably no residual ketonuria
 give glucose so insulin can continue
 replace K+, PO43- as levels drop due to insulin
o Goal is correction of metabolic disturbance with insulin
 Critically ill hyperglycaemic  Critical Illness Glucose Control Guideline
o Goal is prevention of hyperglycaemia per se
 Hyperglycaemia in critical illness follows stress response and may impair recovery
o Start insulin infusion protocol if blood [glucose] exceeds 10mmol/l
o Target = blood [glucose] 8mmol/l
o Terminate infusion if blood [glucose] below 5mmol/l
o Never reduce feeds in adults to reduce hyperglycaemia – feed fully, give glucose
 Acute hypoglycaemia (<3.5mmol/l) = emergency
o Stop any insulin infusion
o Adults: Administer 20ml (only) of 50% dextrose
 Larger doses may result in hyperglycaemia, and rebound hyperinsulinism
o Repeat glucose testing after 10 minutes and rebolus as necessary
o Look for cause!
 Recurrent hypoglycaemia (more than 3 boluses of dextrose needed in 1 hour)
o May be a problem in liver failure, severe inflammatory response
o Manage with infusion of 50% dextrose via CVP
 Start with 0.1ml/kg/hr infusion and titrate to maintain glucose 6-8mmol/L

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 31 of 34

ABCDEFGHIJ FASTHUGSSS

S : Steroids

 Evaluate specific indications for disease-modifying glucocorticoids

o bacterial meningitis
o asthma
o some cases of community-acquired pneumonia
o Pneumocystis jerovicii treatment with co-trimoxazole
o ARDS at 7 days (transition to fibroproliferative phase)
 “Physiological dose” / “Stress dose” steroids
o Standard Dose : Hydrocortisone 50mg q6hr
 Etomidate : Standard Dose x 4 doses
 Goal: Cover 24-hour period of adrenosuppression
 Catecholamine infusions > 6hrs : Standard Dose while on inotrope and/or
vasopressors
 Goal: Limit adrenoceptor downregulation
 If < 12 doses, terminate when inotropes terminated
 If > 12 doses, taper as below
 Septic shock requiring inotropes : 5-7 day course Standard Dose + taper
 Goal: Modulate inflammatory response : early cessation causes rebound
 Second goal: possibly modulate “relative Addisonian” state that may develop
in some patients with septic shock
 Taper dose at end : 25mg q6h x 4 doses, then 25mg q12h x 4 doses.

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 32 of 34

ABCDEFGHIJ FASTHUGSSS

S : Statins

 Statins specifically indicated post myocardial infarction

o Atorvastatin preferred
 If patient is on statin pre-admission, attempt to restart as soon as enteral tolerance re-established
 Acute statin use for general pleiotropic anti-inflammatory activity not yet recommended.

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 33 of 34

ABCDEFGHIJ FASTHUGSSS

S : Seizures

 Seizure control is an emergency

 Be aware of the possibility of Non-Convulsive Status Epilepticus in patients who are not awakening.
 If a patient has repeated new-onset seizures, or has focal seizures an urgent CT brain is mandatory
 Prophylactic phenytoin should be administered to all patients with Moderate or Severe Traumatic
Brain Injury for 7 days post-injury.
o Make sure that therapeutic drug levels are achieved while the patient is in ICU
 Status epilepticus / recurrent seizures : follow detailed Status Epilepticus guideline, get Neurology
advice, get neuroimaging studies
o Control seizures initially with bolus benzodiazepines.
o If repeated seizures, load with either
 Intravenous phenytoin
 Intravenous sodium valproate
o If repeated seizures
 Consider midazolam infusion
 Check if levels of phenytoin / valproate therapeutic and correct if not
 Note: TDM well established with phenytoin, but exact toxic and therapeutic
levels not well-established with valproate
 Consider loading with the other agent (valproate / phenytoin)
o If repeated seizures, consider propofol (preferred) or thiopentone infusion
 Note extremely long period of sedation is to be expected with thiopentone
 Don’t forget possibility of tetanus spasms, and rabies, as differential diagnoses for seizures.

“10 FASTHUGSSS” v3.0 : January 2014 Dr RP von Rahden Page 34 of 34