Alterations in body temperature Flashcards
(98 cards)
1
Q
NORMAL TEMPERATURE
A
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
2
Q
preferred for Children
A
Rectal
3
Q
ORAL:
A
preferred for Adults
4
Q
AXILLARY:
A
common for Adults
5
Q
Fever associated with various changes.
A
○ Vasoconstriction
○ Shivering
○ Behavioral changes
6
Q
PYROGENS
A
● Any substance causing fever
● May be caused by infection (development of antigens)
● Stimulates the production of pyrogenic cytokines
● Antibiotics may cause fever!
7
Q
PYROGENIC CYTOKINES
A
● 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
8
Q
PGE2
A
● 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).
9
Q
Induction of Fever
A
Infection → activate monocytes & macrophages → release
pyrogens, ILs, cytokines → stimulate hypothalamus →
release prostaglandin (PGE2) → set hypothalamic set
point higher → FEVER
10
Q
PGE2:
A
stage where you will develop fever
11
Q
HYPERPYREXIA
A
● 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
12
Q
Rare causes of elevated hypothalamic set point
A
○ Local trauma, hemorrhage, tumor or intrinsic hypothalamic malfunction
○ Sometimes even medications
13
Q
TREATMENT of Hyperpyrexia
A
● 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
14
Q
Medications
A
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
15
Q
ANTIPYRECTICS
A
● 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
16
Q
HYPERTHERMIA
A
● 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
17
Q
Cardiovascular
Inefficiency
A
Age extremes Beta/Ca2+ channels blockade Congestive heart failure Dehydration Diuresis Obesity Poor physical fitness
18
Q
Central Nervous
System Illness
A
Cerebral hemorrhage Hypothalamic cerebrovascular accident Psychiatric disorders Status epilepticus
19
Q
Impaired heat
loss
A
Antihistamines
Heterocyclic antidepressants
Occlusive clothing
Skin abnormalities
20
Q
Endocrine
related illness
A
Diabetic ketoacidosis
Pheochromocytoma
Thyroid storm
21
Q
Excessive heat
load
A
Environmental conditions Exertion Fever Hypermetabolic state Lack of acclimatization
22
Q
Infectious Illness
A
Cerebral abscesses Encephalitis Malaria Meningitis Sepsis syndrome Tetanus Typhoid
23
Q
Toxicologic
Illness
A
Amphetamines Anticholinergic toxidrome Cocaine Dietary supplements Hallucinogens Malignant hyperthermia Neurologic malignant syndrome Salicylates Serotonin syndrome Sympathomimetic Withdrawal syndrome (ethanol, hypnotics)
24
Q
Heat stroke
A
can be exertional (playing in the gym
w/o aircon) or non-exertional (has mild
hyperthermic effect
25
Drug-induced
usually illegal drugs
26
Neuroleptic Malignant Syndrome causes
EPS
(extrapyramidal side effects) like catatonia,
rigidity, difficulty of movement from the muscle.
27
Serotonin Syndrome
similar in the production of
| hyperthermia but you could have diarrhea
28
Malignant Hyperthermia Drug-induced
(Haldane, muscle relaxants) hyperthermia, and
| muscle destruction
29
Endocrinopathy causes transient
increase in
body temperature unless properly treated –
Thyroid Storm II
30
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
31
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
32
```
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.
33
FEVER OF UNKNOWN ORIGIN
1. Fever >= 38.3 C (at least two occasions)
2. Illness duration of at least 3 weeks
3. Absence of immunocompromised state
4. No conclusive diagnosis after a thorough assessment via history-taking, physical examination, and laboratory tests for specific parameters.
34
Flowchart to FUO
Read book
35
TREATMENT for FUO
Usually self-limited (no medications)
36
STEPS IN APPROACHING FUO
1. One must observe the 3 first characteristics of
FUO (fever temp., febrile state duration and immunocompetency).
2. Perform thorough physical examination and complete patient history in order to gather PDCs.
3. Stop current antibiotic and glucocorticoid treatment which could mask the presence of other diseases.
4. Perform the tests in characteristic #4 of FUO. This is to eliminate and identify the possible disease as well as to gather PDCs.
5. Thermometer manipulation must be excluded (to discount fraudulent fever)
6. Stop or replace current medication (to discount drug fever).
7. If PDCs are still absent, perform fundoscopy and cryoglobulin tests.
8. Perform Fluorodeoxyglucose positron emission tomography with low-dose CT (FDG-PET/CT) scans or a Scintigraphy.
9. If still no remarkable PDCs, redo history and physical examination.
10. Perform PDC-driven invasive testing.
11. Conduct chest and abdominal CT scans.
12. If the patient is in stable condition up to this point:
provide NSAID treatment and follow-up for new PDCs.
13. If the patient deteriorates, perform further testing and consider therapeutic trials.
37
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.
38
*Note that in the Philippines, Tuberculosis is one of the
| most common underlying causes of
FUO
39
MACULE
- Flat, colored lesion
- <2 cm in diameter,
not
- raised above the
surface of the
surrounding skin
- similar to freckles,
usually skin
discolorations
40
PATCH
- Flat, large lesion
- >2 cm
- Color different from
the surrounding
skin
- Differs from macule
only in size
- Birthmark;
hyperpigmentation
41
PAPULE
- Small, solid lesion
- <0.5 cm
- Raised above the
surface of the
surrounding skin
- No fluid inside
- Maculopapular
Rash: a rash that
has flat, nodular,
raised solid lesions
42
PLAQUE
```
- Large, flat-topped,
raised lesion
- >1cm
- Distinct edges,
gradually blend
with surrounding
skin
```
43
VESICLE
```
- Small, fluid-filled
lesion
- <0.5 cm
- Raised above the
plane of
surrounding skin
- Fluid is often
visible, and the
lesions are
translucent
```
44
PUSTULE
Leukocyte-filled
| vesicle
45
BULLA
```
- Fluid-filled, raised,
often translucent
lesion
- >0.5 cm
- An allergic reaction
- Self-limiting lesions
```
46
WHEAL
```
- Raised,
erythematous,
edematous papule
or plaque
- Usually
representing shortlived vasodilatation
and
vasopermeability
- Usually seen
among allergic
reactions. A
plaque-like lesion
that disappears
```
47
NON-PALPABLE
| PURPURA
```
PURPURA
- Flat lesions due
to bleeding in the
skin
- Petechiae: <3mm
- Ecchymoses:
>3mm
- Petechial rash:
non-blanching —
does not fade when
pressed‖
- Ecchymoses:
bruise
```
48
PALPABLE
| PURPURA
```
- Raised lesions due
to inflammation of
the vessel wall
- Will blanch when
you apply pressure
```
49
CENTRALLY DISTRIBUTED MACULOPAPULAR
| ERUPTIONS
Rubeola
Rubells
Erythema Infectiosum
Exanthem subitum
50
Rubeola
Usually, this is the result of you not being
vaccinated when you’re young and some
classmates have measles, so you get
infected as well. Could develop fever, other
symptoms more sever like diarrhea
51
Rubella
Forscheimer spots, unlike measles which
usually appear in a febrile episode, when the
rashes erupt, the fever usually goes down
52
Erythema infectiosum
○ Manifested by fever usually in young
| individuals with a slightly “slapped” cheek appearance. Sometimes, they could have a lacey pattern.
53
Exanthem subitum
○ Here’s when the problem comes in because most of the related viruses usually resolved
for about 2-3 days so it’s very difficult to
diagnose unless you do the viral studies.
○ If you’re not sure of the diagnosis because they’ll tell you that they got rashes but they feel better, the rashes is not, you could just
tell them that it is a viral fever. Similarly, it is common with children below 3 years old and they usually get better after.
54
PERIPHERAL ERUPTIONS
● Prominent peripherally or begin at the (peripheral)
acral areas before spreading centripetally
● May be from the head → down, legs → up
55
Rocky Mountain spotted fever
○ Manifestation is from peripheral going down.
It is treatable but if it has been diagnosed
late, the mortality is very high.
56
Secondary syphilis
Condyloma latum – are moist flat-topped
papules that appear about 6 months after
infection
57
Chikungunya fever
Chikungunya Fever – very common in the
Philippines a few years ago. Most prominent
feature is that the fever is accompanied by
migratory arthralgias or non-inflammatory
joint pain that spreads from one joint to
another. These rashes are very painful that
you might feel like you have rheumatoid
arthritis. Same vector with the Dengue virus.
58
Erythema multiforme (EM)
Consist of target lesions similar to a dart
board. If involves the mucus membrane, it is your Erythema multiforme major. It is very severe and has high mortality. Some drugs like allopurinol and antibiotics can cause these lesions
59
Bacterial endocarditis
Presenting as fever and you might not see
the nodular lesions often. Instead, you must
look for the presence of anemia, heart
murmur and fever. The thing that you need
to watch out for and the thing that you
probably will give you an idea is new and
changing murmurs. Diagnosis is usually via
2D –Echo and Esophageal Echocardiogram.
60
CONFLUENT DESQUAMATIVE ERYTHEMAS
Diffuse erythemas followed by desquamation
61
CONFLUENT DESQUAMATIVE ERYTHEMAS examples
● Scarlet fever
● Kawasaki disease
○ Because of the absence of immunoglobulins,
we give these patients very high doses of
aspirin in order to improve them, but now,
immunoglobulin is the drug of choice. Look
for the presence of “strawberry tongue”
● Streptococcal toxic shock syndrome
● Staphylococcal toxic shock syndrome
● Staphylococcal scalded-skin syndrome
● Exfoliative erythrodema syndrome
○ You might mistakenly diagnose this as very
severe psoriasis then check for the clinical
symptoms.
● Stevens-Johnson Syndrome (SJS)
62
VESICULOBULLOUS OR PUSTULAR
● Rash can be of different sizes, some vesicle-like or
a bullous configuration, some are smaller while
some are bigger
63
Varicella
```
Most of the time it occurs in younger age or
when you’re in college. These are
progressive, usually self-limiting.
Immunocompromised children with present
with more sever symptoms
```
64
Pseudomonas
– hot-tub folliculitis
65
Variola
Similar to your chickenpox, however more
diffused. Can also affect your
mucocutaneous areas.
66
Primary herpes simplex virus (HSV) infection
Very painful lesions, usually sexually
| transmitted
67
Disseminated herpes virus infection
Shingles. Not diffused, they follow a certain dermatomal line and are very painful
68
URTICARIA-LIKE LESIONS
```
● If with fever, are often associated with vasculitis
● Nodular eruptions
● It may appear in healthy people or in
immunocompromised hosts
● Sign of disseminated infection
```
69
NODULAR ERUPTIONS
Erythema nodosum
○ Type of vasculitis that could usually present in the lower extremities. They would present to the nodular erythematous lesions that are
very painful and may present with fever. It
could be secondary to an infection.
● Sweet syndrome
○ Secondary to Yersinia infection.
Management is antibiotics.
70
PURPURIC ERUPTIONS
● May reflect a sever underlying condition
71
Acute meningococcemia
A severe infection that would present initially
with fever, myalgia, and more severely to
hypertension, DIC. Mortality is very high.
Usually, these patients are rushed in with
fever, very septic looking, with bluish …
rashes.be very careful because this is very easily disseminated and prophylaxis is usually given to employees exposed.
72
PURPURIC ERUPTIONS
● Purpura fulminans
● Disseminated gonococcal infection
● Cutaneous small-vessel vasculitis
73
ERUPTION WITH ULCERS OR ESCHERS
Anthrax or Tuleremia or Ricketssialpox
74
HYPOTHERMIA
● Unintentional drop in the body’s core temperature
| below 35 C (95 F)
75
PRIMARY ACCIDENTAL HYPOTHERMIA
○ Direct exposure of a previously healthy individual to cold
76
SECONDARY HYPOTHERMIA
○ A complication of a serious systemic disorder
77
RESPONSE TO COLD
AUTONOMIC NERVOUS SYSTEM
○ Release of norepinephrine – tachycardia;
trying to pump as much blood to the body
○ Increased muscle tone
○ Shivering – increase core temperature
○ Direct reflex vasoconstriction – as the body
is trying to warm up
78
ENDOCRINE
○ Increased metabolic rate
79
Risk Factor for Hypothermia
Age, Environmental, Toxicologic, pharmacologic, Insufficient Fuel, ENdocrine, Neurologic, multisystemic
80
Mild:
renal and endocrine compensation is much better
| than cardiovascular.
81
Moderate:
decreased consciousness
82
Severe:
comatose state, renal dysfunction, high chance of mortality
83
DIAGNOSIS of Hypothermia
```
● Measure core temperature in two sites
● Rectal probes
○ 15 cm and not adjacent to cold feces
● Esophageal probes
○ 24 cm below the larynx
○ You might have to intubate the patient if they are not breathing
```
84
MANAGEMENT of Hypothermia
● Cardiac monitoring – to check for arrhythmias
○ If there is arryhtmia, defibrillate
● Defibrillation (do not do multiple defibrillation if the
patient does not respond to the initial
defibrillation)
● Crystalloid/colloid infusion
○ To achieve a MAP of 60mmHg – to increase
blood pressure
○ Use of low dose dopamine/ low dose IV
nitroglycerin – to open highly constricted
blood vessels
● Gastric tube insertion
● Indwelling catheter – to monitor renal function
● Rewarm the patient
● Cardiac resuscitation
● Empiric antibiotics
85
PASSIVE EXTERNAL REWARMING
○ Covering and insulating the patient in a warm environment at 0.5-2C per hour
○ Truncal heat application
■ To prevent – afterdrop
86
ACTIVE REWARMING
```
○ Core temperature <32 C
○ Cardiovascular instability
○ Age extremes
○ CNS dysfunction
○ Hormone insufficiency
○ Secondary hypothermia
```
87
ACTIVE EXTERNAL REWARMIN
■ Forced-air heating blankets
■ External heat exchange packs
■ Radiant heat source
■ Hot packs
88
ACTIVE CORE REWARMING
```
■ Airway rewarming with humidified
oxygen at 40- 45 C
■ Heated crystalloids at 40-42 C
■ Heated irrigation of the GI and UB
■ Closed thoracic lavage
■ Most efficient
■ Peritoneal lavage at 40-45 C
```
89
Poor prognosis of hypothermia
● K+
levels > 10mmol/l
● Core temperature <10-12 C
● pH <6.5
● Evidence of intravascular thrombosis with fibrinogen value
● <50 mg/dl
● Chances to survival are minimal, no recucitate
90
FROSTBITE
● Tissue temperature drops <0 C
● Ice crystals destroy cellular architecture
● Stasis → microvascular thrombosis → Dermal ischemia → edema → thrombosis → ischemia → superficial necrosis → mummification and demarcation
91
SUPERFICIAL FROSTBITE
● Does not entail tissue losS
● Causes anesthesia and erythema
● Subcutaneous tissue is pliable
● Dermis can be rolled over bony prominences
92
DEEP FROSTBITE
● Waxy, mottled, yellow or violaceous appearance
● Vesiculation with edema and erythema
● Hemorrhagic vesicles
93
TREATMENT of FB
● Amputation or debridement
● Delayed until signs of mummification, demarcation, sloughing or infection occurs
● prevent partial thawing and freezing
● During thawing, give analgesics, NSAID because frostbite is very painful
● if pain is refractory, give opioid analgesics – give drugs for thrombolysis if there is already vascular coagulation in the digit
94
SEQUELAE
```
● Paresthesia
● Thermal misperception
● Hyperhidrosis
● Nail deformities
● Cutaneous carcinoma
● Epiphyseal damage in children
```
95
PERIPHERAL COLD INJURIES
Chilblain
| Trench foot
96
Chilbain (pernio)
```
○ Neuronal and endothelial damage from
repeated exposure to dry cold
○ Erythema, mild edema and pruritus
○ Plaques, blue nodules and ulceration
○ Seen in patients with lupus or Reynaud’s
phenomenon
```
97
Immersion (trench) foot
○ Repetitive immersion to wet cold
○ Cyanotic, cold and edematous
○ Bullae, ulceration and liquefaction gangrene
○ Hyperhidrosis, cold sensitivity and painful
ambulation
98
TREATMENT
| Chilbain Syndrome
```
Chilbain Syndrome
● Supportive
● Nifedipine
● Steroid
● Limaprost (PGE Analogue)
```
