Disordered temperature regulation is a common manifestation
of acute and critical illness. Hyperthermia occurs secondary to heat generated
by hypermetabolism that accompanies inflammation. This is associated with altered central nervous system
thermoregulation resulting in an upward adjustment of the hypothalamic
thermostat.
Fever has both beneficial and harmful
effects. Fever is a beneficial
survival mechanism that enables the body to combat infection. Endogenous pyrogens stimulate
production of T & B lymphocytes which increases antibody production
twenty-fold. The harmful effect of
fever is a result of increased metabolic activity which in turn increases
oxygen consumption. The goal of
therapy should be aimed at allowing the body’s defense mechanism to help combat
the infectious organism without compromising tissue oxygenation. If the
fever is not compromising tissue oxygenation, it is not necessary to treat
fever.
Diagnosis and source of infection are often
difficult to identify in the acutely or critically ill patient in whom many
potential sources of fever may exist.
Also, there are many non-infectious clinical conditions that produce
hyperthermia that should be considered when attempting to identify the source
of fever.
The following algorithm was designed to assist
the resident and the nurse in clinical decision making for appropriate
intervention and treatment of the acutely/critically ill febrile patient.
Other etiologies of fever should
be investigated:
Miscellaneous
etiologies:
Alcohol withdrawal
Deep venous thrombosis
Drug withdrawal
Drugs *
Hematoma
Neuroleptic hyperthermia
Pancreatitis
Subarachnoid hemorrhage
SIRS (secondary to shock, trauma)
Tissue necrosis
Transfusions
*Drugs:
Allopurinol
Antibiotics (penicillin, sulfonamide,
cephalosporins)
Antihistamines
Dobutamine
Hydralazine
Methyldopa
Procainamide
Phenytoin
Quinidine
Possible Sites of
Infection Seen in the Surgical or ICU Patient
Pneumonia: (The
most common nosocomial infection in the ICU). Risk factors include prolonged intubation, ,supine posture,
oral cavity colonization, aspiration, chest trauma and ARDS. Pathogens commonly found include: gram
negative enteric organisms (Haemophilus, E coli, Klebsiella, Pseudomonas, and
Enterobacter) and/or gram positive organisms (Staphylococcus aureus, other
strep species and Enterococcus).
Urinary Tract Infection: Usually associated with Foley catheterization. Pathogens commonly found
include: E. coli, Enterococcus, Klebsiella, Pseudomonas, Enterobacter, Proteus
and Candida species.
Wound Infection: The wound may be erythematous with or without purulent drainage, or
subcutaneous crepitus. A surgical
wound infection may not be clinically apparent until 5 to 7 days
post-operatively.
Vascular Catheter Related
Infection: The risk of line infection
increases with the length of time the vascular cannula has been in place.
Factors associated with reduced infection include proper insertion technique,
maintenance of an intact Biopatch and dressing and cleansing hubs prior to
accessing them.
Sinusitis: The risk factors include: nasogastric tube, nasotracheal tube, nasal
packing, facial fractures, recumbent positions, and high dose steroids.
Intraabdominal Infection: The risk factors include: peritoneal contamination by GI contents,
ascites, or presence of intraabdominal hematoma. If a patient develops bacteremia with Klebsiella,
Enterobacter, E. coli, B fragilis, or Enterococci species, an intraabdominal
source should be considered and investigated.
Acalulous Cholecystitis: Any critically ill patient is at risk. Contributing factors include: opiates, fasting, TPN and shock.
Empyema: The risk factors include: pneumothorax, hemothorax, penetrating chest
trauma, unrecognized diaphragmatic perforation and pneumonia.
Tracheitis: Usually associated with tracheal intubation. Manifestations may include foul smelling purulent tracheal
secretions.
Fungal Infection: This is usually seen in immunocompromised patients or in patients who
have been critically ill for a prolonged period of time and have been on
extended courses of broad spectrum antibiotics.
Vascular Grafts: Manifestations of vascular graft related infections include: wound
drainage, wound infection, graft thrombosis, septic emboli and pseudoaneurysm.
Endocarditis: Central venous catheters can be an etiologic factor. Common pathogens include: Staphylococcus
and Streptococcus.
Mediastinitis: Can be seen after surgical procedures performed through a median
sternotomy and with injuries to the aerodigestive tract.
Central Nervous System Infection: The risk factors include CSF leak (following craniotomy or basilar
skull fracture), craniotomy, intraventricular catheter or penetrating spinal
cord injury.
Nursing Guidelines
The goal
of therapy is to allow temperature elevation considering the possible benefits
of immune functioning, but be aware of the harmful effects that require immediate
interventions.
1. Tissue
oxygenation: Keep ScvO2 > 65, SaO2 > 90, in the
absence of shivering
2.
Hydration: PCWP > 10, CVP > 8, UOP > 30cc/hr are general (not strict)
guidelines
3.
Nutrition: Consult R.D. to ensure metabolic needs are being met with current
feeding regimen.
4.
Pain/Sedation/Monitor for signs and symptoms of pain and assess need for
sedation. Adequate sedation will help control shivering. If unsuccessful, shivering
will need NMBA.
5.
External cooling should only be used if temperature is > 40° C.
AND the patient is receiving a NMBA and is properly sedated.
6.
Antipyretics may be given if patient temperature is > 39.0°C
and adequate tissue oxygenation cannot
be achieved.
7. Nasopharyngeal
or tracheal temp probes may be preferred if the patient does not have a temp-sensing
Foley catheter or pulmonary artery catheter.
8. Blood
cultures should be obtained peripherally unless impossible to do so, per Hosp
policy.
9. When
obtaining blood cultures, wipe down the tops of the
culture bottles, stick the skin only after sterile prep, and do not allow the
top of the culture bottle to touch anything after prep.
External Cooling:
Hyperthermia is a natural adaptive mechanism in critical illness.
Hypothalamic temperature regulation is adjusted upward to accommodate the
hyperthermia associated with hypermetabolism and infection. Under these
circumstances, attempts to lower temperature to normal can be harmful because
CNS autoregulation has been reset at a higher core temperature. External cooling will produce increases
in sympathetic tone that markedly increase oxygen consumption. The body will attempt to restore
temperature, during external cooling by stimulating skeletal muscle, producing
shivering, will increase tissue oxygen consumption. External cooling will cause peripheral vasoconstriction.
This will shunt heat deeper and make it more difficult to cool. Recognizing the role of hyperthermia in
critical illness, a more permissive attitude is taken towards temperature
elevation. Modest rise in core
temperature is monitored without treatment, and moderate temperature elevation
(>102.2°) is
treated with antipyretics.
External cooling is reserved for extreme temperature elevation (>104°) when compromise of tissue
oxygenation and/or direct tissue damage may occur. More aggressive temperature control can and should be
employed when marginal tissue oxygenation occurs with lower temperatures.
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Revised: 12/13
