Download Fever in the ICU

Document related concepts

Sarcocystis wikipedia , lookup

West Nile fever wikipedia , lookup

Orthohantavirus wikipedia , lookup

Sepsis wikipedia , lookup

Clostridium difficile infection wikipedia , lookup

Anaerobic infection wikipedia , lookup

Traveler's diarrhea wikipedia , lookup

Hepatitis C wikipedia , lookup

Carbapenem-resistant enterobacteriaceae wikipedia , lookup

Gastroenteritis wikipedia , lookup

Chickenpox wikipedia , lookup

Trichinosis wikipedia , lookup

Hepatitis B wikipedia , lookup

Dirofilaria immitis wikipedia , lookup

Human cytomegalovirus wikipedia , lookup

Pandemic wikipedia , lookup

Oesophagostomum wikipedia , lookup

Yellow fever wikipedia , lookup

Typhoid fever wikipedia , lookup

Schistosomiasis wikipedia , lookup

Marburg virus disease wikipedia , lookup

Neonatal infection wikipedia , lookup

1793 Philadelphia yellow fever epidemic wikipedia , lookup

Leptospirosis wikipedia , lookup

Yellow fever in Buenos Aires wikipedia , lookup

Rocky Mountain spotted fever wikipedia , lookup

Coccidioidomycosis wikipedia , lookup

Hospital-acquired infection wikipedia , lookup

Transcript
FEVER IN THE ICU
Dr. Ankit Jain
DEFINITIONS

Normal Body Temperature
37°C (98.6°F)
 Diurnal Variation 1.3°C
 Core Body Temperature vs Peripheral Measurements
 Elderly Subjects have lower body temperatures.

DEFINITIONS

Fever in the ICU
Body Temperature ≥ 38.3°C (101°F)
 Body Temperature ≥ 38.0°C (100.4°F) in
Immunocompromised patients, neutropenia.

THERMOMETRY – WHERE TO MEASURE?

Thermistor Equipped Catheters (Core Body
Temperature)
Pulmonary Artery
 Oesophagus
 Urinary Bladder

More Accurate
 Continuous Monitoring

THERMOMETRY – WHERE TO MEASURE?

Peripheral Temperature

Rectal
CBT < 0.2 to 0.3 than Rectal temp
 Avoid in Neutropenic Patients


Oral
CBT > 0.5
 Measure with Electronic Probes not Mercury
 Cold Liquids


Tympanic Membrane
Head Injury/Stroke?
 Cerebral Temp vs Core Temp

Axillary
 Temporal Artery

THE FEBRILE RESPONSE
Inflammatory Cytokines – Endogenous Pyrogens.
 Reset of the Hypothalamic Thermostat
 Neuroecndocrine Control Mechanisms.

THE FEBRILE RESPONSE
Fever is a sign of Inflammation not Infection.
 Infection is most significant cause of
Inflammation.
 Severity of Fever ≠ Severity of Infection

FEVER VS. HYPERTHERMIA

Hyperthermia
Abnormal Temperature Regulation.
 Eg: Heat Exhaustion, Heat Stroke, MH, NMS,
Serotonin Syndrome.


Fever
Thermoregulatory Centre is Intact i.e Normal
Temperature Regulation.
 But Operating at a Higher Set Point.
 Adaptive Response.
 Eg: Infectious and Non Infectious causes of Fever.

INITIAL APPROACH
New Onset Fever in the ICU
INFECTIOUS OR NON INFECTIOUS?
50:50
 Medical and Surgical
 Noninfectious causes once Infectious Causes are
Ruled Out!
 Infectious Causes?? Likely if the Risk Factors are
Present.
 Fever>38.9C(102.2)more likely Infectious
 Fever>41.1 (105.9)more likely non
infectious/neurological.

ASSESSMENT OF RISK FACTORS

Risk Factors for Nosocomial Microbial Infections
in the ICU
PATIENT FACTORS
SOURCES OF
INFECTION
Advanced Age
Intravascular Catheters
Severe Underlying Disease Intubation and
Mechanical Ventilation
Neutropenia
Bladder Catheters
Immunosuppression
Nasogastric Tubes
Neurological Disease with
Impaired Consciousness
Surgical Drains
Stress Ulcer Prophylaxis
Prosthesis
Prolonged ICU Stay
Bed Sores
RISK FACTORS
4 Infections account for 3/4th of ICU Acquired
Infections
 3 of these involve indwelling plastic devices

Pneumonias – 83% in Intubated Patients
 UTI – 97% in Catheterized patients
 Bloodstream Infections – 87% from IV Catheters.
 Surgical Site Infections.

(Richards MJ, Edwards JR, Culver DH, Gaynes RP. The National Nosocomial
Infections Surveillance System. Nosocomial infections in combined medicalsurgical intensive care units in the United States. Infect Control Hosp Epidemiol
2000; 21:510–515)
VENTILATOR ASSOCIATED
PNEUMONIA
VENTILATOR ASSOCIATED PNEUMONIA

Suspect:
Fever
 Pt. on Ventilator
 Increased Volume of Respiratory Secretions
 Change in Character of Secretions


Lab Clues
Leukocytosis/Leukopenia
 CXR: New or Progressive Infiltrate

VAP
Limited Diagnostic Accuracy of Clinical Criteria
 Non Specific Nature of Pulmonary Infiltrates
 Conditions other than pneumonia are the most
frequent causes of pulmonary infiltrates in ICU
patients
 Non Infectious Causes of Pulmonary Infiltrates

Pulmonary Oedema
 ARDS
 Atelectasis


Sensitivity OF CXR?? Vs CT

Diagnosis of Pneumonia cannot be ruled out with a
portable CXR.
VAP
New Clinical Criteria
 National Healthcare Safety Network
 No involvement of CXR Findings.

Deterioration in Arterial
Oxygenation
Change In Body
Temperature/ WBC
VAP
MICROBIOLOGICAL EVALUATION
 Sample

Tracheal Aspirate
 BAL

Before Antibiotics
 Role of Blood Cultures

VAP - PREVENTION
Aspiration – of Oropharyngeal flora.
 Oral Decontamination – Oral Chlorhexidine
Gargles
 Routine Airway Care – Reduce Endotracheal
Suctioning.
 Clearance of Subglottic secretions.

CATHETER ASSOCIATED
URINARY TRACT INFECTIONS
URINARY TRACT INFECTIONS

Suspect
Fever
 Urinary Catheter (Most patients in ICU)


Majority are Colonizers
NOT NECESSARILY
•
•
•
•
A
UTI
Common symptoms of UTI such as dysuria and
frequency are not relevant in catheterized patients, and
the usual signs of infection (fever, leukocytosis) can lack
specificity in catheterized patients.
Fever or Leucocytosis (Another Infection?)
Cloudy Urine
White Blood Cells in Urine(But absence of Pyuria
against CA-UTI )
CA-UTI DAIGNOSIS
Catheter <30 days - urine through the catheter port or
catheter tubing. Catheter > 30 days- catheter should
be replaced before collecting the urine specimen.
 Significant bacteriuria in catheterized patients ≥105
cfu/mL. How-ever, over 90% of patients with
significant bacteriuria have no other evidence of
infection (asymptomatic bacteriuria) (8).

CA-UTI DAIGNOSIS

Catheter-associated urinary tract infection (CAUTI) is defined as a urine culture that grows
>103 cfu/mL in a patient with clinical signs of a
symptomatic UTI. These can include:





Bacteremia with the same organism isolated in blood
and urine.
New costovertebral tenderness.
Rigors.
New onset of delirium or depressed consciousness.
Increased spasticity in patients with spinal cord
injuries.
CA-UTI PREVENTION
Remove catheter when no longer needed.
 DO NOT use prophylactic antibiotics.
 ? Antibiotic Impregnated Urinary Catheters

CA-UTI TREATMENT
Change catheter
 Empirical Abx
 Abx as per C/S

UTI - CANDIDURIA
Colonization
 Disseminated Candidiasis
 Candiduria the result not Cause.
 Candiduriathe only evidence of Disseminated
Candidiasis.
 Blood Cultures inrevealing in >50%
 Assess clinical condition of Patient.

UTI - CANDIDURIA

Asymptmatic Candiduria
Remove Catheter when possible.
 Repeat Cultures
 No treatment (Unless neutropenic.)
 Persistant Candiduria – Blood, Kidney.


Symptomatic Candiduria
Blood Cultures
 Kidney Imaging
 Antifungals

CATHETER RELATED
BLOOD STREAM
INFECTIONS
VASCULAR CATHETER RELATED
INFECTIONS

Suspect:
Fever
 Leucocytosis
 Catheter >3days
 Local Signs of Infection

WHAT IS NOT A CRBSI

Local Signs of Infection
No Predictive value of presence of Septicemia.
 Purulent drainage uncommon – Exit site infection without
blood stream infection

WHAT IS??

Diagnosis with Cultures.
(Mermel LA, Allon M, Bouza E, et al. Clinical practice guidelines for the diagnosis
and management of intravascular catheter-related infection: 2009 update by the
Infectious Diseases Society of America. Clin Infect Dis 2009; 49:1–45.)
WHICH METHOD TO USE?

Leave the Catheter Alone
Most evaluations of CRBSI do not confirm the
daignosis.
 Guidewire Replacements have adverse effects.


Replace Catheter over Guidewire
Risk of dislodging clot.
 Difficult Access.


Remove and insert new catheter at new site

Prosthetic Valves, Indwelling pacemaker wires,
purulent discharge, neutropenia.
PERSISTENT SEPSIS

Persistent fever/sepsis after 72 hrs of Abx
Suppurative Thrombophlebitis/Intravascular Abscess
 Endocarditis

SURGICAL SITE
INFECTIONS
SURGICAL SITE INFECTION

Versus Normal Response to trauma
Starts almost immediately.
 Less than 2 days.
 Fever < 38.5Lasts


Suspect
Fever > 38.5
 Lasts longer than 2 days.
 Starts on 3rd post op day. (Exception – Necrotizing Wound
Infections)
 Local Signs (Remove Dressing and see)


Treatment
Surgical Opinion.
 Surgical Debridement
 Antibiotics.

CLOSTRIDIUM DIFFICILE INFECTION

Suspect
New Onset Diarrhoea
 Acid Suppression with PPI

Diagnosis
 Stool Cultures Unreliable
 ELISA to detect Cytotoxins



Two stool samples better than One. (85 vs 95%
Sensitivity)
Treat
Antibiotics
 Stop Antiperistaltic agents
 Discontinue PPIs

OTHER CAUSES OF INFECTIOUS
FEVER
SINUSITIS

Suspect:
Nasogastric Tubes
 Nasal Intubation
 Orotracheal Tubes
 Sinus Tenderness


Investigate
Bedside Plain Radiograms
 CT PNS
 Needle Aspiration with Microscopy C/S.


Treat
Antibiotics
 FESS

ACUTE ACALCULOUS CHOLECYSTITIS
Often Missed
 Complications: Gangrenous Cholecystitis,
Perforation.
 Pain and RUQ tenderness absent in 1/3rd
patients
 Fever, Elevated Bilirubin.
 Ix: USG, CT.
 Tx: Cholecystectomy, Percutanious Drainage,
Antibiotics.

NON INFECTIOUS CAUSES OF
FEVER IN ICU.
EARLY POST OPERATIVE FEVER
Due to Tissue Injury and Inflammation.
 Suspect

Fever on First Postop day.
 No Apparent Infection.
 Resolves in 24-48 hours.

VENOUS THROMBOEMBOLISM

Suspect


Risk Factors for VTE
Acute Pulmonary Embolism can cause fever that
lasts upto 1 week.
BLOOD TRANSFUSIONS

Mechanism
Even in Absence of Infection or Hemolysis.
 Antileukocyte Ab in recepient that react with donor
leucocytes.


Suspect
More Common with Platelet Transfusions
 Fever during or upto 6 hrs after transfusion.


Treat
Stop BT
 Send Donor and Recipient Sample for Ix.

DRUG FEVER

Suspect
No other cause
 Onset of fecver: Few hours to 3weeks after starting
drug
 ?Hypersensitivity reaction(Rash, Eosinophilia,)
absent in >75%.
 Common Drugs

DRUG FEVER

Treatment
Stop Offending Drug if possible
 Fever should stop within 2-3 days
 Can Persist for upto7 days

ADRENAL FAILURE

Mechanism

Spontaneous Adrenal Hemorrhaging in
Anticoagulation therapy, DIC.
IATROGENIC FEVER
Faulty Regulators
 Check Temperature settings on Air Mattresses
Forced air Warmers

ANTIPYRETIC THERAPY
SHOULD FEVER BE TREATED??
BENEFITS OF FEVER
Fever as a Host Defense Mechanism
 Fever is a normal Adaptive response that
enhances the ability to eradicate infection.

FEVER AS HOST DEFENCE
Arons MM, Wheeler AP, Bernard GR, et al.
Effects of ibuprofen on the physiology and
survival of hypothermic sepsis. Critical Care Med
1999; 27:699–707.
 Clemmer TP, Fisher CJ, Bone RC, et al.
Hypothermia in the sepsis syndrome and clinical
outcome. Crit Care Med 1990; 18:801–806.

WHEN IS FEVER HARMFUL?
Tachycardia – Patients with Heart Disease.
 Post Cardiac Arrest and Ischemic Stroke:
Aggravates Ischemic Brain Injury.
 Hyperpyrexia : Temp > 42 C for greater than 1 hr
– Non Ischemic Brain Damage.

COOLING BLANKETS AND FEVER

Understand the Febrile Response
Cutaneous Vasoconstriction
 Increased Skeletal Muscle Activity (Shivering and
Rigors)

Body behaves like it is already wrapped in a
cooling blanket
 Ineffective!!
 Appropriate in Hyperthermia

HYPERTHERMIA
DRUG INDUCED HYPERTHERMIA

Source of thermal stress
Heat Stroke : environment. Unlikely in the ICU.
 Versus Drug induced metabolic Heat production.


Examples
Malignant Hyperthermia
 Neuroleptic Malignant Syndrome
 Serotonin Syndrome

MALIGNANT HYPERTHERMIA

Suspect:








In OT
Exposure to Halogenated Inhalation Agents, NM Blocking
Agents
Sudden Rise in EtCO2
Generalized Muscle Rigidity (Rhabdomyolisis,
Myoglobinuria )
Hyperthermia >104 F
Altered Mental Status
Autonomic Instabiity
Treatment
Discontinue offending agent
 Supportive Care
 Dantrolene

NEUROLEPTIC MALIGNANT SYNDROME

Suspect Drugs
(Inhibit Dopaminergic Transmission)
Antipsychotics HALOPERIDOL (Serenase)
 Antiemetics eg Metaclopramide, prochlorpreazine
 CNS Stimulants: Amphetamines
 TCAs

Discontinuation of Dopaminergic Drugs eg:
Levodopa, Bromocriptine
 No Relation between Intensity or Duration of Tx.

NMS

Suspect:






Muscle Rigidity (Myoglubinuria)
Altered Sensorium
Symptoms 24-72 hrs after onset of tx.
Hyperthermia following Muscle Rigidity >41 C
Autonomic Instability
Labs
CPK > 1000 U/L
 Can Mimic Sepsis with TLC >40K

SEROTONIN SYNDROME

Suspect
Recent ingestion of Seritonergic Drugs.(Linezolid)
 Usually within last few Hours
 Maybe upto 5 weeks
 Hyperkinesis, Hyperreflexia and Clonus.
