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Elevation of the set point steps up the mechanisms of heat production

and inhibits the mechanisms for heat loss. The
endogenous pyrogens include interleukin-1 ( and ), inerleukin-2,
tumor necrosis factor ( and ) and interferon .

August and
09, 2010

- most common complaint; usually self-managed; not always due to
- a state of elevated core temperature, which is often, but not
necessarily, part of the defensive responses of the multicellular
organism (host) to the invasion of the live microorganisms or inanimate
matter recognized as pathogenic or alien by the host (from the
International Union of Physiological Sciences Commission for Thermal
Physiology, 2001)
- elevation of the body temperature above the normal circadian range in
response to a new temperature set point that has been established in
the thermoregulatory center located in the hypothalamus
- inc. Hypothalamic set point activation of vasomotor center
vasoconstriction (shunting of blood from the periphery to the internal
organs) dec heat loss from skin person feels cold shivering
or non shivering heat production temp of blood surrounding
hypothalamus = new set point continuous febrile state dec. in
pyrogen conc. Or antipyretics downward reset of hypothalamic set
- hyperprexia

- The physiologic response to fever may be adequate or inadequate. In

the immunocompetent, other symptoms will be present aside from
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- unchanged setting of the thermoregulatory center in conjunction with
an uncontrolled increase in body temperature that exceeds the bodys
ability to lose heat
- can be rapidly fatal and characteristically does not respond to
antipyretics (paracetamol or any relative agents)
- does not involve pyrogenic molecules
- can develop from 24 hours to 48 hours after the operation(drug fever)
Causes of Hyperthermia syndromes

o fever of > 41.5 degrees celcius

o due to severe infections or CNS hemorrhages
normally a normal thermal ceiling of 106 degrees farenheit is
observed, this is mediated by neuropeptides (central antipyretics)

Heat stroke
o caused by thermoregulatory failure in association with a
warm environment
o can be terminal or can be secondary terminal

o caused by exercise in higher-than-normal heat and/or
o can also be precipitated by dehydration or OTC
antihistamines with anticholinergic side effects

o occurs in high heat or humidity in patients taking
anticholinergics (including antihistamines);
antiparkinsonian drugs; diuretics; phenothiazines

- complex physiologic reaction to disease, involving not only cytokinemediated rise in core temperature but also the generation of acute
phase reactants, and the activation of numerous physiologic,
endocrinologic and immunologic systems (tachycardia, tachypnea,
hypotension, oliguria)
- Physiologic means that aside from a high temperature, you would
expect your patients to have competitor response= Heart rate,
respiratory rate, basal metabolic rate.


o caused by drugs such as MAO inhibitors, tricyclic
antidepressants, amphetamines, cocaine,
phencyclidine, LSD, sallicylates, lithium
o can increase heart rate, and basal metabolic rate


Neuroleptic malignant syndrome

o caused by neuroleptic agents such as phenothiazines,
butyrophenones (haloperidol, bromperidol), fluoxetine,
loxapine, tricyclic dipenzodiazepines, metoclopramide,
domperidone, thioxetine, molindone
o consists of lead-pipe muscle rigidity, extrapyramidal side
effects, autonomic dysregulation, hyperthermia


Malignant hyperthermia
o systemic response to halothane and other inhalational
anesthetics in patients with genetic abnormality (in
skeletal muscle sarcoplasmic reticulum)
o increased intracellular Calcium -> increased muscle
rigidity -> increased thrombogenesis
o also in post-operative patients
o patients prone to develop CV instability and acidosis


Serotonin syndrome
o caused by selective serotonin reuptake inhibitors,
monoamine oxidase inhibitors, tricyclic antidepressants
o additional symptoms: diarrhea, tremor, myoclonus

Endocrinologic, catecholamines= heart rate, glucagon

- Immunologic System, blood will respond to febrile reaction and there will
be an increase in inflammatory cells(WBC).
- The anterior hypothalamus acts as the heat-loss center. The posterior
hypothalamus acts as the heat-producing center.
- Can be caused by:

exogenous pyrogens lipopolysaccharide endotoxin,

outside the body

endogenous pyrogens induced by exogenous pyrogens

interleukin-1, TNF

prostaglandin E2
o in CNS: raises hypothalamic set point
o in peripheral tissues: causes myalgia, arthralgia
Fever results when exogenous pyrogens (bacteria, viruses, fungi, other
microorganisms, allergens, etc.) or pyrogenic factors (immune
complex, lymphokines from sensitized lymphocytes, etc.) encounter
circulating monocytes and monocyte-derived tissue macrophages, the
major sources of biologically defined endogenous pyrogens.
Endogenous pyrogens increase prostaglandin synthesis, which
stimulates the thermostat center, thereby elevating the set point.

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o caused by thyrotoxicosis, pheochromocytoma
o increased basal metabolic rate
CNS Damage
o caused by cerebral hemorrhage,
epilepticus, hypothalamic injury



Elevated temperature in hyperthermia is NOT decreased

by antipyretics

Diagnosis of hyperthermia is difficult but should be

o Events immediately preceding the elevation of
core temperature (eg. Heat exposure or
treatment with drugs that interfere with
o Physical findings of dry skin, hallucinations,
delirium, pupil dilation and muscle rigidity

*Fever an am temp of >37.2 C or a pm temp of

37.7 C
Types of thermometer
oral has a longer probe than rectal
gives the most reliable reading
placed under the tongue
axillary same as oral
rectal has a more blunt end
tympanic membrane
- always consider:
power source affects the reading
calibration must be properly

status of patient
check responsiveness and coherence
if not coherent: severe infection
check vital signs (BP, HR, RR, temp)
ask when the last urination was. monitor urine
check other signs that would suggest an
headache: CNS infection
cough (productive) then fever:
bacterial pneumonia
fever then cough: viral flu
dry cough: influenza
rashes: dengue


requirement for isolation procedures

in viral infections


requirement for immediate antimicrobial therapy

not necessary in viral infections
different approach in the immunosuppressed

**Factors affecting Heat production

a. Basal metabolism
b. Muscular activity (voluntary shivering)
c. Thyroxin and epinephrine (stimulating effects on
metabolic rate)
d. Specific dynamic action of food
e. Chemical reaction
**Factors affecting Heat conservation
a. Vasoconstriction
b. Insulation of heat by means of thick clothing
**Factors affecting Heat loss
a. Vasodilation (radiation, conduction, convection)
b. Evaporation (sweat, insensible water loss)
c. Urine and feces

factors that may influence hemostatic measurement:

1. Observer variability

Anatomic variability:

Oral / tympanic membrane > rectal > axillary


Physiologic variability:
mean oral temp for healthy people
aged 18-40 y/o = 36.8 +/- 0.4 C
lowest at 6am = 37.2 C

highest at 4-6pm = 37.7 C


Diagnostic Approach
1. fever characteristics
a. onset
b. pattern
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intermittent with normalization and recovery to

remittent doesnt go back to baseline even with
intake of paracetamol
eg, Salmonella, typhoid, bacterial
continuous or sustained eg, severe infection,
CNS, viral
relapsing longer periods of afebrile state
eg, vivax, malaria
septic or hectic erratic, more exaggerated; can
go down to normal with intake of paracetamol

dietary proclivities
household pets
sexual orientation and practices include
precautions taken/not taken
use of tobacco, marijuana, IV drugs, alcohol
drug allergies and hypersensitivities
season of the year
Physical Examination

general appearance
vital signs
signs of toxicity
focus of infection
skin lesions
presence and location of adenopathy
presence and morphology of genital, mucosal, or
conjunctival lesions
detection of hepatosplenomegaly (malaria)
presence of arthritis
signs of nuchal rigidity, meningismus or neurologic
rectal exam imperative
penis, prostate, scrotum, testes for males
pelvic exam part of complete PE of females

Laboratory Tests
2. chronology of symptoms
If fever comes first before dry cough along with
muscle pain, and joint pains, there is viral flu
If non productive cough occurred first then after 2
days becomes productive with chest pain then it is a
bacterial infection like pneumonia
3. antecedent events and precipitating factors
underlying medical illness (eg. valvular heat
disease, COPD, diabetes)
surgical and dental procedures
previous or recent hospitalizations
prescription drugs, supplements, herbs taken
without physicians supervision
factors affecting immunologic status (eg, cancer)
travel and residential history include locations
during military service; travel to Palawan:
consider malaria
occupational history exposure to animals; toxic
fumes; potential sinfectious agents; possible
antigens; febrile or infected individuals in the
home, workplace, school
immunizations flu shot: llocal soreness at
injection site + low-grade fever
STD exposure
family history and ethnicity
unusual hobbies

1. Tempo and complexicity of work-up depend on:

diagnostic considerations
pace of illness
immune status
2. clinical pathology
blood smears
routine analysis of important body fluids (sputum
evaluation, CSF exam)
histopathological studies
joint fluid exam
stool exam
bone marrow biopsy
3. chemistry
electrolyte, glucose, BUN, creatinine
4. radiology
chest x-ray
CT scan
5. microbiological studies most important
smears and cultures (throat, urethra, anus, cervix,
Therapeutic Management
- antibiotic therapy when needed
- use of antipyretics
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4. Neuromuscular blockers
1. Fever
oral aspirin, acetaminophen (preferred) , NSAIDs
2. Hyperthermia
physical cooling with the use of sponging, cooling
blankets, fans, ice baths
administration of IV fluids etc
gastric or peritoneal lavage w/ iced saline
for malignant cases: dantrolene, procainamide,
bromocriptine, levodopa, amantidine, nifedipine
for muscle paralysis: curare and pancuronium

Unintentional drop in the bodys core temperature below

35C (95F)
Primary result of the direct exposure of a previously
healthy individual to the cold
Secondary complication of a serious disorder

A. Age extremes
Elderly and neonates are vulnerable to
1. Elderly
- diminished thermal perception
- more susceptible to immobility, malnutrition &
systemic illnesses that interfere with heat generation
or conservation
2. Neonates
- high rates of heat loss due to their increased surfaceto-mass ratio
- lack of effective shivering & adaptive behavioral
B. Environmental exposure
- Occupational
- Sports related
- Inadequate clothing
- Immersion
C. Drugs and intoxication
1. Ethanol
causes vasodilation, which increases heat loss,
reduces thermogenesis & gluconeogenesis and
may impair judgement or lead to obtundation
2. Phenothiazines, barbiturates, benzodiazepines, cyclic
Reduce centrally mediated vasoconstriction
3. Anesthetics
Can block shivering responses

D. Endocrine related
1. Hypothyroidism
particularly when extreme (myxedema coma)
reduces metabolic rate & impairs thermogenesis
and behavioral responses
2. Adrenal insufficiency & hypopituitarism
Increase susceptibility to hypothermia
3. Hypoglycemia
Most commonly caused by insulin or other
Result of neuroglycopenic effects on
hypothalamic function
4. Uremia, diabetic ketoacidosis & lactic acidosis
Can lead to altered hypothalamic regulation
E. Neurologic-related
1. Trauma, cerebrovascular accident (ex. Stroke),
subarachnoid hemorrhage or hypothalamic lesions
increases susceptibility to hypothermia
2. Agenesis of corpus callosum, Shapiro syndrome
cause of episodic hypothermia
characterized by profuse perspiration followed by
rapid fall in temperature
3. Acute spinal cord injury
disrupts autonomic pathways that lead to
prevents cold-induced reflex vasoconstrictive
4. Parkinsons disease
F. Multisystem
1. Malnutrition, Trauma
2. Sepsis
3. Shock
4. Hepatic or renal failure
Decreased glycogen stores & gluconeogenesis
Diminished shivering responses
5. Acute myocardial infarction
low cardiac output
G. Burns, psoriasis, erythrodermas, & exfoliative dermatologic
increased peripheral blood flow
excessive heat loss
H. Immobility or debilitation
Preoptic anterior hypothalamus
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handles thermoregulation

ANS immediate defense

a. release of NE
b. increased muscle tone
c. shivering leading to thermogenesis
d. increased basal metabolic rate
e. peripheral vasoconstriction
Endocrine system delayed control
A. History
1. Exposures
2. Underlying diseases/problems
3. Other associated symptoms
B. Physical Exam
patients may be confused or combative
maladaptive behavior
C. Diagnosis
Measure the core temperature at 2 sites
rectal probe & esophageal probe
Sole determination by infrared tympanic
thermography not reliable
D. Stabilization process
1. Cardiac monitoring along with attempts to limit further
heat loss
2. If patient is in ventricular fibrillation 1 sequence of
3 fibrillation attempts (2j/kg)
3. Supplemental oxygenation leftward shift of oxyHb
dissociation curve
4. Pulse oxymetry unreliable in patients with
5. Endotracheal intubation if protective airway
reflexes are absent
6. Prevention of ventricular arrythmias by adequate
7. Gastric tube insertion prevents dilatation secondary
to decreased bowel motility
8. Foley catheter insertion
9. Rehydration
10. Maintenance of acid-base and electrolyte balance
A. Passive
- For acute, mild hypothermia
- involves covering and insulating the patient in a
warm environment
- usually 0.5 2.0C per hour

B. Active
- for moderate (28-32C)
- necessary under the following conditions:
cardiovascular instability, age extremes, CNS
dysfunction, endocrine insufficiency, or any suspicion
of secondary hypothermia
1. External
Best accomplished with forced-air heating
Prevent use of electric blankets
Radiant heat sources / hot packs
2. Core
- Airway rewarming with heated humidified
oxygen (40C - 45C) via mask or endotracheal
C. Intensive
- For intense (<28C)
- Use extracorporeal blood rewarming techniques

A. CV stabilization
Achieving a mean arterial pressure of at least
60mmHg should be an early objective
Perfusion of vasoconstricted CV system with low
dose IV nitroglycerin
Monitoring of atrial arrythmias
B. Endocrine balance
Look for clues of hypothyroidism
If myxedema is the cause, Achilles tendon reflex is
prolonged more than the contraction phase
C. Empiric antimicrobial therapy
If infection is identified as the cause
D. Preventive measures
Layered clothing
Adequate shelter
Increased caloric intake
Avoidance of ethanol


Management Challenge
Presence of rash + clinical syndrome

Immediate diagnosis

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Administration of life-saving therapy

Critical infection control interventions



type of rash, including the site of onset, direction and rate

of spread
associated symptoms
immune status
recent medications taken
travel history
immunization status
animal exposure
cardiac abnormalities
presence of prosthetic material
recent exposure to ill individuals
STI exposure

Physical Examination
Salient features:

1. Type of rash
Macule flat, raised, erythematous, <5mm
Papule raised, <5mm
Plaque plateau-like, raised, irregular borders, >5mm
Nodule - round
Vesicle- round, w/ fluid inside
Bulla- larger than vesicle, w/ fluid inside
Pustule w/ pus
Purpura: Palpable vs Non-palpable
Ulcer w/ concavity
Eschar necrotic center; in bed sores
2. Configuration
3. Arrangement diffuse or localized
4. Distribution
- The presence of rash may indicate a life-threatening or a
highly contagious disease.
- Different types of rashes may co-exist in one clinical
1. Centrally distributed maculopapular eruptions
most common type of eruption

primarily truncal
rashes due to measles vs German measles
* Both have maculopapular rashes but the
rashes do not coalesce in German
erythema infectiosum
Parvovirus B19
slapped cheeks appearance
with perioral pallor
Exanthem subitum
herpesvirus 6
Rose-pink macules and
papules that rarely coalesce
drug-induced eruptions
2. Peripheral eruptions
prominent peripherally or begin in peripheral or
acral areas
Meningococcemia, disseminated gonococcal
Rocky Mountain Spotted Fever prominent in
wrist, hand, dorsum
Secondary syphilis- on palms, soles
Hand, Foot, and Mouth Disease (HFMD)
Erythema multiforme, usually drug-induced
hyperpigmentd on center
3. Confluent desquamative erythemas
diffuse erythema followed by desquamation
Toxin-mediated syndromes
Staphylococcus aureus
Group A Streptococcus
Toxic Epidermal Necrolysis (TEN), StevensJohnson Syndrome (SJS)
4. Vesicobullous eruptions
could suggest a highly contagious condition
Prominent on the trunk
Pseudomonas (pruritic appearance)
occluded by bathing suits
Variola (small pox)
Prominent on the face and
Herpes Simplex Virus
HSV1: oral
HSV2: genital
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Dengue fever
5. Urticarial Eruptions
typically look like hives
usually due to a hypersensitivity reaction to a drug
without associated fever
lasts up to 5 days
Drug-induced urticaria
Urticarial vasulitis
6. Nodular eruptions
suggestive of widespread infection in
immunocompromised hosts
Erythema nodosum (septal panniculitis)
Sweets syndrome with concomitant
vesiculobulbar eruptions
Disseminated infection
7. Purpuric eruptions
occurs prominently in the distal areas or

8. Eruptions with ulcers and/or eschars

occurrence of an ulcer along with a widespread
eruption provides an important diagnostic clue
Scrub typhus


Fever and hypothermia are important manifestations

that indicate lots of possibilities
The onset, timing & pattern, along with the
associated signs & symptoms, including the
presence of rashes, could provide additional clues
Aggressive management must be instituted as soon
as possible, including appropriate infection control
measures as necessary

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