Download Temperature management in critically ill patients

Temperature management in critically ill
patients
Matthew Faulds BMedSci (Hons) MBChB FRCA
Tim Meekings BMedSci (Hons) MBChB MRCP FRCA DICM FFICM
Key points
Disruption of
thermoregulation is
common in the critically ill.
Severe hyperthermia should
be treated promptly to
avoid multiorgan failure.
Hypothermia should usually
be corrected no faster than
0.58C per hour.
Therapeutic hypothermia
can improve the outcome
after cardiac arrest and
perinatal asphyxia.
Both hypothermic and
hyperthermic patients may
have underlying medical
conditions that require
treatment before
temperature can be
corrected.
Thermoregulation is a dynamic part of homeostasis controlled by the anterior hypothalamus.
Temperature in mammals will vary diurnally
within a narrow range and temperatures outside
this can have a profound effect at both a biological and clinical level. Biochemical sequelae
can include acid –base disturbance, electrolyte
derangement, fluid shifts, alteration of intraand extracellular enzymatic function, and variations in energy production and consumption.
Clinical manifestations can also vary widely
with potential neurological, cardiorespiratory,
metabolic and infective compromise.
In the critically ill population, thermoregulation is often disrupted. This may be inadvertent (e.g. hypothermia in a trauma patient), part
of a disease process such as fever or for therapeutic benefit, such as induced hypothermia
after cardiac arrest. The close monitoring, manipulation, and regulation of body temperature
forms an important part of the care of the critically ill patient (Table 1).
Definitions
Temperature
Matthew Faulds BMedSci (Hons)
MBChB FRCA
Specialty Registrar in Anaesthesia and
Intensive Care
Sheffield Teaching Hospitals
Sheffield
South Yorkshire S5 7AU
UK
Tim Meekings BMedSci (Hons) MBChB
MRCP FRCA DICM FFICM
Consultant in Anaesthesia and Intensive
Care
Critical Care Directorate
Chesterfield Royal Hospital
Calow
Chesterfield S44 5BL
UK
Tel: þ44 (0)1246 512284
Fax: þ44 (0)1246 512607
E-mail: tim.meekings@chesterfieldroyal.
nhs.uk
(for correspondence)
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Heat energy is the kinetic energy of the particles within a substance. Heat can be transferred
from a hotter substance to a colder substance.
By measuring this ability for heat to be transferred, we can quantify the heat energy. That
measurement is temperature and is proportional
to the mean kinetic energy of the particles in
the substance.
There are three major temperature scales;
Kelvin, Celsius, and Fahrenheit. The
International System of Units (SI) unit of temperature is the Kelvin, which has a value of 0
K at absolute zero. The Celsius scale has units
of the same magnitude as Kelvin (18C¼1 K),
but the values are based on properties of water,
for example, the triple point of water is 0.018C
or 273.16 K and the boiling point of water is
1008C or 373.15 K. Therefore, in clinical
1A01, 2C01, 3C00
practice, it is more convenient to use the
Celsius scale. In some countries, notably the
United States, the Fahrenheit scale is still in
common use.
Temperature homeostasis
Heat is produced by metabolism and homeostatic mechanisms maintain core temperature.
The thermoneutral zone is the ambient temperature range over which normothermia is
maintained without any changes to basal metabolic rate. In humans, this has been defined as
27–318C for a naked 70 kg male.
Heat production can be increased from basic
metabolic rate by food consumption, exercise
and, paradoxically, by an increase in body temperature. Normal muscle activity is the main
method of increasing heat generation but, as a
last resort, shivering in the adult can increase
heat production by 2–5 times. However, there
is no mechanism for reducing the metabolic
rate when overheating has occurred.
Heat loss occurs through five routes: radiation (40%), convection (30%), evaporation
(15%), conduction (5%), and respiration (10%).
Radiation, convection, and evaporation can be
reduced by increasing ambient temperature and
covering exposed skin—behavioural responses
to low temperature. Further reductions of heat
loss are achieved through reflex mechanisms
such as vasoconstriction to reduce skin perfusion. The converse is true to increase heat loss;
reflex vasodilation, sweating, uncovering, and
reducing ambient temperature all contribute to
cooling.
Normothermia
In humans, normal core temperature is between
35.5 and 37.58C, depending on factors such as
the time of day, site, and method of measurement. In part, this is because of diurnal variation, +0.58C, with lower temperatures in the
morning and higher in the evening. There is
doi:10.1093/bjaceaccp/mks063
Advance Access publication 18 January, 2013
Continuing Education in Anaesthesia, Critical Care & Pain | Volume 13 Number 3 2013
& The Author [2013]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia.
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Temperature management in critically ill patients
Table 1 Complications of hyperthermia and hypothermia
Aetiology
Hyperthermia
Hypothermia
Dehydration
Nausea and vomiting
Hypotension
Hyperkalaemia
Tachycardia
Hypercarbia and metabolic acidosis
Rhabdomyolisis
Renal failure
Confusion
Seizures
Coma
Death
Shivering
Hyperglycaemia
Hypovolaemia
Hypokalaemia and hypomagnesaemia
Bradycardia and other cardiac arrythmias
Coagulopathy
Reduced drug clearance
Immunocompromise
Pressure sores
Confusion
Coma
Death
The causes of fever in critical care patients are diverse and range
in incidence from very common to extremely rare. A full account
of the wide range of causes of fever in the critically ill patient is
beyond the scope of this article; the focus will therefore be on
some of the more commonly found causes and rarer causes that
require specific treatment.
also a large difference between the core (brain, thoracic, and abdominal organs) temperature and body surface temperature; the
latter is lower than core temperature with a range of 32– 358C.
Hypothermia
Hypothermia is generally accepted to mean a core body temperature ,358C. This can then be further subdivided into mild (32–
358C), moderate (28 –328C), and severe (,288C) hypothermia.
However, these terms can be confusing because of variable ranges
used in the literature and guidelines. For example, during the perioperative period, the National Institute for Health and Clinical
Excellence (NICE) classify normothermia as being a core temperature between 36.5 and 37.58C, with mild, moderate, and severe
hypothermia defined as 35 –35.98C, 34– 34.98C, and ,348C,
respectively.1
Hyperthermia
This is a core temperature over 388C. Fever is a type of hyperthermia caused by an elevation of the thermoregulatory set point by a
process such as infection and is defined as a core temperature
.38.38C (1018F). Hyperpyrexia is a very high temperature 408C
that is considered life-threatening when 41.58C.
Hyperthermia
Epidemiology
Fever has been found to be present in a range of 15–50% of
patients after surgery, in some this represents the development of
infection whereas in the remainder this is simply a marker of a
postoperative inflammatory response.2 A significant proportion of
patients will have a core temperature .388C recorded either at admission or during their stay in critical care. As raised temperature
is a contributory factor when calculating either the APACHE II
and SAPS II physiology scores in critically ill patients, it is likely
this demonstrates that hyperthermia is associated with adverse outcomes in these patients.
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Systemic inflammatory response syndrome (SIRS)
as a result of infection
The cytokine response to infection from a variety of sources
results in fever—this can occur in characteristic patterns in certain
infections (e.g. the cyclical fevers of malaria).
SIRS because of other causes
The systemic activation of the inflammatory cascade can also be a
result of other pathologies unrelated to infection. These include
trauma, burns, ischaemia, and connective tissue diseases. An inflammatory response can also occur after surgery. All these processes involve a cytokine response that usually produces a fever.
Malignant hyperthermia
This inherited disorder of calcium metabolism in skeletal muscle
results in the rapid development of an uncontrolled hypermetabolic
state after exposure to succinylcholine or volatile anaesthetic
agents. The clinical features include hypercarbia, sinus tachycardia,
generalized muscular rigidity, and an elevated temperature.
Heatstroke
This is defined as altered mental status, anhydrosis, and a temperature .40.68C. Classic heat stroke is most common in the elderly
and has a reported mortality five times higher in people aged 65
years and over.3 Exertional heatstroke is more common in younger,
athletically active individuals. As the pathophysiology of both conditions is similar, there is a possibility that both malignant hyperthermia and a susceptibility to heatstroke are related disorders,
which are both caused by abnormalities in muscle physiology.
Neuroleptic malignant syndrome and serotonin
syndrome
These are both adverse drug reactions that include hyperthermia as
a clinical feature. They can be distinguished by slightly different
clinical presentations and a different onset time. Neuroleptic malignant syndrome is characterized by bradykinesia or akinesia and
an onset over several days. In contrast, the serotonin syndrome typically evolves rapidly over a matter of hours and manifests as
tremor, hyperreflexia, and clonus.
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Temperature management in critically ill patients
Management
The sequelae of worsening multiorgan failure that results when
core temperature exceeds 40.58C indicate that fever above this
limit should be treated promptly and aggressively. There is controversy regarding whether milder degrees of fever secondary to infection or the systemic inflammatory response syndrome should be
treated in critical care patients, as it may be part of a beneficial
host response and treating it may not alter outcome.4 An elevated
core temperature in certain subgroups of patients such as in traumatic brain injury and post cardiac arrest syndrome appears to be
associated with poorer neurological recovery and increased mortality—patients in these subgroups may benefit from avoidance of
hyperthermia and in some cases the induction of therapeutic hypothermia (TH).
Initially, any potential trigger agents must be removed, for
example volatile anaesthetic agents in malignant hyperthermia.
The subsequent management of hyperthermia can be divided into
physical and pharmacological methods of inducing cooling.
Fever associated with infections on intensive care also require
specific antimicrobial therapy; this should be tailored to the
patient’s culture results and local resistance patterns in consultation
with a medical microbiologist.
Dantrolene is a skeletal neuromuscular blocking agent that acts
by blocking calcium efflux from sarcoplasmic reticulum.
Malignant hyperthermia is the only specific indication for dantrolene in hyperthermic patients. In this situation, an immediate i.v.
bolus of 2.5 mg kg21 should be given. This is followed by 1 mg
kg21 boluses as required every 5–10 min up to a maximum of 10
mg kg21.
The use of dantrolene has also been described for the treatment
of neuroleptic malignant syndrome. Pharmacological management
of the neuroleptic malignant syndrome can also include the use of
dopamine agonists such as bromocriptine. In the serotonin syndrome, 5-HT2A antagonists such as cyproheptadine may be used to
provide blockade of the serotonin receptors.
Hypothermia
Epidemiology
Physical methods of cooling
Initially simple methods can be instituted, such as uncovering the
patient whilst preserving their dignity and using cold towels placed
across the patient or in the axillae. If ice packs are used, care must
be taken to ensure that the ice does not come into direct contact
with the patient’s skin and cause subsequent thermal injury.
Cooling blanket systems utilize circulated cold water and a feedback control system monitoring the patient’s core temperature to
achieve and maintain normothermia.
In refractory cases of hyperthermia, more invasive methods of
cooling may need to be implemented. This begins with rapid infusion of cooled i.v. fluids. Other invasive methods of cooling
include the installation of cold fluid into body cavities such as the
stomach, pleura, bladder, and peritoneum. The inherent complications and infection risks of this strategy mean that it is not widely
practiced in the UK. Other invasive options for cooling include the
use of intravascular cooling catheters, haemodialysis, or haemofiltration and ultimately cardiopulmonary bypass. These methods are obviously dependent upon the resources and equipment available locally.
Pharmacological methods of cooling
Nonspecific medication used to reduce heat production in the critically ill patient includes sedative agents and neuromuscular blocking agents. More specific antipyretic medications include
paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs).
Paracetamol acts by selective inhibition of the cyclooxygenase-3
enzyme (COX-3); this results in reduced production of fevergenerating prostaglandins. With a relatively limited side-effect
profile in most patients, paracetamol is widely used in critical care
patients with fever. The other major group of antipyretics are
NSAIDs—the risks of exacerbation of renal impairment and
gastric ulceration with the use of these drugs mean that they are
often relatively contraindicated in the critically ill population.
Hypothermia is commonly found on presentation to medical care,
but its true incidence is not known. Although death rates in the
UK increase by 1560 per week during the winter months, little
of this is thought to be directly as a result of hypothermia. It is
clear that those at highest risk are the elderly, those with low
socio-economic status and trauma patients. Five percent of patients
over 65 years of age attending a Scottish Accident and Emergency
department in winter were hypothermic and this group had a mortality of 34%.5 Around 13% of major trauma patients are hypothermic and this triples their risk of death.6 Unfortunately,
hypothermia also occurs in hospital with up to 70% of postoperative patients found to be hypothermic.1
Aetiology
Increased heat loss
This is the most common cause of low core temperature and can
cause primary or secondary hypothermia. In the United States,
around 650 people each year die from primary hypothermia but
these represent only the minority of cases. There is usually an
underlying medical or surgical cause; of particular interest to the
intensivist are trauma, immersion, burns, and the perioperative
period.
Trauma patients are especially at risk of hypothermia as they
tend to be exposed for long periods of time both before and after
arrival in hospital. They may also be wet and have obtunded
thermoregulatory responses. Hypothermia is very important to recognize and control in these patients—the mortality of a patient
with a core temperature of 328C is 23% but a trauma patient at the
same temperature has a mortality of 100%.7
Immersion in water loses heat more rapidly than exposure to air
as the thermal conductivity of water is higher and once extracted,
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Temperature management in critically ill patients
body temperature decreases even further because of evaporative
losses. Similarly, burns patients may be cold as a result of initial
irrigation, increased evaporative losses, and inability to effectively
modulate peripheral blood flow. Both of these groups of patients
have a high coincident rate of trauma, adding to their risk of being
hypothermic.
Inadvertent perioperative hypothermia has been of interest in
recent years because of its high incidence and the increased morbidity and mortality seen in hypothermic patients. Increased heat
loss is caused by both general and neuraxial anaesthesia, predominantly through vasodilatation, and also by surgical techniques that
involve open body cavities or require large skin areas to be uncovered. Efforts must be made to monitor and control temperature
appropriately.
Decreased metabolic rate
A variety of endocrinological conditions may cause decreased heat
production, for example hypopituitarism, hypoadrenalism, and
hypothyroidism. Rewarming may be difficult in these patients
without treating the underlying pathology, for instance, with drugs
such as triiodothyronine, steroids, or both. Patients who have
severe malnutrition or hypoglycemia also have a low metabolic
rate. Others, such as the very young and very old, do not have the
ability to increase their metabolic rate because of the lack of shivering reflex or low muscle mass.
Impaired thermoregulation
A wide array of causes may impair thermoregulation. In general,
the end result is failure of the hypothalamus to regulate core body
temperature, often as a result of direct effects on the central
nervous system. Examples where this occurs include brain and
spinal cord trauma, stroke, intracranial haemorrhage, central
nervous system tumours, Parkinson’s disease, Wernicke’s encephalopathy, and multiple sclerosis. Sepsis and uraemia may also alter
the hypothalamic set point resulting in hypothermia.
Drugs such as general anaesthetic agents, beta-blockers, neuroleptics, and meperidine may disrupt thermoregulation. Ethanol,
sedatives, and phenothiazines obtund the responses to low ambient
temperatures.
Therapeutic hypothermia
Therapeutic hypothermia aims to improve the outcome by reducing
metabolic oxygen demands. In the operating theatre, TH can be
instituted for neuroprotection before primary insult, for example in
aortic root repair when the cerebral circulation is interrupted.
Postoperatively, these patients require specialist management on
the cardiac intensive care unit. TH to ameliorate the secondary
insult is more common, with the best evidence for its use after
either cardiac arrest or perinatal hypoxia. Trials looking at TH in
traumatic brain injury and ischaemic stroke have produced equivocal results to date and consequently use in these conditions is not
recommended at present.
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In 2002, two studies of TH after out-of-hospital cardiac arrest
demonstrated significantly improved outcome with a number
needed to treat (NNT) of 6– 7. Consequently, the International
Liaison Committee on Resuscitation (ILCOR) recommended that
the management of all unconscious patients who have suffered an
out-of-hospital cardiac arrest with a shockable rhythm should
include 24 h of TH at 32 –348C, initiated as soon as possible after
return of circulation.8 However, building on the ILCOR statement,
the 2010 Resuscitation Council (UK) Guidelines now stipulate that
non-shockable and in-hospital arrests should also be considered for
TH although there is limited evidence to support this.
Perinatal hypoxia occurs in around 2 in 1000 births and causes
major morbidity and mortality. Ten randomized controlled trials of
TH in these neonates showed a reduction in poor outcome with 72
h of TH at 33– 348C (NNT¼9) and its use is recommended by
NICE (IPG347).9
Management
Therapeutic hypothermia
Induction of TH should be achieved as quickly as possible and in
most cases will begin before arrival on the ICU. Initial strategies
include covered ice packs and peripheral infusion of cold i.v. fluids
unless there are signs of significant fluid overload. Further cooling
and maintenance of TH is achieved using devices that provide
either surface or core cooling, often using an automated feedback
control system that responds to changes in the patient’s temperature. Most commonly, these are water-filled cooling blankets or
suits, but there are also methods of providing localized cooling to
the brain. These include the use of cooling helmets or caps in
newborn infants with perinatal hypoxia and nasal probes designed
to provide rapid intranasal cooling in adult patients suffering
cardiac arrest.
Shivering must be prevented during TH as it increases oxygen
demand and generates heat. This is achieved using sedation and
boluses or infusions of neuromuscular blocking agents until the
temperature is ,33.58C when the shivering reflex itself is
obtunded.10
The hypothermic patient
Hypothermia affects nearly all the systems of the body. Cardiac irritability increases as temperature decreases and arrhythmias are
frequently seen ,308C. Maintenance of intravascular volume and
electrolytes is important as hypovolaemia, hypokalaemia, and
hypomagnesaemia are common especially in head injuries where
mannitol may worsen the effects of cold diuresis. Although the coagulation cascade and platelet function are impaired during hypothermia, reports of spontaneous bleeding are rare. However, if
surgical intervention is planned or if spontaneous bleeding occurs,
supportive treatment in the form of blood products and related
therapies may be required. Other complications include respiratory
secretion retention as a result of ciliary dysfunction and pressure
sores.
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Temperature management in critically ill patients
the period after rewarming and may have been an underlying cause
of the hypothermia.
Table 2 Methods of warming the hypothermic patient
Non-invasive
Invasive
Ensure dry
Cover skin
Cover/close wounds
Raise ambient temperature
Radiant warmer
Forced air warmer
Warmed IV fluids
Luminal lavage
Haemodialysis/haemofiltration
Cardiopulmonary bypass
Cardiac arrest in a hypothermic patient presents several problems; ventricular fibrillation and ventricular tachycardia may be refractory to defibrillation and drugs may have unpredictable
efficacy, even becoming toxic secondary to reduced metabolism
and clearance. Below 308C it is advised to deliver a total of three
shocks and withhold inotropic or antiarrhythmic drugs until the
core temperature increases to .308C. The drug administration
interval time should be doubled between 30 and 358C. If the arrest
is survivable, declaration of death is not possible until a core temperature of 328C has been achieved unless rewarming attempts
fail.
Summary
Temperature is not only an important clinical marker of severity of
illness but also an independent predictor of morbidity and mortality in critically ill patients. Close monitoring and regulation to
avoid extremes of body temperature is particularly important in the
critically ill patient. This will prevent the uncontrolled disruption
of homeostasis and associated subsequent organ dysfunction and
failure.
Declaration of Interest
None declared.
References
1. Perioperative hypothermia (inadvertent). Clinical guidelines CG65.
National Institute for Health and Clinical Excellence 2008
2. Barone JE. Fever: fact and fiction. J Trauma 2009; 67: 406–9
Rewarming
In general, rewarming (Table 2) should not be faster than 0.58C
h21 to avoid localized temperature differences (cerebral thermopooling), cerebral hypoxia, and impaired cerebrovascular reactivity.
An initial decrease in core temperature may be seen on commencement of rewarming as peripheral tissues become reperfused and
colder blood returns to the core. In practice, this is only clinically
significant when treating severe hypothermia.
Hypotension secondary to vasodilatation is countered by the administration of fluid boluses and vasoconstrictor infusions. As
rewarming progresses, particular attention must be given to potassium and glucose levels. Hyperkalaemia caused by shifts from the
intracellular to the extracellular compartment is common. Insulin
sensitivity may increase rapidly because of both a decrease in
insulin resistance and the return of pancreatic function.
Hypoglycaemia may result if blood glucose and insulin infusion
rates are not monitored closely.
Once the core temperature is 338C, the level of sedation and
muscle relaxation in place will require additional consideration as
activation of the shivering response increases oxygen consumption
and may lead to systemic hypoxaemia and metabolic acidosis.
Once normothermia is reached, active maintenance of this temperature is necessary to avoid rebound hyperthermia. Temperature
control is further complicated by infection, which is common in
3. Ellis FP. Mortality from heat illness and heat aggravated illness in the
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4. Gozzoli V, Schottker P, Suter PM, Ricou B. Is it worth treating fever in intensive care unit patients? Arch Int Med 2001; 161: 121– 3
5. Pedley DK, Paterson B, Morrison W. Hypothermia in elderly patients
presenting to accident and emergency during the onset of winter. Scott
Med J 2002; 47: 10– 11
6. Ireland S, Endacott R, Cameron P, Fitzgerald M, Paul E. The incidence
and significance of accidental hypothermia in major trauma—a prospective observational study. Resuscitation 2011; 82: 300–6
7. Tsuei BJ, Kearney PA. Hypothermia in the trauma patient. Injury 2004;
35: 7– 15
8. Nolan JP, Morley PT, Vanden Hoek TL, Hickey RW, ALS Task Force.
Therapeutic hypothermia after cardiac arrest. An advisory statement by
the Advanced Life Support Task Force of the International Liaison
Committee on Resuscitation. Resuscitation 2003; 57: 231– 5
9. Edwards AD, Brocklehurst P, Gunn AJ, Halliday H, Juszczak E, Levene M,
Strohm B, Thoresen M, Whitelaw A, Azzopardi D. Neurological outcomes at 18 months of age after moderate hypothermia for perinatal
hypoxic ischaemic encephalopathy: synthesis and meta-analysis of trial
data. Br Med J 2010; 340: c363
10. Polderman KH, Herold I. Therapeutic hypothermia and controlled normothermia in the intensive care unit: Practical considerations, side
effects, and cooling methods. Crit Care Med 2009; 37: 1101–20
Please see multiple choice questions 5– 8.
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