MODULE-1: HISTORY OF

VETERINARY MEDICINE
Learning objectives

• To know about how the art and science of animal healing eveolved in
India and around the globe.
• To understand the contributions of Indians for the development of
Veterinary Medicine and Animal Health Care as well as the
international contributions for the animal health care.
• History repeats itself! At the end, the learner must be able to evolve
himself / herself for a dedicated carrier, following the innovations of
the past and endeavouring to innovate further for a better
future.

HISTORY OF VETRINARY MEDICINE IN INDIA

The World's First Animal Hospital was established in India(Emperor
Asoka's Period).The Practice of Animal Healing, existed in India even
centuries prior to the Emperor Asoka's regime, as evident from the life of
the ancient saints of the Tamil Kingdoms & Dravidian Civilizations and
from the Rishi’s & Sadhu’s of Aryan Civilizations in Northern
India. Keeping these rich traditions alive for several centuries and even
today, the Indian Subcontinent boasts one of the richest biodiversity of
animal and plant life in India.
Father of Veterinary Medicine - RENATUS VEGETIUS (450-500 A.D.)
Why the Indian Veterinary
History is important...
• According to Somvanshi's
Documentation(2006)on
Indian History of Veterinary
Medicine, Cattle husbandry
was well developed during
the Rigvedic period (1500–
1000 BC)
• Atharvaveda provided
an interesting information
about ailments of animals,
herbal medicines, and cure
of diseases.
• Shalihotra, the first known
veterinarian of the world,
was an expert in horse
husbandry and medicine and
composed a text Haya
Ayurveda.
• Sage Palakapya was an
expert dealing with
elephants and composed a
text Gaja Ayurveda.
• In Mahabharata period
(1000 BC), Nakula and
Sahadeva, the two Pandava
brothers were experts of
horse and cattle husbandry,
respectively.
• Lord Krishna was an expert
caretaker and conservator of
cow husbandry. Gokul and
Mathura were famous for
excellent breeds of cows,
high milk production,
quality curd, butter, and
other products.
• Buddha was a great
protector of all kinds of
animals and birds (including
game) in ancient India as he
preached lessons of non-
violence to masses.
• Graeco-Romans imported
livestock from India after
invasion by Alexander.
These descriptions are
available in Indika, a book
authored by Megasthenes,
the ambassador of Seleucus
Nikator, king of Mecedonia
in the court of Chandragupta
Maurya.
• The great king Ashoka (300
BC) erected the first known
veterinary hospitals of the
world. He arranged
cultivation of herbal
medicines for men and
 animals in his empire and
adjoining kingdoms.
• In a famous text, the
Arthashastra (science of
economics) composed by
Kautilya, the guide and
political advisor of emperor
Chandragupta Maurya, a lot
of information is available
about different animal
(elephant, horse, and cow)
departments, grazing lands,
rules of meat science,
livestock products like skin
and fur, and veterinary
jurisprudence. This
knowledge flourished during
the great Hindu kings of the
Gupta period up to 800 AD
before Islamic followers
invaded India.

HISTORICAL DEVELOPMENTS IN HARAPPAN

PERIOD & VEDIC AGE
Historical Developments in Harappan Culture
• Excavations
of Harappa in
Montgomeri
district,
Punjab and
Mohenjo-
daro in
Larkana
district, Sindh
(now in
Pakistan) in
1920–22
provided
valuable
archaeological
evidence of a
well
developed
civilization,
which was
5000 to 6000
years old. The
famous Indus
Valley
civilization
was better
known for
highly
developed
culture and
 organized
society.
• People of
Indus Valley
civilization
were familiar
with dogs,
bulls, sheep,
goats,
buffaloes,
horses, and
elephants.
They were
also aware of
a number of
wild-game
and animal
products,
such as milk,
curd, ghee,
and meat.
• Fish was their
main animal
food. These
people were
fond of
mutton, beef,
chicken, and
meat of
tortoise. Seals
recovered
 from Indus
valley
provided
knowledge of
bulls,
buffaloes,
goats,
elephants,
ibex, and
many other
animals. The
script on
these seals
has not been
fully
deciphered so
far.

Historical Developments in Vedic age

• A lot of information is available on keeping of animals in the

Vedic Age in the Rigveda, which is the oldest holy book of
Aryans. In Rigveda, animals were considered as wealth.
Aryans maintained their cattle on pastures, which were near
to their dwellings. They cut the jungles and grazed cattle
there. The cows were milked thrice a day. Castration of males
was practiced and oxen were used for farm transport. It
appears that Aryans preferred cows. Buffalo was not a
commonly used animal by them. They kept dogs for guarding
houses and for hunting of boars. Sheep were kept mostly for
wool and goats for milk. Oxen were used for plowing and
irrigation also. The cow has been defined as aghanya, i.e., not
to be killed, indicating the high sanctity of the cow in the
 Vedic period. In Rigveda, barley, sugarcane, and leftovers of
sesame after extraction of oil were used for feeding of
animals.
• Masters of philosophy searched the secrets of life and the
universe and developed “cow science”. Virtually “cow
science” is a unique gift of India to the whole world. Learned
people of ancient India considered that whole cow family or
“gau vansh” was essential for existence of humanity, its
protection, nourishment, development, and culture. Cow
milk provided special energy, strength, and intelligence. Cow
dung and urine nourished agriculture farming. Bullock
power helped in development of techniques in agriculture
like carrying draft,
transportation, and cottage industry. Skin from dead animals
supported the leather industry and handicrafts. Therefore,
cow husbandry was always core-point in the Indian lifestyle
and economy during the Vedic period.

ANIMAL AYURVEDA & DEVELOPMENTS

DURING EPIC ERA
Animal Ayurveda in Vedic period

• The Vedic Society in India was dominated by the ‘cow

culture’ and Vedic people adored the cow and regarded it as
the source of their good fortune, happiness, and good health
(Rigveda 6.28.1, 6).
• It is believed that the religious priests, who had the
responsibility of maintaining cattle, were the first animal
healers or veterinarians.
• A number of Vedic hymns indicate medicinal values of the
herbs and it is likely that these priests were also apt to it and
used their medical knowledge to keep the sacred cattle free
from ailments.
 • The Atharvaveda mentions about healing herbs and drugs.
The Ayurveda (the science of life) deals with the knowledge
of medicine possessed by the Vedic saints.

Epic period

• Ramayana is the oldest literature of Sanskrit, although no

written history is available of that period. The treatment of
various ailments using medicinal herbs and surgical
procedures are described at length.
• Various uses of oil as preservative and treatment are
mentioned.
• Surgical procedures like caesarean section, hysterectomy,
etc. were known to be performed by trained vaidhyas or
physicians.
• Fruit juices, flower extracts, and wines made from fruits
were said to have great medicinal properties.
• Medicinal herbs like arjuna (Terminalia arjuna), kutaja
(Holarrhena antidysenterica), kadamba (Anthocephalus
cadamba), sarja (Vateria indica), neem (Azadirachta indica),
ashoka (Saraca asoca), asana (Pterocarpus marsupium), etc.
were used widely to cure ailments of men and animals.
• Diseases like leprosy, tuberculosis, mental disorders, etc.
were described along with treatment. The herbs found in the
mountains of Kanchanjunga and Kailash (now in China) are
said to possess good medicinal quality.

DEVELOPMENTS IN MAURYAN AGE AND

THEIR INTERNATIONAL RELEVANCE
Historical Developments in Mauryan Age

• Animal husbandry made great progress in the Mauryan age

(322–232 BC). The Mauryan age preceded the period of
Buddha and Mahavir, who preached non-violence towards
animals.
• The earliest Buddhist text “Suttanipata” describes cattle as a
giver of food, beauty, and happiness (annada, vannada, and
sukhada) and therefore deserves to be protected.
• According to Kautilya’s Arthashastra, cow was a worshiped
animal. It was one of the first duties of the King to worship
the cow with her calf and bull. The killing of cow was a
deadly sin.
• Buffalo also became a recognized dairy animal by this period.
• In the Arthashastra, goat has been described as an important
milch animal like cows and buffaloes. Sheep were raised for
wool.
• According to Arthashastra, in a breeding herd, 4 bulls should
be provided for every 10 cows/buffaloes. Feeding of animals
on pasture was the main practice. It was the duty of the King
to identify and provide enough land for pastures near each
village. The Gopa (village accountant) was supposed to keep
the details of the pasturelands. \
• In Arthashastra, there is separate mention of capital
punishment for stealing or hurting a cow. When a person
caused a bull to fight with another bull, he was fined. If any
person injured a bull, he was heavily fined. Similiar
punishents were also describe in Code of Hamurabhi
(Egypt)
 • Veterinary services were essential services during the
Mauryan period. In this period, asses were used to carry
loads. Horses were used to yoke different kinds of chariots
like festival chariots, battle chariots, and traveling chariots.
In the stables, different kinds of horses were kept separately.
Horses were regularly trained for warfare. There were horses
of many breeds.
• Arthashastra has graded them as best, middle, and ordinary
quality. Thoroughbred horses were recommended parched
rice, drippings, minced meat, red rice-powder, and grasses.
Mules have also been mentioned in Arthashastra, indicating
their presence in the Mauryan period. Elephants were very
important animals in the Mauryan period. They were used in
warfare, as they were very useful for storming fortresses;
breaking upon massive doors and to move even in dense
forests and marshy lands. There were about 6000 elephants
with Nandas and 9000 with Chandragupta Maurya.
Elephants for war and riding were housed inside the fort.
Whoever killed an elephant was sentenced to death. Tusks of
an elephant were considered precious.

ASOKA PERIOD
The Golden Era for Veterinary Medicine in the Ancient
Word
• The present-day Veterinary Council of India adopted its
insignia, the sculpture of a bull and a part of the text of the
stone edict from the period of Emperor Ashoka (around 300
BC), which projected the veterinary profession as its “best
heritage”.
• Ashoka, the grandson of Chandragupta, who turned to
Buddhism after Kalinga war gave veterinary science a new
turn in India. It is described that the first veterinary hospital
existed in Ashoka’s [Link] ‘Baniyan Hospital’ of Suratis
 is believed to be one of them, which consisted of a large piece
of land enclosed by high walls. Provision for keeping indoor
patients was made inside to accommodate animals.

Animal Surgery

• From primitive therapeutics, the early man turned to

primitive surgery. “Susruta Samhita” is the earliest known
work dealing with surgery. According to evidence with
Indian scholars, Dhanvantari’s direct disciple Susruta
belonged to 600 BC.
• He made great improvement in the general techniques of
surgery and performed many new and major operations.
Susruta Samhita testifies to the great scientific knowledge of
the ancient Indian surgeons.
• It was translated into Arabic before the end of 800 AD and
was called ‘Kitab-Show-Shoon-a-Hindi’ or ‘Kitab-i-Susrud’;
Cellars translated into Latin and Hassler into German. The
students were taught surgical techniques first on dummies
and later on dead bodies. Before Susruta’s time, knowledge
and practice of surgery in India was more or less of the same
standard as in contemporary civilizations like Egypt,
Mesopotamia, and Greece.
• Almost all aspects of surgery were dealt in ancient medical
veterinary treatises. Some of these aspects were preliminary
surgical methods, dressing and bandaging of wounds,
symptoms to predict prognosis of the surgical cases, etc.
Special methods include application of cautery, removal of
foreign bodies and obstructions, surgical grafting, and
treatment of fractures, dislocations, and fistula. Methods of
suturing and plastering and duties of physicians, surgeons,
and nurses have been dealt in detail. General principles of
surgery described include preparatory measures and
principal measures (including surgery and post-operative
measures). However, there appears to be no mention of
anaesthetic techniques. Surgical treatment of animal disease
 was very much developed during Vedic period. Skilful
surgeons treated animals with precision and great
perfection. Various techniques of surgical operations along
with instruments have been dealt in detail in Shalihotra’s
and Palakapya’s works. Treatment of sinus fistula, burns and
scalds, snakebite, fractures, ailments of ligaments/tendons,
dystocia, removal of dead foetus, extraction of teeth and
fractures were routinely done during Vedic period (Singh,
2002b).
The Animal Haealth Care & Treatise on Animal Health

• Animals received good medical care in ancient India.

Physicians treating human beings were also trained in the
care of animals. Indian medical treatises like Charaka
Samhita, Susruta Samhita, and Harita Samhita contain
chapters or references about care of diseased as well as
healthy animals. There were, however, physicians who
specialized only in the care of animals or in one class of
animals only; the greatest of them was Shalihotra, first
known veterinarian of the world and the father of Indian
veterinary sciences. The treatment of animal diseases in
ancient India was well developed and carried out with great
care and precision by well-trained personnel.
• The treatment of animal diseases using Ayurvedic medicine
has been mentioned in Agni Purana, Atri-Samhita, Matsya
Purana and many other texts. The treatment of a variety of
ailments: infection of horns, ears, tooth, throat, heart, and
navel, rheumatism, haemorrhagic enteritis, dysentery,
digestive ailments, cold, parasitic/verminous diseases,
stomach worms, rabies, abscess, anaemia, wounds,
medicines to increase milk production, epistasis, retention of
urine, urinary colic, constipation, lacrimation, arthritis,
rhinitis, sprain, haematuria, and skin infection has been
given in detail (Somvanshi, 1993).
 ETHNO VETERINARY MEDICINE AND
FOOD SAFETY IN ANCIENT INDIA
Ethno Veterinary Medicine

• Before the advent of modern allopathic system of medicine,

it seems possible that the healing art was almost the same
throughout the world including India. This system of
medicine has given the term ethno-medicine (when implied
to human treatment) and ethno-veterinary medicine (in the
context of animal treatment). In India, ethno-veterinary
practices were in vogue since time immemorial. In ancient
India, the Vedic literature, particularly Atharvaveda is a
repository of traditional medicine including prescriptions for
treatment of animal diseases. Scriptures such as Skanda
Purana, Devi Purana, Matsya Purana, Agni Purana, Garuda
Purana, Linga Purana, and books written by Charaka,
Susruta, Palakapya (1000 BC), and Shalihotra (2350 BC)
documented treatment of animal diseases using medicinal
plants. Vedic texts also describe divine healing powers.
Yajurveda cites importance of growth and development of
medicinal plants and Atharvaveda mentions about the value
of medicines in curing the diseases. Shalihotra undoubtedly
appears to be the first veterinarian of pre-historic times. The
ancient Indians were so apt with the knowledge of herbals,
even Alexander acquired some of the skills used by Indians,
particularly for treatment of snakebite.

Food Safety in Ancient India

• Although milk, fruits, vegetables, and grains formed bulk of

their food, Vedic Indians were meat eaters. Slaughter of
animals was more or less a sacrificial act. Goat and sheep
meat were consumed by men and offered to their gods.
During Rigveda, cow slaughter was banned. However,
 horseflesh was eaten occasionally at the time of religious
sacrifice called Ashvamegha yagna. Dogs were used for
hunting wild boars. In later Vedic period, meat eating was
fairly common but killing of cow was a deadly sin. Vedic
Aryans did not prefer fish while the Indus Valley people had
a special liking.
• During Ashoka period, non-violence or ahimsa was a policy
of the state but meat eating was not banned. Slaughterhouse
was located at a distant place towards south of the palace
and regulated by a superintendent. Pregnant or milking goat,
sheep, pig, and piglets up to 6 months of age were banned
from slaughter. Butchers selling meat derived from sick or
dead animals and adulterated or spoiled meat were severely
punished. This shows that meat science had a sound basis in
ancient India.

ELEPHANT MEDICINE, EQUINE & BOVINE

MEDICINE - THE ANCIENT INDIAN
EXPERTISE
Elephant Medicine or Gaja Ayurveda

• Palakapya, an ultimate authority on elephant medicine

belonged to the Rigvedic period 2000–4000 BC. The
Gautam Samhita, the Ashva Ayurveda, and Hastya Ayurveda
are the only treatises on animal science till now. Palakapya
wrote Hastya Ayurveda or Gaja Ayurveda dealing with
elephant medicine and dedicated to Lord Ganesha. Elephant
medicine and surgery were divided into four parts by
Palakapya, viz., Maha Rogsthan or major diseases, Ksudra
Rogasthan or minor diseases, Salyasthan or surgery, and
materia medica-diet and hygiene. He classified various
ailments of elephants into: Adhyatmika (physical) and
Agantuka (accidental or incidental); physical classes of
ailments were called Manasa (caused by mental diseases)
 and Dosaja [caused by disorder of bodily humors – vata
(air), pitta (bile), and kapha (phlegm)]. Hastya Ayurveda also
mentions about anatomy of elephant, treatment of different
kinds of diseases, training of elephant, and also classification
of elephants on the basis of a number of characteristics.

Equine Medicine or Haya Ayurveda

• There is no legend of horses in the seal of Mohanjo-daro,

Harappa, Kalibangan and in Indus Valley culture. Amongst
18 gems recovered in Samudramanthan by gods and
demons, the horse named Ucchasrava was possibly the first
known horse of puranik (ancient) India. The Aryans
introduced horses for rapid transportation. Pack, riding,
chariot, war, race, and even plowing horses were frequently
mentioned in the Vedic age (1500–1000 BC). The Aryans
took advantage of the trained horses to march into the fertile
land of Iran and Mesopotamia. The Aryan chariot (ratha) is
depicted at Sanchi. In the later Vedic period (1000–600 BC),
Buddhist period (600 BC), and Mauryan period (400 BC),
the use of horses was well documented. In the Mauryan age
(322–232 BC), equine husbandry made tremendous progress
and these were used for riding and for war.
• The royal horses were under the charge of a superintendent
of horses (Asva adhyakacha), who used to register the breed,
age, color, and place of origin. Detailed accounts of housing
and feeding of horses were mentioned in Arthashastra.
Veterinary doctors and horse trainers were assigned free
endowment. In the Gupta dynasty (300–550 AD), horses
were given more importance than elephants in
Samudragupta’s army because of their speed and easy
maneuvrability. He also performed Ashvamedha yagna to
proclaim his imperial power and issued a gold coin depicting
a horse. Skandagupta (455–467 AD) was shattered by Huns,
who were expert horse riders. The Kannauj empire (606–647
 AD) has also been mentioned to use saddled horses in
warfare.

Bovine Husbandry , Health Care and Medicine

• Cows were regarded as wealth and were the backbone of the

economy of ancient Indians, i.e., Aryans. Wars were fought
for acquiring cows. Cattle were one of the most frequently
used animals described in Vedas. Cows were regarded as
mother (“Gau-mata”) and referred to as Aghanya. Prayers
were offered to Agni (God of Fire) to kill with his flame all
those evil dwellers, who stole milk of cows. Those demons
may not get the nectar (milk of cows). Voluminous treatises
are also available on cows, e.g., ‘Gau Ayurveda’. During
Pauranik period, cow (Kamdhenu) emerged out of Samudra
manthan, was considered so valuable that devatas fought
with demons and acquired them.
• Mantras in Vedas (Shala Nirman and Goshth Suktas of
Atharvaveda) describe that the animal houses (Goshth) and
their management were of good quality. Pashu Samvardhan
Sukta of Atharvaveda indicates that Vrihaspati Deva knew
the animal behavior and management well. Cows were high
milk-yielders and were milked thrice a day by women
(Duhitras). They knew the animal feeding practices and fed
them with dry hay and green fodder. The herb arundhati (a
climber, not identified) not only treated several disease
conditions but also increased milk yield in cows. Prayers
were offered to Aditi Deva to discover medicines for health
improvement of humans and calves. It shows that Aditi was
one of the researchers of medicine. Treatment of weak,
infertile, and unproductive cows for making them productive
was well described. Castration of males by crushing the
testicles between two stones was also practiced.

Cow prosperity and protection

 • Cow worship, cow keeping, and cow protection were the
three stages through which the prosperity of the mother cow
occurred from time to time. Beef eating in ancient India has
been a controversial subject. Due to availability of natural
facilities of breeding, feeding, and grazing, cattle flourished
in the ancient times. Cow prosperity started declining with
increasing human population and socioeconomic conflict. In
case of buffalo, it is the utility of the buffalo that has
increased its prospects.
Legends of cow-bulls in coins of ancient India

• In ancient India, cow was addressed as “Gau-mata” or

mother cow. Rulers from 600 BC used to inscribe pictures of
bulls (rarely cows) on coins, which show their importance
and utility. Round coins (occasionally rectangular or square)
weighing 5–7 g made up of copper, silver, lead, or gold were
used as currency. The best and rare inscription of cow was
seen in the coins of King Anshu Verma, ruler of ancient
republic of Lichavvi (Nepal). Inscriptions of standing right
facing (rarely left facing) humped bulls are seen on the coins
of punch-mark, Airan, Audumbar, Ayodhya, Kaushambi,
Saatvahan, Ujjaini, Chatrapa, Yaudhey, Krishnaraj
(Kalchuri), etc.

Buffalo
• Reference of buffaloes in the form of a furious demon,
Mahishasur and docile beast, the ride of death God Yamraj
has been made in the prehistoric ancient Indian literature.
Taming and domestication of buffalo has been mentioned
during the epic era of Ramayana and Mahabharata and true
domestication during the Indus Valley civilization. Several
types of buffaloes have been described in different parts. The
Indian subcontinent is the richest habitat of riverine
buffaloes (dairy) whereas East and Southeast Asian countries
 are dominated by draft type swamp buffaloes. In South India
buffaloes were used for plowing lands after which they
wallow in the pond to reduce tiredness. Buffalo keeping was
a symbol of prosperity in Southern India.

Goat

• Goats and sheep were first domesticated near Iraq and

United Arab Emirates 8700 years ago, much earlier than the
advent of agriculture. People who belong to Chalcolithic age
were found in the Indian states of Madhya Pradesh,
Maharastra, and Rajasthan and they reared goats and other
animals. Goats were domesticated earlier, and served
mankind for longer period for their milk and other products.
• During Pre-Harappan period, wild ancestors of goats were
found in barren hills of Baluchistan and Western Sindh.
Gaddi goats resembling the ancestral wild goats are still used
for carrying goods in the higher Himalayan region of India.
The greatest artistic creations of Harappan culture are seals
resembling goats, which greatly supported the animal
husbandry in Indus Valley civilization. Goats serve mankind
providing meat, milk, fiber and therefore, appropriately
called poor man’s cow.

Sheep

• Sheep was domesticated about 8700 BC. The original center

of domestication was the Aralo-Caspian steppe and
Turkestan. From there, sheep keeping spread early into Iran
and later into Mesopotamia and Baluchistan. The sheep kept
in India, Tibet, and other countries of East and South Asia
were of western derivation and basically of Urial stock.
• In India, sheep keeping was practiced evidently from Pre-
Harappan period through to Mauryan Age. The dominant
form of sheep rearing still remained of nomadic nature.
Domestication of sheep, besides ensuring a permanent meat
 supply, also improved the supply of skin, hair (wool), fat, and
bones. Although these animal by-products are available from
other sources, production of wool, however, remained a
monopoly of the sheep. Sheep rearing is an exclusive
occupation of a class of herders traditionally marked out as a
pastoral caste.

Fowl

• People of the Indus Valley civilization were quite familiar

with domesticated fowl. In the seals of the Indus Valley, two
Sonarati red cocks with fighting gesture were identified. At
the same place, small pieces of earthen hen toys were
recovered. One of these birds, which was adjoining to feed
pot, was considered as hen. This indicates that captive
breeding of birds was practiced during those days.
• Domestic fowl was also found in Harrappa. From this place,
two earthen birds (one male and the other female) were
recovered. From Kanhudaro also, small-sized figures of birds
belonging to the family of domestic fowl were recovered.
Possibly these were the images of quails. It is accepted that
Indus Valley people kept birds for games and breeding for
meat, possibly started afterwards. When Aryans invaded
India around 2500 BC, they appreciated cocks.
• Cock is mentioned in Atharvaveda and Yajurveda, but not in
Rigveda. During 1000 BC, eating hen meat was prohibited,
possibly for religious reasons. The study of Northwest Indian
coins indicates that cocks were favored. During 310 BC,
Softitus, a Prince of Punjab presented a few silver coins to
Alexander, which had legends of cocks along with spur.
Satyamitra (100–200 AD) engraved fowl on coins with palm
leaves. During this period, India had trade with Western
Asia, Arabia, and Egypt through sea and land route, which
was instrumental in the dissemination of red jungle fowl
throughout the world.
 SCOPE OF VETERINARY MEDICINE

Clinical practice
• All veterinarians have a professional responsibility to
the community and an important part to play in the
economic and social well being of the nation. The
primary responsibility of veterinarians in practice is to
serve the public through the provision of high quality
care for the health and welfare of their animals,
whether these animals are kept as pets or for leisure
activities, are working animals, farm livestock, or
wildlife.
• Veterinary practices are distributed through the
country in towns and rural areas. These may involve
one veterinarian working on their own but, more
commonly, several veterinarians work together. The
type of practice varies according to the location. In
large cities, for example, practices may deal only with
companion animals such as dogs, cats and caged
birds. This is commonly referred to as 'small animal'
or 'companion animal' practice. In farming areas, the
emphasis is on farm livestock such as cattle, sheep,
deer and pigs, although other animals such as dogs,
cats and horses will also be dealt with ('large animal'
or 'mixed' practice). Some practices, particularly in
areas where there are large numbers of horses, may
deal mainly or solely with them ('equine practice').
• Veterinarians in clinical practice in today generally
operate from well-equipped clinics containing x-ray
equipment, surgery and animal hospital facilities and
laboratory equipment for conducting clinical
 pathology. There are also private and government-run
laboratories that provide diagnostic services for
practitioners through the testing of samples of various
kinds from their animal patients. These can be for
bacteriology, parasitology, virology, pathology,
biochemistry and so on. These laboratories commonly
employ veterinarians with advanced training.
• Clinical practice offers an interesting career with
plenty of variety. Apart from other veterinary skills, it
requires an ability to assess facts in investigating
outbreaks of disease in order to arrive at a satisfactory
diagnosis. Common sense, independence and the
ability to work with people of the farming community
or other animal owners are necessary. The graduate
engaged in this work has ample opportunity to
exercise and extend knowledge and practical skills
gained during university education.
Some special characteristics of particular types of
practice
• Large animal (Farm animal) practice
o Diagnosing and treating disease in individual

animals is an important part of all clinical

practice and in some cases it is the major
concern. In farm animal practice, however, the
veterinarian has additional responsibilities
centred on the flocks and herds that make up
farming enterprises. Veterinarians have an
important contribution to make to the
productivity of these flocks and herds by assisting
with the planning and development of flock and
 herd health programmes, monitoring the health
status and production of the animals, often
working in collaboration with other animal
production advisers. Veterinarians in these
practices also have an important part to play in
national disease control and eradication schemes,
in maintaining the quality of animal products in
keeping a lookout for exotic diseases or pests that
may be brought into the country and in ensuring
and promoting animal welfare.
• Equine Practice
o Some private practitioners practice only in the

care of horses, which makes a valuable

contribution to the economy. Success in racing
requires absolute fitness and by helping to
achieve this, veterinarians have significantly
contributed to the outstanding reputation of
gallopers and trotters. They also play an
important part in keeping horses that are used for
other sporting and leisure activities fit and well.
• Companion Animal Practice
o In larger towns and cities, ample opportunity

exists for restriction of practice to companion

animal work including cats, dogs and other
family pets. Most urban small animal practices
use similar techniques to those available at a
public hospital. In the field of medicine this
involves the diagnosis and treatment of such
widely differing diseases as diabetes, dysentery,
and cancer. Abdominal, thoracic and orthopaedic
surgery is routine, although some procedures
 require specialised equipment that not every
practice may have. The use of techniques such as
blood transfusion, fluid therapy and advanced
procedures for repairing bone fractures are
examples of skills that can be expected of a
veterinarian providing surgical services. Within
companion animal practice, specialisation is
becoming increasingly common so that specialist
veterinary ophthalmologists, dermatologists,
behaviourists and surgeons accept referrals from
other companion animal veterinarians.
Food Safety Authority
• This newly setup authority sets standards for food
safety for exports of animal (and horticultural)
products, and for meat and dairy products for
domestic consumption. It is a food safety assurance
organisation that provides food evaluation,
verification, and certification services to the food
production industries. It is concerned with quality
control and hygiene in meat and other animal
products. Many veterinarians can work in meat
processing establishments and are responsible for the
standards of hygiene and meat inspection in meat
processing establishments to ensure that meat and
meat products are fit for human consumption, and
can be certified for export or domestic consumption.
Ministry of Agriculture and Forestry
 • There are many career opportunities for veterinarians
in the Ministry of Agriculture and Forestry in various
cadres.
Veterinary Diagnostic Services
• Diagnostic Services are provided by government and
privately owned laboratories. They are staffed by
veterinarians, with advanced training in disciplines
such as diagnostic pathology, microbiology, virology,
parasitology, clinical biochemistry and haematology.
Veterinary Education
• An important employer of veterinary graduates is the
education sector, with the different kinds of
Veterinary and Animal Science Programmes , being
the major employer in this area. Veterinary staff are
responsible for most aspects of the training of BVSc
undergraduates, diploma students and postgraduate
veterinary studies up to doctoral level. An important
aspect of the work of the staff is the conduct of
research and supervision of postgraduate student
research.
Veterinary Research and Technical Services in
Industry
• As you would expect in any economy which is so
firmly based on animal production, a considerable
industry exists in certain packets of India(eg. Poultry
in Namakkal District of Tamilnadu) to provide
veterinary pharmaceuticals, feedstuffs, and other aids
 to the maintenance of animal health and production.
This industry requires the professional skills of
veterinarians, and there are posts available in such
fields as technical advisory services and research.
Many of these can lead to senior executive
management roles.
International Veterinary Science & Service
• There are development projects for livestock
industries in overseas countries. A number of
veterinarians are involved in projects concerned with
this development, with some projects being on a very
large scale.
• A veterinary degree can lead to a great diversity of
other careers including employment in animal
welfare, conservation biology, specialist clinic
construction, animal feed formulation and
manufacture, and zoological parks.
Other career opportunities
</object >
COMMON QUESTIONS
• Who is the Father of Veterinary Medicine?
• Who is the Father of Clinical Medicine?
• Describe about Code of Hamurabi?
• Briefly describe about Ancient Indian contributions
in Veterinary Medicine.
 • What are the treatise on animal health from
ancient India?

MODULE-2: CONCEPTS OF ANIMAL DISEASES

Learning objectives

• To understand the concept of disease and to know about

the various theories regarding the disease.
• To learn the evolution of disease concept from the age old
humoral theory to the current concept of diseases.

WHAT DOES DISEASE MEANS?

Disease is defined as an abnormal condition affecting the body of
an organism. It is also a pathological condition of a part, organ or
system of an organism that results from different causes like
infection, genetic defect or environmental stress.

The term disease have a variety of definition, but it has a common

concept. It is a term for any condition that impairs normal
functioning of an organism or body. Not just human beings alone;
but also the Plants and animals have diseases.

Diseases are classified into three categories:

• Intrinsic,
• Extrinsic and
• Unknown origin.

Intrinsic is defined as coming from within the body and is more

familiar to us now a days. Examples of intrinsic diseases are
autoimmune disorders, cancers, stress-related, hereditary and
conditions resulting from malnutrition.
Extrinsic or infectious simply means coming from the outside or
external organism such as parvovirus, distemper and many
others. Extrinsic diseases are diseases that are triggered by
external factors like bacterial organisms, which entered into body
and affect the normal function of healthy organisms inside.

The third category is of unknown origin, like Alzheimer's

disease in Human beings. Until now doctors and scientist failed to
know the main cause of Alzheimer's disease and this is greatly
affecting elderly human population. Some of the animal examples
included Pyrexia of Unkown Origin(PUO).

CONCEPT OF ANIMAL DISEASES

• Disease is the result of complex interactions (some would say
imbalance) between the triad of the agent (toxic or
infectious), the host and the environment. The components
of this interaction differ depending upon the specific
circumstances of each group of affected animals. Particularly
for agricultural animals, this triad is strongly influenced by
husbandry and management factors, which are often the
most important. For vector-borne diseases, vector factors are
also linked to the other factors.
• Recognizing the different components of this triad is
important because they are the source of opportunities to
reduce disease at multiple points in the transmission cycle. A
common mistake is to focus on only one aspect of the triad
for disease control or prevention and to overlook the others.
• Examination of the past historical and contemporary
writings on disease suggested that disease concepts were
viewed as causal networks that represent relations among
the symptoms, causes, and treatment of a disease.
Conceptual change concerning disease is primarily driven by
changes in causal theories about diseases.
• The most famous thories on diseases include
 o The Humoral Theory
o The Contagion Theory &
o Germ Theory
• All of which were now superseded by the current medical
advances.
• Ancient Greek viewed of diseases, whose concepts are closely
connected to the humoral theory of the causes of disease.
The same view dominated european medical thought until
the development of the germ theory of disease, which was
first hinted at in the sixteenth century but not developed and
generally accepted until the nineteenth.
• Fracastoro, an Italian physician, wrote the first important
work on contagion in 1546, but the modern germ theory of
disease developed with the research of Pasteur, Lister, Koch,
and others in the 1860s and 1870s.
• Transition from the humoral to the germ theory of disease
required a major conceptual revolution, involving many
kinds of conceptual change including a fundamental shift in
how diseases are classified. Less radical conceptual changes
occurred in the twentieth century with the discovery of
genetic, nutritional, and immunological causes of disease.

Agent Factor Examples

• Dose
• Environmental hardiness
• Virulence (microbial)
• Infectivity (microbial)
• Toxicity (poisons)

Host Factor Examples

• Innate resistance (e.g. gastric barrier, mucocilliary transport

mechanism)
• Previous exposure
• Passive immune status (neonates)
 • Vaccination status and response
• Age
• Gender
• Behavior (e.g. mutual grooming, dominance, pica)
• Production status (e.g., lactating vs. non-lactating)
• Reproductive status (e.g., pregnant vs. non-pregnant, sterile
vs. intact)
• Genetics

Intrinsic (non-changeable in the individual)

• Age is very important because the risk of many diseases

change widely over the animals life time due to underlying
physiological changes that are associated with age. Neonates
are very susceptible to many enteric and respiratory
infections but resistance increases as the animals mature. As
immune function declines with advanced age, susceptibility
begins increasing again.
• Clinical disease due to ubiquitous agents, such as the viral
scour agents, can be reduced by delaying the neonate's
exposure to the agent (innate resistance increases with age)
and reducing the infectious dose by changing the
environmental factors.
• Due to genetics different breeds have different risks for
diseases, such as hip dysplasia in German Shepherds. Within
breeds, some infectious diseases occur due to underlying
genetic defects (e.g., Holstein BLAD, Arab CID, Quarter
Horse HPP).

Extrinsic (changeable in the individual)

• Intact bitches are at risk of pyometra and mammary gland

tumors than spayed (excluding stump pyometras) are not.
Intact dogs behave differently than non-intact dogs, tending
to roam more and thus being at higher risk of being hit by
cars and of acquiring communicable infectious diseases.
 • Vaccination increases an individual’s resistance to disease
but the protection is not absolute for most biologics.

Environmental Factor Examples

• Animal stocking density

• Animal movement between groups
• Housing (e.g. ventilation, sanitation)
• Environmental conditions (e.g. temperature, humidity, wind
velocity, precipitation)
• Nutrition (protein, energy and macromineral and
micromineral adequacy)
• Many infectious agents are susceptible to the ultraviolet (UV)
in direct sunlight and to desiccation. Many infectious agents
survive for long periods in damp environments.
• Strangles (Strep. equi) in horses appears to occur more
frequently during damp cold weather. This is likely because
the agent is able to survive longer in damp environments.
• Salmonellosis in all animals including humans occurs more
frequently during summer than during other times of the
year. This is likely because the agent is able to replicate to
infectious doses in moist feedstuffs at summer temperatures.
• Bluetongue virus grows more rapidly in Cuilicoides
variipennis at higher temperatures. A strong association has
been shown between bluetongue infection in cattle and both
temperature and rainfall.
• These factors interact in complex ways that are often under
the control of man.
• Eg: Increased animal density may lead to increased
microbial load in the environment, a roof may prevent
exposure of microbe to killing UV, low ventilation may
increase humidity from animal respiration which in turn
increases environmental survival of the organism which in
turn increases exposure dose and infects more animals.
• It has been said that:
 o "Bovine mastitis is a disease of man with signs in the
cow."
o "Bad management will overwhelm the best
immunology."

The "Iceberg" Concept

• In outbreaks of most disease in animal groups, both clinical

cases (the tip of the iceberg) and subclinical cases
(unobserved beneath the ocean surface) are present in the
group.
• For many infectious agents, particularly those that are
endemic, more of the infections in a group are subclinical
(silent) than are clinical. For some exceptions, such as rabies,
few if any subclinical infections occur and almost all if not all
clinical infections end in death. This iceberg concept of
severity distribution also holds for most induced, non-
infectious diseases affecting a group, such as
hypomagnesemia, ketosis and hypocalcemia. Disease in an
individual is often evidence of a group phenomena because
the factors that caused the disease in that individual are
usually affecting others adversely as well.
• For most groups, the response to the host-agent-
environment interaction that results in disease is usually not
an either / or, black or white phenomenon. Instead, it is
usually a continuum, with different individuals expressing
different degrees of severity at different times as determined
by the unique combinations of agent – host – environment
risk factors that they experience. For each problem outbreak,
the "shape" of this iceberg (the proportion affected, the
proportion of the affected that become clinical and the
proportion of these that die) at any point in time depends on
the specific combination of agent, host, environment, vector
(if one is involved), and human husbandry / management
factors acting in that specific situation.
• Because these factors change over time (e.g., animal immune
responses eliminate the infection, humans change their
management practices, the environment changes both
seasonally, day-to-day and year-to-year), this "shape"
changes over time. This does make outbreak investigation
and problem solving both challenging and rewarding for the
clinician.

HIPPOCRATES AND THE HUMORAL THEORY

• The quotes from
Hippocratic treatises
concisely summarized
the humoral theory:
o The human body
contains blood,
phlegm, yellow
bile, and black
bile. These are the
things that make
up its constitution
and cause its
pains and health.
Health is
primarily a state
in which these
constituent
substances are in
the correct
proportion to
each other, both
in strength and
quantity, and are
well mixed.
o All human
diseases arise
from bile and
phlegm; the bile
and phlegm
produce diseases
when, inside the
body, one of them
becomes too
moist, too dry, too
hot, or too cold;
they become this
way from foods
and drinks, from
exertions and
wounds, from
 smell, sound,
sight, and venery,
and from heat and
cold.
• Diseases arise because
of humoral imbalances.
For example, too much
bile can produce
various fevers, and too
much phlegm can cause
epilepsy or angina.
Imbalances arise from
natural causes such as
heredity (phlegmatic
parents have
phlegmatic children),
regimen (diet and other
behavior), and climate
(temperature, wind,
and moisture
conditions).
• Different kinds of
imbalance produce
different diseases with
symptoms and
development that were
acutely observed by the
Hippocratics. They
described in detail not
only the symptoms of
patients with a
particular disease, but
also the ways that the
patients tended to
develop toward
recovery or death.
• The course of a disease
was affected by the
development of a
particular humor,
 producing crises that
signaled basic changes
in patient outcome.
Fevers were classified
as tertian, quartan, and
so on based on the
number of days before a
crisis occurred.

FRACASTRO AND THE CONTAGION THEORY

• Fracastoro,
the Italian
Physician
suggested
that the
persons can
contract
infections
even if their
humors are
normally
balanced. He
defined a
contagion as
a "corruption
which
develops in
the substance
of a
combination,
passes from
one thing to
another, and
is originally
caused by
infection of
the
imperceptible
particles".
 • He called the
particles the
seminaria
(seeds or
seedlets) of
contagion. He
described
how
contagion can
occur by
direct
contact, by
indirect
contact via
clothes and
other
substances,
and by long-
distance
transmission.
In addition,
he stated that
diseases can
arise within
an individual
spontaneousl
y.

PASTEUR, LISTER, KOCH AND THE GERM THEORY

 • The germ theory viewed
diseases in terms of a causal
network similar to that of
Fracastoro, but with much
more detail about the nature of
germs and possible
treatments. The Hippocratics
were largely confined to a
taxonomy of diseases in terms
of symptoms, and Fracastoro'
theory allowed only a limited
causal classification based on
kinds of contagion; but the
germ theory of disease made
possible a detailed and
clinically powerful taxonomy
of diseases in terms of their
microbial causes. Today,
infectious diseases are
typically classified as bacterial
(e.g. tuberculosis,), viral (e.g.
herpes), protozoal (e.g.
trypanosomes), and so on.

CURRENT CONCEPTS OF ANIMAL /

HUMAN DISEASES
• While many diseases are infectious, research in the twentieth
century has revealed other kinds of cause of disease: genetic,
nutritional, immunological, metabolic, and cytological. The
Hippocratics saw some traits such as being phlegmatic as
hereditary, but the first demonstration of the genetic basis of
a disease was Archibald Garrod's work on alkaptonuria in
1901. Many other kinds of genetic disorders have been
identified, and in recent years genetic engineering has
offered the possibility of new kinds of treatment for such
disorders.
• Hippocrates placed great emphasis on diet as a factor on
disease, and the value of citrus fruits in preventing scurvy
was established in 1747, but identification of vitamin C as a
nutritional requisite of health occurred only in 1932.
Diseases caused by nutritional deficiencies can easily be
treated by providing the missing vitamins or other nutrient.
• Knowledge of the immune system advanced rapidly in the
1950s, making possible the understanding of diseases that
arise from attacks by the immune system on the body's own
organs, as occurs in diseases such as lupus erythematosus.
• Metabolic disorders such as diabetes have become
increasingly understood as knowledge increases of the
physiology of organs such as the pancreas, but causality in
such cases is complex, involving an interaction of hereditary
and environmental factors.
• Similarly, although knowledge is developing rapidly
concerning the nature of the cells and genes involved in the
growth of cancers, the causal interactions are enormously
complex and hard to identify.
• Currently the authoritative Textbooks of Medicine are
divided into parts that implicitly classify diseases in two
complementary respects: organ systems and pathogenesis.
Most of these are organized around physiological systems,
such as the cardiovascular and respiratory systems. But there
are also parts that group diseases in terms of pathogenetic
mechanisms that can affect various organ systems: oncology,
metabolic diseases, nutritional diseases, infectious diseases,
and so on. Some diseases are naturally discussed in more
than one part, as when myocarditis occurs both under
cardiovascular diseases and infectious diseases. Modern
medical classification thus blends two overlapping
taxonomies of disease.
o Cardiovascular diseases
o Respiratory diseases
o Renal diseases
 o Gastrointestinal diseases
o Diseases of the liver, gall bladder, and bile ducts
o Hematologic diseases
o Oncology
o Metabolic diseases
o Nutritional diseases
o Endocrine and reproductive diseases
o Diseases of the bone and bone mineral metabolism
o Diseases of the immune system
o Musculoskeletal and connective tissue diseases
o Infectious diseases
o HIV and associate disorders
o Diseases caused by protozoa and metazoa
o Neurology
o Eye diseases
o Skin diseases
• The shift from the humoral to the germ theory of disease
required a conceptual revolution: the old conceptual and
explanatory system was replaced by a radically different one.
In contrast, the development in the twentieth century of
concepts of genetic, nutritional, immunological, and
metabolic diseases were relatively conservative extensions of
the nineteenth century ideas: new causes were introduced
without denying that the germ theory was right about the
causes of diseases to which it had been applied.

COMMON QUESTIONS

1. What are the

components of the triad
pertaining to a disease?
2. Explain about the
iceberg concept,
endemic stability
 concept and the herd
immunity concept?
3. Define prognosis and
its importance in
clinical practice?
4. Enlist the various
records maintained in a
veterinary hospital and
the advantages of
maintaining them.

MODULE-3: CONCEPTS OF DISEASE -

DIAGNOSIS, DIFFERENTIAL DIAGNOSIS AND
PROGNOSIS

Learning
objectives
• To understand
concept of
diagnosis
• To know how to
make a
differential
diagnosis
• To understand
arriving at a
diagnosis
 • To know how to
decide upon the
prognosis

CONCEPT OF DIAGNOSIS
• A Veterinary health care provider's job is to know the animal
body and its functions in terms of normality (homeostasis).
The four cornerstones of diagnostic medicine, each essential
for understanding homeostasis, are: anatomy (the structure
of the human body), physiology (how the body works),
pathology (what can go wrong with the anatomy and
physiology) and psychology (thought and behavior). Once
the provider knows what is normal and can measure the
patient's current condition against those norms, she or he
can then determine the patient's particular departure from
homeostasis and the degree of departure. This is called the
diagnosis.
• Once a diagnosis has been reached, the health care provider
is able to propose a management plan, which will include
treatment as well as plans for follow-up. From this point on,
in addition to treating the patient's condition, the provider
educates the patient about the causes, progression,
outcomes, and possible treatments of his ailments, as well as
providing advice for maintaining health.

Diagnostic procedures

• The diagnostic process is fluid in which the provider gathers

information from the patient and others, from a physical
examination of the patient, and from medical tests
performed upon the patient.
• There are a number of techniques used by providers to
obtain a correct diagnosis:
o Exhaustive method
 o Every possible question is asked and all possible data is
collected.
o Algorithmic method
o The provider follows the steps of a proven strategy.
o Pattern-recognition method
o The provider uses experience to recognise a pattern of
clinical characteristics.

Differential diagnosis

• The health care provider uses the hypothetico-deductive

method, a systematic, problem-focused method of inquiry.
• The advanced clinician uses a combination of the pattern-
recognition and hypothetico-deductive approaches.
• The presence of some medical conditions cannot be
established with complete confidence from examination or
testing. Diagnosis is therefore by elimination of other
reasonable possibilities, referred to as the diagnosis of
exclusion.
• The process of diagnosis begins when the animal owner with
the animal patient consults the animal health provider and
presents a set of complaints (symptoms). If the patient is
unconscious, this condition is the de facto complaint. The
provider then obtains further information from the patient
owner and from those who know the animal patient, if
present, about the animal patient's symptoms, their previous
state of health, living conditions, and so forth.
• Rather than consider the myriad diseases that could afflict
the patient, the provider narrows down the possibilities to
their illnesses likely to account for the apparent symptoms,
making a list of only those disease (conditions) that could
account for what is wrong with the patient. These are
generally ranked in order of probability.
• The provider then conducts a physical examination of the
animal patient, studies the patient's medical record, and asks
further questions in an effort to rule out as many of the
 potential conditions as possible. When the list is narrowed
down to a single condition, this is called the differential
diagnosis and provides the basis for a hypothesis of what is
ailing the patient.
• Unless the provider is certain of the condition present,
further medical tests are performed or scheduled such as
medical imaging, in part to confirm or disprove the diagnosis
but also to document the patient's status to keep the patient's
medical history up to date. Consultations with other
providers and specialists in the field may be sought. If
unexpected findings are made during this process, the initial
hypothesis may be ruled out and the provider must then
consider other hypotheses.
• Despite all of these complexities, most animal patient
consultations are relatively brief, because many diseases are
obvious, or the providers experience may enable him or her
to recognize the condition quickly. Another factor is that the
decision tree is used for most diagnostic hypothesis testing
are relatively short.
• Once the provider has completed the diagnosis, the
prognosis is explained to the patient and a treatment plan is
proposed which includes therapy and follow-up
consultations and tests to monitor the condition and the
progress of the treatment, if needed, usually according to the
medical guideline provided by the vetrinary medical field on
the treatment of the particular illness.
• Treatment itself may indicate a need for review of the
diagnosis if there is a failure to respond to treatments that
would normally work.
• A laboratory diagnosis is either a substitution or complement
to the diagnosis made by examination of the patient. For
instance, a proper diagnosis of infectious diseases usually
requires both an examination of symptoms, as well as
laboratory characteristics of the pathogen involved.
 CONCEPT OF DIFFERENTIAL DIAGNOSIS
• In Veterinary Medicine, differential diagnosis (abbreviated
DDx, ddx, DD, or ΔΔ) is a systematic method used to identify
unknowns. This method, essentially a process of elimination,
is used by physicians, physician assistants, and other trained
medical professionals to diagnose the specific disease in a
patient.
• Not all veterinary medical diagnoses are differential ones:
some diagnoses merely name a set of signs and symptoms
that may have more than one possible cause, and some
diagnoses are based on intuition or estimations of likelihood.
• Careful differential diagnosis involves first making a list of
possible diagnoses, then attempting to remove diagnoses
from the list until at most one diagnosis remains. In some
cases, there will remain no diagnosis; this suggests the
physician has made an error, or that the true diagnosis is
unknown to medicine. Removing diagnoses from the list is
done by making observations and using tests that should
have different results, depending on which diagnosis is
correct.
• In Veterinary Medicine, differential diagnosis is the process
whereby a given condition or circumstance, called the
presenting problem or chief complaint, is examined in terms
of underlying causal factors and concurrent phenomena as
discerned by appropriate disciplinary perspectives and
according to several theoretical paradigms or frames of
reference, and compared to known categories of pathology or
exceptionality.

Differential diagnosis allows the physician to

• More clearly understand the condition or circumstance

• Assess reasonable prognosis
• Eliminate any imminently life-threatening conditions
• Plan treatment or intervention for the condition or
circumstance
• Enable the patient and the family to integrate the condition
or circumstance into their lives, until the condition or
circumstance may be ameliorated, if possible.
• If the patient's condition does not improve as anticipated
when the treatment or therapy for the disease or disorder
has been applied, the diagnosis must be reassessed.
• The method of differential diagnosis is based on the idea that
one begins by first considering the most common diagnosis
first: a head cold versus meningitis, for example. As a
reminder, medical students are taught the adage, "When you
hear hoofbeats, don't look for zebras," which means look for
the simplest, most common explanation first. Only after the
simplest diagnosis has been ruled out should the clinician
consider more complex or exotic diagnoses.
• At one time doctors ordered only particular blood tests, but
now a full blood chemistry profile is standard, which can
speed up the process of diagnosis as well as uncover sub-
clinical conditions.
• With the advent of better radiological studies like MRI and
the wider use of nuclear medicine, it has become more likely
that unexpected findings will emerge and will be further
studied, though such findings may not be supported by
further investigation.
• Such findings are a valuable tool but not infallible; often it
still takes a veterinary physician or veterinary medical team
to track down either a more common illness with a rare
presentation or a rare illness with symptoms suggestive of
many other conditions. Sometimes a definitive diagnosis
might take years.

CONCEPT OF PROGNOSIS
• Prognosis is a veterinary medical term to describe the likely
outcome of an illness. When applied to large populations,
prognostic estimates can be very accurate: for example the
statement "45% of patients with severe septic shock will die
within 28 days" can be made with some confidence, because
previous research found that this proportion of patients died.
However, it is much more difficult to translate this into a
prognosis for an individual patient: additional information is
needed to determine whether a patient belongs to the 45%
who will succumb, or to the 55% who survive. A complete
prognosis includes expected time, function, and a
description of the disease course such as progressive decline,
intermittent crisis, or sudden, unpredictable crisis.
• Prognosis tells about

o The expected course of a disease.

o The patient's chance of recovery.

• The prognosis predicts the outcome of a disease and

therefore the future for the patient, for example, good /
favourable /unfavourable /grave etc. The word prognosis
comes from the Greek prognostikos (of knowledge
beforehand). It combines pro (before) and gnosis (a
knowing). Hippocrates used the word prognosis, much as we
do today, to mean a foretelling of the course of a disease.

CLINICAL DIAGNOSIS
• Clinical diagnosis is the science of clinical methods of
examination of animals in order to identify the affected
organ or system that is the cause of disease.
• Externally visible or appreciable changes in the body of an
animal or one of its organs is an indicator of disease. The
recognition of such changes using inspection, palpation,
percussion or auscultation is called clinical or physical
examination.
 • Physical examination is an integral part of clinical diagnosis,
which is crucial for the management of disease conditions.
• The determination of the causes of disease may be termed
aetiological diagnosis whereas symptomatic diagnosis is used
when the cause of the disease cannot be determined.

Some definitions

• Symptoms are any visible functional disturbances of various

body systems (e.g. increased body temperature).
• Syndrome , a group of clinical signs that constitute a group of
diseases that cannot be traced to a single aetiological factor
(e.g. feline urologic syndrome).
• Prognosis , anticipating the outcome of the disease or
condition (e.g. recovery or death).
• Three main categories should be taken into account when
clinically examining the animal, these are:
o Case history.
o Examination of the environment.
o Examination of the animal.

CLINICAL EXAMINATION - MODEL

RECORD
 •

GENERAL METHODS OF EXAMINATION

• These include inspection, palpation, percussion and
auscultation.

Inspection

• Means observing the animal from a distance, simple and

widely used in veterinary medicine it helps obtaining an idea
about the general characters of diseased animal.
• The following information can be obtained by inspecting the
animal:
 o General demeanor, posture and gait.
o Body score of the animal (thin, emaciated, obese).
o Depression, anxiety or frenzy.
o Skin diseases and lesions.
o Lameness.
o Abnormal odour.
o Type of respiration, rate and rhythm.
• Inspection should always be performed in daylight except in
emergency where artificial light may be used.
Palpation

• Using the sense of touch to obtain information about the

organs examined, this is called direct palpation. Indirect
palpation can sometimes be used by means of a probe.
• When palpating an organ or a lesion, the following
information can be obtained:
o Sensitivity (pain and tenderness)
o Temperature (hot, cold or normal)
o Consistency (resilient, doughy, firm, hard, fluctuating
or emphysematous).

Percussion

• Obtaining information about internal organs using a plexor

and pleximeter (indirect percussion) or using the fingers
(direct percussion).
• Tapping on the area of examination and noting the sound is
used to obtain information about the physical condition of
certain organs.
• It also reveals the sensitivity of this organ.
• Percussive sounds
o Resonant
▪ This is the sound heard over a normal lung and
indicates presence of air in tissues.
o Tympanic
 ▪ Sound produced by percussion over a hollow organ
containing gas (e.g. Rumen).
o Dull
▪ The sound heard in case of percussion of solid
tissues containing no air.
▪ A change of percussive sound (e.g. change from
resonant to dull over the lung area) indicates
disease of the organ.

Auscultation

• Listening to sounds produced by the functional activity of an

organ.
• Organs that can be auscultated are
o The heart.
o The lungs.
o The rumen.
• Direct auscultation is performed by using the ear, whereas
indirect auscultation is performed by means of a
stethoscope.

COMMON QUESTIONS
• What are the cornerstones of a diagnosis?
• What are the techniques used by the clinician to make a
diagnosis?
• Explain the basis for forming a differential diagnosis?
• What advantages of forming a differential diagnosis ?
• Define the following: clinical diagnosis, symptoms,
syndrome and prognosis?
• Explain briefly about the general methods of examination?

MODULE-4: GENERAL AND SYSTEMIC STATES

-I
 Learning objectives
• To understand the
concepts of the
generalized states
affecting all body
systems
• To know about
their clinical
findings, diagnosis
and treatment
• To know about
medical
management
pertaining to the
general systemic
states such as
o Hypothermia

o Hyperthermia

o Fever

o Electrolyte

Imbalnces
o Acid-Base

Disorders

HYPOTHERMIA
• Hypothermia is a lowering of the body's temperature in
animals or human beings.
• At a rectal temperature of less than 28 C (82 F), the ability to
regain normal temperature is lost, but the animal will
continue to survive if external heat is applied and the
temperature returns to normal. It is important to observe
 and measure the vital signs: pulse, breathing, mental status
and rectal temperature.
• To know the severity of hypothermia is valuable to decide the
re-warming technique to be used for treatment.
• On the basis of body temperature, hypothermia can be
classified as Mild (86 -89 F or 30 - 32 C), Moderate (71- 77 F
or 22 -25 C) and Severe (32- 46.5 or 0 - 8 C). There are three
rewarming techniques (Passive external, Active external, and
Active internal) which should be used according to severity
of hypothermia.
• When the skin or blood is cooled enough to lower the body
temperature in non-hibernating animals, the metabolic and
physiological processes slow down. In the hypothermic state,
the oxygen need of cells, particularly neurons is greatly
reduced, and the circulation can be stopped for relatively
long periods.
• At a rectal temperature of less than 28 C (82 F), the ability to
regain normal temperature is lost, but animal will continue
to survive if external heat is applied and the temperature
returns to normal. Hypothermia is a condition of general
body cooling in contrast to frostbite, which is localized.
• A fall in body temperature can be due to accidental exposure
to external cold, effect of drugs, or failure of internal
temperature regulating mechanisms.
• The simplest way to determine whether the patient is
hypothermic or not, is to assess body temperature by placing
a bare hand against the skin (preferably in axilla or groin
region) of the patient. If the skin feels warm, hypothermia is
unlikely.
• Patients with cold skin should have rectal temperatures
taken with a low reading thermometer.

What to expect in a hypothermic animal?

• As the body core temperature drops, more body systems

suffer from the effects of cold.
 • The signs and symptoms can assess the presence and
severity of hypothermia.
• In the cold patient, a rectal temperature is one of the most
important signs and is useful for assessing and treating
hypothermia, however there is a tremendous variability in
physiological responses at specific temperatures among
individuals and species.
• Once it is established that an animal is hypothermic it is
important to observe and measure the following most
important signs: pulse (slow to none); breathing (slow to
none); mental status (responsive to unconsciousness); cold
skin; low rectal temperature.
• Severally hypothermic animals may have other problems,
which are not easily detected. e.g. change in blood chemistry;
irregular heart beat; dehydration; difference in temperature
between deep body tissues and superficial body tissues.

Classification on the basis of severity

• On the basis of body temperature, hypothermia can be

classified as Mild (86 -89 F or 30 - 32 C), Moderate (71- 77 F
or 22 -25 C) and Severe (32- 46.5 or 0 - 8 C).

Management of a hypothermic animal

• The primary goals in the treatment and handling of a

hypothermic animal are: keep the animal alive by warming,
avoid any further exposure to cold, and then transport the
animal to a site of complete veterinary care.
• In order to treat the hypothermic animal appropriately, one
should first know that the animal is in fact hypothermic.
• If so, then the severity of hypothermia e.g. mild, moderate or
severe.
• Once this is determined, one has to decide the re-warming
technique to be used for treatment.
 EXAMINATION OF HYPOTHERMIC
ANIMAL
• To examine a hypothermic animal, one should proceed as
follows:
o Attention to ABCD:
▪ A. Airway;
▪ B. Breathing;
▪ C. Circulation;
▪ D. Degrees.
o One should make sure that the animal has an open
airway, is breathing, and has a heart beat and assess
rectal temperature.
• Brief history (e.g. duration of exposure, regarding
circumstances in which animal found etc.).
• Brief physical examination including
o feel of body temperature
o level of consciousness and neurological examination
o cardio-pulmonary examination
o associated trauma
o weight of animal
• Depending upon the availability of staff and equipment,
chest x-ray, urinalysis, complete blood work, and arterial
blood gases are also recommended.
• If there is a high probability that the animal is severely
hypothermic, breathing and heart rate may be slow, shallow
and very hard to detect, therefore, take a full minute or more
to measure these vital signs.
• Hypothermic patients with any measurable pulse or
respiration obviously do not require Cardio - pulmonary
Resuscitation (CPR). However, if both pulse/heart beat and
respiration are absent then commence CPR.
• Evaluate the animal's level of consciousness, size of pupil,
ability to respond if conscious and ability to walk.
 • When any of these characteristics are abnormal, suspect
severe hypothermia and treat accordingly.
• While treating the hypothermic animal, also check the
animal for other possible injuries. The best chances of
recovery are as a result of early diagnosis and treatment.
• In accidental hypothermia, the animal should be brought
into a heated environment and allowed to warm slowly to its
normal temperature. Rewarming and maintenance of normal
body temperature can be accomplished externally or
internally (see Rewarming techniques).
• Neonates not only require rewarming but careful attention to
nutrition should also be given.

Mild Hypothermia

• Prevent further heat loss, insulate from the ground, protect

from the wind, cover the head and neck, and move the
animal to a warm environment. Rewarming through the
application of insulated heat packs to high heat loss areas
such as head, neck, between legs, side of chest wall to
prevent heat loss. Consider warm showers and warm bath, if
the patient is alert (see passive external and active external
rewarming techniques)

Moderate Hypothermia

• Keep the patient warm e.g. warm bottles, blankets, immerse

patient in tub of warm water.
• Continue rewarming efforts until animal's core temperature
is restored to normal (see active external rewarming
methods).

Severe Hypothermia

• Animal in severe hypothermic state, can erroneously thought

to be dead as no pulse, no heart rate, and no respiration is
apparent. It is wise to follow the same criteria as in human
 medicine which suggests " the hypothermic patient is not
dead until the patient is warm and dead."
• Animals with severe hypothermia should be treated by
putting heat directly into the core areas (see active
rewarming methods).
• If the heart beat and respiration is not detectable after
checking for up to 1 minute then commence CPR: Mouth to
mouth or mouth to mask breathing during CPR is best
because this provides warm, humidified air or oxygen.
• One can also use an apparatus to ventilate the animal with
100% heated, humidified air or oxygen.
• Reassess the animal's physical status periodically while
performing CPR.
o CPR is less likely to have a significant effect on the
survival of a hypothermic animal, if
▪ The animal has been under the water for more
than 1 hour.
▪ The animal with a core temperature below 60 F
(15.5 C).
▪ The animal is frozen e.g. ice formation in the
airway.
▪ The animal's chest wall is so stiff that compression
is impossible

• Treatment that stimulates peripheral circulation (i.e.

wrapping in a blanket, massaging extremities etc.) must be
avoided in cases of severe hypothermia.
• These activities will likely increase flow of cold blood from
the periphery (muscle pumping) which can cause after drop,
increasing the depth of hypothermia in critical core tissues,
especially the heart.
• Stimulating the peripheral circulation also reduces the blood
volume in the body core, causing rewarming shock, which
increases the workload on the heart.
 • The blood returning from the periphery can also include
metabolic waste products that can cause a fatal heart
arrhythmia.

REWARMING TECHNIQUES
• There are three classes of rewarming techniques:

Passive external

• The animal's own metabolic processes continue to produce

heat spontaneously so no external heat is required.
• Shivering is an example of thermogenesis.
• This is simplest and slowest rewarming method but is
sufficient for mild hypothermic patients.

Active external

• This system includes warm water baths, hot water bottles,

blankets, heating pads, radiant heaters.
• This method of rewarming is safe only for mild hypothermia
because externally applied heat stimulates peripheral
circulation.

Active internal

• These rewarming methods are usually more complex and

need to be carried out by professionals
(Veterinarians/Animal health technicians).
• These include inhalation rewarming (ventilation of patient
with heated, humidified air or oxygen), circulation of heated
fluids (40.5 - 43.5 C) in body cavities (gastric, thoracic and
peritoneal lavage), and heated intra venous solutions
preferably dextrose as this provides energy to meet increased
metabolic demands (contribute little heat due to
vasoconstriction in cold extremities).
 • Inhalation rewarming is the only method, which can be used
by a layman and does not require much training (mouth to
mouth breathing). Inhalation of warm-saturated air delivers
heat directly to the lungs and heart.
• The brain is also warmed from this blood flow and from
conductive heat flow from the respiratory and nasal cavities.
• This method also assists in re-hydration as an added benefit.

PRECAUTIONS
Precautions while treating hypothermic animals

• Be cautious about assuming that animal can not be

resuscitated. As in resuscitation, a positive attitude is
important.
• The hypothermic animal may appear to be beyond help
because of, skin and membrane colors, pupil dilatation and
depressed vital signs.
• Avoid direct application of hot objects or excessive pressure
(e.g. uninsulated hot water bottles, tourniquets etc.).
• Ensure that items such as oxygen and fluids coming into
contact with the animal are warmed.
• Do not put severely hypothermic animal in a shower or bath.
• Drug treatments are not useful in treating severe
hypothermic animals since the cold heart will not respond as
expected.
• If administered, drugs will not be metabolized normally by
the liver and kidneys; instead these will accumulate in the
body and become active as it warms.
• Do not use Lactated Ringers because the hypothermic liver
may not be able to metabolize the lactate normally.
• Do not administer cold fluids.

HYPERTHERMIA
 • Hyperthermia is an elevated body temperature in mammals.
The effects of hyperthermia, or heat stroke, if left untreated,
can cause permanent internal organ damage or even death.
• Hyperthermia is an elevated body temperature due to failed
thermoregulation.
• Hyperthermia occurs when the body produces or absorbs
more heat than it can dissipate.
• When the elevated body temperatures are sufficiently high,
hyperthermia is a medical emergency and requires
immediate treatment to prevent disability and death.
• The most common causes are heat stroke and adverse
reactions to drugs.
• Heat stroke is an acute condition of hyperthermia that is
caused by prolonged exposure to excessive heat and/or
humidity.
• The heat-regulating mechanisms of the body eventually
become overwhelmed and unable to effectively deal with the
heat, causing the body temperature to climb uncontrollably.
• Hyperthermia is a relatively rare side effect of many drugs,
particularly those that affect the central nervous system.
• Malignant hyperthermia is a rare complication of some types
of general anesthesia.
• Hyperthermia can be created artificially by drugs or medical
devices.
• Hyperthermia therapy may be used to treat some kinds of
cancer and other conditions, most commonly in conjunction
with radiotherapy.
• Hyperthermia differs from fever in the mechanism that
causes the elevated body temperatures: a fever is caused by a
change in the body's temperature set-point.

Signs and Symptoms

• Hot, dry skin is a typical sign of [Link] inability to

cool the body through perspiration causes the skin to feel
dry.
 • Other signs and symptoms vary depending on the cause. The
dehydration associated with heat stroke can produce
vomiting, and low blood pressure. This can lead to fainting
or dizziness, especially if the person stands suddenly.
• In the case of severe heat stroke, the animal or person may
become confused or hostile, and may seem intoxicated.
• Heart rate and respiration rate will increase (tachycardia and
tachypnea) as blood pressure drops and the heart attempts
to supply enough oxygen to the body.
• The decrease in blood pressure can then cause blood vessels
to contract, resulting in a pale or bluish skin color in
advanced cases of heat stroke.
• Some, especially young animals, may have seizures.
Eventually, as body organs begin to fail, unconsciousness
and coma will result.

Heat Stroke

• Heat stroke is due to an environmental exposure to heat,

resulting in an abnormally high body temperature.
• In severe cases, temperatures can exceed 40 °C (104 °F).
• Heat stroke may be exertional or non-exertional, depending
on whether the animal or person has been exercising in the
heat.
• Significant physical exertion on a very hot day can generate
heat beyond a healthy body's ability to cool itself, because the
heat and humidity of the environment reduces the efficiency
of the body's normal cooling mechanisms.
• Other factors, such as drinking too little water, can
exacerbate the condition.
• Non-exertional heat stroke is typically precipitated by
medications that reduce vasodilation, sweating, and other
heat-loss mechanisms, such as anticholingeric drugs,
antihistamines, and diuretics.
 • In this situation, the body's tolerance for the excessive
environmental temperatures can be too limited to cope with
the heat, even while resting.

Diagnostic Approach

• Hyperthermia is generally diagnosed in the presence of an

unexpectedly high body temperature and a history that
suggests hyperthermia instead of a fever.
• Most commonly this means that the elevated temperature
has appeared in a animal that was working in a hot, humid
environment (eg. equine heat stroke) or that was taking a
drug for which hyperthermia is a known side effect (drug-
induced hyperthermia).
• If fever-reducing drugs lower the body temperature, even if
the temperature does not return entirely to normal, then
hyperthermia is excluded.

Prevention & Mitigation

• In cases where heat stress is caused by physical exertion, hot

environments or wearing protective equipment it can be
prevented or mitigated by taking frequent rest breaks,
staying hydrated and carefully monitoring body temperature.
However, in situations demanding prolonged exposure to a
hot environment or wearing protective equipment, a
personal cooling system is required as a matter of health and
safety.
• A variety of active or passive technologies personal cooling
systems exist which can be categorized by their power
sources and whether they are animal or vehicle-mounted.

Treatment

• Treatment for hyperthermia depends on its cause, as the

underlying cause must be corrected.
• Mild hyperthemia caused by exertion on a hot day might be
adequately treated through measures, such as allowing to
drink more water and resting in a cool place.
• Hyperthermia that results from drug exposures is frequently
treated by cessation of that drug, and occasionally by other
drugs to counteract them. Fever-reducing drugs such as
paracetamol and aspirin have no value in treating
hyperthermia.
• When the body temperature is significantly elevated,
mechanical methods of cooling are used to remove heat from
the body and to restore the body's ability to regulate its own
temperatures.
• Passive cooling techniques, such as resting in a cool, shady
area and removing clothing can be applied immediately.
• Active cooling methods, such as sponging the head, neck,
and trunk with cool water, remove heat from the body and
thereby speed the body's return to normal temperatures.
• Making the animal to drink water and turning a fan or
dehumidifying air conditioning unit on the affected animal
may improve the effectiveness of the body's evaporative
cooling mechanisms (sweating).
• Placing the animal in a bigger bathtub or pool of tepid or
cool water (immersion method) can remove a significant
amount of heat in a relatively short period of time. However,
immersion in very cold water is counterproductive, as it
causes vasoconstriction in the skin and thereby prevents heat
from escaping the body core.
• In exertional heat stroke, studies have shown that although
there are practical limitations, cool water immersion is the
most effective cooling technique and the biggest predictor of
outcome is degree and duration of [Link] superior
cooling method found for nonexertional heat stroke.
• When the body temperature reaches about 40 C, or if the
affected animal is unconscious or showing signs of
confusion, hyperthermia is considered a medical emergency
 that requires treatment in a proper veterinary medical
facility.
• In a veterinary hospital, more aggressive cooling measures
are available, including intravenous hydration, gastric lavage
with iced saline, and even hemodialysis to cool the blood.

FEVER
• Fever (also known as pyrexia or controlled hyperthermia) is
a common medical sign characterized by an elevation of
temperature above the normal range due to an increase in
the body temperature regulatory [Link] increase in
set-point triggers increased muscle tone and shivering.
• As an animal's temperature increases there is generally a
feeling of cold despite an increasing body temperature.
• Once the new temperature is reached there is a feeling of
warmth.
• A fever is one of the body's immune responses which
attempts to neutralize a bacterial or viral infection.
• A fever can be caused by many different conditions ranging
from benign to potentially serious.
• With the exception of very high temperatures, treatment to
reduce fever is often not necessary; however, antipyretic
medications can be effective at lowering the temperature,
and this may improve the affected person's comfort.
• Fever differs from uncontrolled hyperthermia, usually just
referred to as hyperthermia, in that hyperthermia is an
increase in body temperature over the body's
thermoregulatory set-point, due to excessive heat production
and/or insufficient thermoregulation.

Classification/Types of Fever
 • Fever continues - A
• Fever continues to abrupt onset and remission - B
• Fever remittent - C
• Intermittent fever - D
• Undulant fever - E
• Relapsing fever - F

Hyperpyrexia

• Hyperpyrexia is a fever with an extreme elevation of body

temperature greater than or equal to 41.5 °C (106.7 °F).[12]
Such a high temperature is considered a veterinary medical
emergency as it may indicate a serious underlying condition
or lead to significant side effects.
• The most common cause is a intracranial hemorrhage. Other
possible causes include sepsis,malignant syndrome, drug
effects, serotonin syndrome, and thyroid storm.
• Infections are the most common cause of fevers as the
temperature rises other causes become more common.
 • Hyperpyrexia differs from hyperthermia in that in
hyperpyrexia the body's temperature regulation mechanism
sets the body temperature above the normal temperature,
then generates heat to achieve this temperature, while in
hyperthermia the body temperature rises above its set point.

Pathophysiology

• Temperature is ultimately regulated in the hypothalamus. A

trigger of the fever, called a pyrogen, causes a release of
prostaglandin E2 (PGE2). PGE2 then in turn acts on the
hypothalamus, which generates a systemic response back to
the rest of the body, causing heat-creating effects to match a
new temperature level.
• In many respects, the hypothalamus works like a
[Link] the set point is raised, the body increases
its temperature through both active generation of heat and
retaining heat. Vasoconstriction both reduces heat loss
through the skin and causes the person to feel cold.
• The liver produces extra heat. If these measures are
insufficient to make the blood temperature in the brain
match the new setting in the hypothalamus, then shivering
begins, to use muscle movements to produce more heat.
• When the fever stops, and the hypothalamic setting is set
lower, the reverse of these processes (vasodilation, end of
shivering and nonshivering heat production) and sweating
are used to cool the body to the new, lower setting.
• This contrasts with hyperthermia, in which the normal
setting remains, and the body overheats through undesirable
retention of excess heat or over-production of
[Link] is usually the result of an excessively hot
environment (heat stroke) or an adverse reaction to drugs.
• Fever can be differentiated from hyperthermia by the
circumstances surrounding it and its response to anti-pyretic
medications.
Pyrogens

• A pyrogen is a substance that induces fever. These can be

either internal (endogenous) or external (exogenous) to the
body.
• The bacterial substance lipopolysaccharide (LPS), present in
the cell wall of some bacteria, is an example of an exogenous
pyrogen.
• Pyrogenicity can vary, as in extreme examples some bacterial
pyrogens known as superantigens can cause rapid and
dangerous fevers.
• Depyrogenation may be achieved through filtration,
distillation, chromatography, or inactivation.

Endogenous Pyrogens

• Cytokines (especially interleukin 1) are a part of the innate

immune system, are produced by phagocytic cells, and cause
the increase in the thermoregulatory set-point in the
hypothalamus. Other examples of endogenous pyrogens are
interleukin 6 (IL-6), and tumor necrosis factor-alpha.
• These cytokine factors are released into general circulation
where they migrate to the circumventricular organs of the
brain due to easier absorption caused by the blood-brain
barrier's reduced filtration action there. The cytokine factors
then bind with endothelial receptors on vessel walls, or
interact with local microglial cells. When these cytokine
factors bind, the arachidonic acid pathway is then activated.

Exogenous Pyrogens

• One model for the mechanism of fever caused by exogenous

pyrogens includes LPS, which is a cell wall component of
gram-negative bacteria.
• An immunological protein called lipopolysaccharide-binding
protein (LBP) binds to LPS.
 • The LBP–LPS complex then binds to the CD14 receptor of a
nearby macrophage.
• This binding results in the synthesis and release of various
endogenous cytokine factors, such as interleukin 1 (IL-1),
interleukin 6 (IL-6), and the tumor necrosis factor-alpha.
• In other words, exogenous factors cause release of
endogenous factors, which, in turn, activate the arachidonic
acid pathway.

PGE2 release

• PGE2 release comes from the arachidonic acid pathway.

• This pathway (as it relates to fever), is mediated by the
enzymes phospholipase A2 (PLA2), cyclooxygenase-2 (COX-
2), and prostaglandin E2 synthase. These enzymes ultimately
mediate the synthesis and release of PGE2.
• PGE2 is the ultimate mediator of the febrile response. The
set-point temperature of the body will remain elevated until
PGE2 is no longer present. PGE2 acts on neurons in the
preoptic area (POA) through the prostaglandin E receptor 3
(EP3).
• EP3-expressing neurons in the POA innervate the
dorsomedial hypothalamus (DMH), the rostral raphe
pallidus nucleus in the medulla oblongata (rRPa) and the
paraventricular nucleus (PVN) of the hypothalamus .
• Fever signals sent to the DMH and rRPa lead to stimulation
of the sympathetic output system, which evokes non-
shivering thermogenesis to produce body heat and skin
vasoconstriction to decrease heat loss from the body surface.
• It is presumed that the innervation from the POA to the PVN
mediates the neuroendocrine effects of fever through the
pathway involving pituitary gland and various endocrine
organs.

Hypothalamus
 • The brain ultimately orchestrates heat effector mechanisms
via the autonomic nervous system. These may be:
• Increased heat production by
o Increased muscle tone, shivering and hormones like
epinephrine.
o Prevention of heat loss, such as vasoconstriction.
• The autonomic nervous system may also activate brown
adipose tissue to produce heat (non-exercise-associated
thermogenesis, also known as non-shivering thermogenesis),
but this seems mostly important for babies.
• Increased heart rate and vasoconstriction contribute to
increased blood pressure in fever.

EPHEMERAL FEVER OR THREE DAY

FEVER
• Ephemeral fever is an insect-transmitted, noncontagious,
viral disease of cattle and buffalo. Inapparent infections can
develop in goats also.

Etiology

• Ephemeral fever virus is classified as a Rhabdovirus (single-

stranded, negative sense RNA).
• It is best isolated from infected cattle by inoculation of
mosquito ( Aedes albopictus ) cell cultures with defibrinated
blood, followed by transfer to baby hamster kidney (BHK-21)
or monkey kidney (Vero) cell cultures after 15 days.
• The virus can be transmitted from infected to susceptible
cattle by IV inoculation; as little as 0.005 mL of blood
collected during the febrile stage is infective.
• Although the virus has been recovered from several
Culicoides species and from Anopheline and Culicine
mosquito species collected in the field, the identity of the
major vectors has not been proved. Transmission by contact
 or fomites does not occur, and the virus does not appear to
persist in recovered cattle.
• Most recovered cattle have a lifelong immunity.
• The prevalence, geographic range, and severity of the disease
vary from year to year, and epidemics occur periodically.
• During epidemics, onset is rapid; many animals are affected
within days or 2-3 wk.
• Ephemeral fever is most prevalent in the wet season in the
tropics and in summer to early autumn in the subtropics or
temperate regions (when conditions favor multiplication of
biting insects); it disappears abruptly in winter.
• Morbidity may be as high as 80%; overall mortality is usually
1-2%, although it can be higher in lactating cows, bulls in
good condition, and fat steers (10-30%).

Clinical Findings

• Signs, which occur suddenly and vary in severity, include

biphasic to polyphasic fever, shivering, inappetence,
lacrimation, serous nasal discharge, drooling, dyspnea, atony
of forestomachs, depression, stiffness and lameness, and a
sudden decrease in milk yield.
• Affected cattle may become recumbent and paralyzed for 8
hr to >1 wk.
• After recovery, milk production often fails to return to
normal levels until the next lactation. Abortion, with total
loss of the season’s lactation, occurs in ~5% of cows pregnant
for 8-9 mo.
• The virus does not appear to cross the placenta or affect the
fertility of the cow.
• Bulls, heavy cattle, and high-lactating dairy cows are the
most severely affected, but spontaneous recovery usually
occurs within a few days.
• More insidious losses may result from decreased muscle
mass and lowered fertility in bulls.
Diagnosis

• Diagnosis is based almost entirely on clinical signs in an

epidemic.
• All clinical cases have a neutrophilia with the presence of
many immature forms, although this is not pathognomonic.
• Laboratory confirmation is by serology, rarely by virus
isolation.
• Whole blood should be collected from sick and apparently
healthy cattle in affected herds.
• Samples must be sufficient to provide 2 air-dried blood
smears, 5 mL in anticoagulant (not EDTA), and 20 mL for
serum.
• Isolated viruses are identified by neutralization tests using
specific ephemeral fever virus antisera and by ELISA using
specific monoclonal antibodies.
• The neutralization test and the blocking ELISA are
recommended for antibody detection and give similar
results.
• A 4-fold rise in antibody titer between paired sera collected
2-3 wk apart confirms infection.

Treatment and Control

• Complete rest is the most effective treatment, and recovering

animals should not be stressed or worked because relapse is
likely.
• Anti-inflammatory drugs given early and in repeated doses
for 2-3 days are effective.
• Oral dosing should be avoided unless the swallowing reflex is
functional. Signs of hypocalcemia are treated as for milk
fever .
• Antibiotic treatment to control secondary infection and
rehydration with isotonic fluids may be warranted.

PYREXIA OF UNKNOWN ORIGIN (PUO)

 • In both veterinary patients, fever may indicate infectious,
inflammatory, immune-mediated, or neoplastic disease.
• In most cases, the history and physical examination reveal
the cause of the fever, or the fever resolves spontaneously or
in response to antibiotic therapy.
• However, in a small percentage of patients, the cause of fever
is not readily apparent, and the problem becomes persistent
or recurrent.
• These patients are said to have pyrexia of unknown origin
(PUO).
• The classical PUO is defined as fever >101ºF (38.3ºC) on
several occasions over a period >2-3 wk with no diagnosis
established after 3 outpatient visits or 3 days in the hospital.

Body Temperature Regulation

• Body temperature is regulated by the hypothalamus. This

area of the brain acts as a thermostat to maintain
temperature as close as possible to a normal set-point.
• The hypothalamus receives input from internal and external
thermoreceptors, and it activates physiologic and behavioral
activities that influence heat production, heat loss, and heat
gain.
• Hyperthermia refers to any increase in body temperature
above the normal range.
• Fever is a particular form of hyperthermia in which the heat
loss and heat gain mechanisms are adjusted to maintain
body temperature at a higher hypothalamic set-point; thus,
fever is essentially a regulated hyperthermia.
• In nonfebrile cases of hyperthermia (eg, heat stroke,
exercise-induced hyperthermia, malignant hyperthermia,
seizure), body temperature is elevated by abnormal and
unregulated heat loss, heat gain, or heat production, and the
hypothalamic set-point is not altered.
• Depending on their severity, these conditions can potentially
result in body temperatures ³106ºF (41.1ºC).
 • In comparison, most patients with true fever have body
temperatures in the range of 103-106ºF (39.5-41.1ºC).
• Elevation of the hypothalamic set-point may be initiated by
exogenous pyrogens, which include drugs, toxins, and viral
or bacterial products (eg, endotoxin).
• These pyrogenic stimuli lead to the release of cytokines,
termed endogenous pyrogens, from inflammatory cells.
• Ultimately, locally synthesized prostaglandin E2 in the
hypothalamus is responsible for elevating the set-point,
resulting in fever.

TOP

Etiology and Pathogenesis

• PUO may be defined as fever that does not resolve

spontaneously in the period expected for self-limited
infection and for which a cause cannot be found despite
considerable diagnostic effort.
• This excludes patients that respond to antibiotic therapy
(and do not relapse) and patients in which the cause of fever
is determined from initial history, physical examination, or
laboratory tests, or in which fever resolves spontaneously.
• Infectious, immune-mediated, and neoplastic disease are the
most common causes of PUO in dogs.
• In a study of 101 dogs with fever, 22% had immune-mediated
diseases, 22% primary bone marrow abnormalities, 16%
infectious diseases, 9.5% neoplasia, 11.5% miscellaneous
conditions, and 19% had genuine FUO.
• In cats, the cause is more likely to be infectious, but there are
fewer published data on feline cases compared with canine
cases.
• In a case series of horses with PUO, 43% had infectious
disease, 22% had neoplasia, 6.5% had immune-mediated
disease, 19% had miscellaneous causes, and in 9.5% the
cause was not determined.
 • In farm animals, the most likely causes of PUO are infectious
or inflammatory diseases such as pneumonia, peritonitis,
abscesses, endocarditis, metritis, mastitis, polyarthritis, and
pyelonephritis.

Diagnosis

• The key to diagnosis of PUO is to develop and follow a

systematic plan that allows for the detection of both common
and uncommon causes of fever.
• Clients should be informed that diagnosis of PUO may
require considerable time and patience and may demand
more advanced or expensive diagnostic tests. Nevertheless,
simple and inexpensive tests may also reveal diagnostic clues
that eventually point to the cause of the fever.
• A staged or tiered approach to diagnosis can assist in
choosing appropriate tests.
• The first stage should include history, physical examination,
ophthalmic and neurologic examinations, CBC, fibrinogen,
serum chemistry profile, urinalysis and urine culture, feline
leukemia virus and feline immunodeficiency virus tests
(cats), and usually thoracic and abdominal radiographs in
small animals.
• In the second stage, some first-stage tests may be repeated
(particularly the physical examination) and additional
specialized tests are performed.
• These may be dictated by abnormal findings in the first stage
of testing or may be determined by consideration of the most
common known causes of PUO.
• Tests included in this stage include blood cultures,
arthrocentesis, abdominal ultrasound, lymph node
aspiration, aspiration of other organs or masses, analysis of
body fluids (eg, fluid from body cavities, milk samples,
reproductive tract secretions), fecal culture,
echocardiography (in the presence of a murmur), long-bone
and joint radiographs, contrast radiographs, and serology.
 • The third stage again may repeat earlier tests, as well as
additional specialized procedures.
• These procedures are most likely to be chosen on the basis of
previous findings, but may also be considered when all
previous testing has been unrewarding.
• Examples include echocardiography (in the absence of a
murmur), dental radiographs, bone marrow aspiration,
bronchoscopy and bronchoalveolar lavage, CSF analysis,
computed tomography (CT), MRI, laparoscopy,
thoracoscopy, biopsies, exploratory surgery, or trial therapy.

TOP

History and Physical Examination

• Epidemiologic characteristics such as vaccination, parasite

control, and travel history should always be reviewed.
• The response to previous medications should be determined,
as well as the presence of illness in other animals or humans.
• Clients should be questioned carefully about specific clinical
signs as these may help localize the source of the fever.
• The physical examination should be detailed and repeated
frequently.

CBC and Serum Chemistry Profile

• The CBC and chemistry changes in FUO patients are often

nonspecific, but may suggest further diagnostic tests.
• The CBC should always be accompanied by blood smear
evaluation to detect parasites or morphologic changes.

Urine Culture

• This test is always indicated to evaluate FUO in small

animals, regardless of the appearance of the urine sediment.

Radiography and Advanced Imaging

 • Thoracic and abdominal radiographs are useful screening
tools for the early localization of fever.
• Skeletal radiographs and contrast radiographs may
subsequently be considered, depending on initial findings.
• For example, myelography may be used to investigate back
pain.
• The use of advanced techniques such as CT and MRI is
determined by the results of initial diagnostic testing or by
consideration of the body system of interest, eg, MRI is
particularly useful for evaluating the CNS.

TOP

Ultrasonography and Echocardiography

• Abdominal ultrasound may reveal a source of fever in the

abdomen, such as neoplasia, peritonitis, pancreatitis, or
abscesses.
• The thoracic cavity, limbs, and retrobulbar areas may also be
examined by ultrasound.
• Echocardiography is indicated at the early stages of
evaluation of the PUO patient with a murmur.
• This may aid in the detection of endocarditis, although this
diagnosis should also be based on signalment, onset of the
heart murmur, and blood culture results.

Bone Marrow Evaluation

• Bone marrow cytology and histology should be evaluated in

any patient with unexplained CBC abnormalities.
• Bone marrow disease is a common cause of FUO in small
animals; therefore, bone marrow aspiration should also be
included in the second stage of diagnostic testing in these
patients.

Arthrocentesis
 • Because immune-mediated polyarthritis is a common cause
of FUO in dogs, arthrocentesis is included in the second
stage of diagnostic testing in this species, even if the joints
are normal on palpation.
• Some dogs with steroid-responsive meningitis-arteritis also
have concurrent immune-mediated polyarthritis; therefore,
arthrocentesis should be performed in dogs with spinal pain.
• Infectious polyarthritis is more commonly recognized in
large animals, in which arthrocentesis is an important
diagnostic test.

Blood Culture

• Blood cultures are recommended in all patients with

unexplained fever.
• The techniques used should allow the collection of
adequately large volumes of blood under aseptic conditions.
• If the size of the patient allows collecting more than one
blood culture set, using appropriately sized aerobic and
anaerobic bottles increases the sensitivity and specificity of
the test.

TOP

Serology

• Serologic tests are available for the diagnosis of many

infectious diseases and some immune-mediated disorders.
• Selection should be based on the signalment, clinical signs,
and epidemiologic characteristics of the patient.
• Interpretation of test results requires an understanding of
disease prevalence, vaccination history, and sensitivity and
specificity of the test.
• The use of immune panels or autoantibody screens in small
animal patients with FUO is discouraged.
 • Neither antinuclear antibody or rheumatoid factor titers
alone are sensitive or specific enough to diagnose systemic
lupus erythematosus or rheumatoid arthritis, respectively.

Microbiology, Cytology, and Histology

• Fine-needle aspirates are safe and simple to obtain from

effusions, masses, nodules, organs, tissues, and body fluids.
• Fluids should be examined cytologically and also submitted
for microbiologic testing.
• Tissue biopsies are generally obtained in the second or third
stages of diagnostic testing, after clinical signs or initial
diagnostic tests have localized the fever.
• When biopsies are obtained, sufficient samples should be
submitted for histopathology, appropriate culture (aerobic
and anaerobic, fungal, mycoplasmal, mycobacterial, etc), and
special stains. If exploratory surgery is performed, biopsies
should be obtained from several sites.

Treatment

• In some PUO cases a specific diagnosis is not reached, or

diagnostic testing is discontinued, leading to consideration of
therapy in the absence of a diagnosis.
• Options include antibiotics, antifungal agents, and anti-
inflammatory or immunosuppressive therapy (usually with
corticosteroids).
•
• Trial therapy may resolve the patient’s clinical signs or may
confirm a presumptive diagnosis, but it is also associated
with significant risk.
• Before pursuing a therapeutic trial, the client should be
informed of the potential risks and should be committed to
careful monitoring of the patient for an appropriate length of
time.
 • The therapeutic trial should be based on a tentative
diagnosis and should define the parameters to be followed
and the criteria used to determine treatment success or
failure.
• In true fever, the elevation in body temperature is regulated;
therefore, cooling methods such as water baths work against
the body’s own regulatory mechanisms.
• It is also likely that fever itself has some beneficial effects,
particularly in infectious diseases.
• However, fever can lead to anorexia, lethargy, and
dehydration.
• Thus, PUO patients may benefit from IV fluid therapy or
from the use of antipyretic medications.
• Examples include NSAID such as aspirin, carprofen,
ketoprofen, and meloxicam (small animals) and flunixin
meglumine or phenylbutazone (large animals).

ELECTROLYTE IMBALANCES-CONCEPTS

Elecrolytes

• Major concepts
o Electrolyte concentrations in serum are the net result of:
▪ intake
▪ excretion
▪ shifts between the ICF and ECF
▪ must consider hydration state with [Na+] and [Cl-]

REPRESENTATIVE ELECTROLYTE
CONCENTRATIONS
IN THE BODY FLUID COMPARTMENTS (mEg/L)
 Intracell
Electrol Extracell Intersti ntravasc
ular
ytes ular Fluid tial ular
Fluid
Cations - - - -
Sodium 15 147 142 -
Potassium 155 4 5 5
Calcium 2 2.5 - -
Magnesiu
27 1 2 -
m
Anions - - - -
Bicarbona
10 30 27 -
te
Chloride 1 114 103 -
Phosphat
100 2 2 -
e
Sulfate 20 1 1 -
Organic
1 7.5 - 5
acids
Protein 62 0 16 -

• Major functions of electrolytes

o Na+
▪ - H2O conservation (osmotic effect in kidney
tubules)
▪ As a measure of hydration status
▪ hypothalmic osmoreceptors
▪ renal volume receptors
 o Cl-
▪ Gastric fluid (HCl)
▪ linked to the renal generation of HCO3-

volume effects

• hypovolemia - ↑ pituitary antidiuretic hormone (ADH)* → ↑

CT H2O resorption
• hypervolemia - ↓ pituitary antidiuretic hormone (ADH)* → ↓
CT H2O resorption

Note : *at atrial and carotid baroreceptors (ADH)

• hypoosmolality:
o inhibit thirst centers → ↓ H2O intake
o CT H2O resorption↑ ADH* →
• hyperosmolality
o stimulate thirst centers → ↑ H2O intake
o ↑ ADH* → ↑ CT H2O resorption

Note : * at hypothalmic osmoreceptors

SPECIFIC IMBALANCES
Sodium

• Approximately 1/2 of the total body concentration of sodium

is found in ECF.
• The quantity of sodium in the body is controlled by dietary
intake and loss.
• The most important route for sodium excretion is through
the kidney. Most sodium presented to renal tubules is
reabsorbed in a process controlled by aldosterone.
• Renal reabsorption of sodium requires an equivalent passage
of hydrogen or potassium ions in the opposite direction.
• Sodium is also lost in sweat and in digestive tract secretions.
 • In carnivores and most herbivores, sodium is reabsorbed in
the lower intestinal tract.
• In herbivores with large quantities of fluid in the feces, such
as the cow and the horse, there may be considerable fecal
loss of sodium.
• A decrease in plasma sodium concentration (hyponatremia)
occurs most frequently because of excessive sodium loss.
• from the gastrointestinal tract through diarrhea or vomition
• in renal disease in which the sodium conservation
mechanism is operating deficiently because of tubular
damage
• Hyponatremia may occur with hyperglycemia due to
increased sodium excretion to prevent hyperosmolarity.
• An increase in plasma sodium concentration
(hypernatremia) is rare and can occur when there is
restricted water intake with excessive sodium intake, in
advanced chronic renal failure with a low glomerular
filtration rate, and with primary hyperaldosteronism.

Potassium

• Potassium concentration is low in ECF and high in most

cells of the body.
• Most potassium is excreted by the kidneys through
glomerular filtration and tubular secretion.
• Aldosterone facilitates excretion of potassium since it causes
increased sodium reabsorption by promoting the exchange
of sodium in tubular fluid for potassium in the tubular cell.
• Potassium excretion by the kidneys is also controlled by
competition between potassium and hydrogen ions for
reabsorption.
• Alterations in serum potassium levels occur when there is a
disturbance in the equilibrium between potassium in
the ICF and potassium in the ECF.
• In alkalosis, potassium moves into the cell in exchange for
hydrogen ions and may cause hypokalemia.
 • In acidosis, potassium moves out of the cell in exchange for
hydrogen ions and may cause hyperkalemia.
• Plasma potassium increases about 0.6 mEq/L for
each 0.1 unit decrease in blood pH. Therefore, if an acidotic
animal has a normal plasma potassium level, it should be
considered hypokalemic and corrective therapy should be
initiated.
• In addition to its role in maintaining the tonicity of the ICF,
potassium is of great importance in the mechanism of
neuromuscular transmission.
• Low concentrations of K+ in the ECF result in profound
muscular weakness and ECG abnormalities.
• High concentration of K+ in the ECF (10-12 mEq/L) result
in severe myocardial disturbances and death due to cardiac
arrest.

Chloride

• Chloride concentration is low in ICF and high in ECF.

• Excretion, absorption and distribution of chloride are
passive processes in association with active sodium
transport.
• Unusual reduction in chloride concentration in the absence
of comparable change in sodium, usually reflects
sequestration of gastric juice in the stomach or vomiting.

Bicarbonate

• Bicarbonate is mostly of endogenous origin in that it comes

from the hydration of carbon dioxide to carbonic acid which
then dissociates to bicarbonate and hydrogen ions.
• Bicarbonate is lost through secretions to the digestive tract
and in the urine.
• Bicarbonate levels are regulated by respiratory and
metabolic (kidney) processes.
 ACID-BASE BALANCE AND DISORDERS
Major concepts

• Acidosis and alkalosis refer to the pathophysiologic process

that cause net accumulation of acid or alkali (base) in the
body
• Acidemia and alkalemia refer specifically to the pH of the
blood
• Buffer - a substance that is able to take up or release H+ so
that drastic changes in [H+] are minimized; a depot for H+.

Physiologically relevant buffer systems

• Bicarbonate (HCO3-/H2CO3) – most important

quantitatively; easily measured;
• Can be effectively regulated in response to acidosis or
alkalosis through Mmtabolic (renal) or respiratory (lung)
compensation
• Red cell hemoglobin
• Plasma and intracellular proteins
• Organic and inorganic phosphates (HPO42-, / H2PO4-)
• Bone carbonate (CO32-)

Bicarbonate system

CO2 + H2O → H2CO3 → H+ + HCO3-

Respiratory Metabolic
Component Component

• Measurements of the above components, and more, are

performed on a blood gas analyzer
• CO2 - Respiratory Acid; HCO3- - Metabolic Base
• Samples are collected in a heparinized syringe with the
needle closed with a rubber stopper to prevent exposure to
air
 • Analysis should be done within minutes
• Analytes of a standard blood gas include pH, pCO2, HCO3-,
TCO2, pO2, and Base Excess (BE)

pH

• pH is necessary to determine if the patient is acidemic or

alkalemic
• Remember that small changes in pH represent large changes
in [H+] since it is measured on an logarithmic scale

pCO2

• Partial pressure of CO2 dissolved in plasma (mmHg)

• Respiratory component – regulated by the lungs
• Respiratory acidosis is characterized by ↑ pCO2
(hypercapnia) caused by alveolar hypoventilation
• Respiratory alkalosis is characterized by ↓ pCO2
(hypocapnia) caused by alveolar hyperventilation

HCO3-

• Bicarbonate concentration (mmol/L)

• Metabolic component – regulated by the kidney
• Metabolic acidosis is characterized by ↓ [HCO3-], due either
to HCO3- loss or HCO3- buffering of acid (titration)
• Metabolic alkalosis is characterized by ↑ [HCO3-], due to H+
loss or rarely iatrogenic HCO3- administration
• pH [H+] Primary Compensatory
• Metabolic acidosis ↓ ↑ ↓ [HCO3-] ↓ pCO2
• Metabolic alkalosis ↑ ↓ ↑ [HCO3-] ↑ pCO2
• Respiratory acidosis ↓ ↑ ↑ pCO2 ↑ [HCO3-]

Respiratory alkalosis ↑ ↓ ↓ pCO2 ↓ [HCO3-]

Total CO2 (TCO2)

 • TCO2 ~ HCO3- ; TCO2 ≠ pCO2
• TCO2 is the sum of all substances in serum which can be
converted to CO2 gas after the addition of a strong acid;
dissolved CO2, H2CO3, and HCO3-
• Approximately 95% of TCO2 is HCO3-
• Can be performed on serum/plasma and may be run several
hours after collection; however, values will decrease over
longer periods

Anion gap (AG) = (Na+ + K+) − (HCO3- + Cl-)

• Represents the major electrolytes in serum

• Law of electroneutrality → all anionic charges = all cationic
charges
• AG measures the major electrolytes and compares to
reference range

Abnormal AG - change in an ion(s) not normally present to that

degree or at all in health

In practice is used to detect unmeasured anions :

• lactic acid
• ketoacids
• uremic acids (PO42-, SO42-, and citrate)
• ethylene glycol metabolites (glycolate and oxalate)
• massive rhabdomyolysis (PO42- and lactic acid)
• ↓ AG is rare and not likely of clinical significance; substantial
hypoalbuminemia can lower AG somewhat.

Metabolic Acidosis

• Addition of H+ (unmeasured acids):

o ↑AG, normochloremic -
o organic acids:
o lactic acidosis (hypoxia)
o ketoacidosis (DKA, ketosis)
 o anionic toxins: (ethylene glycol, salicylate, methanol,
paraldehyde, etc.)
• Decreased removal of H+:
o inorganic acids:
o PO42-, SO42-, citrate (renal failure, urinary
obstruction, uroabdomen)
o renal distal tubular acidosis
• HCO3- loss:
o normal AG, hyperchloremic
o GI (diarrhea, vomiting, sequestration, salivation in
ruminants)
o renal proximal tubular acidosis

respiratory compensation (immediate) → hyperventilation → ↓

pCO2

Metabolic Alkalosis

• Loss of H+:
o hypochloremic
o GI (vomiting, pyloric obstruction, abomasal
displacement)
• Addition of HCO3-:
o iatrogenic with fluid administration (NaHCO3, lactate,
citrate)

respiratory compensation (immediate) → hypoventilation → ↑

pCO2

Respiratory acidosis

↑ pCO2 from hypoventilation: Iinhibition or dysfunction of

medullary respiratory center

• drugs (anesthetics, sedatives, narcotics)

• brain stem disease
• alkalemia
 • inhibition or dysfunction of respiratory muscles (tick
paralysis, tetanus, botulism, myasthenia gravis,
hypokalemia, succinylcholine
• upper airway dysfunction (foreign body, vomitus)
• impaired gas exchange (lung/thoracic disease)
• inappropriate mechanical ventilation

metabolic compensation (days) → ↑ H+ secretion and ↑ HCO3-

production

Respiratory Alkalosis

• ↓ pCO2 from hyperventilation

o altered respiratory control (fear, convulsions, fever,
heat exposure, hepatic encephalopathy)
o hypoxemia (lung disease, hypotension)
o inappropriate mechanical ventilation
• Metabolic compensation (days) → ↓ H+ secretion and ↓
HCO3- production
• Mixed acid/base - coexistence of multiple primary acid/base
abnormalities
• Compensating responses to simple acid-base disturbances do
not correct pH to normal

First type

• A normal pH with abnormal HCO3- and/or pCO2 represents

a mixed acid/base disturbance. e.g. HBC → uroabdomen +
extremely painful (panting):
o Low normal pH
↓ [HCO3-]
↓ pCO2
↑ AG
o Uroabdomen → primary metabolic acidosis
o Panting → primary respiratory alkalosis
 • An extremely high or low pH can occur if the [HCO3-] and
pCO2 levels go in opposite directions, i.e. both representing
primary acidoses or both representing primary alkaloses.
• These can be grave situations.

COMMON QUESTIONS
1. What are the basic factors affecting the electrolyte balance?
2. What are the functions of the electrolytes?
3. Define respiratory acidosis and alkalosis?
4. Define hypothermia, how is it classified, enumerate the
consequences of hypothermia?
5. Explain breifly the management of hypothermia?
6. What are the different forms of rewarming techniques used,
explain ?
7. What is hyperthermia, explain briefly the various causes for
heat stroke and its medical management?
8. What is the difference between hyperthermia and fever?
Describe the pathophysiology of fever?
9. Enumerate the clinical findings of ephemeral fever, how to
diagnose the condition and what is the line of treatment for
the disease?
10. Define pyrexia of unknown origin, explain the
pathogenesis and line of treatment to be followed?

MODULE-5: GENERAL AND SYSTEMIC

STATES - II
Learning objectives

• To know about their clinical findings, diagnosis and

treatment of common generel systemic states such as
septicemia and shock.
• To know about the medical management pertaining to the
general systemic states such as
 o Septecemia
o Toxaemia
o Shock
o Dehydration

SEPTICEMIA
• Septicemia is the presence of bacteria in the blood
(bacteremia) and is often associated with severe infections.

Causes

• Septicemia is a serious, life-threatening infection that gets

worse very quickly.
• It can arise from infections throughout the body, including
infections in the lungs, abdomen, and urinary tract.
• It may come before or at the same time as infections of the
bone (osteomyelitis), central nervous system (meningitis),
heart (endocarditis), or other tissues.

Symptoms

• Septicemia can begin with spiking fevers, chills, rapid

breathing, and rapid heart rate.
• The symptoms rapidly progress to shock with fever or
decreased body temperature (hypothermia), falling blood
pressure, confusion or other changes in mental status, and
blood clotting problems that lead to a specific type of red
spots on the skin (petechiae and ecchymosis).
• There may be decreased or no urine output.

Examinations and Tests

• A physical examination may show:

• Low blood pressure
• Low body temperature or fever
 • Signs of associated disease (such as meningitis, epiglottitis,
pneumonia, or cellulitis)

Tests that can confirm infection include

• Blood culture
• Blood gases
• CBC
• Clotting studies
• PT
• PTT
• Fibrinogen levels
• CSF culture
• Culture of any suspect skin lesion
• Platelet count
• Urine culture

Treatment

• Septicemia is a serious condition that requires a vetrinary

hospital stay.
• The animal patient may be admitted to an intensive care unit
(ICU).
• Fluids and medicines are to be given by IV to maintain the
blood pressure.
• Oxygenneeds to be be given. Antibiotics are used to treat the
infection.
• Plasma or other blood products may be given to correct any
clotting abnormalities.

Prognosis

• What to expect depends on the organism involved and how

quickly the patient is hospitalized and treatment begins.
• The death rate is high -- more than 50% for some organisms.

Possible Complications
 • Septicemia can rapidly lead to adult respiratory distress
syndrome (ARDS), septic shock, and death.
• Septicemia associated with meningococci can lead to shock
or adrenal collapse.

Prevention

• Appropriate treatment of localized infections can prevent

septicemia.
• In certain cases, animals who are in close contact with
someothers with septicemia may be prescribed preventative
antibiotics.

SEPTICEMIA IN EQUINE NEONATES

• Septicemia is a systemic disease involving the presence and
persistence of bacteria or their toxins in the blood.

• The condition implies an extensive, whole body insult from a

single or multiple sources of infection.

Etiology and Pathogenesis

• The predominant bacteria involved in neonatal foal

septicemia are the gram-negative organisms Escherichia coli
 , Klebsiella spp , Enterobacter spp , Actinobacillus spp , and
Pseudomonas spp .
• About 50% of infections also involve gram-positive bacteria,
with Streptococcus spp being the most common isolates.
• Anaerobic pathogens are involved in 30% of cases.
• The routes of entry for these bacteria include the placenta,
umbilicus, lungs, and GI tract.
• Clinical Signs of septicemia and septic shock mainly result
from the release of endotoxins related to gram-positive
infections.
• Endotoxins stimulate macrophages to release an array of
cytokines (eg, IL-6, IL-1, TNF-α) and activate pro-
inflammatory enzymes (eg, phospholipase A2).
• Together, these factors lead to signs of inflammation such as
fever, vasodilation, hypoglycemia, myocardial depression,
procoagulant activity, and eventually disseminated
intravascular coagulation (DIC).
• Bacterial infection accounts for nearly one third of all foal
mortality. Septicemia is the second most common problem
of equine neonates, second only to failure of passive transfer
of maternal antibodies.
• Certain immunologic and management factors predispose
foals to septicemia. Although foals can respond
immunologically in utero to bacterial or viral infections, their
ability to do so is less than that of adults.
• The major risk factor for septicemia in foals is failure to
receive an adequate quality and quantity of colostral
antibodies.
• Other factors that influence disease incidence include
unsanitary environmental conditions, gestational age of the
foal (prematurity), health and condition of the dam,
difficulty of parturition, and the presence of new pathogens
in the environment against which the mare has no
antibodies.
Clinical Findings

• Clinical signs largely depend on the stage of the animal’s

illness and the primary body systems involved.
• Frequently affected organ systems include the umbilical
remnants, CNS, respiratory, cardiovascular, musculoskeletal,
renal, ophthalmic, hepatobiliary, and GI organs.
• Foals in the early stages of sepsis display some degree of
depression and lethargy and may lie down more than usual.
• The mare’s udder is often distended with milk, indicating
that the foal is not nursing with normal frequency.
• In the advanced stage of illness (septic shock), foals are
severely depressed, recumbent, dehydrated, and tachycardic.
• The mucous membranes are muddy, and hypotension, which
manifests clinically as cold extremities, thready pulse, and
poor capillary refill time, is evident.
• Foals may be hyper- or hypothermic. In septicemia, bacteria
spread hematogenously to various organs, such as the lungs,
intestines, eyes, CNS, bones, and joints.
• The foal may show evidence of single or multiple organ
dysfunction. Sepsis can manifest as respiratory distress,
pneumonia, diarrhea, uveitis, meningitis, osteomyelitis, or
septic arthritis.

Diagnosis

• A good perinatal history and physical examination can

provide clues in the diagnosis.
• Depending on the specific organ systems involved, an
umbilical, abdominal, and synovial ultrasound examination;
arterial blood gas analysis; arthrocentesis; cerebrospinal
centesis; and chest, abdominal, and distal limb radiographs
may be indicated. Advanced diagnostic imaging techniques
(eg, computed tomography of the distal limbs) may further
serve as a prognostic aid.
 • Septic foals are often neutropenic with a high ratio of band to
segmented neutrophils.
• The neutrophils may exhibit toxic changes, which are highly
suggestive of sepsis. Foals <24 hr old are often
hypoglycemic.
• Fibrinogen levels >600 mg/dL in a foal <24 hr old is
indicative of an in utero infection.
• Other chemistry abnormalities that may be evident include
azotemia due to inadequate renal perfusion and increased
bilirubin secondary to endotoxin damage to the liver.
• A high anion gap (>20 mEq/L), hypoxemia, hypercapnia,
and a mixed respiratory and metabolic acidosis may be
found on arterial blood gas analysis.
• Because of the high correlation between failure of passive
transfer of antibodies and septicemia, serum IgG levels
should be measured in any questionably sick equine neonate.
IgG levels <200 mg/dL indicate complete failure of passive
transfer of maternal antibodies. IgG levels >800 mg/dL are
optimal.
• A definitive diagnosis of neonatal sepsis is based on clinical
signs, laboratory data, and evidence of failure of passive
antibody transfer. These data can be combined to determine
the animal’s sepsis score, which helps synthesize laboratory
results into a coherent whole.
• A positive blood culture also correlates to sepsis, but a
negative culture does not rule out the possibility of infection.
• Differential diagnoses include hypoxic ischemic
encephalopathy (Hypoxic Ischemic Encephalopathy:
Introduction), hypoglycemia, hypothermia, neonatal
isoerythrolysis (Hemolytic Anemia), white muscle disease
(Nutritional Myopathy of Calves and Lambs), prematurity,
neonatal pneumonia, and uroperitoneum (Uroperitoneum in
Foals).

Treatment
• Foals suspected of being septic should be placed on broad-
spectrum antibiotics active against both gram-positive and
gram-negative organisms.
• Penicillin (22,000 IU/kg, IV, qid) in combination with
amikacin sulfate (20-25 mg/kg, IV, sid) provides good initial
coverage until culture results are available.
• Metronidazole (10-15 mg/kg, PO or IV, tid) may be necessary
if an anaerobic infection (eg, Clostridium ) is suspected.
• A third- generation cephalosporin (eg, ceftiofur, 4.4-6
mg/kg, IV, bid-qid) may be used as a broad-spectrum agent
in patients with compromised renal function.
• In all cases of neonatal sepsis, immunologic support, in the
form of IV plasma transfusions (1-2 L), to raise the IgG levels
to >800 mg/dL is important.
• Effective IV fluid therapy is needed to combat endotoxic
shock.
• Foals may require 100 mL/kg/day of maintenance therapy
using polyionic isotonic crystalloid fluids (eg, lactated
Ringer’s solution) after fluids have been administered for
shock. Because many foals are hypoglycemic, dextrose
should be added to make a 2.5-5% dextrose solution.
• Isotonic bicarbonate solution may be given to help correct
moderate to severe metabolic acidosis, but can worsen
respiratory acidosis.
• In these cases, mechanical ventilation should be used to
decrease PaCO2 before giving bicarbonate.
• Treatment with hyperimmune antiendotoxin serum should
be considered in patients with endotoxemia.
• Antiprostaglandin drugs counteract several of the clinical
and hemodynamic changes associated with endotoxemia and
septic shock.
• Low doses of flunixin meglumine (0.25 mg/kg, IV, tid) may
help reduce signs of endotoxemia.
• Additionally, administration of low doses of polymyxin B
(6,000 IU/kg, diluted in 300-500 mL of saline, slow IV) is
 an investigational treatment used to neutralize systemic
endotoxin.
• Because sepsis creates a catabolic state in the foal,
nutritional support is important.
• If the foal is not nursing adequately, it should be fed mare’s
milk or a milk substitute at 15-25% of its body weight over
each 24-hr period. An indwelling nasogastric tube should be
placed in foals with a decreased suckle reflex.
• Parenteral nutrition may also be helpful to provide adequate
nutrients.
• Administration of gastric protectants (eg, ranitidine,
cimetidine, omeprazole) has been proposed as an adjunct
therapy in sick neonates.
• System-specific therapy includes lavaging septic joints with
sterile fluids and providing nasal oxygen (2-10 L/min) or
ventilation for foals with septic pneumonia.
• Corneal ulceration may be treated with low doses of topical
atropine (although it may cause ileus), NSAID, and broad-
spectrum topical antimicrobials. Entropion generally
requires mattress sutures of the lower eyelid.
• Surgical removal of infected umbilical remnants may be
indicated.
• Recovery from neonatal sepsis depends on the severity and
manifestation of the infection.
• Current survival rates are 50-65% in referral centers. A
minimum of 1-4 wk of intensive care should be expected.
• Early recognition and intensive treatment of neonatal sepsis
improves the outcome.
• If the foal survives the initial problems, it has the potential of
becoming a healthy and useful adult.

TOXEMIA
• Toxemia is a generic term for the presence of toxins in the
blood. It is not necessarily the same as Bacteremia.
 • The toxins released by bacteria can enter the blood stream
and can move throughout the body without any bacteria
entering the blood stream.
• Pre-eclampsia, a serious condition in pregnancy that
involves hypertension and proteinuria, may be caused by
toxemia.

Septicemic Disease (Colisepticemia)

• Septicemia caused by Escherichia coli is a common disease

of calves, and to a lesser extent lambs, <1 wk old.
• It may present with signs of acute septicemia or as a chronic
bacteremia with localization.
• The disease is caused by specific serotypes of E coli that
possess virulence factors enabling them to cross mucosal
surfaces and produce bacteremia and septicemia.
• However, the main determinant of the disease is deficiency
of circulating immunoglobulins as the result of a failure in
passive transfer of colostral immunoglobulin; septicemic
disease due to invasion by E coli occurs only in
immunoglobulin-deficient calves.
• Colisepticemia is seen during the first week of life, most
commonly at 2-5 days of age.
 • Chronic disease with localization can be seen up to 2 wk of
age. The disease is usually sporadic and is more common in
dairy than beef calves.

Transmission and Pathogenesis

• Invasion occurs primarily through the nasal and

oropharyngeal mucosa but can also occur across the intestine
or via the umbilicus and umbilical veins.
• There is a period of subclinical bacteremia that, with virulent
strains, is followed by rapid development of septicemia and
death from endotoxemic shock.
• A more prolonged course, with localization of infection,
polyarthritis, meningitis, and less commonly uveitis and
nephritis, is seen with less virulent strains.
• Chronic disease also develops in calves that have acquired
marginal levels of circulating immunoglobulin.
• The organism is excreted in nasal and oral secretions, urine,
and feces; excretion begins during the preclinical bacteremic
stage.
• Initial infection can be acquired from a contaminated
environment.
• In groups of calves, transmission is by direct nose-to-nose
contact, urinary and respiratory aerosols, or as the result of
navel-sucking or fecal-oral contact.

Clinical Findings and Diagnosis

• In the acute disease, the clinical course is short (3-8 hr), and
signs are related to the development of septic shock.
• Pyrexia is not prominent, and the rectal temperature may be
subnormal.
• Listlessness and an early loss of interest in sucking are
followed by depression, poor response to external stimuli,
collapse, recumbency, and coma.
 • Tachycardia, a poor pulse pressure, and a prolonged
capillary refill time are seen.
• The feces are loose and mucoid, but severe diarrhea is not
seen in uncomplicated cases.
• Mortality approaches 100%. With a more prolonged clinical
course, the infection may localize.
• Polyarthritis and meningitis are common; tremor,
hyperesthesia, opisthotonos, and convulsions are seen
occasionally, but stupor and coma are more common.
• A moderate but significant leukocytosis and neutrophilia are
seen early, but leukopenia is marked in the terminal stages.
• The joint fluid contains increased inflammatory cells and
protein, and the CSF shows pleocytosis and an increased
protein concentration; organisms may be evident on
microscopic examination.
• Less commonly, other bacteria, including other
Enterobacteriaceae, Streptococcus spp , and Pasteurella spp ,
produce septicemic disease in young calves.
• These organisms are more common in sporadic cases than as
causes of outbreaks.
• They produce similar clinical disease, but they can be
differentiated by culture.
• As with colisepticemia, the primary determinant of these
infections is a failure of passive transfer of immunoglobulins.
• The diagnosis is based on history and clinical findings,
demonstration of a severe deficiency of circulating IgG, and
ultimately, demonstration of the organism in the blood or
tissues.
• Zinc sulfate or total protein estimation can be used for rapid
estimation of IgG ( Nutritional Requirements).

Treatment

• Treatment requires aggressive use of antibiotics.

 • Because there is no time for sensitivity testing, the initial
choice should be a bactericidal drug that has a high
probability of efficacy against gram-negative organisms.
• Antibacterial therapy should be coupled with aggressive
fluid, drug, and other therapy for endotoxic shock. Mortality
is high despite aggressive treatment.

Control and Prevention

• Calves that acquire adequate concentrations of

immunoglobulin from colostrum are resistant to
colisepticemia.
• Therefore, prevention depends primarily on management
practices that ensure an adequate and early intake of
colostrum.
• The adequacy of the farm’s practice of feeding colostrum
should be monitored, and corrective strategies applied as
required.
• In dairy herds, natural sucking does not guarantee adequate
concentrations of circulating immunoglobulins, and calves
should be fed 2-4 L of first-milking colostrum, using a nipple
bottle or an esophageal feeder, within 2 hr of birth, followed
by a second feeding at 12 hr.
• The circulating concentration of immunoglobulin required to
protect against colisepticemia is low; however, high
concentrations of circulating immunoglobulins are desirable
because they decrease susceptibility to other neonatal
infectious diseases.
• When natural colostrum is not available for a newborn calf,
commercial colostrum substitutes containing 25 g IgG will
provide sufficient immunoglobulin for protection against
colisepticemia if fed early in the absorptive period.
• Plasma containing at least 4 g and preferably 8 g IgG,
administered parenterally, will provide some protection for
older calves that have not been fed colostrum and are unable
to absorb immunoglobulins from the intestine.
 • Small-volume hyperimmune serum is of benefit only when it
contains antibody specific to the particular serotype
associated with an outbreak.
• The risk of early infection should be minimized by hygiene in
the calving area and disinfection of the navel at birth.
• To minimize transmission, calves reared indoors should be
in separate pens (without contact) or reared in calf hutches.

PRINCIPLES OF ANTIMICROBIAL
THERAPY
Penicillins

• β-Lactams. G+, easy G-, anaerobes. Bactericidal. Inhibit cell

wall synthesis. Safe. Elimated via kidney, good for UTIs.
• Natural penicillins – G+, poor G-, spirochetes, destroyed by
penicillinase. PenG and PenV. Penicillinase-resistant
penicillins – Penicillinase producing G+ cocci, esp.
Staphylococcus.

• Cloxacillin, dicloxacillin. Aminopenicillins – Broad

spectrum, ↑ G- activity. Ampicillin, amoxicillin. Extended
spectrum penicillins – addl G- activity, Pseudomonas.
• Carbenicillin, ticarcillin, piperacillin. Potentiated penicillins
- Developed to inactivate β-lactamases.
• Clavomox, timentin. Don’t use penicillins in rodents and
lagomorphs; elimination of G+ gut flora can lead to fatal
colibacillosis.
Cephalosporins
• β-Lactams. G+, some G- (more with each generation),
anaerobes. Bactericidal. β-lactam antibiotics. Inhibit cell wall
synthesis.
• More effective against actively growing bacteria.
Classifications – 1st generation cepholosporins include
cephalothin, cefazolin, cephapirin, cephadine, cephalexin,
cefadroxil. Activity against most G+, poor G- activity. 2nd
generation cepholosporins - not very popular, same G+
activity, expanded G-. 3rd generation cepholosporins – same
G+ activity, much expanded G- activity; cefotaxime,
moxolactom, cefoperazone, ceftiofur (BRD, no withdrawal
time).

Aminoglycosides

• 1° G- aerobes. Some G+. Pseudomonas, staphylococcus,

atypical mycobacterium (nocardia/actinomyces).
• Irreversibly bind to 30S ribosomal unit and inhibits protein
synthesis. Bactericidal.
• Includes amikacin (SID, parvo pups), gentamicin, neomycin,
and spectinomycin.
• Inactive against fungi, viruses and most anaerobic bacteria.
Accumulate in inner ear and kidneys.
• Elimination via glomerular filtration. Adverse Effects –
Nephrotoxic.
• Casts in urine, increased BUN and Cr. Nephrotoxicity
reversible when drug discontinued. Ototoxic. 8th cranial
nerve toxicity.
• Auditory and vestibular symptoms may be irreversible.

Fluoroquinolones

• Good G- aerobes, facultative anaerobes, atypical

mycobacterium, chlamydia, mycoplasma, ehrilichia, BRD.
 • Bactericidal. DNA gyrase inhibitor, prevent DNA synthesis.
Enrofloxacin (SID, prostate, RMSF, deethylated to cipro),
ciprofloxacin. Variable activity against Streptococci – not
recommended. Contraindicated in young animals due to
cartilage defects. Baytril associated with blindness in cats.

Sulfonamides
• G+, easy G-, anaerobes; nocardia and actinomyces.
Bacteriostatic.
• Inhibit folic acid pathway (PABA/pteridine not converted to
DHFA). Broad spectrum.
• Many bacteria have developed resistance. Potentiated
sulfonamides – TMPS.
• Bactericidal, inhibits bacterial thymidine synthesis in folic
acid pathway.
• Excellent tissue distribution. Most drug side effects of all
Abs, allergic reactions, hepatotoxic, KCS, hypothroidism,
crystalluria, thyrotoxic, anemia, BM toxicity (aplastic
anemia, thrombocytopenia hypoprothrombinemia).

Tetracyclines

• G+, easy G-, Mycoplasma, spirochetes, chlamydia,

Rickettsia, Hemobartonella, Brucellosis. Bacteriostatic.
• Inhibits protein synthesis by binding to the 30S ribosomal
unit. Safe.
• Prostate. Includes doxycycline (biliary excretion),
oxytetracycline, tetracycline. Resistance ↑.
• May cause esophagitis. Chloramphenicol – G+, G-.
Bacteriostatic.
• Binds to the 50S ribosomal subunit preventing protein
synthesis.
• Penetrates everything. Can cause aplastic anemia in humans.

Lincosomides
 • G+ aerobes, anaerobes. No G-. Often combo w/
aminoglycosides. Lincomycin, clindamycin.
• Bacteriostatic or bactericidal. Bind to the 50S ribosomal
subunit.
• Distribute well, biliary elimination. Contraindicated in
rabbits, rodents, horses, ruminants due to serious GI effects.

Macrolides
• G+, selected G-. Bacteriostatic. Bind 50S ribosomal subunit.
[ ] in alveolar macrophages, great for pulmonary infections.
• Erythromycin, tylosin, tilmicosin. Erythromycin is used in
the treatment of Rhodococcus equi in combo w/ rifampin.
• Can cause increase in GI motility. Tilmicosin – used in BRD;
CV toxicity in primates, horses, swine.

Metronidazole
• Bactericidal and antiprotozoal. Obligate anaerobes.
• Disrupts DNA and nucleic acid synthesis.
Immunolmodulator in IBD.

Rifampin
• Bactericidal or bacteriostatic. Inhibits DNA-dependent RNA
polymerase.
• Used for treatment of Rhodococcus equi in combo w/
erythromycin.

Antifungal Agents

Amphotericin B
• Polyene macrolide. Binds to fungal sterols, altering
permeability of membrane.
• Fungistatic. Dimorphic fungi (histo, blasto, crypto, coccidio).
 • Because of the risk of severe toxicity reserved for
disseminated, progressive, potentially fatal fungal infections.
Nephrotoxic, anaphylactoid.

Imidazoles
• Fungistatic. Inhibit ergosterol/steroid synthesis (blocks
cytochrome p450), ↑ cell membrane permeability, ↓ cell
membrane fluidity.
• Use for dermatophytes, yeast, dimorphic fungi. Impairs
steroid sythesis, so sometimes used in hyperadrenocorticism
and prostate diz.
• Ketaconazole – Fairly safe (hepatotoxicity), give w/ food.
Short t½. Not got w/ dimorphic fungi, esp. blasto.
• Itraconazole – more effective spectrum. Fluconazole –
Crosses BBB.

Flucytosine
• Ancoban. Inhibits DNA synthesis (antimetabolite, competes
with uracil, interfering with pyrimidine metabolism and
protein synthesis).
• Limited spectrum - Cryptococcus, Candida. Rapid
absorption, excellent distribution. Synergistic effect with
amphotericin B.
• Adverse effects include BM depression (pancytopenia), GI
disturbances, rashes, oral ulceration, increased liver
enzymes.

Griseofulvin

• Inhibits fungal mitosis by disrupting mitotic spindle, inhibit

nucleic acid and fungal wall sythesis.
• Limited to dermatophytes only. Give w/ fatty food to ↑
absorption. [ ] in keratin. Side effects include GI, teratogenic
and carcinogenic at ↑ doses, bone marrow dyscrasias.
 • Do not give to pregnant animals.

Antiseptic Agents
• Agents applied to the body vs. disinfectants which are used
on inanimate objects.

Alcohol

• Protein denaturation. 70% is effective against G+ and G-

bacteria.
• Good bactericidal, fungicidal, virucidal. Most rapid acting
but least residual action.
• Fast kill, defatting agent. Evaporates quickly. 2 min for max
effect. May be drying or irritating.
• May cause cytotoxicity. Often used in combo w/ povidone
iodine.

Chlorhexidine

• Cytoplasmic membrane disruption. 0.05% soln effective

against Gram+ and Gram-.
• Persists on skin to give cumulative antibacterial effect. Less
irritating.
• Not inactivated by organic matter. 0.05% is 1:40 dilution,
most bactericidal and least toxic to tissues.

Hydrogen peroxide

• Poor antiseptic. Short-acting germicidal effect through

release of nascent O2, irreversibly alters proteins.
• Effective sporicide. Effervescent action mechanically
removes pus and bacteria.

Iodine
 • One of most potent antiseptics. Bactericidal, virucidal,
fungicidal. Takes 15 min for sporicidal action.
• Organic matter inactivates free I in PI. Iodine Soln USP has
little to no stinging on broken skin.
• Iodine tincture USP (I in alcohol) is even more effective, but
stings and irritates skin.
• Rare HPS rxns. Povidone iodine often used in conjunction
w/ alcohol. Use PI in 0.1 to 1% [ ]; more dilure solns have ↑
free I and faster, potent bactericidal activity.
• Dilute stock solution 1:100 or 1:10. Don’t use I scrub on open
wounds –damage tissue and ↑ infection.

Iodophors
• Betadine. Aqueous complex of iodine, less bactericidal but
also less irritating. Gram-, gram+.
• Do not require repeated application for optimal
antimicrobial effect.
• Contact time 10 min for max effect.

Hexachlorophene
• Gram+ bacteria. Only effective after days of use once film
deposition on skin, long contact time.
• CNS toxin if absorbed, esp in young. Not used much
anymore.
Quaternary ammonium compounds

• Changes in cell membrane permeability. G+.

• Inactivated by organic debris and soaps. Not recommended.

DEHYDRATION - CONCEPTS AND

ASSESSMENT
Dehydration is one of the most commonest general systemic state,
encountered in majority of the diosders /diseases and Fluid
therapy is the most imporntant therapeutic strategy, not only in
day to day veterinary practice, but also as a cornerstone in
emergency and critical care medicine practice.

Body Fluid Distribution

• The total body water ranges from 55-70% of the lean body
weight. In the average adult dog the total body water is about
60%. Thus in a 15 Kg dog the total body water will equal
about 9 liters.
• Total body water is distributed into 2 main compartments:
o The intracellular fluid space, and
o The extracellular fluid space.
• About 66% of the total body water resides in the intracellular
fluid space and 33% in the extracellular fluid space.
• The extracellular fluid space is further subdivided into two
fluid containing compartments:
o The interstitial space (containing 75% of the
extracellular fluid space water) and
o The intravascular space (containing 25% of the
extracellular fluid space water).
 • When water is added to one compartment, it distributes
evenly across the total body water and the amount of volume
added to any given compartment, is proportional to its
fractional representation of the total body water. Thus, if one
liter of free water is placed in the intravascular space, there
will be a minimal increase in the intravascular volume after
equilibrium takes place. In fact, approximately 30 minutes
after rapid volume infusion of free water, only 1/10th of the
volume infused remains in the intravascular space.
FLUID MOVEMENT

• A. Into and out of cells. Determined by concentration

gradient in freely diffusible substances (ie: urea)
o Tonicity dictates water movement in “nonpermeable”
substances. (ie: Na/K, proteins)
• B. Between vascular and interstitial spaces
• C. Governed by starling forces
• D. Influenced by integrity of capillary endothelium
(inflammation causes increased vascular permeability).
• E. Forces favoring fluid into vessel (reabsorbtion)
o Tissue hydrostatic pressure
o Plasma oncotic pressure
• F. Forces favoring fluid out of vessel (filtration)
o Vascular hydrostatic pressure
o Tissue oncotic pressure
• G. Net: Filtration at arteriolar end of capillary, reabsorption
at venule end (also some fluid goes into lymphatic system).

DETERMINING THE PERCENTAGE OF DEHYDRATION

• The percentage of dehydration can be subjectively estimated

based on the presence and degree of loss of body weight,
mucous membrane dryness, decreased skin turgor, sunken
eyes, and altered mentation. These parameters are largely
 subjective because they can also be affected by decreased
body fat and increased age.

Estimated Physical Examination

Percentage Findings
Dehydration
<5 History of fluid loss but no
findings on physical examination
5 Dry oral mucous membranes but
no panting or pathological
tachycardia
7 Mild to moderate decreased skin
turgor, dry oral mucous
membranes, slight tachycardia,
and normal pulse pressure.
Moderate to marked degree of
decreased skin turgor, dry oral
10
mucous membranes, tachycardia,
and decreased pulse pressure.
12 Marked loss of skin turgor, dry
oral mucous membranes, and
significant signs of shock.

• The more severe stages of dehydration are also accompanied

by signs of hypovolemic shock. Other factors, including
hemorrhage and third spacing of body fluids, can also result
in a decrease in intravascular circulating volume, resulting in
signs of hypovolemia.
• Severe hypovolemia resulting in more than a 15% depletion
of effective circulating volume leads to a transcompartmental
 fluid shift from the interstitial to the intravascular
compartments, which occurs within one hour of fluid loss.6
When fluid loss is so severe that intravascular fluid volume is
affected, hypovolemia can result in tachycardia, prolonged
capillary refill time, decreased urine output, and
hypotension.
• The vascular space is sensitive to changes in the amount of
circulating volume. During states of normovolemia,
baroreceptors in the carotid body and aortic arch sense
vascular wall tension and send pulsatile continuous feedback
via vagal afferent stimuli to decrease heart rate.
• In the early stages of hypovolemic shock, the baroreceptors
sense a decrease in vascular wall stretch or tension and blunt
the tonic vagal stimulation. This allows sympathetic tone to
increase heart rate and contractility in an attempt to
normalize cardiac output.
• Later, decreased blood flow and sodium delivery to receptors
in the juxtaglomerular apparatus activate the renin-
angiotensin-aldosterone axis, stimulating sodium and fluid
retention to replenish intravascular fluid volume.

DEHYDRATION : CORRECTING FLUID

IMBALANCES
CORRECTING FLUID IMBALANCES

• When there are clinical signs of hypovolemic shock,

intravascular fluids must be replaced immediately.
Calculated fluid volumes for patients in shock are 90 ml/kg
for dogs and 44 ml/kg for cats. A simple guideline to follow
in day to day practice is to replace one-fourth of the
calculated fluid volume as rapidly as possible and then
reassess perfusion parameters including heart rate, blood
pressure, capillary refill time, and urine output.
• About 80% of the volume of crystalloid fluid infused will re-
equilibrate and leave the intravascular space within one hour
of administration. A constant-rate infusion of a crystalloid
fluid is recommended to provide continuous fluid support in
patients that are dehydrated and have ongoing losses. In
some cases, the fluid required to restore intravascular and
interstitial volume can cause hemodilution and dilution of
oncotically active plasma proteins, resulting in interstitial
edema formation. In such cases, a combination of a
crystalloid fluid along with a colloid-containing fluid can
help restore oncotic pressure and prevent interstitial edema.
• Once immediate life-threatening fluid deficits are replaced,
provide additional fluid based on the estimated percentage of
dehydration and maintenance needs. Basic dehydration
estimates can be calculated based on the fact that 1 ml water
weighs about 1 g and by using the following formula:
• Body weight in kg × estimated percent dehydration × 1,000
ml/L
• This formula helps to determine the amount of fluid deficit
in liters. A frequent mistake when replenishing fluid deficits
is to arbitrarily multiply a patient's daily water requirement
by a factor of two or three to replenish intravascular and
interstitial deficits. This practice frequently underestimates a
patient's fluid needs and does little to treat volume depletion
and interstitial dehydration. Instead, it is better to use the
formula above and add the result to daily maintenance fluid
requirements and ongoing losses.
• Eighty percent of the calculated fluid deficit can be replaced
in the first 24 hours. More rapid administration of an
animal's estimated fluid deficit can result in diuresis and loss
of the fluid administered. After successfully treating
hypovolemic shock and replacing fluid deficits estimated
based on the percentage of dehydration, we need to
administer only maintenance fluids until the animal can
maintain hydration on its own, provided no signs of
 dehydration or ongoing excessive fluid losses are present. An
objective way to assess whether the fluid volume is adequate
is to evaluate body weight regularly throughout the day.
Acute weight loss is commonly associated with fluid loss and
can be used to determine whether the patient is at risk of
becoming dehydrated again.
• Vomiting results in loss of H2O, H+, Cl-, Na+, K+, and
HCO3-. If vomit is primarily stomach contents, 1o loss is HCl,
H2O.
• Most vomit includes proximal duodenal contents, therefore
HCO3- also lost.
• Conclusion: H2O is consistently lost in vomiting, other
electrolytes/acid base are best assayed.
• Diarrhea results in loss of H2O and electrolytes, resulting in
dehydration, electrolyte depletion/imbalance, acid-base
imbalance, and shock.
• Intestinal contents are basically ECF; also can lose large
amounts of K+.
• Fluid losses from diarrhea can be particularly severe in the
cow and horse (salmonellosis, neonatal calf diarrhea).
• The primary acid-base disturbance is metabolic acidosis.

Plasma osmolality

• Ratio of body solute to body water.

Effective circulating volume

• Part ECF in the vascular space Depends on SNS, angiotensin

II, and renal sodium excretion.
• Regulates by increasing vasoconstriction, and renal sodium
resorption (RATS).
• Hypovolemia causes activation of RATS. If < 5%, PE is
normal. If 5%, dry mm but no panting. If 7%, decreased skin
turgor, dry mm, mild tachycardia.
 • If 10%, dec skin turgor, tachycardia, dry mm, dec pulse
pressure.
• If > 12%, marked loss of skin turgor, dry mm, shock.
• In mild dehydration, s/c route (isotonic fluids, max. 5 to 10
ml/lb at each injection site).
• Need multiple sites. I/p route is quick, easy but can cause
dyspnea. IV route indicated with dehydration < 7%.

Amount of fluid

• The deficit volume - only 75% to 80% of the deficit should be

replaced during the first 24 hours, as it can worsen
dehydration.
• Total Deficit Replacement Volume (24 hrs) = Deficit
Volume(% dehydration x body weight (lb/kg) x 454/1000 x
0.80) + Maint. Volume

Maintenance volumes

• 2/3 sensible (urine and feces) and 1/3 insensible (panting or

sweating). (30 X BWKg) + 70.
• A 22-lb (10 kg) dog, 7% dehydrated will need - Volume (ml)
required = deficit volume + maintenance volume= [0.07 x 22
lb x 454 x 0.80] + [(10 x 30) + 70]= [560] + [370] = 930 ml

Continuing losses during the replacement

• Estimate the volume of fluid loss and then double this

estimate.
• How to know if animal is receiving an inadequate fluid
volume.
• If the animal is losing body weight while being given
crystalloid fluids, the animal is likely receiving inadequate
volumes of fluid.
• One group of patients where body weight may fool you is in
animals that are third-spacing fluids (peritonitis,
pyometritis, pleural effusions).
 • In these animals the animal may still be dehydrated but the
body weight may not have changed.
• Additionally, if renal function is adequate, an animal which
is dehydrated will have a urine specific gravity above 1.025.

Clinical signs of overhydration

• Increased serous nasal discharge, followed by chemosis, and

finally pulmonary congestion will be ausculated before
edema ensues.
• Clinically, pulmonary edema is the terminal event of
overhydration!
o non-respiratory acidosis (HCO 3-). may result from:
excess ingestion of H+, decreased elimination of
H+ (renal), increased production of H+ (anaerobic
metabolism), or increased elimination of HCO 3- . It is
the most common acid-base disturbance in dogs, cats,
and horses.
o non-respiratory alkalosis ( HCO 3-) excess ingestion of
HCO3-, excess admin. of HCO3-, excess loss of
H+ (vomiting), or sequestration of H+ (functional
3rd space loss). This acid-base disturbance is common in
the cow (displaced abomasum).
o respiratory acidosis (CO2) hypoventilation. This is
common in the anesthetized horse.
o respiratory alkalosis (CO 2). hyperventilation, pain,
excitement, and artificial ventilation that is excessive.

• Shock therapy with crystalloid fluid: (no head trauma or

pulmonary edema) - Dog – 90 mL/kg/hour. Cat – 60
mL/kg/hour
• Blood transfusion (PCV < 20%): 20 ml/kg fresh whole blood.
15-30 ml/kg Oxyglobin.
• Shock therapy for head trauma or pulmonary contusions:
Hypertonic saline + Hetastarch or dextran. Total dose = 5
ml/kg. Draw up 1/3 volume as 23% saline, 2/3 as colloid.
 • Small volume resuscitation: 5ml/kg IV hetastarch or
dextran. Repeat every 5-10 minutes until HR, pulses and
color improves.
• Crystalloids: Run very fast. Doesn’t stay in vascular space, so
need to give 3-4 times what they have lost.
• Avoid in animals w/ interstitial edema (head trauma,
pulmonary contusions, hypoproteinemia).
• RL - Buffered pH of about 7.4 which is good for acidosis, The
lactate is converted to bicarb for acidosis, Lactate is
metbolized in the liver and has calcium.
• Avoid in cows (alkalosis). Normalsol R - Buffered pH of
about 7.4 which is good for acidosis, The acetate in
normalsol R is converted to bicarb for acidosis.

• Colloids: Help in retention of fluid in the vascular space.

Increases oncotic pressure b/c are not filtered in the
glomerulus. Give smaller volume to restore circulation.

Indications

• Hypoproteinemia, 3rd space loss, Head trauma, pulmonary

edema, leaky capillaries, SIRS.
• Eg. Hetastarch, Dextran 70, Whole blood – if PCV drops
below 20% and TP < 3.5 (1 mL of blood per pound will raise
hematocrit 1%) then give 20 mL/kg,

Oxyglobin

• Same as above at a rate of 15-30 ml/kg, Whole plasma

• If there is evidence of ongoing blood loss into the abdominal
cavity, a snug compressive bandage should be applied, being
careful not to impair respiration.

NEONATAL DIARRHEA
• Diarrhea is the most important disease of neonatal calves
and results in the greatest economic loss due to disease in
this age group in both dairy and beef calves.

• Neonatal diarrhea in calves is a complex, multifactorial

condition with factors such as pathogen exposure, strain
variation, environmental and management conditions,
nutritional state and immune status playing a major role in
production of disease.
• Most of these factors are related to biosecurity in the calf
rearing area and must be considered before developing a
treatment plan for individual cases of the disease.

• Diarrhea is an increase in frequency, volume or fluidity of

bowel movements.
• Fluidity is much less important in cattle than in other
species.
• Cattle normally produce 15-28 Kg of feces per day that is 75-
85% water.
• Mechanisms of diarrhea are one of more of the following:
Malabsorption- decreased or damaged cellular absorptive
area; Osmotic- increased number of particles within the
lumen of the bowel holds water; Secretory- cyclic AMP and
prostaglandin mediate active secretion into the bowel;
Abnormal motility- increased or decreased transit time;
Hydrostatic- increased blood to lumen pressure gradient
such as with cardiac problems or inflammatory bowel
disease.
• Pathogenesis of diarrhea is related to either increased
secretion or decreased absorption.
• The normal bovine GI system absorbs only slightly more
than what is secreted per day.
• Normal secretory amounts are equal to, or exceed the
extracellular fluid amounts.
• Clinical signs of diarrhea are associated with dehydration,
acidosis, depression, failure to nurse, weight loss, cardiac
arrhythmias, sepsis and endotoxemia.
• Dehydration should be scored as a percentage of body weight
and results in profound loss of circulatory volume.
• Acidosis increases vascular resistance, impairs cardiac
function, and blocks catecholamine action.
• Hyperkalemia causes cardiac arrhythmias due to myocardial
potassium imbalances.
• Shock and sepsis occur frequently in severe diarrheic cases.
Signs of sepsis in calves include hypopion, arthritis,
hyperesthesia, rigid neck, fever, and scleral injection.
• Remember that calves are born and raised in a wide diversity
of environments and housing condition, which will affect the
risk of enteric infectious disease.
• Ventilation is inadequate in many cases resulting in high
humidity. Vermin such as flies and rodents are often present
 in high numbers and these vectors can become a significant
factor in disease transmission.
• The most frequently recognized agents causing calf diarrhea
include E. coli, rotavirus, coronavirus, cryptosporidia,
coccidia and Salmonella.
• With the exceptions of Salmonella and specific strains of E.
coli these organisms are ubiquitous in the environment and
present within the GI tract of most healthy, mature cattle
without clinical signs of infection.

SHOCK
• Shock is inadequate cellular respiration due to inadequate
tissue perfusion, due to any number of causes It is defined as
oxygen delivery to the tissue that is insufficient to meet
tissue requirements. This may be due to altered
hemodynamics, such that the circulatory system is unable to
provide adequate pressure to drive perfusion. Or, shock can
occur when tissues are receiving adequate flow, but there is
either not enough oxygen in the blood or the tissues are
unable to extract and utilize the oxygen.
 • Shock is a syndrome of clinical signs that has multiple
underlying causes.
• Classically, the signs that indicate the shock state are:
o Tachycardia (although bradycardia often occurs in cats)
o Tachypnea
o Pale mucous membranes
o Cold extremities
o Poor peripheral pulses
o Altered mentation

Brief Pathophysiology

• Shock is genearlly associated with a decrease in cardiac

output, venous return, and arterial blood pressure (sepsis is
an important exception to this rule).
• The decrease in CO and MABP may lead to a self-
perpetuating cycle and downward spiral. The ¯ CO and ¯
MABP stimulate the sympathetics, baroreceptors, and the
renin-angiotensin system in an attempt to restore MABP.
• Stimulation of these systems results in an heart rate and
intense vasoconstriction. The result of the vasoconstriction
and ¯ MABP is ¯ capillary perfusion resulting in
deterioration of the microcirculation, stasis of blood,
endothelial damage, capillary permeability, development of
microthrombi, and disseminated intravascular coagulation.
The resultant tissue ischemia results in cellular hypoxia and
anaerobic metabolism.
• Anaerobic metabolism is energy inefficient (94% energy loss)
and associated with a lactic acidosis, metabolic acidosis, ¯
cell function, and tissue autolysis. All of these results tend to
further depress cardiac output and blood pressure, thus
worsening the shock cycle.
• The clinically observed effects of vasoconstriction are:
• Decreased blood flow to skin causes cold skin temperature
• Decreased blood flow to splanchnic vasculature leads to GI
hypermotility, followed by stasis and mucosal necrosis ®
 bacterial proliferation, absorption of bacteria, toxins, etc.,
and septic shock
• Decreased renal blood flow results in decreased urine output,
renal ischemia, tubular necrosis
• Decreased blood flow to liver (hepatic artery, portal vein)
leads to anaerobic metabolism and the resultant clostridia,
toxins
• Decreased blood flow to pancreas results in MDF
• Initially, peripheral vascular beds will vasoconstrict to shunt
flow to the "essential organs" (brain and heart). This results
in reduced perfusion and oxygen delivery to the affected
vascular beds.
• In the dog, the GI tract is considered the shock organ since it
takes the brunt of vasoconstriction. Unless shock is rapidly
reversed, tissue beds enter an anaerobic state.
• The products of cellular metabolism build up in tissues,
including lactate, acids, nitric oxide, CO2 and adenosine. As
ATP stores decrease, membrane pumps are unable to
maintain electrochemical gradients, leading to cellular
edema.
• Over time, cellular death will occur, resulting in cell lysis,
inflammation, free radical formation and local activation of
coagulation. As the by-products of cellular metabolism
continue to accumulate, these local factors can eventually
overwhelm the vasoconstriction induced by the sympathetic
nervous system. This results in vasodilation, systemic
hypotension, decompensate, and entry of metabolic
byproducts, cytokines, free radical and activated white blood
cells into systemic circulation.
• Many compensatory mechanisms are induced in the shock
state. The goals of the compensatory mechanisms are to
maintain perfusion to the core organs and restore vascular
volume. These include:
o Mobilization of fluid from the interstitial to
intravascular space. This occurs primarily in shock
 states with low blood volume, especially hypovolemic
shock, but can potentially occur in all shock states.
o Activation of the sympathetic nervous system (SNS).
This results in release of norepinephrine and
epinephrine. There are many effects of the SNS,
including tachycardia, vasoconstriction which may
preferentially affect certain tissue beds, and positive
inotropy. Activation of the SNS also results in retention
of sodium (and therefore water) by the kidneys.
o Activation of the renin-angiotensin-aldosterone system
(RAAS). This results in multiple effects, the most
important (and immediate) of which are retention of
sodium and water by the kidneys, and peripheral
vasoconstriction.
o Release of Antidiuretic hormone (ADH). This results in
retention of water and urine concentration. ADH is also
a powerful vasoconstrictor.

Stages of shock

• The earliest stage of shock is the compensated phase. During

this period of time, compensatory mechanisms are able to
maintain blood flow to the important organs through
peripheral vasoconstriction. Clinical signs are the "classic"
signs of shock, and include pale mucous membranes, poor
pulse quality and cold extremities secondary to
vasoconstriction. Tachycardia is a result of SNS activation, as
the body tries to maintain cardiac output. Blood pressure is
usually normal to high as a result of vasoconstriction.
Remember that the overall goal of compensation is to
maintain blood pressure, and a normal blood pressure does
NOT mean that perfusion is normal.
• Over time, the body is either able to "fix" the blood volume
and return to normal homeostasis, or it goes into
decompensated shock. This phase occurs when local tissue
beds that were vasoconstricted begin to vasodilate.
 Vasodilation leads to pooling of blood and maldistribution of
flow to "non-essential" organs. Clinical signs include grey
mucous membranes, bradycardia, loss of vasomotor tone
leading to hypotension, and severely altered mentation. The
patient is often stuporous to comatose. Ventricular
arrhythmias can be seen on an ECG. It is important to realize
that the progression from compensated to decompensated
shock can occur over minutes to hours depending on the
cause and severity of injury, and that patients can present
anywhere along this spectrum.
• Cats present a special challenge since they do not always
display the classic signs of shock like dogs do. The shocky cat
often presents with bradycardia, hypothermia and
hypotension, even in the early stages of shock. The causes for
this are unknown, although it is documented that cats have
species specific alterations in vascular tone and in vascular
response to injury.
• Treatment of the decompensated shock patient may result in
resolution of clinical signs of shock, but the patient may
decompensate again soon after resuscitation. This is the
result of inflammatory mediators and free radicals being
flushed back into systemic circulation, setting up DIC and
the systemic inflammatory response syndrome, and
eventually multi-organ dysfunction. In short, there was
simply too much tissue damage to fix despite appropriate
shock therapy.

STAGES OF SHOCK
• The earliest stage of shock is the compensated phase. During
this period of time, compensatory mechanisms are able to
maintain blood flow to the important organs through
peripheral vasoconstriction.
• Clinical signs are the "classic" signs of shock, and include
pale mucous membranes, poor pulse quality and cold
 extremities secondary to vasoconstriction. Tachycardia is a
result of SNS activation, as the body tries to maintain cardiac
output. Blood pressure is usually normal to high as a result
of vasoconstriction.
• Remember that the overall goal of compensation is to
maintain blood pressure, and a normal blood pressure does
NOT mean that perfusion is normal.
• Over time, the body is either able to "fix" the blood volume
and return to normal homeostasis, or it goes into
decompensated shock. This phase occurs when local tissue
beds that were vasoconstricted begin to vasodilate.
• Vasodilation leads to pooling of blood and maldistribution of
flow to "non-essential" organs. Clinical signs include grey
mucous membranes, bradycardia, loss of vasomotor tone
leading to hypotension, and severely altered mentation.
• The patient is often stuporous to comatose. Ventricular
arrhythmias can be seen on an ECG. It is important to realize
that the progression from compensated to decompensated
shock can occur over minutes to hours depending on the
cause and severity of injury, and that patients can present
anywhere along this spectrum.
• Cats present a special challenge since they do not always
display the classic signs of shock like dogs do. The shocky cat
often presents with bradycardia, hypothermia and
hypotension, even in the early stages of shock. The causes for
this are unknown, although it is documented that cats have
species specific alterations in vascular tone and in vascular
response to injury.
• Treatment of the decompensated shock patient may result in
resolution of clinical signs of shock, but the patient may
decompensate again soon after resuscitation.
• This is the result of inflammatory mediators and free radicals
being flushed back into systemic circulation, setting up DIC
and the systemic inflammatory response syndrome, and
eventually multi-organ dysfunction. In short, there was
 simply too much tissue damage to fix despite appropriate
shock therapy.

CAUSES AND CLASSIFICATION OF SHOCK

• Multiple classification systems and etiologies of shock have
been described. The classic approach will be used here

Hypovolemic shock

• It is one of the most common etiologies, and means that

blood volume is low. This can be due to two major causes:
hemorrhage (either external or internal) and dehydration.
Dehydration does not always cause hypovolemia, but in
severe cases can lead to it. The categories of hemorrhagic
shock are listed below:
Cardiogenic shock
• It occurs when the heart is unable to put enough blood
forward to maintain perfusion and oxygen delivery.
Examples of cardiogenic shock include dilated
cardiomyopathy, mitral regurgitation and myocardial
failure Obstructive shock
• It occurs when there is an obstruction to flow. Usually this is
an obstruction to venous return, although arterial
obstruction (such as with a saddle thrombus) can also cause
obstructive shock. GDV, pericardial effusion, venous
thrombosis and tension pneumothorax are all causes of
obstructive shock.

Distributive shock

• It is a combination of various types of shock.

(Mal)distributive shock usually occurs as a result of sepsis,
although anaphylaxis can cause it as well. The hallmark of
distributive shock is peripheral vasodilation and vascular
pooling.
 • The patient may have red instead of pale mucous
membranes.
• Patients with septic shock may also have elements of
hypovolemia (from fluid losses or tissue edema), cardiogenic
(from myocardial dysfunction) and obstructive (from DIC)
shocks.

Hypoxemic and anemic shock

• It occurs when there is insufficient oxygen content to meet

tissue needs. This can be that there are not enough red blood
cells to carry the oxygen (anemic), or that the oxygen cannot
get into the blood (hypoxemic). Hypoxemic shock is usually
the result of pulmonary pathology.

Neurogenic shock

• It is a specialized form of distributive shock. Massive

sympathetic release causes severe systemic vasoconstriction,
which results in decreased forward flow and signs of shock
despite adequate blood volume.
• Causes are severe spinal cord or CNS injury, head trauma,
status epilepticus, strangulation and airway obstruction.

Metabolic shock

• It is caused when the cells have sufficient oxygen for normal

metabolism, but are unable to use that oxygen. This is
usually the result of disruption of the Krebs cycle or the
electron transport chain.
• Causes include hypoglycemia, cyanide toxicity or
mitochondrial dysfunction (as occurs with sepsis).

MANAGEMENT OF SHOCK
• Management of shock depends on rapid determination of the
underlying cause. The causes and treatment principles of the
various shock categories are listed below.
o Hypovolemic shock can be treated by replacing blood
volume, either with crystalloids, colloids, or blood
products as indicated. More information on this will be
presented in the next session.
o Cardiogenic shock can be treated by reducing vascular
volume (Furosemide 2mg/kg in dog; 1mg/kg in cats;
PRN), causing peripheral vasodilation if indicated
(nitroglycerin) or improving inotropy (Dobutamine).
o Obstructive shock can only be treated by relieving the
obstruction, whether that is by decompressing the GDV,
tapping the pericardial effusion or the pneumothorax,
or otherwise de-obstructing flow. Vascular loading with
IV fluids can also be of benefit, especially if decreased
regional blood flow is the cause of shock (as occurs with
GDV).
o Distributive shock can be very difficult to diagnose and
treat. If vasodilation and hypotension are present,
treatment with vasopressors (such as dopamine,
vasopressin or norepinephrine infusions) can be
beneficial. These patients may also respond to fluid
loading, which is the first line treatment for septic
shock.
o Anemic or hypoxemic shock can be treated with relative
ease. RBC transfusions or Oxyglobin can be given in
cases of anemia shock (more on this later). Hypoxemic
shock will usually respond to supplemental oxygen,
although mechanical ventilation may be indicated in
more severe cases.
o Neurogenic shock is difficult to treat. The only known
treatment is to treat the underlying cause. This may
include administration of mannitol 1 g/kg IV or
 hypertonic saline in case of head trauma or CNS disease
to reduce intracranial pressure.
o Treatment of metabolic shock is also aimed at
correcting the underlying cause. Give dextrose 0.5g/kg
IV bolus for hypoglycemia, but otherwise treatment is
symptomatic and supportive.
• In Practice scenario, unfortunately, the cause of shock is not
always readily apparent. With the exception of cardiogenic
shock, it is never wrong to try an IV bolus of crystalloids. The
"shock dose" of crystalloids should be given in ¼ - 1/3
aliquots over a 10-15 minute period. If cardiogenic shock is
suspected (heart murmur on auscultation +/- crackles), a
test dose of furosemide can be administered. The test dose
for dogs is 2 mg/kg IV or IM, and for cats is 1 mg/kg IV or
IM. IV fluids should not be routinely administered in
cardiogenic shock.

SUPPORTIVE THERAPY FOR SHOCK

Steroids

• The proposed benefit of steroids include stabilization of

lysosomal membranes, prevention of lipid peroxidation,
scavenging and stabilization of free radicals, and
maintenance of adrenoreceptor function.
• Disadvantages are many, and include alterations of GI blood
flow (especially in an already compromised GI tract),
immunosuppression, vasodilation, and impaired wound
healing. Multiple studies have failed to show any benefit of
high dose steroid administration in any shock state. Low
dose steroid administration (at physiologic doses) may be
beneficial in anaphylactic or septic shock.

Antibiotics
 • They should be administered only when indicated. In dogs,
severe shock states are associated with GI tract
hypoperfusion. This may cause ischemia-induced sloughing
of the mucosal barrier, which allows bacteria to translocate
from the gut lumen to the blood vessels. This often manifests
as raspberry jam-like diarrhea which may have flecks of
mucosa. If bloody diarrhea accompanies shock, broad
spectrum antibiotics may be indicated.

Analgesia

• It is always indicated if shock is accompanied by pain. The

physiologic response to pain is similar to that to shock, in
that SNS activation causes tachycardia and peripheral
vasoconstriction.
• Not administering opioids can make shock resuscitation
more difficult since the physical manifestations of the pain
response can easily be confused with prolonged shock. If the
animal seems painful, opioids should be administered.
• The opioids are typically cardiovascularly sparing and can be
titrated to effect. Hydromorphone, oxymorphone,
buprenorphine, fentanyl or morphine (except in cats) can all
be used with success.
• Butorphanol is generally not sufficient for treatment of
severe pain. NSAIDs should be avoided in the shocky dog
due to alterations in GI blood flow.

MONITORING OF SHOCK
• Shock resuscitation is aimed at improving tissue oxygen
delivery such that homeostasis can be maintained. Therapy
should always be titrated to effect and halted once the
endpoints of resuscitation are achieved.
• Over-zealous fluid administration can cause more harm than
good, and complete shock volumes should not be given
unless necessary. Therefore, it is important to constantly
 monitor endpoints of resuscitation during shock therapy.
These include:

Heart rate

• This is the easiest modality to measure. For the patient in

compensated shock, the heart rate should decrease during
resuscitation. In cats, heart rate should increase to normal if
presented with bradycardia. Unfortunately, ongoing pain or
stress can obscure the response to therapy.

Pulse quality

• This should improve with shock therapy. However, pulse

quality is a relatively imprecise indicator of blood pressure
since pulse pressure is merely the difference between the
systolic and diastolic pressures. A normal pulse quality does
not mean that the animal is fine, but a poor pulse quality
usually indicates ongoing issues.

Mucous membrane color

• MM color reflects the degree of tissue perfusion. If there is

on-going vasoconstriction, MM color will remain poor.
However, vasodilatory conditions such as sepsis may cause
normal color even in the face of severe shock. Additionally,
ongoing pain can contribute to peripheral vasoconstriction
even without shock.

Mental status

• Improvements in mentation often lag behind normalization

of other parameters, so it should not be used as the sole
measure of shock resuscitation. However, improvements in
mentation are expected as shock is resolved. Mental status
can be difficult to asses in patients with CNS disease or head
trauma.
Arterial blood pressure

• This modality is one of the most frequently used to assess

shock states, but the astute clinician also should realize the
limitations of blood pressure measurement.
• A normal blood pressure does not mean that the patient is
fine, and an abnormal blood pressure definitely means that
something is not right. Out of all parameters, blood pressure
is the most protected by compensation for shock.
• Normalization of blood in conjunction with normalization of
heart rate, mucous membrane color and mentation indicate
the shock resuscitation has been successful.

PCV/TS

• These are insensitive indicators of shock resuscitation. Even

with severe blood loss, redistribution of fluid from the
interstitial to intravascular compartments takes time.
• Further changes in PCV will occur with fluid administration,
or PCV can be falsely elevated due to splenic contraction.
PCV can be useful for determining the need for blood
transfusions.

Urine output and specific gravity

• Urine output is an excellent indicator of renal blood flow,

provided that the patient does not have pre-existing renal
disease. The normal urine output for a patient on IV fluids is
1-2 ml/kg/hr.
• The well-hydrated patient should have a urine SG of 1.012-
1.020. Unfortunately, shock states can cause acute renal
failure or impaired concentrated ability, which limit the
usefulness of this as a monitoring tool.
• Additionally, evidence of good renal perfusion does not
necessarily equal normal perfusion in other tissues.

Acid-base balance
 • Shock states are usually associated with metabolic acidosis.
Successful treatment of shock should cause an improvement
in pH and base excess back towards normal. Failure of base
excess to return to normal is associated with a worse
prognosis.

Lactate

• This is a good marker of tissue perfusion, especially in the GI

tract. Lactate is produced by tissues undergoing anaerobic
metabolism. Remember that the measured value is the
balanced between lactate production and clearance.
• Decreased clearance (i.e., liver disease) can cause elevations
in lactate. Additionally, severely underperfused tissue can
have lactate trapped, resulting in falsely low blood
concentrations. Lactate has been shown to be an important
prognostic marker. Failure to reduce lactate concentrations
have been strongly correlated with a worse prognosis for
multiple diseases.
The important point is that multiple parameters should be
assessed to judge response to shock resuscitation. No single
marker has been shown to be strongly correlated with
successful treatment, therefore, the entire patient should be
reassessed frequently (every 10-15 minutes) during the
resuscitation period.

COMMON QUESTIONS
1. Differentiate between septicemia and toxemia.
2. What are the complications of septicemia. Enumerate the
measures used to control toxemia?
3. What is the line of treatment for septicemia?
4. Explain about fluid therapy?
5. What are the mechanisms of diarrhea?
6. Define hyperpnoea,polypnoea and oligopnoea?