FEVER IN ICU
Surg SLt LO Majolagbe
DEPT OF ANAESTHESIA/ICU
NNRH OJO
OUTLINE
 INTRODUCTION
 EPIDEMIOLOGY
 CAUSES
 EVALUATION
 MANAGEMENT
Introduction
 Fever is a common problem in the ICU
 It could be infections, non-infectious or mixed
Definition
 It is defined as a coordinated neuro-endocrine,
autonomic and behavioral response that is adaptive
and an essential part of acute-phase response to
immune stimulus or tissue injury.
Definition
 It is coordinated by the Hypothalamus (Thermostat).
 Neural input from peripheral thermoreceptors.
 Humoral stimulus from inflammation or infection.
 Hypothalamic set point – 37 °C. Varies through the
course of the day. Rises up by 0.5 as the day goes by
(evening).
What is a fever?
 Society of Critical Care Medicine(SCCM) and
Infectious disease society of America(IDSA):
 Normal : 98.2 °F (36.8 °C)
 Elevation in body temperature above normal range
from increase in temperature regulatory set point :
99.5 - 100.9 °F (37.5 – 38.2 °C)
 Hyperpyrexia:
 104 - 106.7 °F (40 – 41.5 °C).
 Hyperthermia (Set point not affected).
 Hypothermia 95 °F (35 °C)
Fever of Unknown Origin (FUO)
 Fever on several occasions, persisting without
diagnosis for at least 3 weeks in spite of at least 1
week’s investigation in hospital.
Introduction
 30% of medical patients will be febrile during their
stay in ICU.
 90% of critically ill patients with severe sepsis will
experience fever during their stay in ICU.
 The acquisition of fever in the ICU is associated with
adverse outcomes.
Introduction
Epidemiology
 The incidence of fever in the ICU ranges from 28%
to 70%.
 Infectious as well as noninfectious etiologies
contribute almost equally to the causation of febrile
episodes.
 35-55% are infectious.
 At least 50% of febrile episodes are non-infectious.
Merits of Fever
 It helps to rid of the host from invading pathogens:
e.g. Plasmodium species, Spirochaetes, Bacteria such
as Streptococcus pneumoniae and Treponema
pallidum.
 Enhances parameters of immune function
 Improves antibody production
 Activates T-cell
 Produces cytokines
 Enhances neutrophil and macrophage function
Demerits of Fever
 Increase in cardiac output
 Increase oxygen consumption (10% per 1°C)
 Increase carbon dioxide production
 Poor neurological outcomes in patients with stroke
and traumatic brain injury
 Increase basal metabolic rate
 Fever is poorly tolerated in patients with reduced
cardio-respiratory reserve
Fever versus hyperthermia
 Fever: resetting of the thermostatic set-point in the
anterior hypothalamus and the resultant initiation of
heat-conserving mechanisms until the internal
temperature reaches the new level
 If acute (and less commonly chronic), infection unless
proven otherwise
 Hyperthermia: an elevation in body temperature that
occurs in the absence of resetting of the hypothalamic
thermoregulatory center
 Usually not mediated by infectious diseases
Pathogenesis
 Pyrogens (endogenous and exogenous) trigger fevers
via release of prostaglandin E2  hypothalamic
stimulation  vasoconstriction, then shivering 
temp rise
 Endogenous: IL1, 6,8, TNF, IFNa,b,g  arachidonic
acid pathway activated
 Can be released in collagen vascular, malignancy
 Exogenous: i.e. LPS  binds to lipopolysaccharide
binding protein  release of IL-1
 Typically infectious
Causes
 Infectious, Non – Infectious or Both.
 Most noninfectious disorders usually do not lead to a
fever >38.9°C (102°F)
Non Infectious causes
Non Infectious causes - Drugs
Non Infectious causes - Drugs
Non Infectious causes - Drugs
 Remember to always document drug related fever as
an allergy!
Fever Associated With Drug Withdrawal
 Fever may occur several hours or days after
discontinuation of a medication.
 Patient will have Fever, Tachycardia, Diaphoresis,
Hyperreflexia.
 Offenders are Alcohol, Opiates, Barbiturates
Benzodiazepines.
Febrile Transfusion Reactions
 Complicate about 0.5% of blood transfusions.
 It is more common following platelet transfusion.
 It usually begin within 30 mins to 2 hrs. after a blood
product transfusion.
 The fever generally lasts between 2 to 24 hrs. and
may be preceded by chills.
Other Non – Infectious causes
 ICU Environment
 Specialized Mattresses
 Hot Lights
 Cardiopulmonary Bypass
 Peritoneal Lavage
 Dialysis
 Post Op fever
Other Non – Infectious causes
 Hyperthermic Syndromes
 Neuroleptic Malignant Syndrome
 Malignant Hyperthermia
 Environmental (heatstroke) – Tropics
 Serotonin Syndrome
 Endocrine: Thyrotoxicosis, Pheochromocytoma and
Adrenal Crisis
MH - NMS
NMS
 Neuroleptic Malignant Syndrome (3 major or 2 major
+ 4 minor)
 Major Criteria: Insidious onset of hyperthermia,
Muscle rigidity, Elevated CPK
 Minor criteria: Tachycardia, Tachypnea, Altered
sensorium, Abnormal BP, Leukocytosis.
Infectious causes of fever
whilst in ICU
 Ventilator associated pneumonia
 Catheter related blood stream infections
 Urosepsis
 Intra-abdominal infections
 Sinus infections
 Diarrhea
Infectious causes
 Community acquired pneumonia
 Acute CNS infection
 Urinary tract infection
 Abdominal focus of infection
 Wound infection/ Pus collections
Infectious causes
 Fungal infections including candidemia
 Surgical wound infections
 Acalculous cholecystitis
 Endocarditis
 Meningitis
Ventilator Associated Pneumonia
 Pneumonia in a patient who has been on ventilator
for >48 hours
 Risk of VAP highest early in the course of hospital
stay
 3%/day for first 5 days
 2%/day from 5 to 10 days &
 1%/day thereafter
 Mortality in Pt with VAP twice than pts without VAP
(33 and 50%).
Ventilator Associated Pneumonia
System
System
Evaluation
 Is this a complication of the underlying reason for
admission?
 Untreated, relapsed, or metastatic focus of infection •
Post-surgical infection (surgical site infection, intra-
abdominal abscess)
 Is this a separate nosocomial process? • Hospital-
acquired (VAP, aspiration) • CA-UTI • Catheter-
Related Bloodstream Infection (CRBSI) • Clostridium
 Is this non-infectious? • Drug fever • Others
Evaluation
Head to Toe Approach
Evaluation
Evaluation
 Bloods –counts, procalcitonin
 Imaging – CXR scans as indicated
(abdomen, sinus, CT brain)
 Cultures as appropriate- ETA, BAL,
Urine, Blood cultures (peripheral
and through lines), cultures from
pus, wound etc., Stool for
clostridium
Evaluation
 Assess if lines are “old” and if there is
any evidence of line sepsis – re-site line
if indicated
 Change urinary catheter
 May need NG change- if sinus infection
suspected
Procalcitonin
 Procalcitonin can be used as an adjunctive to
microbiological tests for identifying infective diseases.
 SIRS 0.6 to 2.0 ng/mL
 Severe sepsis 2 to10 ng/mL
 Septic shock ≥10 ng/mL
 Viral infections, recent surgery, and chronic
inflammatory states are not associated with any
increment
C-Reactive Protein
 Originally named for its ability to bind the C
polysaccharide of Streptococcus pneumoniae
 CRP is mostly synthesized by hepatocytes in response
to IL-6, IL-1 and TGF-ß. The plasma level of CRP
rises within 6 hrs., double every 8 hrs. and peak at
50 hrs. in systemic inflammatory stimulus
C-Reactive Protein
 Normal level in healthy adults is <10 mg/L.
 May rise up to a 1000-fold in response to an
inflammatory stimulus.
Management
 Relative risk-benefits should be evaluated in
individual patient.
 Treat with acetaminophen if: Temperature > 38°C
 External cooling useful in cases of hyperthermia
rather than fever.
External cooling techniques
Conclusion
 Prompt and adequate evaluation and treatment is
key in critically ill patients with fever to avoid further
deterioration and adverse outcomes.
THANK YOU FOR YOUR RAPT
ATTENTION

Fever IN ICU.pptx

  • 1.
    FEVER IN ICU SurgSLt LO Majolagbe DEPT OF ANAESTHESIA/ICU NNRH OJO
  • 2.
    OUTLINE  INTRODUCTION  EPIDEMIOLOGY CAUSES  EVALUATION  MANAGEMENT
  • 3.
    Introduction  Fever isa common problem in the ICU  It could be infections, non-infectious or mixed
  • 4.
    Definition  It isdefined as a coordinated neuro-endocrine, autonomic and behavioral response that is adaptive and an essential part of acute-phase response to immune stimulus or tissue injury.
  • 5.
    Definition  It iscoordinated by the Hypothalamus (Thermostat).  Neural input from peripheral thermoreceptors.  Humoral stimulus from inflammation or infection.  Hypothalamic set point – 37 °C. Varies through the course of the day. Rises up by 0.5 as the day goes by (evening).
  • 6.
    What is afever?  Society of Critical Care Medicine(SCCM) and Infectious disease society of America(IDSA):  Normal : 98.2 °F (36.8 °C)  Elevation in body temperature above normal range from increase in temperature regulatory set point : 99.5 - 100.9 °F (37.5 – 38.2 °C)  Hyperpyrexia:  104 - 106.7 °F (40 – 41.5 °C).  Hyperthermia (Set point not affected).  Hypothermia 95 °F (35 °C)
  • 7.
    Fever of UnknownOrigin (FUO)  Fever on several occasions, persisting without diagnosis for at least 3 weeks in spite of at least 1 week’s investigation in hospital.
  • 8.
    Introduction  30% ofmedical patients will be febrile during their stay in ICU.  90% of critically ill patients with severe sepsis will experience fever during their stay in ICU.  The acquisition of fever in the ICU is associated with adverse outcomes.
  • 9.
  • 10.
    Epidemiology  The incidenceof fever in the ICU ranges from 28% to 70%.  Infectious as well as noninfectious etiologies contribute almost equally to the causation of febrile episodes.  35-55% are infectious.  At least 50% of febrile episodes are non-infectious.
  • 11.
    Merits of Fever It helps to rid of the host from invading pathogens: e.g. Plasmodium species, Spirochaetes, Bacteria such as Streptococcus pneumoniae and Treponema pallidum.  Enhances parameters of immune function  Improves antibody production  Activates T-cell  Produces cytokines  Enhances neutrophil and macrophage function
  • 12.
    Demerits of Fever Increase in cardiac output  Increase oxygen consumption (10% per 1°C)  Increase carbon dioxide production  Poor neurological outcomes in patients with stroke and traumatic brain injury  Increase basal metabolic rate  Fever is poorly tolerated in patients with reduced cardio-respiratory reserve
  • 13.
    Fever versus hyperthermia Fever: resetting of the thermostatic set-point in the anterior hypothalamus and the resultant initiation of heat-conserving mechanisms until the internal temperature reaches the new level  If acute (and less commonly chronic), infection unless proven otherwise  Hyperthermia: an elevation in body temperature that occurs in the absence of resetting of the hypothalamic thermoregulatory center  Usually not mediated by infectious diseases
  • 14.
    Pathogenesis  Pyrogens (endogenousand exogenous) trigger fevers via release of prostaglandin E2  hypothalamic stimulation  vasoconstriction, then shivering  temp rise  Endogenous: IL1, 6,8, TNF, IFNa,b,g  arachidonic acid pathway activated  Can be released in collagen vascular, malignancy  Exogenous: i.e. LPS  binds to lipopolysaccharide binding protein  release of IL-1  Typically infectious
  • 15.
    Causes  Infectious, Non– Infectious or Both.  Most noninfectious disorders usually do not lead to a fever >38.9°C (102°F)
  • 16.
  • 17.
  • 18.
  • 19.
    Non Infectious causes- Drugs  Remember to always document drug related fever as an allergy!
  • 20.
    Fever Associated WithDrug Withdrawal  Fever may occur several hours or days after discontinuation of a medication.  Patient will have Fever, Tachycardia, Diaphoresis, Hyperreflexia.  Offenders are Alcohol, Opiates, Barbiturates Benzodiazepines.
  • 21.
    Febrile Transfusion Reactions Complicate about 0.5% of blood transfusions.  It is more common following platelet transfusion.  It usually begin within 30 mins to 2 hrs. after a blood product transfusion.  The fever generally lasts between 2 to 24 hrs. and may be preceded by chills.
  • 22.
    Other Non –Infectious causes  ICU Environment  Specialized Mattresses  Hot Lights  Cardiopulmonary Bypass  Peritoneal Lavage  Dialysis  Post Op fever
  • 23.
    Other Non –Infectious causes  Hyperthermic Syndromes  Neuroleptic Malignant Syndrome  Malignant Hyperthermia  Environmental (heatstroke) – Tropics  Serotonin Syndrome  Endocrine: Thyrotoxicosis, Pheochromocytoma and Adrenal Crisis
  • 24.
  • 25.
    NMS  Neuroleptic MalignantSyndrome (3 major or 2 major + 4 minor)  Major Criteria: Insidious onset of hyperthermia, Muscle rigidity, Elevated CPK  Minor criteria: Tachycardia, Tachypnea, Altered sensorium, Abnormal BP, Leukocytosis.
  • 26.
    Infectious causes offever whilst in ICU  Ventilator associated pneumonia  Catheter related blood stream infections  Urosepsis  Intra-abdominal infections  Sinus infections  Diarrhea
  • 27.
    Infectious causes  Communityacquired pneumonia  Acute CNS infection  Urinary tract infection  Abdominal focus of infection  Wound infection/ Pus collections
  • 28.
    Infectious causes  Fungalinfections including candidemia  Surgical wound infections  Acalculous cholecystitis  Endocarditis  Meningitis
  • 29.
    Ventilator Associated Pneumonia Pneumonia in a patient who has been on ventilator for >48 hours  Risk of VAP highest early in the course of hospital stay  3%/day for first 5 days  2%/day from 5 to 10 days &  1%/day thereafter  Mortality in Pt with VAP twice than pts without VAP (33 and 50%).
  • 30.
  • 31.
  • 32.
  • 33.
    Evaluation  Is thisa complication of the underlying reason for admission?  Untreated, relapsed, or metastatic focus of infection • Post-surgical infection (surgical site infection, intra- abdominal abscess)  Is this a separate nosocomial process? • Hospital- acquired (VAP, aspiration) • CA-UTI • Catheter- Related Bloodstream Infection (CRBSI) • Clostridium  Is this non-infectious? • Drug fever • Others
  • 34.
  • 35.
    Head to ToeApproach
  • 36.
  • 37.
    Evaluation  Bloods –counts,procalcitonin  Imaging – CXR scans as indicated (abdomen, sinus, CT brain)  Cultures as appropriate- ETA, BAL, Urine, Blood cultures (peripheral and through lines), cultures from pus, wound etc., Stool for clostridium
  • 38.
    Evaluation  Assess iflines are “old” and if there is any evidence of line sepsis – re-site line if indicated  Change urinary catheter  May need NG change- if sinus infection suspected
  • 39.
    Procalcitonin  Procalcitonin canbe used as an adjunctive to microbiological tests for identifying infective diseases.  SIRS 0.6 to 2.0 ng/mL  Severe sepsis 2 to10 ng/mL  Septic shock ≥10 ng/mL  Viral infections, recent surgery, and chronic inflammatory states are not associated with any increment
  • 40.
    C-Reactive Protein  Originallynamed for its ability to bind the C polysaccharide of Streptococcus pneumoniae  CRP is mostly synthesized by hepatocytes in response to IL-6, IL-1 and TGF-ß. The plasma level of CRP rises within 6 hrs., double every 8 hrs. and peak at 50 hrs. in systemic inflammatory stimulus
  • 41.
    C-Reactive Protein  Normallevel in healthy adults is <10 mg/L.  May rise up to a 1000-fold in response to an inflammatory stimulus.
  • 42.
    Management  Relative risk-benefitsshould be evaluated in individual patient.  Treat with acetaminophen if: Temperature > 38°C  External cooling useful in cases of hyperthermia rather than fever.
  • 43.
  • 44.
    Conclusion  Prompt andadequate evaluation and treatment is key in critically ill patients with fever to avoid further deterioration and adverse outcomes.
  • 45.
    THANK YOU FORYOUR RAPT ATTENTION