Alterations in body temperature Flashcards
NORMAL TEMPERATURE
NORMAL TEMPERATURE ● Core body temperature ○ 36.5-37.5 C ● Variability exists ○ 36.8 ± 0.4 C at 6 am ○ 37.2 C – 37.7 C at 4-6 pm ● Timing of fever is important! ○ High in the afternoon ○ Low in the morning ● Rectal temp is 0.4 C higher than oral temp
preferred for Children
Rectal
ORAL:
preferred for Adults
AXILLARY:
common for Adults
Fever associated with various changes.
○ Vasoconstriction
○ Shivering
○ Behavioral changes
PYROGENS
● Any substance causing fever
● May be caused by infection (development of antigens)
● Stimulates the production of pyrogenic cytokines
● Antibiotics may cause fever!
PYROGENIC CYTOKINES
● Small proteins that regulate immune, inflammatory, and hematopoietic processes
● IL-1 (most common for autoimmune problems: px always has fever), IL-6, TNF, CNTF and IIFNα
● May be released in infections, inflammatory processes, trauma, tissue necrosis, and antigenantibody complexes
● Needed to differentiate progenitor cells
● Normally has physiologic effects but pathologic in excess (ex., gout)
● Needed to stimulate blood and immune production.
However, overproduction can also lead to an inflammatory response
PGE2
● Stimulation by the cytokines increases the hypothalamic set point as well as induces other s/sx (ex., arthralgia & myalgia)
● Vasodilation, GIT effects
● PGE2 is produced centrally and peripherally.
Peripheral production causes arthralgia and myalgia, central production causes fever. However, it is not the PGE2 itself that would cause the fever,
but the stimulation of the cAMP (neurotransmitter).
Induction of Fever
Infection → activate monocytes & macrophages → release
pyrogens, ILs, cytokines → stimulate hypothalamus →
release prostaglandin (PGE2) → set hypothalamic set
point higher → FEVER
PGE2:
stage where you will develop fever
HYPERPYREXIA
● Fever >41.5 C
● Severe infections or CNS hemorrhage
● Usually secondary to CNS problem
● Changing of hypothalamic set point to a higher level
● Very high fever with several complications
● >41.5C – look for s/sx of CNS infxn; ideally perform CT scan
Rare causes of elevated hypothalamic set point
○ Local trauma, hemorrhage, tumor or intrinsic hypothalamic malfunction
○ Sometimes even medications
TREATMENT of Hyperpyrexia
● Usually self-limited (no medications)
● In some bacterial infections, assessment of fever
patterns can help correctly give diagnosis and
treatment (for prolonged fever)
○ Normal fever: ↑temp = ↑pulse rate
○ Typhoid fever: ↑temp = no increase in pulse
rate
○ That’s why proper assessment is necessary
Medications
Paracetamol (acetaminophen) – effects
mainly on the hypothalamic set point by action of cyclooxygenase. Acts only on the brain, not in the body. Good effect is only when it reaches the brain.
○ IL-1 – only affect IL 1, only good if fever is secondary to autoimmune process ○ ASA ○ Ibuprofen and Coz-2 inhibitors ○ Glucocorticoids ■ acts on inflammation (cortisol) ■ acts on the brain by lowering the set point
ANTIPYRECTICS
● Reduces inflammation → ↓ cytokines → (-) fever
● Stops any inflammation, shotgun treatment, not supposed to be used only to treat fever
○ ASA (Acetyl Salicylic Acid or – aspirin),
NSAIDS (Non-Steroidal, Anti-Inflammatory Drugs), Acetaminophen (Paracetamol), Steroids
HYPERTHERMIA
● Uncontrolled increase in body temperature that
exceeds the body’s capability to lose heat.
● The set point is not changed and does not involve
pyrogenic molecules
● Exogenous heat exposure and exogenous heat
production
● core temp is going up w/o necessary stimulus – no
change in the set point but problem lies
exogenously
● Mostly exogenous depending on the type that
induces hyperthermia
Cardiovascular
Inefficiency
Age extremes Beta/Ca2+ channels blockade Congestive heart failure Dehydration Diuresis Obesity Poor physical fitness
Central Nervous
System Illness
Cerebral hemorrhage Hypothalamic cerebrovascular accident Psychiatric disorders Status epilepticus
Impaired heat
loss
Antihistamines
Heterocyclic antidepressants
Occlusive clothing
Skin abnormalities
Endocrine
related illness
Diabetic ketoacidosis
Pheochromocytoma
Thyroid storm
Excessive heat
load
Environmental conditions Exertion Fever Hypermetabolic state Lack of acclimatization
Infectious Illness
Cerebral abscesses Encephalitis Malaria Meningitis Sepsis syndrome Tetanus Typhoid
Toxicologic
Illness
Amphetamines Anticholinergic toxidrome Cocaine Dietary supplements Hallucinogens Malignant hyperthermia Neurologic malignant syndrome Salicylates Serotonin syndrome Sympathomimetic Withdrawal syndrome (ethanol, hypnotics)
Heat stroke
can be exertional (playing in the gym
w/o aircon) or non-exertional (has mild
hyperthermic effect
Drug-induced
usually illegal drugs
Neuroleptic Malignant Syndrome causes
EPS
(extrapyramidal side effects) like catatonia,
rigidity, difficulty of movement from the muscle.
Serotonin Syndrome
similar in the production of
hyperthermia but you could have diarrhea
Malignant Hyperthermia Drug-induced
(Haldane, muscle relaxants) hyperthermia, and
muscle destruction
Endocrinopathy causes transient
increase in
body temperature unless properly treated –
Thyroid Storm II
APPROACH to Hyperthermia
● Complete History
○ Esp. in those on Anti-cytokine therapy
○ Drugs, antibiotics, smoker, previous
exposure, family history, poorly controlled,
history of head trauma, allergy, etc
○ (autoimmune d/o) stops TNF production,
lowers immune system, & can cause fever
(ex., Tuberculosis)
● Complete physical examination & vital signs
● Laboratory tests to determine if infectious,
inflammatory or other causes of fever. Do after
complete history
TREATMENT
● Treatment of hyperthermia must be aggressive –
cool the patient bec px cannot cool on their own. No
lowering of set point bec set point is not affected
● Treating fever (Antipyretics)
○ Physical cooling
○ Sponging, fans, cooling blankets, and ice
baths
○ IV hydration (watch out for congestion)
○ Vascular resuscitation
○ Control tachyarrhythmias (bec pulse rate
would be very high)
○ Check for Coagulopathies and treat with FFP
(DIC)
○ Shivering, discomfort and agitation bt short
acting benzodiazepines (sedate the patient)
● Rarely necessary unless malignant hyperthermia or
not controlled w/ the prior mgmt – the you become
invase:
○ Gastric or peritoneal lavage, invasive and
rarely necessary
○ Hemodialysis or CP bypass rarely necessary
● Acetaminophen can also be used but its action is
very dependent & similar to NSAIDs via inhibition of
the Cox pathway, inhibiting prostaglandin release
● Treat underlying cause
Px with Dengue presents with a 40C fever of 2 days duration, what will you give? a. Ice bath b. Paracetamol c. antibiotics?
● Dengue is viral infxn - no need for antibiotics
● Ice bath is for hyperthermia (>41c)
● Give paracetamol.
FEVER OF UNKNOWN ORIGIN
- Fever >= 38.3 C (at least two occasions)
- Illness duration of at least 3 weeks
- Absence of immunocompromised state
- No conclusive diagnosis after a thorough assessment via history-taking, physical examination, and laboratory tests for specific parameters.
Flowchart to FUO
Read book
TREATMENT for FUO
Usually self-limited (no medications)
STEPS IN APPROACHING FUO
- One must observe the 3 first characteristics of
FUO (fever temp., febrile state duration and immunocompetency). - Perform thorough physical examination and complete patient history in order to gather PDCs.
- Stop current antibiotic and glucocorticoid treatment which could mask the presence of other diseases.
- Perform the tests in characteristic #4 of FUO. This is to eliminate and identify the possible disease as well as to gather PDCs.
- Thermometer manipulation must be excluded (to discount fraudulent fever)
- Stop or replace current medication (to discount drug fever).
- If PDCs are still absent, perform fundoscopy and cryoglobulin tests.
- Perform Fluorodeoxyglucose positron emission tomography with low-dose CT (FDG-PET/CT) scans or a Scintigraphy.
- If still no remarkable PDCs, redo history and physical examination.
- Perform PDC-driven invasive testing.
- Conduct chest and abdominal CT scans.
- If the patient is in stable condition up to this point:
provide NSAID treatment and follow-up for new PDCs. - If the patient deteriorates, perform further testing and consider therapeutic trials.
TREATMENT OF FUO
ANTIBIOTICS AND ANTI-TB THERAPY
● Consider antibiotic therapy if hemodynamic
instability or neutropenia is observed.
● If TST/IGRA positive or there is presence of
sarcoidosis or anergy, consider Anti-TB medication.
(disease may be rare, military tuberculosis). If fever
does not respond to treatment, consider other
diagnosis.
COLCHICINE, NSAIDS, AND GLUCOCORTICOIDS
ANAKIRA- a recombinant form of the naturally occurring
Interleukin-1 receptor antagonist that blocks both
IL-1A and IL-1B.
● Effective in treating auto-inflammatory syndromes
like familial Mediterranean fever, TNF receptor
associated periodic syndrome, hyper IgD
syndrome, and Schnitzler syndrome.
*Note that in the Philippines, Tuberculosis is one of the
most common underlying causes of
FUO
MACULE
- Flat, colored lesion
- <2 cm in diameter,
not - raised above the
surface of the
surrounding skin - similar to freckles,
usually skin
discolorations
