This document provides an overview of fever (pyrexia), including its introduction, mechanism, pathogenesis, patterns, approach to patients, and treatment. It discusses the difference between hyperpyrexia and hyperthermia. Fever is caused by an increased hypothalamic set point and occurs in conjunction with infections or non-infectious causes like trauma or vaccines. Different fever patterns include continuous, remittent, intermittent, relapsing, and drug fever. The approach involves a physical exam, labs like CBC and CRP, and treating the underlying cause while withholding antipyretics in some cases.

1. APPROACH TO CASE
OF PYREXIA
DR.MOHAMAD HUSAIN
PGJR-2
DEPARTMENT OF MEDICINE
TOTAL NO. OF SLIDE-28
1

2. OVERVIEW
• INTRODUCTION
• MECHANISM
• HYPERPYREXIA VS HYPERTHERMIA
• PATHOGENESIS
• PATTERN OF FEVER
• APPROACH TO A PATIENT
• TREATMENT 2

3. INTRODUCTION
3

4. 4
Tympanic membrane Thermometers:
• use an otoscope-like probe that is inserted into the
external auditory canal to detect and measure thermal
infrared energy emitted from the tympanic membrane.

5. Menstruating Females: the morning
temperature is generally lower during the 2
weeks before ovulation.
it then rises by ~0.6°C (1°F) with ovulation
and stays at that level until menses occur.
5

6. MECHANISM OF FEVER
• Fever occurs in conjunction with an increase in the
hypothalamic set point (e.g., from 37°C to 39°C).
• Once this hypothalamic center is active the
neurons and vasomotor center are activated which
leads to vasoconstriction of peripheral circulation
(hand & feet cooling). 6

7. Mechanisms to raise the core temperature to new set
point in hypothalamus.
(heat conservation) by Cutaneous Vasoconstriction
 (heat production)
• Shivering
• Non shivering Thermogenesis
• Behavioural Adjustments (like putting more clothes)
7

8. When the hypothalamic set point is again reset
downward:
• Vasodilation
• Sweating
With every 1°F rise of temperature, above 100°F,
• the pulse rate increases by 10, the respiratory rate
by 4,and BMR by 7.
• Oxygen consumption increases by 13%.
8

9. PATHOGENESIS
Pyrogens
• Any substance that causes fever.
1. Exogenous Pyrogens:
• Derived from outside the patient.
• Microbes or their Products.
• eg-(endotoxin) of Gram-ve bacteria, Enterotoxins of S. aureus.
2. Pyrogenic Cytokines
• Cytokines which cause fever aka Endogenous Pyrogens IL-1, IL-
6, TNF, IFN a, Ciliary Neurotrophic Factor.
9

10. • Can be induced by:
• Infective Cause: Bacterial, Fungal, Viral
Infection
• Non Infective Cause: Pericarditis, trauma,
Stroke, Vaccination.
10

11. 11

12. HYPERPYREXIA VS HYPERTHERMIA
HYPERPYREXIA:
It is an elevation of body core temperature, above 41°C
(106°F), due to inadequate dissipation of heat.
HYPERTHERMIA:
Hyperthermia is characterised by an unchanged setting of
the thermoregulatory centre with an uncontrolled increase in
body temperature that exceeds body’s ability to lose heat.
12

13. HYPERPYREXIA HYPERTHERMIA
CAUSE Cns haemorrhage (pontine
hemorrhage)M/C
Microbes
Toxin
Increase environmental
temp.(heat stroke)
Or
Increase heat production by
muscle(malignant hyperthermia)
MECHANISM Increase hypothalamic set point
(Increase PGE2)
Hypothalamic set point normal
SWEATING Present (cold skin) Hot &dry skin
VALUE >41.5 c(>106.7 F) >40.5 C
TREATMENT Underlying cause + NSAID Water therapy 13

14. • Causes of Hyperpyrexia
• 1. Pontine haemorrhage
• 2. Rheumatic fever
• 3. Meningococcal meningitis
• 4. Septicaemia
• 5. Cerebral malaria.
• Treatment It is treated with parenteral anti-
pyretics to set the elevated thermostat set point
to a lower level. 14

15. Malignant hyperthermia
• Is an inherent abnormality of skeletal muscle
cell sarcoplasmic reticulum which is unable to
store calcium ion.
• There is an increase in the intracellular
myoplasmic calcium, leading to activation of
myosin ATPase.
• which converts ATP to ADP there by producing
hyperthermia. 15

16. • Hyperthermia is triggered by use of inhalation
anaesthetics (Halothane, Cyclopropane) and muscle
relaxants (Succinylcholine).
 Seratonin syndrome:
It is seen with selective serotonin uptake inhibitors –
monoamine oxidase inhibitors and other seratonergic
medications.
It consists of hyperthermia, diarrhoea, tremor and
myoclonus.
16

17. PATTERNS OF FEVER
1. Continuous Fever
• The temperature remains elevated above normal without
touching the baseline and the fluctuation does not exceed 0.6°C
(1°F) (diurnal variation).
 Lobar pneumonia.
 Infective endocarditis.
 Enteric fever.
2. Remittent Fever
• The temperature fluctuation exceeds 0.6°C (1°F), but without
touching the baseline. 17

18. 3.Intermittent fever
• The elevated temperature touches the baseline in
between.
• In hectic or septic type of intermittent fever, the diurnal
variation is extremely large, as occurs in septicaemia.
4.Relapsing Fever
• Febrile episodes are separated by normal temperature
for more than one day,
e.g. Borrelia infection, rat bite fever.
18

19. Tertian fever - occurs on the first and third day,
e.g. Plasmodium vivax, ovale, falciparum.
 Quartan fever - occurs on first and fourth day,
e.g. Plasmodium malariae.
 Pel-Ebstein fever- Is a type of fever lasting
for 3–10 days followed by an afebrile period of
3–10 days.
e.g. Hodgkins and other lymphomas.
19

20.  Saddle back fever: Initially fever lasts for 2–3
days followed by a remission lasting for 2 days
and the fever reappears and continues for 2–3
days.
e.g. Dengue fever.
 Cyclic neutropenia: Cyclic neutropenia
accompanied with fever occurs every 21 days.
20

21. 21

22. Fever with Relative Bradycardia
1. Typhoid fever
2. Meningitis
3. Viral fever (Influenza)
4. Brucellosis
5. Leptospirosis
6.Drug induced fever
Fever with Exanthems
1.Rash appearing on first day of fever—Chickenpox.
2.Rash appearing on fourth day of fever—Measles.
3.Rash appearing on seventh day of fever-Typhoid. 22

23. DRUG FEVER
• It is prolonged fever and may belong to any febrile
pattern.
• There is relative bradycardia and hypotension.
• Pruritus, skin rash and arthralgia may occur.
• It begins 1–3 weeks after the start of the drugs
and persists 2–3 days after the drug is withdrawn.
• Eosinophilia may be present.
23

24. • Almost all drugs can produce fever.
• Important commonly used drugs producing fever are:
Sulphonamide
Procainamide
Penicillins
Iodides
Anti-TB drugs
Propylthiouracil
Methyldopa
Anticonvulsants
24

25. • Fever can Subside in the Following Ways
Crisis - Elevated temperature settles down to
the baseline immediately after starting
treatment. It may be accompanied by
diaphoresis, diarrhoea or diuresis, e.g.
Pneumonia.
Lysis : Elevated temperature settles down to
the baseline in a step ladder fashion, after
starting treatment, e.g. Typhoid fever. 25

26. APPROACH TO PATIENT
 Physical Examination:
• Same site should be used consistently to monitor
the temperature
• Active Infection in the absence of fever can be
present in
• Newborns & Elderly
• Chronic Hepatic or Renal failure
• Patients taking Glucocorticoids or Anticytokine
therapy.
26

27.  Laboratory Tests
• CBC with Differential Count
• C Reactive Protein
• Erythrocyte Sedimentation Rate
27

28. TREATMENT
 Most fevers- self limited infections (viral)
• With holding Antipyretics can be helpful:
• For evaluating the effectiveness of Antibiotic &
• Pattern of certain diseases helpfull for
diagnosis.
• Treat underlying cause of Fever.
28

29. 29