Disturbances in body Temperature

introduction

Homeothermy:is thermoregulation that maintains a relatively stable

internal body core temperature regardless of external influences.

through behavioral and physiological mechanisms. The heat regulating

functions are controlled by hypothalamus.

Bes oneCeG ioko Canbes

These mechanisms maintain the balance between the heat loss and

gain.

Homeothermy:

Heat loss➡️ Balance ➡️ Heat gain

_ Radiation. _ Radiation.

_ Conduction. Environment&. _ Conduction.

_ Convection. _ Convection.

_ Evaporation.

* Milk removal. * Exercise.

* Fecal elimination. Metabolic activity. * Maintenance.

* Urine elimination. * Growth, feeding, lactation,
gestation.

-Hypothermia:
It means body temperature is lower than normal.

Causes:

1. General causes:

ExCessive heat loss.

Exposure to excess cold air.

Insufficient heat is produced.

Insufficient feed intake & body reserves.

2-Specific causes: Secondary to diseases or other conditions:

During anésthesia & sedation.

Reduction of metabolic activity as in terminal stages of some diseases as

parturient paresis & acute ruminal acidosis.

3. Combination between excessive heat loss & insufficient production:

starvation of newborn in cold environment.

4. Secondary to other diseases:

Not marked.
With Milk fever in cattle.

Temperature return to normal after successful treatment with calcium salts.

Neonatal Hypothermia,;
Newborn farm animals (calves-Lambs).

It is a major cause of mortalities.

Cause:

Neonates at first few hours (6 hours) of life cannot maintain their rectal
temperature at normal value in cold conditions.

Changes from a stable thermal environment to a variable one (10-15 °C colder).

Coat is wet with placental fluid &low insulated Energy loss increased by
evaporation.

Low immunity against environmental pathogens.

Risk factors:

in calves:

Reared outdoors in cold climates.

Enteritis.

Dystocia:

➡️ Weak calyes.

➡️Weak teat-seeking activity.

➡️Poor suck reflex.

➡️Colostrum deprivation (energy-immunity).

 ➡️Failure of passive Immunoglobulin's transfer.

In lambs:

* Starvation, dystocia, multiple births.

* Low birth weight, birth injuries, sparse hair coat.

* Ewe of poor condition, young or aged.

Pathogenesis:

Cold temperature + risk factors ➡️ Subnormal body temperature (Rectal below

37 °C to 30 °c):

* Muscular weakness.

* Mental depression, convulsions.

* Respiratory failure.

* Bradycardia, weak pulse, cool oral mucosa.

* Cold extremities.

* Recumbency.

* Collapse, death.

Prognosis

If animal has suffered from previous febrile condition then a sudden fall in body
temperature occurs this is called a pre-mortal fall and in this Case the hypothermia
is considered of poor or unfavorable prognosis.
Treatment of Hypothermic neonates:

* Dry off calf-lamb to reduce heat loss.

* Place in a shelter with ewe or cow.

* Give ewe or cow colostrum by stomach tube or feeder (50 mi/kg BW).

* Colostrum or milk should be warmed.

* 1/V fluid therapy (dextrose) (1 ml of 50% dextrose/kg BW).

* Glucose Intra-peritoneal.

* Monitor rectal temperature every 30 min.

Control of Hypothermia in neonates:

* Change in calving season to a warmer time.

* Provide dry, draft free place for calving or lambing.

* Protective shelter for pairs (cow-calf) during first week.

* Minimize incidence of dystocia.

* Ingestion of adequate colostrum as soon as possible after birth.

2. Hyperthermia-(heat stroke) - Heat exhaustion-(Heat stasis):

It means elevation of body temperature.

Causes: Physical:

* High environmental temperature.

* Severe muscular exertion, high humidity.

* Fat animal, heavy hair coat.

* Confinement indoor with inadequate ventilation as shipping or transportation.

Predisposing factors:

A difference between animals breeds in tolerance to environmental temperature.

Ex.Water bufalo/& lactating are less tolerant.

Other causes:

* Neurogenic: damage to hyothalamus as in spontaneous hemorrhage.

* Dehydration insufficient tissue fluids so cannot accommodate heat by

evaporation.

* Specific mycotoxins: Claviceps purpurca.

* Poisoning: levamisole.

* Malignant hyperthermia.

* Hyperthermia can be: For short period.

For prolonged period.

Critical temperature exceed the critical one.

Pathogenesis: Hyperthermia causes imbalance between heat gain and loss so

results in many effects on body system.

1. Hyperthermia For short period: Useful in infectious diseases and causes:

➡️ Impairment of organism's viability.

➡️ Stimulation of immune system & phagocytosis.

2- Hyperthermia For prolonged period:

Have harmful effects on body as illustrated in the following diagram:

1. ➡️ Metabolic rate 40-50%➡️ ➡️ Liver glycogen store.➡️ Endogenous metabolism of
protein.

2. Difficult respiration, ➡️Rate & depth,Dryness of mouth➡️ anorexia and thirst ➡️

Loss of body weight, Hypoglycemia, ➡️Muscle strength

3. Peripheral vasodilation ➡️ ➡️ renal blood flow and blood pressure ➡️ ➡️ urine

secretion, albuminuria and ➡️ heart rate.

3. Hyperthermia with critical temperature:

Have devastating effects on body:

CNS depression, respiratory center depression, myocardial weakness+ irregular

heart rate, endogenous metabolism+ anorexia, extensive degeneration in most
tissues ➡️➡️ respiratory failure+ circulatory failure ➡️ death.

Clinical findings:

* Rectal temperature exceeds39.5.

* Heart & respiratory rates, weak pulse.

* At the beginning sweating & salivation.

* Restless, dullness, tend to-be recumbent.

* Early stage thirst, seek cool places.

* If reach 41°C. (labored shallow & irregular respiration, rapid & weak pulse).

* Collapse, convulsions & terminal coma.

* Death occurs if core temperature exceed normal by 5 °C.

* If heat stress is prolonged it can lead to:

* In sheep abortion and embryonic mortalities.

* In cattle reduced breeding efficiency.

Clinical findings in horse:

* Rectal temperature usually exceed 42°C:

* Fatigue.

* Excessive sweating leads to profound fluid & electrolyte loss, and finally results
in hypotonic dehydration.

* Hyponatremia leads to loss desire to drink and dehydration.

* Increased Heart & respiratory rates.

* Reduced performance, depression, weakness.

* Hypocalcemia, metabolic alkalosis results in synchronous diaphragmatic

flutter(SDF).

* In extreme cases:(Coma & death).

Treatment of hyperthermia:

* Adequate drinking water, Cooled (2-8°C) with or without electrolytes.

* Frequent monitoring of rectal temperature during cooling.

* I/V administration of fluids as 0.9% NaCl in weak, recumbent & dehydrated

animals.

* Horse need I/V (20-40 L)over first few hours.

In case of synchronous diaphragmatic flutter give I/V calcium therapy.

Oral electrolytes solution by nasogastric tube (NaCl & KCI) to adult horse.

Antipyretic preparation.
Control of hyperthermia:

* Provide cool and clean water.

* Continuous application of water to increase humidity.

* Use shades & intermittent sprayer.

* Enhance airflow by fans.

* Provide mounds for cattle to stand on.

* Feed a larger percentage of ration in evening (cooler weather).

* Reduce handling during periods of heat stress.

* Select cattle based on breed & coat characters.

3-Fever (Pyrexia):

It is elevation of [core body temperature. It is combination of hyperthermia &

infection or, inflammation and it is dependent on ambient temperature.

Causes of fever:

1. Septic fever: (the most common), caused by inrection with bacteria, viruses,
protozoa or fungi.

* Localized infection such as abscess.

* Systemic infection as bacteremia, endocarditis (fever is intermittent).

* Systemic as septicemia (fever is consistent).

2. Aseptic fever:

* Chemical fever as injection of foreign protein.

* Surgical fever due to breakdown of tissue & blood.

* Tissue necrosis due to breakdown of muscles.

* Rapidly growing neoplasms cause extensive necrosis.

* Lymphosarcoma in cattle.

* Immune reactions, anaphylaxis.

* Severe hemolytic crisis.

Stages of fever

1- Increment or the onset (chill).

2- Fastigium or the period of constant temperature.

3- Decrement or deferveścence.

Mechanisms of action during stages of fever:

1- Increment or the onset (chill): It is the immediate response characterized by

cutaneous vasoconstriction to prevent heat loss and increase the heat production
and reflected by the following clinical findings:

* Cold extremities.

* Dryness of skin.

* Muscular shivering.

* Absence of sweating

* Minimize urine formation.

* Increase in temperature, pulse and respiratory rates.

2- Fastigium: the period of constant temperature that is characterized by
cutaneous vasodilatation through mechanisms of heat dissipation & heat
production returns to normal and reflected clinically by:

* Flushing of skin & mucosa.

* Sweating (may be severe).

* Diuresis.

* Reduce fore-stomach motility.

* Increase metabolism and tissue wasting may occur.

3- Decrement: During this period the erfects of pyrogenic substances are removed,
this period is characterized by marked vasodilatation so the excess of stored heat
is dissipated and reflected clinically by:

* Sweating (may be severe).

* Muscle flaccidity.

* Fall in body temperature.

Note: In Severe cases (Toxemia + hyperthermia) the tissue ability to respond to

heat production are lost and results in collapse and death.

Degree of fever:

Mild fever: about 1 degree above normal.

Moderate fever (pyrexia): 1.7 above normal.

Severe fever (Hyperpyrexia): 2 above normal.

Types of fever:
1. Simple.

2. Continuous.

3. Sustained: no-signifieant diurnal (within daytime) variations.

4. Remittent: increase diurnal variations.

5. Intermittent: fever peak lasts for 2-3 days combined with normal Periods.

6- Recurrent.

7. Atypical: temperature variations are irregular.

8. Biphasic fever.

Treatment of fever: Treat the primary cause.

Antimicrobial agent.

Antipyretic and analgesic.

Anti-inflammatory.

Fluid therapy.

Immuno-stimulants, Vitamin C.

Toxemia & Endotoxemia

It is the circulation of toxins in the blood stream (produced by Bacteria, Parasites
body cells), this does not include (plants or insects, ingested organic or inorganic
poisons).

Causes:

- Antigenic toxins: produced by bacteria, parasites. It can be:

Exotoxins.

Endotoxins.

- Metabolic toxins: produced by abnormal body metabolism.

As ketone bodies & histamine.

Pathogenesis:

Have the following effects on metabolism of:

1. CHO: ➡️ Blood sugar level, ➡️ Liver glycogen, ➡️ Blood pyruvate & Lactate.

2. Protein: ➡️ Tissue breakdown, ➡️ Blood-NPN, ➡️ Antibody production ➡️ Total serum

protein.

3. Minerals: ➡️ Cu, ➡️ Fe, ➡️ Zn.

4. Damage to liver & Kidney Parenchyma & tubules ➡️ Albuminuria.

5. Weakness of muscles & myocardium ➡️ Response to stimuli.

6. Depression of hemopoiesis.

7. Hypersensitivity reaction: ➡️ Leukocytes.

Clinical findings:

* Depression.

* Hyperthermia followed by hypothermia.

* Anorexia.

* Pulse rapid, weak irregular.

* Heart rate increase (tachycardia) with weak sound.

* Systemic blood pressure reduced.

* Cool skin & extremities.

* Congested mucosa & increase Capillary refilling time.

* Diarrhea.

* Renal faiture: Anuria & albuminuria.

* Muscular weakness: recumbency, coma,..death.

Treatment:

* Specific antitoxin with supportive treatment.

* Intensive fluid & electrolytes therapy (1/V).

* Broad spectrum antibiotic.

* Parenteral nutrition.

* Glucose, corticoids 1 mg/kg Bwt 1/V daily.

* NSA: Acetylsalicylic acid, phenyl-butazone. 15 mg/kg Bw initially then 10 mg/kg/6

or 12 hrs.

Septicemia / Viremia
Toxemia + hyperthermia + infectious MOs. (large Number) in blood stream.

Bacteremia (Transient).

Septicemia (all over the course of disease).

Causes (In all species):

* Pasteurellosis, Salmonellosis, Leptospirosis.

* Rift valley fever.

* Anthrax.

* Pseudomonas pseudomonas.

Pathogenesis:

Infectious agent ➡️ release exotoxin and endotoxin causing fever and toxaemia.

Endothelial damage and hemorrhage ➡️ localisation in tissues ( heart, joints, eyes,

meninges).

Pain
Can be classified to:

1-Superficial: Skin or SC tissues.

2-Deep: Muscles, Joints, Bones, CT.

3-Visceral: Viscera.

Motor response to pain changes in:

* Posture & demands.

* Restlessness.

* Reluctance to move.

* Prolonged recumbency.

* Vocalization.
* Self-mutilation.

Aspect Visceral Parietal Referred

Cause Localized damage Stimulation of Site distant from

as ischemia, nociceptors. actual lesion.
infection.

_ stretch of wall as
obstruction or
tension.

Origin Thoracic or Pleura, Viscera.

abdominal cavity. peritoneum,
pericardium.

Degree Severe rhythmic Stabbing. Sharp on surface,

cramps. tender in cavity.

Localize Difficult Well localized. Can not.