Fever/ Pyrexia

Fever is an elevation of body temperature above the normal circadian range as the result of a change in the thermoregulatory center located in the anterior hypothalamus

Max normal oral temp in morning is 37.2*C (98.9*F)

Max normal oral temp in evening is 37.7*C (99.9*F)

Rectal temp is 1*F higher

Given these criteria, an a.m. temp >98.9*F or a p.m. temp of > 99.9*F would define fever.

Febrile response is a complex physiological reaction to an illness, involving a cytokine mediated rise in core temp, the generation of acute phase reactants, & the activation of numerous physiologic, endocrinologic and immunologic systems

Pattern of fever

Sustained fever/continuous fever

Typhoid, pneumococcal

Intermittent fever

Pyogenic abcess, malaria

Remitting fever

Viral infections. mycoplasma

Relapsing fever –Lymphoma, Dangue

Fever – pulse Disparity– Typhoid, legionella

Drug fever

Current evidence

Indicates  fever is a primitive immunologic response with long phylogenetic history

Studies show that fever & its direct consequences are adaptations and natural selection

1. Specifically to fight infections  both by increasing the phagocytic activity—Neutrophils
2. Optimizing cytotoxic activity of Lymphocytes

Cost of fever

For each 1*C  rise:

• Increase in 13% O2 consumption
• Increase in caloric needs
• Induction of temp infertility in men
• Accelerate muscular catabolism
• Antipyretics frequently used without compelling medical reason
• In most febrile illness there is no evidence that fever is detrimental & that antipyretics offer any benefit

Whom to be treated first ?

1. Pregnant women— a hypermetabolic state can be dangerous
2. Children with hx of febrile seizures
3. Patients who cannot tolerate a rise in intracranial pressure
4. Physicians should treat fever only when the expected benefit outweigh the possible risks

Pathogenesis

With >37.2*C the body responds:

1. Muscle shivering, vasoconstriction & piloerection–chills
2. Thereby body conserving temp followed by
3. Vasodilatation, muscle spasm—-sweeting

Exogenic toxins/pyrogens (Bacteria, viruses, parasites)

Endogenic toxins (cytokines, bacterial products IL-1, IL-6, TNF-a)

1. Both affect on thermosensitive neurons on Hypothalamus
2. Thereby increasing heat production & decreasing heat loss
3. Temp rises till the new set point
4. This info is conveyed by the temp of the blood flowing around hypothalmus

• The pyrogens trigger synthesis of prostaglandins of group E from arachdonic acid (PGE2) which through cyclic AMP resets the central thermostat
• NSAIDS/antipyretics inhibit PGE2 thru inhibiting Cyclo-oxigenase pathway
• Glucosteroids inhibit all pyrogens thru lipo-oxygenase pathway (IL & TNF-a)
• Cytokines stimulate immune response at 39.5*C
• They also recruit neutophils & enhance their functions Indicating fever as a positive factor

Diagnostic approach

History taking

Complete physical examination

Investigations

Management

Complete physical examination

Do not overlook:

1. Rash or skin nodules
2. Eyes
3. Optic fundi
4. Upper airways
5. Rectal examination

Investigations

• CP with ESR, C-reactive protein
• Chest radiograph
• Malaria films, Urinalysis
• Blood culture, urine culture, faeces culture
• Sputum RE & Culture
• Ultrasound exam of abdomen
• Serological tests for viruses, bacteria, fungus and parasites
• LFTs, RFTs
• Blood sugar, CPK, Bone biochemistry
• ECG/Echocardiogram
• Biopsies- Liver, bone marrow
• Immunological tests-  auto-antibodies, PCR, TB serology