8/1/2016
ICU CONDITIONS
S. Lawler
Deep vein thrombosis
• Patients requiring intensive care are at risk for the development
of deep venous thrombosis and pulmonary embolism (PE).
• Risk factors include immobility, venous stasis, poor
circulation, major surgery, malignancy and pre-existing illness.
• Over and above these well-known factors, intensive care itself
is an independent risk factor (sedation and ventilation)
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• in critically ill patients, 95% of DVTs are clinically silent
• ICU patients may require mechanical or chemical prophylaxis
depending on risk factors for bleeding
Pulmonary embolism
• Pulmonary thromboembolism is common in immobile,
critically ill, traumatised and postoperative patients.
• The effects range from mild discomfort and shortness of
breath to sudden profound collapse and cardiac arrest.
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Management
• Oxygenation : high inspired oxygen; intubate/ventilate as
necessary.
• Optimisation of cardiovascular status
• Major embolism: thrombolysis, e.g. streptokinase
• For smaller embolism- anticoagulation, eg heparin infusion
Shock
• The primary function of the cardiovascular system is to
maintain the perfusion of organs and tissues with oxygenated
blood.
• When these mechanisms fail, ‘shock’ ensues, which, if
uncorrected can result in organ failure, prolonged ICU stay and
death.
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Shock
• Definition:
• Shock is a syndrome of cardiovascular system failure resulting in
inadequate tissue perfusion.
• Hypotension is a common but not universal feature.
Types
• Cardiogenic- impaired left ventricular function leads to
decrease in stroke volume, low blood pressure and inadequate
tissue perfusion this results in a sympathetic response of
vasoconstriction and increased SVR so patients peripheries
will be cool, and urine output will be poor.
• Hypovolaemic- blood/blood/plasma loss from an organ or
tissue injury. Decreased intravascular volume,decreased
venous return decreased stroke volume/CO/BP/TP
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• Septic- Severe sepsis in the presence of hypotension
unexplained by cardiovascular insufficiency.causes are
organisims such as Klebsiella;enterobacter, E.Coli and
opportunistic fungi
• An immune response is triggered releasing macrophages
monocytes and neutrophils that interact with the vascular
endolthelial cells, releasing chemicals and toxins resulting in
microvascular injury vasodilation of capillary bed ,capillary
leak tissue ischaemia decreased circulating volume and
decreased oxygen delivery and consumption
Classification
Underlying cause
Hypovolaemia
Dehydration
Haemorrhage
Burns
Sepsis
Cardiogenic
Mycocardial infarction/ischaemia
Valve disruption
Mycocardial rupture (e.g. VSD)
Altered systemic vascular resistance
Sepsis
Anaemia
Anaphylaxis
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Clinical features
• The clinical features vary depending on the cause and the
physiological response. Two patterns are typically recognised,
although there is a continuum from one to the other:
 Warm pink vasodilated, hyperdynamic patient with high
cardiac output and hypotension.
 Cold, grey, sweaty, vasoconsricted, peripherally shut down
patient with low cardiac output. Blood pressure may be
maintained in the early stages.
Features
Other features of shock may include increased or decreased core
temperature, hypoventilation or hyperventilation, renal and
hepatic dysfunction, disseminated intravascular coagulation, and
altered mental status
(Rapid shallow breathing, decreased urine output, confusion,
tachycardia, profound hypotension, cold clammy skin)
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Management
 Optimisation/restoration of oxygen deliveryoxygen therapy
 Optimisation of cardiac output-intravenous
fluid administration and RBC transfusion
 Optimisation of blood pressure- Vasoactive
agents and ionotropes
Renal dysfunction
• Renal dysfunction is common in the ICU and frequently occurs
as part of a syndrome of multiple organ failure.
• It is usually manifest as oliguria progressing to anuria, but highoutput renal failure, in which there are large volumes of poorly
concentrated urine, may also occur.
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• The mortality rate for patients in intensive care who develop
ARF is increased to around 50%.
• The high mortality rate probably reflects the seriousness of the
underlying condition, rather than mortality specifically
attributable to renal failure.
• Patients usually die with renal failure rather than from renal
failure.
• Classically, the causes of acute renal dysfunction are divided
into prerenal (inadequate perfusion), renal (intrinsic renal diseaseproblem is with kidney tissue itself) and postrenal (obstruction to
urine out flow).
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Cardiac failure
Heart failure is common and represents an inability of the heart to
maintain sufficient CO despite adequate filling. The clinical
picture may range from mild peripheral oedema and shortness of
breath to florid pulmonary oedema and hypotension.
The principles of management:
 Oxygenation
 CPAP by face mask / non-invasive ventilation.
 Invasive monitoring as necessary- Arterial line, central venous
or pulmonary artery catheter.
 inotropes if required.
Infection
May be primary cause
of admission or icu
aquired
Increased risk of
cross infection
Immune suppressive
effects of drugs
Poor nutrition and
impaired tissue
healing
Effects of sedative
agents and analgesia
eg.suppressed cough
reflex, gi stasis
ETT
Vascular catheters,
urinary catheters and
drains
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Typical signs of infection in
critically ill
Pyrexia
Tachycardia
Hyperventilation
(failure to wean)
Raise in WCC
Non-specific
deterioration in
condition
Systemic inflammatory response syndrome
(Van Aswegen and Morrow,2015)
• SIRS is a systemic inflammatory response to overwhelming
clinical pathologies such as burns, trauma, ischaemia and
inflammation whereas sepsis is a systemic response to
infection.
• Criteria for diagnosing SIRS and Sepsis
Temperature >38* or <36*
HR >90 beats per min
Resp rate > 20 breaths/per min or PaC02< 32mmHg
White blood cell count > 12000 or < 4000
2 or more of the above after severe clinical insults= SIRS
2 or more of above in presence of infection =sepsis
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• During SIRS or SEPSIS an increase in circulating cytokines
result in tissue damage and dysfunction of vital organs.
• Pro inflammatory Cytokines cause a breakdown in muscle
protein and reduction in muscle mass leading to muscle
weakness.
Disseminated intravascular
coagulopathy
• Arises from generalised activation of the inflammatory cascade
often following septic shock, burns, lung contusion
• It involves clotting within the vasculature(fibrin and platelets)
resulting in tissue damage
• Normal clotting fails to take place because of depletion of
clotting factors
• This will give rise to bleeding from the slightest trauma eg.
suction
• Nasopharyngeal suction is contra indicated
• Ett suctioning very cautiously
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Multiple organ dysfunction
syndrome(MODS)
• Presence of a systemic inflammatory response (e.g. SIRS
criteria) and dysfunction of at least 2 organs
• may be mild, or severe resulting in death
• organ dysfunction may present as:
•
•
•
•
•
•
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Acute kidney injury
ARDS
Cardiomyopathy
Encephalopathy
GI dysfunction
Hepatic dysfunction
Coagulopathy and bone marrow suppression
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ICUAW
• Intensive care unit–acquired weakness, develops in
individuals who are admitted to the intensive care unit for
any reasons, commonly including sepsis and ARDS.
• Many of these conditions require interventions that may
limit patients mobility and therefore their function eg.
MV, haemodialysis, ionotropes etc
• Intensive care unit–acquired weakness is a specific term
describing diffuse, symmetrical, widespread muscle
weakness that develops after the onset of critical illness
without other recognisable causes.
• It is associated with increased rates of morbidity and mortality
as it results in respiratory muscle weakness- prolonged
ventilation, increase in the length of ICU stay and therefore
increased risk for secondary complications (El Said, 2014)
• Muscle weakness acquired in the ICU contributes to impaired
physical function and is a common and major long-term
complication in patients with critical illness often seen up to
five years post discharge (Nordon-craft et al, 2011)
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• ICUAW may develop if an individual is on mechanical
ventilation for as little as 4 to 7 days
• Approximately 46% of the patients with severe sepsis,
multiple organ failure, or prolonged mechanical
ventilation will develop ICUAW (Appleton and Kinsella,
2012)
• Complications of bed rest in patients with critical illness
include systemic inflammation, atelectasis, metabolic and
microvascular dysfunction, joint contractures, skin ulcers, and
muscle weakness.
• During bed rest, patients do not receive the beneficial effects
of exercise, which reduces systemic inflammation.
• In patients with critical illness and on bed rest, the loss of lean
body mass in patients has been shown to be approximately 1%
per day, or 7% per week.
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• Patients with ICUAW are often identified either due to
difficulty to wean from ventilation or if the patient displays
severe weakness having unexpected difficulty mobililising
• In order to properly examine the patient physically the patients
co-operation and maximal effort has to be attained.
• This is not always possible as ICU patients are sedated and
delirious with reduced cortical brain function.
• ICUAW is diagnosed in awake and cooperative patients by bedside
manual muscle testing using the Medical Research Council sum score
Probable Risk factors for
ICUAW (Kress and Hall,2014)
• Severe sepsis/septic shock
• Multiorgan failure / Increasing duration of multiorgan
failure
• Prolonged mechanical ventilation/bed rest
• Increasing duration of SIRS
• Hyperglycaemia-by inducing neural mitochondial
dysfunction (Kress and Hall,2014)
• Glucocorticoid and NMBA use
• Female sex
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• ICUAW may be classified as critical illness myopathy
(CIM),
• critical illness polyneuropathy (CIP),
• or a combination of both referred to as critical illness
polyneuromyopathy (CIPNM or CINM).
Signs
• Symmetrical flaccid weakness of the limbs more pronounced in
proximal rather than distal muscles.
• CIP and CIM have similar presentations which cannot be reliably
differentiated clinically.
• The earliest sign may be facial grimacing in response to painful
stimuli without limb movement
• Muscle wasting is frequently disguised by oedema
• The MRC sum score is used to assess muscle power in the awake
patient.
• A score less than 48 out of 60 indicates ICUAW-but cannot
differentiate between CIM and CIP
• Thereafter EMG and nerve conduction studies may be conducted to
determine compound motor action potentials and sensory nerve
action potentials
• Hand dynamometry and grip strength has also been used as an
outcome measure to detect icuaw
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CIP
People with CIP have
impairments of the
neuromuscular system,
including weakness,
reduced deep tendon
reflexes, and impaired
pain, temperature, and
vibratory sense.
Cranial nerves
typically are spared;
however, facial
weakness can occur.
Weakness typically
occurs in a symmetric
pattern in the shoulder
and hip girdles
weakness can include
the respiratory muscles
making weaning from
mechanical ventilation
very difficult
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CIM
Individuals with CIM
display extreme weakness,
particularly of proximal
muscles.
Deep tendon reflexes may
be preserved or
diminished.
However, in contrast to
CIP, sensation is intact.
The MRC scoring system
is used to determine
muscle strength
Evaluation of the level of patient cooperation
Five standard questions
Open and close your eyes
Look at me
Open your mouth and put your tongue out
Nod your head
Raise your eyebrows after I have counted to five
Each correct answer is worth 1 point
A score of 5/5 is required to assess volition muscle
strength
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Medical Research Council Scoring System13.
Amy Nordon-Craft et al. PHYS THER 2012;92:1494-1506
© 2012 American Physical Therapy Association
Criteria for diagnosing ICUAW are the presence of 1, 2, 5, and either 3 or 4
(Appleton and Kinsella, 2012)
1. Weakness developing after the onset of critical illness
2. The weakness being generalized (involving both proximal and
distal muscles), symmetrical, flaccid, and generally sparing the
cranial nerves (e.g. facial grimace is intact)
3. Muscle power assessed by the Medical Research Council
(MRC) sum score of less than 48 (or a mean score of less than 4 in all
testable muscle groups) noted on more than 2 occasions separated by more than 24 hrs
4. Dependence on mechanical ventilation
5. Causes of weakness not related to the underlying critical illness excluded
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• Patients with persistent coma after sedation should undergo cns
studies eg cranial ct scan and mri
• If studies are normal electrophysiological studies/muscle
biopsies should be performed (Kress and Hall,2014)
Diagnostic algorithm
• Please refer to article entitled
“ICU-Acquired Weakness and Recovery from Critical Illness” John P. Kress, and Jesse B. Hall (N Engl J Med 2014;370:162635)
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Management
• Prevention- the aims are aggressive treatment of sepsis, early
mobilization, preventing hyperglycemia with insulin- tight
glyceamic control to reduce catabolic syndrome
• Minimising the use of corticosteroids and neuromuscular
blocking agents even though evidence for this is scarce
• Rehabilitation- prolonged bedrest is harmful contributing to
skin ulceration, compression neuropathies, DVTs, and reduced
muscle size, strength, co-ordination, balance, endurance
function and low mood -deconditioning (Appleton and
Kinsella,2012).
• Passive and active movements as well as sitting up in bed/EOB
sit to stand and standing must commence in the ICU.
Prevention rehab (Hermans &Van
den Berghe, 2015)
• This method is aimed at reducing immobilisation
• Sedation levels have to be decreased to the minimal level
needed for safety or comfort
• Passive/active movements using a bedside ergometer
• 20 mins of bed-cycling 5 times per week from day 5 following
icu admission- this training improved quads strength at
hospital d/c and HRQoL in patients receiving this regime as
opposed to conventional therapy.
• Another approach used early mobs and OT within 72 hours of
initiation of MV.
• training consisted of individual programmes of PROM –
AROM-bed mobs-sitting-t/f training then walking results
showed that early mobs prevented ICUAW
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ELECTRICAL MUSCLE STIMULATION
• A significant number of ICU patients are not able to participate
in early mobs
• EMS has been used in this population to preserve some muscle
function during this phase however evidence for this approach
remains inconclusive (Hermans &Van den Berghe, 2015).
• EMS in conjunction with active exercises for a group of pts
with copd on Mv was found to be more beneficial than the
exercise only group. They demonstrated greater strength gains
and were able to do bed to chair t/f earlier.
• Cycle ergometry for unresponsive patients has also been found
to be greatly beneficial demonstrating greater quads strength
and greater distances in six min walk test (Nordon-craft et
al,2012)
Criteria for Beginning Physical Rehabilitation
• Sufficient evidence is available to recommend safe physical
rehabilitation for individuals with ICU-acquired weakness.
• Rehab may begin as soon as the patients have sufficient
medical stability to cope with the increased vascular and
oxygen demands that accompany the physical examination and
intervention
• Decisions to mobilise or stop treatment requires careful
interpretation of the patients presentation per encounter in
order to ensure that the patient is physiologically capable to
tolerate the rehabilitation
• An algorithim checklist for mobilisation is below
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Criteria for mobilisation (Nordon-Craft et al , 2012)
Physical therapy intervention
techniques (Nordon-Craft et al , 2012)
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Principles of prescription
Recommendations
Exercise Prescription
Frequency
Start with once a day and progress
Intensity
Aerobic:40-70% of Max HR/11-13 on the Borg
scale
Resistance exercises:
Start with 45%-50% of 1RM rogress to 50-70%
1RM
Rest 1-2 mins between exercises
Type
Aerobic exercises: bedside ergometer; walking;
step climbing;treadmill, walking running;
stationery bike
Resistance exercises-body weight,
freeweights,resistance bands,weight machines
Concentric, eccentric and isometric exercises of
the trunk, upper and lower limbs.Uni and bilateral
limb exercises
Single and mulitiple joint exercises
Time
Aerobic:start with 5-10mins and progress to 20
mins
These recommendations are for patients in the acute and
subacute phases of recovery post traumatic surgery
(van Aswegen and Morrow;2015)
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Considerations
• One of the most difficult decisions to make when managing
these patients is how far to push them.
precise clinical guidelines do not really exist and the approach
requires good clinical reasoning and interpretation of changes
Cessation of treatment can be decided on haemodynamic
instability and/or decreasing pulmonary status
Some literature recommends initiating treatment with the least
challenging to most challenging activities, while other literature
suggest the opposite in order for the patient to practice the most
functionally relevant tasks (Nordon-Craft et al , 2012).
Dosage (intensity,duration,frequency) for exercise ranges from
fifteen minutes to one hour 1-2 times per day, 5-7 days per week
A team approach is absolutely necessary for the successful mx of
these patients.
Prognosis
• Impairments of the respiratory, renal and CVS systems generally resolve
however neuromuscular impairments take much longer and resolution is
often incomplete
• Survivors frequently report fatigue, weakness and cognitive changes
including impaired functional ability up to a year post d/c. Activity
limitations can persist for up to years post d/c (Nordon-Craft et al,2012)
• ICUAW has been found to be an independent threat for prolonged
ventilation increased length of ICU stay and increased mortality even
post discharge at one year (Hermans and Van der Berge,2015)
• Approximately 45% of patients with this condition will die in hospital
and a further 20 % in the first year post discharge . Complete functional
recovery only appears in 68% of patients (Appeleton,2012)
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