COURSE OUTLINE

Welcome to the Clinical Medicine Courses !!!

You are to study one of the fundamental courses in clinical medicine. Clinical
medicine is important in the sense that nearly more than 75% of clinical cases you
see in a hospital practice are medical cases and it requires in-depth physical
examination skills, diagnostic and therapeutic skills and upto date knowledge and
clinical management strategies. Moreover, without a clinical examination skill, you
cannot investigate a clinical case in other clinical areas like gynaecology or surgery.
Therefore this course is of atmost importance to your every day practice in the future.

Instructional Goals

Students will begin identifying and accumulating the specialized knowledge, skills
and resources needed for the practice of Veterinary Medicine. This course examines
the causes and effects of important diseases of food animals and companion animals
in India, with an emphasis on ruminant animal medicine. Elements of physiology,
pathology, epidemiology, microbiology, nutrition, and production management are
integrated into a health management approach emphasizing disease prevention. The
course is directed at undergraduate clinical students with interest in, and knowledge
of, farm animal medicine and companion animal medicine.

Course Objectives

At the end of the course, students should be able to:

 Describe health and disease in the context of health management

 Describe the association of common diseases with sub-optimal productivity or
welfare
 Identify the relative importance of common diseases of common farm and
companion animals
 At a basic level, explain the risk factors, etiology, clinical signs,
interrelationships, and approaches to clinical and preventive management of
common diseases of common farm and companion animals prevalent in
Indian veterinary practice situations.
 To independently undertake physical examination, diagnostic investigations,
diagnosis and prognosis and clinical management.

Clinical Course Practicals are an important component of your veterinary training.

This is where you develop the clinical skills you will need in practice and the vast
majority of you will work to a greater degree in farm animal practice and a lesser
degree in small animal practice. The Clinical Practicals will be oriented with the
activities of the Teaching Veterinary Hospitals and you would get a thorough
grounding in farm and small animal medicine. The success of the practical learning,
however, depends on your attitude; the more you contribute the more you will learn.
It is worth emphasising that there is a wealth of material, case records etc, for you to
use in the Teaching Veterinary Hospitals and what you get from the clinical
practicals is very much a function of you.
Expectations

 You are expected to be familiar with these guidelines before you start each
clinical practical.
 You should behave as, particularly to clients, an ‘almost veterinarian’ instead
of simply a clinical veterinary student. A clean white coat and appropriate
name badge (stating your name and that you are a veterinary student) are
mandatory. Reasonable personal discretion in your dress is fine but casual
clothes, e.g. jeans, sandals, trainers etc. are NOT acceptable. Our clients’ first
impressions are all important and you must, therefore, appear and behave in a
professional manner at all times.

Equipment Required

 Clean white coat

 Name badge
 Digital thermometer
 Stethoscope
 Scissors (blunt ended preferably curved)
 Watch with second hand
 Pen and note book
 Pen torch and artery forceps

DESIRED LEARNING OUTCOMES

General Objectives

 Professional conduct and appearance.

 Competent history taking and clinical examination.
 Problem orientated approach.
 Record keeping (case reports, lab records, case summaries).
 Communication skills (clients, clinicians, nurses, office staff, fellow students).
 Presentation skills – daily rounds.
 Case diaries of cases seen in hospitals.

Laboratory Objectives

 Perform PCV, TP, & Staining.

 Basic cytology – make and read blood smear and pull slide of needle aspirate,
ear swab slide, rectal scrape slide, skin scrapes and cytology etc.
 Know how to interpret haematology, serum chemistry and urinalysis reports.
 Have some understanding of “special tests” – e.g., indications and
performance of bedside diagnostic tests like white side test, California mastitis
tests, etc.

CLINICAL MEDICINE SPECIFIC OBJECTIVES

Knowledge
We expect you to be familiar with your lecture notes from the preclinically taught
course before you start the clinical practicals and rotations. The clinical practicals
and rotations are an opportunity to apply this knowledge to problem solving in
clinical cases.

 Medical ‘problems’ – be able to discuss the approach to the following

problems:
o Weight loss Pruritus
o Pyrexia of unknown origin Alopecia
o Seizures/syncope Scaling
o Coughing Ulceration and crusting
o Nasal discharge PU/PD
o Ascites Urinary ‘incontinence’
o Vomiting/regurgitation Anaemia
o Diarrhoea Heart murmur
o Ataxia/paresis/paralysis Masses and neoplastic lesions
o NB – this is not an exclusive list
 Be able to decide on appropriate drugs and calculate dosages for infectious
diseases, immune mediated diseases, gastrointestinal, urinary, respiratory,
reproductive, dermatological, endocrine and cardiac disorders. Understand
the concepts of chemotherapy.
 Be able to select an appropriate fluid therapy regime and rate.
 Be able to decide on an appropriate diet/nutritional supplementation, route
and quantity. Understand the use of parenteral and enteral nutrition. d.
Understand basic concepts of and indications for diagnostic imaging
techniques.

Skills

 Be able to carry out:

o Physical examination including neurological, otic and basic
ophthalmological examinations
o Venipuncture: jugular and cephalic (and saphenous)
o Subcutaneous and intramuscular injections
o Venous catheterisation
o Cystocentesis
o Urinary catheterisation
o Rectal examination – recognise normal/abnormal
o Enema administration
 Understand how (or be able to):
o Nasogastric tube placement
o Thoracocentesis and chest drain
o Transtracheal wash
o Joint tap
o CSF collection
o Fine needle aspirate
o Abdominocentesis
o Blood transfusion
 o Perform and read ECG
 Understand the indications for and concepts of:
o Radiology, including contrast studies
o Endoscopy and colonoscopy
o Ultrasound examination
o Know when to refer a medicine patient to surgery
 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 regime.The ‘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

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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

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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
imperceptibl
e 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
spontaneous
ly.

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 hyperthermia.An 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 hyperthermia.No
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 set-point.This
 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 thermostat.When 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 heat.Hyperthermia 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).

TOP
 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)

Intracellular Extracellular
Interstitial ntravascular
Electrolytes Fluid Fluid

Cations - - - -
Sodium 15 147 142 -
Potassium 155 4 5 5
Calcium 2 2.5 - -
Magnesium 27 1 2 -
Anions - - - -
Bicarbonate 10 30 27 -
Chloride 1 114 103 -
Phosphate 100 2 2 -
Sulfate 20 1 1 -
Organic acids 1 7.5 - 5
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 ↑ ADH* →  CT H2O resorption
 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 Findings

Percentage
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 (HCO3-). may result from: excess ingestion of
H+, decreased elimination of H+ (renal), increased production of H+
(anaerobic metabolism), or increased elimination of HCO3- . It is the
most common acid-base disturbance in dogs, cats, and horses.
o non-respiratory alkalosis ( HCO3-) 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 (CO2). 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?
7. Explain the different variations of the color of the mucus membranes and its
significance.
 MODULE-6: DISEASES OF DIGESTIVE SYSTEM-I

Learning objectives

 In this section, discussion will be made on vomiting, regurgitation, simple

indigestion and ruminal parakeratosis

VOMITING
 Forceful ejection of contents of the stomach and the proximal small intestine
through the mouth is called vomiting
 True vomiting occurs in monogastric animals. True vomiting is not a feature
of gastric diseases in horses.
o The strong cardiac sphincter inhibits the release of stomach contents
o The soft palate and epiglottis combine to affect a seal between the oral
and nasal parts of the pharynx. Hence the stomach contents are
discharged through the nasal cavities and not through the mouth in
case of vomiting in horses.

Vomiting

 Coordinated vigorous contraction of abdominal, thoracic and diaphragmatic

muscle with resultant forceful ejection of vomitus from the mouth is called
vomiting
 Nausea: outward sign of nausea include depression, shivering, hiding,
yawning and lip licking. 
 Retching is second phase of vomiting and consists of forceful contractions of
the abdominal muscles and diaphragm occurring with the glottis closed to
produce negative intrathoracic pressure and positive abdominal pressure.
These pressure changes are associated with movement of gastric contents into
a dilated esophagus. 

PATHWAYS OF VOMITING

 When the vomitus passes through the pharyngeal cavity, nasopharynx and

glottis are closed to prevent aspiration.
 Emetic center : Located in medulla oblongata in brain.
 o Receptors located throughout the abdominal viscera. Diseases or
irritation of the gastro intestinal tract, other abdominal organs or
peritoneum  stimulate vomiting through vagal afferent pathways 
o Receptors in kidney, uterus, urinary bladder send afferent
impulses through sympathetic nerves
o Receptors in pharynx, tonsillar fossae  through afferent fibers of the
glassopharyngeal nerve.
o CNS disease through direct extension of inflammatory stimuli,
hydrocephalus or space occupying lesions. CSF increase, cereblral
edema, infection, neoplasia.
o Fear, stress or pain: Stimulation of higher centers in cerebro cortex-
psychogenic vomiting 
o Cyclic vomiting in dog is associated with an autonomic / visceral
epilepsy arising from limbic region.

CLINICAL APPROACH TO VOMITING

Clinical approach

 History: gagging, coughing, regurgitation, dysphagia

 Young unvaccinated animal- check for infectious diseases- parvo/CD
vaccination/ travel/ medical problem/ medication/ NSAID
 Age of the animal - assess– weaning- vascular ring anomaly; projectile-
gastric outflow obstruction
 Breed: GDVin deep chested dogs- Setter boxer, GSD; pyloric stenosis in
brachycephalic breeds- boxer
 Check for Ingestion of toxins/ foreign bodies
 Rule out Systemic diseases/ metabolic diseases, polyuria/ polydipsia, weight
loss- ketoacidosis, renal failure
 Assess vomiting episode: duration frequency, relationship with eating/
drinking, description of the vomitus
 Dietary clue:  type of diet, change- adverse reaction to food.
 Vomitus with fecal odour- low intestinal obstruction or SIBO
 Bile in vomitus- no pyloric obstruction
 Blood in vomitus: fresh bright red or digested blood that has coffee ground
appearance- GI erosion / ulceration.
 Hematemesis- metabolic related ulcers uremia, NSAID, gastric neoplasms.
 Examination of  oral cavity: icteric mm, uremic breath, ulceration or linear
foreign body around the base of the tongue.
 Fever- infectious/ inflammatory process.
 Bradycardia or cardia arrhythmia sign of metabolic disturbance
 Abdomen palpated for distension and tympany (GDV) effusion

Hematology
   Neutrophilia with left shift- sepsis or inflammatory disease -
pyometra                         

General treatment and management of vomiting animal

 To correct / remove the primary cause

 To control vomiting episode- alleviating further loss of fluid and electrolytes
 To correct fluid and electrolyte or acid- base disturbances.
 NPO (Nothing per os) for 24 hrs
 After 12 hrs offer small amount of water or ice cubes
 After 24 hrs if water is tolerated, introduce bland carbohydrate== cooked
rice, lean minced beef, chicken, cottage cheese, baby food. Avoid diet high in
fat/ protein
 Initially split total daily requirement into 3-4 small meals
 Fluid therapy- loss of sodium, potassium chloride; hypokalemia with
metabolic acidosis
 PCV total protein - animal’ s dehydration status
 Anaemia- bleeding GI lesions, CRF
 Lipase/ amylase- pancreatitis - acute vomiting/ pain - plain radiograph are
inconclusive
 Urinalysis: fractional excretion of sodium
 pH of vomitus - regurgitation - alkaline; vomitus- acidic
 ECG- hypoadrenocorticism vomiting is associated with bradycardia and signs
of hypovolemic shock
 Radiography/ Endoscopy/ laparotomy
 Leukopenia (with or without left shift) gram-negative sepsis salmonella/ viral
infection

VOMITUS IN DOG

Frothy vomitus Vomitus with blood Bilious vomiting

 Praying posture Acute vomiting

Dog with Chronic Vomitting Severely emaciated dog

PATHOPHYSIOLOGY
  Other causes
 Physaloptera – lymphocytic, plasmocytic gastritis
 Pythium (fungal), Insidiosum – Pyo granulomatous gastitis
 Helicobacter
 Enterogastric reflex

 DIAGNOSIS

Based on

 History
 Clinical Signs
 X ray
 Ultrasonography

DIFFERENTIAL DIAGNOSIS
 Dietary indiscretion
 Ingested grass materials: grass or house plants
 Chemical irritation or Toxins like  herbicides, cleaning materials, heavy
materials.
 Drugs : Aspirin, NSAID’s, glucocorticoids
 Viral infections : Parvo virus
 Bacterial infections : Helicobacter
 Parasites : Physanoptesa, Ollulanus tricuspis
 Systemic disorder : ureamia, liner diseases, neurological diseases, sepsis
 Gastric / Pyloric Obstruction: -foreign body, neoplasms or polyps.
 Hepatic diseases 
  Renal failure
 Neurologic -spinal cord diseases in dogs receiving corticosteroids.
 Most cell tumours
 Gastrinoma
 Stress

TREATMENT I
Treatment

 NPO. Rest
 Without food and water for atleast 24 hrs
  If vomiting resolves – bland diet
 Double cooked chicked with rice
 Gradually introduce normal diet.
 Balanced electrolyte solution
 Potassium supplements if there is hypokalemia
 Metabolic acidosis
 Antiemeties:- for symptomatic control and prevention of furher fluid and
electrolyte loss

Phenothiazine Derivatives

 Chlorpromazine - 0.5 mg/kg BW s/c, i/, i/v q 6-8 hrs

 Prochlorperazine - 0.5 mg/kg BW s/c, i/, i/v q 6-8 hrs
 Metaclopromide – 0.2 to 0.4 mg/kg BW, oral, i/m. o/c q 8 hrs
 (or) 1-2 mg/kg BW as constant rate infusion q 24 hrs.
 Promotes gastric emptying, increases tone and amplitude of gastric
contraction and relaxation of pylorus.

Serotonin Antagonists

 Ondansetron – 0.1-0.2 mg/kg BW s/c q 8 hrs 

       (or)          - 0.5 mg/kg i/v as a loading dose and

                                  - 0.5 mg/kg i/v q 1 hr as maintenance dose.

TREATMENT
H2 blockers – decreased gastric acid secretion

 Cimetidine – 5-10 mg/kg BW PO. i/v, q 6-8 hrs

 Ranitidine - 2 mg/kg BW PO, i/v, q 8-12 hrs
 Famotidine – 0.5 – 1 mg/kg BW PO, i/v, q 12-24 hrs
 Nizatidine - 2.5 – 5 mg / kg BW PO, q 24 hrs
 Sucralfate
o 1 g total dose for large dogs 
o 0.5 g total dose for small dogs

Proton Pump Inhibitors

 Omeprazole - 0.7-1 mg/kg BW PO, q 12-24 hrs

 Pantaprazole - 0.7 – 1 mg/kg BW PO or i/v, q 24 hrs

Prostaglandin analogues

 Misoprostol - 3-5 mg/kg BW PO, q 6 hrs

  7.5 – 10 mg/kg BW
 Cizapride – 0.25 – 0.5 mg/kg BW PO, q 6-12 hrs
 Tegaserod – 0.05 – 0.1 mg/kg BW PO
 Erythromycin – 0.5-1 mg/kg BW PO, q 8 hrs
 Antacids: Gelusil – 5-10 ml PO, q 4-6 hrs

REGURGITATION
 Regurgitation is the expulsion through the mouth or nasal cavities of feed,
saliva and other substances, which have not yet reached the stomach.
 Regurgitation of rumen contents through the mouth in cattle is abnormal
and is associated with loss of tone of cardia or inflammation of the cardia
 Naso gastric regurgitation or gastric reflux occurs in the horse. Stomach
contents flow into the esophagus and usually into the nasopharynx and nasal
cavities due to distension of the stomach with fluid.
 Gastric reflux in the horse can be elicited by nasogastric intubation.
Spontaneous reflux of stomach contents is indicative of high volume and
high-pressure fluid distension of the stomach.

Causes

 Terminal vomiting in horse with gastric dilatation

 Vomiting in cattle is really regurgitation occurring in
o Third stage milk fever
o Arsenic poisoning
o Poisoning by plants
o Administration of large quantities of fluids into the rumen
o Cud dropping associated with abnormality of the cardia 
 Regurgitation in all diseases causing dysphagia or paralysis of swallowing.

SIMPLE INDIGESTION
Causes 

 Dietary abnormalities of minor degree like

o Indigestible Roughage, particularly when protein intake is low,
o Moldy, overheated and frosted
o Moderate excesses of grain and concentrate intake.
o Prolonged or Heavy oral dosing with antimicrobials
Primary atony

 Dietary abnormalities
 Increase or decrease pH of the contents:
 Accumulation of indigestible food
 Putrefaction of protein Production of toxic amides and amines - histamine

Clinical findings

 Reduction in appetite
 Milk yield is reduced to a lesser extent.
 Mild depression and dullness.
 Rumination ceases and depressed ruminal movements - in frequency and
amplitude
 Rumen larger than normal  with mild abdominal pain and Discomfort
 Moderate tympany with doughy rumen 
 Dry Feces and quantity reduced. 24 hrs later feces are softer and voluminous
and malodorous.
 No systemic reaction. 
 Spontaneously recovery or with simple treatment

Clinical Pathology

 Urine: ketone, SAT and cellulosed digestion test, pH test are done in rumen
fluid.
 DD : Acetonemia, TRP, Acidosis, LDA, RDA, Abomasal volvulus, vagal
indigestion, phytobezoars, secondary ruminal atony
 Treatment
o Most cases recover spontaneously.
o Feeding of good quality palatable hay
o Rumenatorics: containing nux vomica, ginger and tartar emetic in
powder form.
o Parasympathomimetics:  
 Caramylcholine chloride, physostigmine and neostigmine are
used. Neostigmine @ 2.5 mg/45 kg BW used.
 Metoclopromide :  for hypomotility associated with vagal nerve
damage.
 Epsom salts 0.5 to 1.0 kg/ adult cow
 Magnesium hydroxide @ 400g/ adult cow in acidic conditions
 Acetic acid or vinegar 5- 10 l in rumen alkalinity.
o Reconstition of ruminal microflora

RUMINAL PARAKERATOSIS
Parakeratosis of ruminal epithelium

 Caused by lowered pH and increased VFA

 Papillae are enlarged, leathery, dark in color and adhere to form clumps.
 Increase in the thickness of the cornified epithelium especially on the dorsal
surface of rumen about the level of the fluid ruminal contents.

INDIGESTION IN CALVES FED MILK REPLACERS

Ruminal drinkers

 Occurs in veal calf characterized by recurrent ruminal tympany, inappetence,

unthriftiness, and clay like feces.
 After being placed on milk diet and fed with a bucket.

Cause

 Insufficient closure of reticular groove while drinking milk.

 Milk enter rumen decreasing the pH of rumen and increasing lactate
concentration
 Clinical recovery occurs after retuning to normal feeding. eg weaning onto
hay and concentrates.

Clinical signs

 Temperature, Heart rate, Respiratory rate normal.

 Unthrifty calf.
 Increase in size especially in the ventral half of the abdomen with fluid
splashing sound on ballottment.
 Auscultation of LPF reveals fluid splashing sound when calf is drinking.
 Foul greyish white fluid siphoned off the rumen.
 Casein clot.
 Treated by inducing them to suck on the herdsman's fingers while they are
being fed a small quantity of cows' whole milk or Milk replace.
 MODULE-7: DISEASES OF DIGESTIVE SYSTEM-II

Learning objectives

 Under this section, bloat and its management will be discussed.

RUMINAL TYMPANY
 Ruminal tympany is the excessive retention of gases of
fermentation with abnormal distension of the rumen and reticulum. The gas
may be in the free form or persistent foam mixed with the rumen contents.

Types
  Primary bloat/ Frothy bloat : Production of stable foam traps the normal
gases of fermentation in the rumen. There is inhibition of coalescence of the
small gas bubbles and increase in the intra ruminal pressure as eructation do
not occur
 Secondary bloat/ Free gas bloat: due to physical obstruction of oesophagus or
failure of eructation mechanism 

FROTHY BLOAT
Primary ruminal tympany (frothy bloat)

 Inhibition of Coalescence of the small gas bubbles

 Production of stable foam

Pasture bloat

 The vital factor is the frothiness of ruminal contents. The stable dispersion of

feed particles are responsible for the frothiness. There is also slower clearance
of ruminal contents that enhances microbial activity and gas production. 
Soluble leaf protein may contribute to frothiness. 

Feedlot bloat

 Feedlot bloat is due to feeding finely ground grain. High carbohydrate content
increases encapsulated bacteria that produce slimes. The slime entraps the
gases of fermentation. Maximum stability of foam occurs at pH of about 6. 

ETIOLOGY- SECONDARY BLOAT

Free gas bloat

 Physical obstruction to eructation occurs in esophageal obstruction (foreign

body), stenosis of esophagus or pressure outside the esophagus such as
Tuberculous lymphadenitis or bovine viral leucosis,  bronchial lymph node
enlargement or obstruction of cardia)
 Interference with esophageal groove function as  in vagal indigestion or DH,
tetanus or carcinoma, Actinomyces bovis, granulomatous lesion near
esophageal groove papillomata
 EPIDEMIOLOGY
 Lush young and leaves containing high concentration of soluble protein are
dangerous.
 Outbreaks of feedlot bloat are usually of the frothy bloat
 Sporadic: Free gas type and secondary to lesions which cause dysfunction of
eructation.

Bloating forages

 Alfalfa, red clover, white clover, young green pasture with high protein
content.

Non-bloating forages

 Bloat safe forages contain tannins, which bind with soluble proteins and
inhibit microbial digestion
 Grazing very succulent pasture –immature rapidly growing legumes in the
pre bloom stage 

Risks

 Herbage at vegetative to prebud stages of growth

 Liberal administration of urea to pasture, high intake of glucose, calcium and
magnesium and high nitrogen intake.
 Cool temperature delay the maturation and extend the vegetative growth
phase of forage crops and optimize conditions for bloat
 Salivary protein bSP30 is correlated with susceptibility to bloat 

CLINICAL SIGNS - PRIMARY BLOAT

Primary pasture 

 Signs may develop Within 15 minutes after going on to bloat producing

pasture.  The entire abdomen is enlarged with obvious distension of the upper
left para lumbar fossa. Discomfort with the animal may standing and lying
down frequently, kicking at its abdomen and rolling. Dyspea, open mouth
breathing, protrusion of tongue, salivation and extension of the head,
increased respiratory rate are noticed.
 Mild bloat : LPF is distended , no distress, 5-7 cm of skin over the LPF may be
easily grasped and tented
 Moderate bloat: Animal is Anxious and uncomfortable, and the skin over the
LPF is usually taut
 Severe bloat: Distension of both sides of the abdomen, breathing through
 mouth and protusion of tongue. Animals are uncomfortable, anxious and
staggering. Skin is very tense and cannot be grasped and tented.
 Trocarization or passage of stomach tube releases only small amounts of gas.
 Sudden death in some animals

CLINICAL SIGNS - SECONDARY BLOAT

Secondary bloat

 Excess gas as a free gas cap on top of ruminal contents. There is initial
increase in frequency and strength of contraction and later atony. There is
release of large quantities of gas when stomach tube is passed or trocarization
is done. 
 If esophageal obstruction is present the same may be detected while the
stomach tube is passed.
 Marked elevation of heart rate, systolic murmur and dyspea are noticed.

Laboratory findings

 Non specific

Differenial Diagnosis

 Vagus indigestion
 Tetanus
 Carcinoma and papillomata of the esophageal groove and reticulum; 
 Actinobacillosis of the reticulum 

TREATMENT
First aid emergency measures

 Emergency rumenotomy in severe cases with gross ruminal distension,

mouth breathing with protrusion of tongue and staggering. 
 An  incision of about 10-20 cm in length over the LPF through the skin,
abdominal musculature and directly into the rumen.

Trocar and cannula

 2.5 cm in diameter. If trocar is successful in reducing the pressure,

antifoaming agents are used.
 Promotion of saliva: A stick is tied in the mouth like a bit to promote the
 production of excessive saliva
 Drenching of sodium bicarbonate 150-200 g in one liter of water or any non-
toxic oil.
 Stomach tube: Passage of tube -2 cm in diameter in free gas bloat,  Anti
foaming agents can be administered with the tube in rumen. 

Feedlot bloat

 Swellers/ moderate cases of bloat, will resolve if the cattle are made to walk.

 Antifoaming agents: Non-toxic oil, non biodegradable - 250 to 500 ml per
animal is used.
 Detergent such as dioctyl sodium sulfosuccinate.
 Synthetic surfactant like polaxalene at 25-50 g is recommended
 Alcohol ethoxylate are more effective and faster than oil.

PREVENTION AND CONTROL

 Restricting the grazing to 20 minutes at a time Prior feeding of dry scabrous
hay particularly cereal hay and straw
 Choice of forages: Seeding cultivated pastures to grass-legume mixtures is the
most effective.
 In a grass- legume mixture a legume content of 50% is suggested as the
maximum bloat safe level.
 High energy and high protein supplement increases the incidence of bloat.
 Use of condensed tannins (proanthocynanidins) :  @ 5g/kg DM of CT is
necessary to prevent bloat

Antifoaming agents

 Individual drenching: twice daily dose of 60- 120 ml of oil;Method to be

adopted if practical utility is observed under field conditions

Application to flanks

 Types of oil: most vegetable oils, mineral oil and emulsion tallow are effective.
Choice depends on availability and cost.  This procedure is followed in foreign
countries and may be tried in India if feasible.

Synthetic non-ionic surfactant

 Polaxalene: surface-active agent polyoxythylene polyoxypropylene block

polymer effectively used for prevention of legume pasture @ 2g/100 kg BW.
 Alcohol ethoxylate detergents: foam-reducing qualities, better palatability.
Blocks containing 10% alcohol ethoxylate @ 17-19 g daily consumption.

Feedlot bloat
  Roughage in ration: feedlot high level grain rations should contain at least 10-
15% roughage, which is cut or chopped and mixed into a complete feed.

Dietary salt

 4% salt to feedlot has been recommended.

MODULE-8: DISEASES OF DIGESTIVE SYSTEM-III

Learning objectives

 Details about acidosis in cattle, LDA and RDA will be discussed.

RUMINAL LACTACIDOSIS
Etiology

 The sudden ingestion of toxic doses of carbohydrate rich feed such as grain
 Ruminating cattle, sheep susceptible; most common in feedlot cattle
 Animals fed low energy rations
 A gradual change during a period of 3-5 weeks from forage ration to high
energy lactation rations
 Feeding excessive quantities of concentrate and Insufficient forages result in
fiber deficient ration
 Feeding of excessive amounts of rapidly fermentable carbohydrates.
 Due to breakdown in feed mill/ handling facilities
 Accidental ingestion.
 Morbidity 10-50 %.
 Case fatality may be up to 90% in untreated cases and 30-40% in treated
cases.
 Wheat barleycorn grains, Finely Ground Grain are more toxic. Oats and
sorghum grain are least toxic

CLINICAL SIGNS
 Speed of onset of illness varies with the nature of feed, being more rapid With
ground feed than whole grain.
 Severity increases with the amount of Feed taken.
 Within few hours of engorgement: Distended rumen, abdominal discomfort,
Kicking at belly.
  Mild form: anorectic, bright and alert and soft feces and reduced ruminal
movements. Rumination absent and begin to eat normally after 3-4 days.
 Severe form:  within 24- 48 hrs animals become recumbent, staggering and
stand-alone. Anorectic, apathetic, depressed. Grinding of Teeth and do not
drink water,  noticed in sheep, but cattle engorge with water if it is readily
available.
 Depression, dehydration, inactivity, weakness, abdominal distension,  Temp
below normal, increased H/R.  Shallow respiration. Diarrhoea is profuse with
kernels of grain. Dehydration is severe and progressive. Anuria is a common
finding
 Pitched tinkling and gurgling sounds are audible in auscultation. Ruminal
Fluid is milky green to olive brown color and has pungent acid smell.  pH of
rumen is below 5.
 Severely affected animal: Staggering drunken gait and impaired eyesight.
They bump into object and palpebral reflex sluggish. Acute laminitis with
animal lame in all four feet
 Recumbency after 48 hrs. Lie quietly with heads turned into the flank. A
rapid onset of recumbency suggests an unfavorable prognosis. Evidence of
improvement include fall in H/R , rise in temp, return of ruminal movements
and passage of large amount of soft feces.
 Mycotic rumentitis may occur 
 Chronic laminitis for severe months or weeks or abortion in pregnant cattle
 Sub acute ruminal acidosis in dairy cattle; laminitis, intermittent diarrhea,
Sub optimal feed intake, liver abscess, haemoptysis, epistaxis and pulmonary
haemorrhage. Laminitis is characterized by ridges in dorsal hoof wall, sole
ulceration white line lesion, sole hemorrhage end misshapen hooves.

DIAGNOSIS
Clinical pathology

 Ruminal pH less than 5.

 Absence of Ruminal protozoa.
 Gram-negative bacterial flora replaced by Gram-positive bacteria.
 Hematocrit rise from 30-32 to 50- 60 %
 Blood lactate and inorganic phosphate levels increased
 Blood pH and bicarbonate reduced
 Hypocalcaemia due to malabsorption. ( 6- 8 mg/dl)
 Urine pH fall to 5 and concentrated

Necropsy findings

 Acute cases:  Content of rumen and reticulum are thin and porridge like and
have typical odor of fermentation.
 Cornified epithelium is mushy and easily wiped off leaving dark hemorrhagic
 surface beneath. These  are restricted to ventral half of the sacs. Abomasitis,
pronounced thickening, darkening of blood and visceral vein stand out
prominently.
 Fungal hepatitis and ischemic nephrosis are noticed

Differential diagnosis

 Parturient paresis 
 Peracute coliform mastitis
 Acute diffuse peritonitis
 Simple indigestion

TREATMENT
 Correction of ruminal and systemic acidosis and prevention of further lactic
acid production.
 Restoration of fluid and electrolyte loses and maintenance of circulating
blood volume
 Restoration of fore stomach and intestinal motility to normal.

Prevention of further access to feed

 Not providing water for 12- 24 hours orally

 Supply of good quality of palatable hay ½ the quantity of daily ration
 Exercise to promote movement of ingesta through digestive tract.
 After 18- 24 hours those cattle which continue to eat hay may be allowed to
free access of water.

Rumenotomy

 In severe cases (recumbency severe depression, hypothermia, prominent

ruminal distension with fluid, H/R 110-130/mt and pH of 5 or below)

Sodium bicarbonate

 Systemic acidosis is treated with IV solutions of 5% sodium bicarbonate @ 5l

for 450 kg animal over a period of 30 minutes. Followed by 1.3% sodium
bicarbonate at150ml/kg body weight IV over next 6-12 hrs.
 Following rumenotomy, and fluid therapy animal show improved muscular
strength and begin to urinate within one hour and attempt to stand within 6-
12 hrs.

Rumen lavage

 In less severe cases standing depressed H/R 90-100/mt moderate distension

 and pH 5-6. Warm water is pumped until LPF is distended and rumen is
allowed to empty by gravity flow.
 Alkalinizing agents: 500g of Mg hydroxide per 450 kg animal or Ma oxide in
10 litres of warm water pumped into rumen and kneading done.

Ancillary therapy

 Antihistamines for laminitis, NSAID for shock therapy, thiamin or brewer’s

yeast to promote lactic acid metabolism, parasympathomimetic for
stimulation of gut motility. Calcium borogluconate for hypocalcemia.
 Oral tetracycline to control growth of lactic acid producing bacteria .
 Following treatment the animals should begin eating hay by third day and
some ruminal movements should be present, pass large quantities of feces
and maintain hydration.

PREVENTION AND CONTROL

 Gradual period of adaptation

 Small incremental increases in grain
 Usage of dietary buffer: 2% sodium bicarbonate, sodium bentonite or
limestone Or usage of 10% alfalfa hay

Ionophores

 Salinomycin, monensin and lasalocid provides protective effect. Laidlomycin

reduces the severity of acidosis.
 Ionophores alters VFA profile in the rumen and increases the propionate
production
 Decreases the population of S. bovis in rumen
 Clearance of lactate from rumen and increases ruminal pH
 Decreases ruminal methanogenesis, ruminal ammonia and decreaes blood
levels of ketone bodies.

LEFT - SIDE DISPLACEMENT OF THE ABOMASUM

Etioloy

 Multifactorial.
  Hypomotility and gaseous distension of the abomasum- prerequisite for
displacement of abomasum
  Feeding of high levels of concentrate to dairy cattle

Occurrence

 Most commonly in large-sized, high-producing adult dairy cows immediately

after parturition.
 Case fatality : 21% in cows with LDA and diarrhea than in cows with LDA and
normal feces (8%).

LEFT - SIDE DISPLACEMENT OF THE ABOMASUM

Dietary risk factors

 Negative energy balance prepartum, High body condition scores, suboptimal

feed management, prepartum diets containing >1.65 Mcal of NE/kg of DM,
winter and summer seasons, high genetic merit, and low parity hepatic lipido-
sis
 High-level grain feeding
 A crude fiber concentration < 16-17% in the diet of dairy cows 
 Feeding rations high in carbohydrates,
 Inadequate levels of roughage

ANIMAL RISK FACTORS

 Greatest risk at 4-7 years of age.

 Dairy cattle and Female cattle were at a higher risk
 Occurs throughout the year
 Parturition,  atonic or distended abomasum-common precipitating factors
 Concurrent diseases
 Pre-existing subclinical ketosis
 Hypocalcemia  
 Genetic predisposition
 Unusual activity, including jumping

PATHOGENESIS 

 The atonic gas-filled abomasum gets displaced under the rumen and upward
along the left abdominal wall
  The fundus, greater curvature of the abomasum, pylorus and
duodenum, omasum, reticulum and liver are also displaced to varying
degrees. A reduced rumen volume in the immediate postpartum period allows
this displacement to occur.
 Leads to rupture of the attachment of the greater omentum to the abomasum.
 Compression of the abomasum causing a decrease in the volume of the organ
and interference with normal movements.
 Metabolic alkalosis with hypochloremia and hypokalemia
 Secondary ketosis, abomasal ulceration and adhesions may occur

CLINICAL SIGNS
 Inappetence, or anorexia, a marked drop in milk production and varying
degrees of ketosis.
 The left lateral abdomen appears 'slab-sided'
 Temperature, heart rate and respirations are within normal ranges.
 The feces are reduced in volume and softer than normal but diarrhea may
occur.
 Ruminal movements decreased in frequency and intensity
 Rumen pack is palpable in the left paralumbar fossa.
 Rumen sounds not be audible over an area anterior to the fossa .

Other clinical features

 Rectal examination
o A sense of emptiness in the upper right abdomen is appreciated.
o The rumen is usually smaller than expected
o The distended abomasum may palpable to the left of the rumen..
 Anterior displacement of abomasum
o The characteristic LDA pings cannot be elicited over the typical region.
o Normal rumen contractions can be heard in LPF.
o Gurgling sounds may be audible just behind and above the heart and
on both sides of the thorax.
o The distended abomasum can be felt between the reticulum and
diaphragm, if a rumenotomy is done
 Atrial fibrillation
o A paroxysmal atrial fibrillation

Course of LOA

 The course of an LDA is highly variable. -several weeks or even a few months.
 DIAGNOSIS

 Diagnosis is based on clinical signs. It should be diferentiated from

o Simple indigestion
o Primary ketosis
o Traumatic reticuloperitonitis 
o Vagus indigestion
o Fat cow syndrome at parturition

LDA
 TREATMENT
 Right paramedian abomasopexy and right paralumbar fossa omentopexy are
used for correcting left displacement of the        abomasum.

Closed suture techniques

 In the blind suture technique, the precise location of insertion of the sutures
is unknown.
 Complications: peritonitis, cellulitis, abomasal displacement or evisceration,
complete forestomach obstruction, and thrombophelebitis of the
subcutaneous abdominal vein

Roll-and-toggle procedure

 Rolling the cow

 The cow is cast and laid on her back, then rolled vigorously to the right and
the roll stopped abruptly

Treatment of ketosis

 Parenteral dextrose 
 Oral propylene glycol

RIGHT - SIDE DISPLACEMENT OF THE ABOMASUM (RDA)

AND ABOMASAL VOLVULUS (AV)
Etiology

 Atony is the precursor of dilatation and displacement, and consequently

abomasal volvulus.

Occurrence and incidence

 Lactating dairy cows: within the period 3-6 weeks after calving. Calves:
occurs in young calves from a few weeks of age up to 6 months

Risk factors

 Feeding of high levels of grain to high producing dairy cows in early

lactation .
 The risk increased with increasing age,
 Dairy cattle are at a much higher risk than beef cattle. 
  The case fatality rate for abomasal volvulus - 23.5%
 PATHOGENESIS
Dilatation and displacement phase

 Abomasal atony occurs initially, resulting in the accumulation of fluid and gas
in the viscus
 This leads to gradual distension and displacement in a caudal direction on the
right side (dilatation phase).
 There is continuous secretion of hydrochloric acid, sodium chloride, and
potassium into the abomasum. These causes gradual distension and the
secreations do not evacuate into the duodenum.
 Leading to dehydration and metabolic alkalosis with hypochloremia and
hypokalemia.
 Increased luminal pressure cause mucosal injury by local vascular occlusion
and affect the prognosis.
 In complicated cases : hemoconcentration, hypovolemia and dehydration and
marked metabolic alkalosis with a severely distended abomasum.
 Severe and prolonged abomasal volvulus: paradoxic aciduria with metabolic
alkalosis associated with abomasal disease.

Volvulus phase

 The distended abomasum  twists in a clockwise or anticlockwise (viewed from

the right side) direction in a vertical plane around a horizontal axis.
 Degreeof volvulus is of 180-270* causing a  acute obstruction with local
circulatory impairment and ischemic necrosis of the abomasum.
 Sometimes abomasum and omasum are  distended and form a loop with the
cranial part of the duodenum. Pressure and tension damage to the ventral
vagal nerve trunk and to the blood vessels are responsible for the poor
prognosis in severe cases

CLINICAL SIGNS
Dilatation and displacement phase

 History of calving within the last few weeks, inappetence, decreased milk

production; the feces are reduced in amount and are abnormal. 
 Anorexia, depression, dehydration, no interest in feed, increased thirst and
sometimes muscular weakness.
 The temperature is usually normaland the respirations are usually within the
normal range. The heart  rate will vary from normal to 100/min
 The mucous membrances are usually pale and dry.
 The reticulorumen is atonic and the rumen pack feel excessively doughy. The
distended abomasum is detectable as a tense viscus on palpation immediately
behind and below the right costal arch.
 Ballottement of the middle third of the right lateral abdomen immediately
 behind the right costal arch along with simultaneous auscultation reveals
fluid-splashing sounds suggesting a fluid-filled viscus.
 Percussion and simultaneous auscultation over the right middle to upper
third of the abdomen commonly elicits a characteristic high-pitched ping.

Volvulus phase

 The clinical findings more severe than during the dilatation phase.
 The abdomen is visibly distended, depression , weakness and dehydration
 The heart rate is 100-120/min, and respirations are increased
 Recumbency with a grossly distended abdomen and grunting may occur 
 Rectal examination reveals the partially distended abomasum . In the
volvulus phase, the distended tense viscus is usually palpable in the right
abdomen anywhere from the upper to the lower quadrant.
 The feces are usually scant, soft and dark in color. The soft feces must not be
mistaken for diarrhea. 
 Death usually occurs in 48-96 hours from shock and dehydration.
 Rupture of the abomasum may occur and cause sudden death.

Acute abomasal volvulus (adult cattle)

 A sudden onset of abdominal pain with kicking at the abdomen, depression of

the back and crouching.
 The heart rate is usually increased to 100-120/min, the temperature is
subnormal, and there is peripheral circulatory failure.
 Mucous membranes are pale, dry and cool.
 Abdomen is grossly distended on the right side and auscultation and
percussion reveal the tympanitic sounds of a gas-filled viscus.
 Fluid-splashing sounds are audible on percussion.
 Paracentesis of the distended abomasum -large quantities of bloodtinged
fluid with a pH of 2-4.
 The distended abomasum palpated on rectal examination
 The feces are scant, soft become blood-stained or melenic

Acute abomasal volvulus (calves)

 A sudden onset of anorexia, acute abdominal pain with kicking at the belly,
depression of the back, bellowing and straining.
 H/R 120-160/min, the abdomen is distended and tense
 Auscultation and percussion over the right abdomen reveal distinct high-
pitched pings.
 Palpation behind the right costal arch reveals a tense viscus.

CLINICAL PATHOLOGY
Serum biochemistry

 Hemoconcentration, metabolic alkalosis, hypochloremia and hypokalemia.

 The severity of volvulus can be classified according to the amount of fluid in
the abomasum and the concentration of serum chloride and the heart rate:
o Group 1 - abomasum distended principally with gas
o Group 2 - abomasum distended with gas and fluid, and surgical
reduction possible without removal of fluid
o Group 3 - abomasum distended with gas and fluid, 1-29 L of fluid
removed before reduction of abomasum
o Group 4 - abomasum distended with gas and fluid, more than   30 L of
fluid removed before reduction of torsion.
 Cows classified as group 3 or 4 or those having presurgical chloride levels
equal to or below 79 rnEq/L (79 mmollL) or pulse rates equal to or greater
than 100/min have a poor prognosis.

Urinalysis

 Paradoxic aciduria

Hemogram

 The total and differential leukocyte count --a stress reaction in the early
stages, and in the later stages of volvulus there is leukopenia with a neu-
tropenia and degenerative left shift

Abomasocentesis

 Centesis of the distended abomasum will yield large quantities of fluid without
protozoa and a pH of 2-4.
 The fluid may be serosanguineous when volvulus is present.

Prognostic Indicators

 An anion gap of 30 rnEq/L - poor prognosis and more accurate than either
serum chloride or base excess values.
 The surgical and postoperative findings in cattle with abomasal volvulus are
good prognostic indicators of outcome.
 Cattle with omasal-abomasal volvulus have a worse prognosis than those
without omasal involvement.
 Large abomasal fluid volume, venous thrombosis, and blue or black abomasal
color before decompression are all indicative of a poor prognosis.
 Postoperatively decreased gastrointestinal motility is an unfavorable
prognostic sign.
 DIAGNOSIS 
 Diagnosis is based on clinical signs and physical findings. Ultrasonography is
used nowadays to diagnose displacement of abomasum. The condition should
be differentiated from the following:
 Impaction of the abomasum associated with vagus indigestion. Pings are not
present in abomasal impaction.

Abomasal ulceration

 A laparotomy may be required to distinguish between them Subacute

abomasal ulceration with moderate dilatation of the abomasum.
 The presence of melena suggests abomasal ulcers but these may be present as
secondary complications in dilatation and right-side displacement

Cecal torsion

 Distension of the right flank, tympanitic sounds on auscultation and

percussion,
 Cecum can  be palpated on rectal examination, as a long (60-80 cm), usually
easily movable, cylindrical, tense tube (10-20 cm in diameter), with a blind
sac

Fetal hydrops

 Bilateral distension of the lower abdomen and an enlarged gravid uterus

palpable on rectal examination

Chronic or subacute traumatic reticuloperitonitis.

 The feces are usually firm and dry, the abdomen is gaunt and a mild fever
may be present. A laparotomy is necessary to make the diagnosis.
 Abdominocentesis may be useful.

RDA APPROACH
  

PINGS IN RIGHT ABDOMEN

Dilatation and right-side displacement of the abomasum

 Ping is usually audible between the 9th and 12th ribs extending from the
costochondral junction of the ribs to their proximal third aspects.

 Abomasal volvulus:

 Ping is  larger than that of the rightside displacement and extends more
cranially and caudally. The ventral border of the ping area is horizontal
because of the level of fluid within the abomasum

Cecal dilatation:

 Ping is confined to the dorsal paralumbar fossa and caudal one or two
intercostal spaces.

Intestinal obstruction:

 Presence of multiple, small areas of ping varying in pitch and intensity

Dilatation of descending colon and rectum:

 Ping in the right caudal abdomen just ventral to the transverse processes of
the vertebrae 
Pneumoperitoneum:

 Pings audible over a wide area of the dorsal third of the abdomen bilaterally. 

TREATMENT
Medical therapy for mild cases

 Empirical treatment with 500 mL of 25% calcium borogluconate IV.

  Offered good quality hay but no grain for 3-5 days and monitored daily.
 Surgical correction  not be necessary if the appetite and movements of the
alimentary tract return to normal in a few days. The ping in the right
abdomen may gradually become smaller in 2-3 days and eventually
disappear.
 The cow will usually not regain her appetite until the abomasal atony has
been corrected.
 A combination of hyoscine-butyl bromide and dipyrone and fasting followed .

Deflation of distended abomasum in calves

 Gas is removed from a grossly distended (bloated) abomasum of calves as an

emergency measure.
  The calf is placed in dorsal recumbency and the abdomen is punctured with a
16 gauge 12 cm hypodermic needle at the highest point of the distended
abdomen between the umbilicus and the xiphoid.
 fluid therapy is given

Surgical correction

 Right flank laparotomy for drainage of the distended abomasum and

correction of the volvulus is done
 Intensive fluid therapy is preoperatively and for several days postoperatively
to correct the dehydration, metabolic alkalosis and to restore normal
abomasal motility.
 Rumen transplants to restore rumen function

Fluid and electrolyte therapy

 Dehydration, metabolic alkalosis, hypochloremia and hypokalemia ae

present. Balanced electrolyte solutions containing sodium, chloride,
potassium, calcium and a source of glucose are to be given.
 A mixture of 2 L of isotonic saline (0.85%), 1 L of isotonic potassium chloride
(1.1%) and 1 L isotonic dextrose (5%) given at the rate of 4-6 L/hour IV is also
 recommended and reliable.

Acidifying solutions

 Isotonic solutions -potassium chloride and ammonium chloride (KCI 108 g,

NH4Cl 80 g, H20 20 L) will correct the alkalosis. This solution can be given
IV at the rate 20 L over 4 hours to a 450 kg cow. Followed by the use of
balanced electrolyte solutions at the rate of 1 00-150 mL/kg BW over a 24
hour period.

Oral therapy

 A mixture of sodium chloride (50-100 g), potassium chloride (50 g) and

ammonium chloride (50-100 g) is given orally daily postoperatively along
with the parenteral fluids
 MODULE-9: DISEASES OF DIGESTIVE SYSTEM-IV

Learning objectives  

 In this section, enteritis in animals and megaoesophagus in dogs will be

discussed.

ENTERITIS

 Gastric dilatation and volvulus, small intestinal bacterial overgrowth,

megacolon, proctitis and colitis will be discussed under this head

PATHOGENESIS
Mechanism of diarrhea

o Osmotic diarrhoea
o Exudative diarrhoea
o Secretory diarrhoea
o Abnormal intestinal motility

Osmotic diarrhoea

 Substances within the lumen of the intestine increase the osmotic pressure .
 E.g. saline purgatives, overfeeding indigestible feeds and disaccharides
deficiencies. Incomplete digestion and accumulation of large quantities of
undigested material
 Epitheliotropic viruses E.g. TGF virus, rotavirus, and corona virus: selective
destruction of villous absorptive cells, villous atrophy loss of digestive and
absorptive capacities, diarrhoea, crypt hyperplasia and recovery.

Exudative diarrhea

 Acute or chronic inflammation or necrosis of the intestinal mucosa resulting

in increase in fluid production, inflammatory products,  E.g diseases caused
by bacteria, viruses, fungi, protozoa, chemical agents and tumors.
Salmonellosis, swine dysentery, bovine virus diarrhoea and inorganic
poisoning.

Secretory diarrhoea

 A secretory absorptive imbalance results in a large net increase in fluid

 secretion with little structural change in the mucosal cells. The enterotoxin
elaborated by E. coli results in intestinal hypersecretion. The integrity of the
mucosal structure is maintained and the secreted fluid is isotonic electrolyte
rich alkaline and free of exudates.

Abnormal intestinal motility

 Hyperexcitability, convulsions and the stress of unexpected sudden

confinement may result in diarrhea
 Reduced intestinal absorption due to rapid passage of intestinal fluids in an
otherwise normal intestines.

CLINICAL SIGNS
 Major clinical finding is diarrhea.
 Dehydration, abdominal pain, septicemia and toxemia with fever.
 In acute enteritis, feces are soft or fluid in consistency and unpleasant odor.
 Contain blood, fibrinous casts and mucus/ foreign material –sand.
 Color of feces- pale yellow; sometimes frank blood; hematochezia or melena.
 Distribution of the feces on animal’s perineum:

Systemic changes

 Septicaemia, toxaemia and fever .

 Increase in body temperature, dehydration, tachycardia or bradycardia and
arrhythmia.
 Abdominal pain in heavy inorganic metal poisoning and in acute
salmonellosis.
 Increased peristalsis and fluid rushing sounds

Chronic enteritis

 Feces are soft homogenous in consistency,

 Considerable mucus and do not have abnormal odor.
 Progressive weight loss and runting are common.
 Hypoproteinemia and subcutaneous edema.
 In terminal ileitis there is usually chronic progressive weight loss and mild
diarrhea.

CLINICAL PATHOLOGY
Clinical pathology

 Fecal examination -causative bacteria, helminthes, protozoa, viruses, and

chemical agents.
 Necropsy on selected early-untreated cases of acute diarrhea,
 Hemoconcentration, metabolic acidosis, and decreases in plasma bicarbonate,
hyponatremia, hypochloremia and hypokalemia.
 Digestion and absorption tests: for investigation of chronic malabsorptive
conditions
 Intestinal biopsy for definitive diagnosis of lymphosarcoma, granulomatous
enteritis and JD.

TREATMENT
 Removal of the causative agent;
 Specific treatment - intestinal helminthiasis with anthelmintics,
antiprotozoan agents against diseases like coccidiosis and antimicrobial
agents against bacterial enteritis.

Antimicrobials:

 Orally or parenterally or both. Oral preparation should not be used for more

than 3 days to avoid superinfection.
 Mass medication for the treatment of outbreaks of specific infectious
enteritis.
 If the cause is dietary, the feed should be removed until the animal has fully
recovered.

 Intestinal protectants and adsorbents:

 Kaolin and pectin mixtures

Antidiarrheal drug: antimotility drugs

Antisecretory drug: treatment of hypersecretory activity of enterotoxin. Loperamide

hydrochloride. Anti secretory drugs include chlorpromazine, opiates atropine and
prostaglandin inhibitors. Loperamide should not be given in cats.

Control

 Reduce infection pressure

 Ensure adequate non specific resistance by adequate colostrums intake
 Vaccinate for those diseases for which there is an effective vaccine
 Minimize Managemental and environmental stressors.
 MEGAESOPHAGUS 

 Megaesophagus refers to esophageal dilation and hypomotility.

 It can be a primary disorder or secondary to esophageal obstruction or
neuromuscular dysfunction.

Causes

 Congenital idiopathic megaesophagus

 Esophageal obstruction—esophageal foreign body, stricture, neoplasia,
granuloma, vascular ring anomalies (e.g., persistent right aortic arch),
periesophageal compression
 Neurologic and neuromuscular diseases—myasthenia gravis (focal or
generalized), polymyositis (including systemic lupus erythematosus [SLE]),
polyneuritis/polyradiculoneuritis, botulism, dysautonomia, central nervous
system (CNS) disorders, degenerative, infectious/inflammatory, neoplasia,
traumatic disorders of the brainstem and spinal cord, bilateral vagal damage.
 Miscellaneous—esophagitis, hypothyroidism, hypoadrenocorticism, thymoma
(with secondarily acquired myasthenia gravis), toxicosis (lead, thallium,
acetylcholinesterase inhibitors)

PATHOPHYSIOLOGY

 Esophageal motility is decreased or absent,

 Resulting in accumulation and retention of food and liquid in the esophagus.
 Reflex esophageal motility begins when food stimulates sensory afferents in
the esophageal mucosa, which then sends afferent messages to the brainstem
swallowing center via the vagus nerve.
 Efferent messages from lower motor neurons in the nucleus ambiguus travel
via the vagus to stimulate contraction of esophageal striated and smooth
muscle.
 Lesions anywhere along this pathway, including the myoneural junction, may
result in esophageal hypomotility and distention.

 Hereditary in wire-haired fox terriers and miniature schnauzers

 Familial predispositions reported in the German shepherd, Newfoundland,
Great dane, Irish setter, Sharpei, Pug, Greyhound, and Siamese cats.
 Congenital megaesophagus—signs of regurgitation first appear at weaning
 Acquired forms—reported most often in young adults to middle-aged animals.
 CLINICAL SIGNS
History

 Regurgitation of food and water

 weight loss or poor growth
 hypersalivation and
 a gurgling sound with swallowing
 coughing
 mucopurulent nasal discharge
 dyspnea with concurrent aspiration pneumonia

Clinical findings

 Occasionally normal
 regurgitation
 weight loss
 auscultation of retained fluid and food in the esophagus,
 halitosis
 ptyalism
 bulging of the esophagus at the thoracic inlet
 pain associated with palpation of the cervical esophagus
 respiratory crackles
 tachypnea
 pyrexia
 myalgia
 muscle weakness, muscle atrophy, hyporeflexia
 proprioceptive and postural deficits
 autonomic disorders (mydriasis with loss of pupillary light reflex
 dry nasal and ocular mucous membranes, diarrhea, bradycardia)
 cranial nerve deficits (especially cranial nerves VI, IX, and X)
 paresis or paralysis, and mentation changes.

RADIOGRAPH - MEGAOESOPHAGUS
  

Radiograph: Barium stasis in the oesophagus

DIAGNOSIS
Differential diagnosis
  Obstructive pharyngeal disease (foreign bodies, inflammation, neoplasia,
cricopharyngeal achalasia) and
 palate disorders may produce regurgitation with normal esophageal motility.
 Pharyngeal pain and dysphagia often occur with obstructive pharyngeal
disease.

Laboratory investigation

 No characteristic findings
 Hyponatremia and hyperkalemia suggest hypoadrenocorticism.
 Hypercholesterolemia is usually present with hypothyroidism.
 Acetylcholine receptor antibody titers to screen for acquired myasthenia
gravis
 Antinuclear antibody titers to evaluate for SLE
 ACTH stimulation to evaluate adrenal function
 Free T4/TSH level to evaluate thyroid function
 Blood lead and cholinesterase levels to evaluate for toxicity

Radiograph

 Survey Thoracic Radiographs

o Esophagus dilated with gas, fluid, or ingesta
o The trachea is often displaced ventrally by the distended esophagus.

Other Diagnostic procedures

 Endoscopy—can use to visualize a dilated esophagus, foreign bodies,

neoplasia, and esophagitis;
 Fecal examination for Spirocerca lupi ova

TREATMENT 
 Feeding in upright position (45–90° angle to the floor) and maintaining
position for 10–15 min following feeding
 Feeding a gruel reduces regurgitation
 Patients with severe regurgitation are fed via gastrotomy tube
 There is risk of aspiration pneumonia
 Surgery may be necessary to remove esophageal foreign bodies or neoplasia
or correct vascular ring anomalies
  No drugs are commonly used to treat megaosophagus alone
 Treatment directed at the underlying disease or associated conditions (e.g.,
aspiration pneumonia)
 Sucralfate (0.5–1.0 g/dog PO q8h), H2 blockers (e.g., famotidine 0.5 mg/kg
PO q12–24h in dogs) or omeprazole (0.7 mg/kg PO q24h in dogs) can be used
 if reflux esophagitis is present
 Metoclopramide (0.2–0.5 mg/kg PO q6–8h in dogs)
 Broad-spectrum antibiotics—necessary for patients with aspiration
pneumonia
 Immunosuppressive agents for immune-mediated diseases
 Prednisone and acetylcholinesterase inhibitors (pyridostigmine) are used to
treat myasthenia gravis
 Cisapride (0.1–0.5 mg/kg PO q8–12h in dogs)

MODULE-10: DISEASES OF DIGESTIVE SYSTEM-V

Learning objectives
  Gastric dilatation and volvulus, small intestinal bacterial overgrowth,
megacolon, proctitis and colitis will be discussed under this head

GASTRIC DILATATION AND VOLVULUS (GDV)

 A syndrome of dogs in which the stomach dilates and twists around its central
axis, resulting in complex local and systemic pathologic and physiologic
changes

 Can be due to pyloric outflow obstruction, gastric myoelectric abnormalities,

dynamic movement of the stomach following ingestion of food or water, and
aerophagia.

 Activity following ingestion of large quantities of food or water

 Any intense activity or stress (including hospitalization and surgery)

PATHOPHYSIOLOGY

 Fluid or ingesta accumulates in the stomach (due to a mechanical or

functional obstruction of the gastroesophageal and pyloric orifices)
 Twisting of the stomach may occur without dilation.
 The stomach  twists in a clockwise or counterclockwise direction.
 Direct gastric damage and multiple systemic abnormalities occur secondary to
ischemia and reperfusion injury.
 Acute clinical signs, which include hypovolemic shock and cardiovascular
failure.
 Reperfusion injury

CLINICAL SIGNS
History

 Nonproductive retching
 Ptyalism
 Progressive abdominal distension
 Weakness or collapse
 Depression
  Frequent belching

Clinical Findings

 Tympanic cranial abdomen

 Tachycardia
 Tachypnea
 Rectal body temperature may vary widely.
 Signs of hypovolemic shock

DIAGNOSIS
Differential diagnosis

 Gastric dilation without torsion—due to overdistension, usually from

ingesting excessive quantities of food
 Intestinal volvulus
 sSplenic torsion
 Abdominal effusion or
 Haemorrhage
 Non-GDV conditions 

Laboratory findings

 Expect hemogram abnormalities consistent with acute inflammation and

hemoconcentration/shock
 Electrolyte abnormalities and acid–base alterations are common.
 high urine specific gravity

Imaging

 Abdominal radiography—a “double bubble” compartmentalized stomach is

considered pathognomonic.
 Dorsoventral view—the pylorus may be shifted toward, or located in, the left
cranial abdomen.

Diagnostic procedures

 Abdominocentesis and cytology may help determine if perforation has

occurred.
 TREATMENT

 Shock/fluid therapy ==  isotonic fluids at the rate of 90 mL/kg within the first
30–60 min
 Use of colloid solutions to restore cardiorespiratory function.
 gastric decompression by orogastric intubation
 Decompression by trocarization and indwelling catheters 
 Immediate surgery is indicated in patients unresponsive to cardiorespiratory
stabilization and in all patients following successful stabilization.
 Severely restrict activity prior to surgery and for a minimum of 10–14 days
postsurgery

 Corticosteroids such as dexamethasone sodium phosphate (5 mg/kg slow IV)

or prednisolone sodium succinate (22 mg/kg slow IV
 Cefazolin sodium (20–35 mg/kg IV q8h or every 2 h interoperatively) or
cefoxitin sodium (30 mg/kg IV q6–8h).
 H2-receptor antagonists may ameliorate or prevent gastric ulceration (e.g.,
famotidine 0.5 mg/kg IV or PO q12–24h; ranitidine 1.0 mg/kg IV or PO q12h).

SMALL INTESTINAL BACTERIAL OVERGROWTH (SIBO)

 An increased number of bacteria in the small intestine causes small intestinal

dysfunction
 Almost any bacteria may be responsible
 SIBO differs from colonization of the alimentary tract by known pathogenic
bacteria with virulence factors (i.e., Salmonella spp., Campylobacter jejuni,
etc.) or overgrowth of toxigenic Clostridium perfringens in the colon.

ETIOLOGY

 Idiopathic
 Altered small intestinal anatomy—blind or stagnant loops, partial obstruction
 Exocrine pancreatic insufficiency (EPI)
 Hypochlorhydria or achlorhydria—spontaneous or iatrogenic
 Immunodeficiency and preexisting intestinal disease—suggested, but
unproven
 PATHOPHYSIOLOGY

 When the natural defenses fail and excessive bacteria persist in the upper
small intestine,
 Because the species and numbers of bacteria in the small intestine may vary
between and even within patients, pathophysiology is not consistent.
 Purported mechanisms include deconjugation of bile acids, dehydroxylation
of fatty acids, formation of alcohols, and destruction of brush border enzymes.
 Anaerobic bacteria (e.g., Bacteroides spp. and Clostridium spp.) have been
considered more likely to cause pathology than many aerobic bacteria; SIBO
can cause protein-losing enteropathy.

SIGNS

 Weight loss may occur despite a reasonable appetite—principal sign

 Small bowel diarrhea (e.g., no mucus or blood in the feces, no tenesmus)—
common
 Vomiting and borborygmus—occasional/variable
 May wax and wane or be consistent
 May be evidence of diarrhea
 Intestinal thickening is unexpected unless other infiltrative intestinal disease
is also present.
 Signs typical of infection (i.e., fever, depression) are unexpected.

DIAGNOSIS
Differential diagnosis

EPI - Exocrine pancreatic insufficiency

Malabsorption due to any cause—

 IBD- InflammatoryBowel Disease

 alimentary lymphoma,
 lymphangiectasia,
 dietary intolerance/allergy,
 giardiasis, 
 IBD may mimic and/or be associated with SIBO.
 Intestinal parasites (especially Giardia)
Laboratory investigations

 Hypoalbuminemia—rare;
 Quantitated Culture
o Aerobic and anaerobic bacteria from fasted, upper intestinal fluid—the
“gold standard”

TREATMENT

 Highly digestible, restricted in fat

 Antigen-restricted diets recommended if concurrent dietary
intolerance/allergy is suspected.
 Broad-spectrum, orally administered antibiotics effective against both aerobic
and anaerobic bacteria are preferred.
 Tetracycline (20 mg/kg PO q12h)—good initial choice;
 Tylosin (40–80 mg/kg/day PO divided q12h)
  Amoxicillin (20 mg/kg PO q12h) or amoxcillin with clavulanate        (22
mg/kg PO q12h)—
 Metronidazole (10–15 mg/kg PO q12h)
 Drugs that do not kill anaerobic bacteria (e.g., neomycin) may be less
effective.

MEGACOLON
 A condition of persistent increased large bowel diameter associated with
chronic constipation/obstipation and low-to-absent colonic motility.

ETIOLOGY
1. Idiopathic—cats
2. Mechanical obstruction—pelvic fracture malunion, foreign body or improper
diet, stricture, pseudocoprostasis, prostatic disease, perineal hernia,
neoplasia, anal or rectal atresia
3. Causes of dyschezia—anorectal disease, trauma
4. Metabolic disorders—hypokalemia, severe dehydration
5. Drugs—vincristine, barium, antacids, sucralfate, anticholinergics
6. Neurologic/neuromuscular disease—congenital abnormalities of the caudal
 spine, paraplegia, spinal cord disease, intervertebral disk disease,
dysautonomia, sacral nerve disease, sacral nerve trauma, trauma to colonic
innervation

Risk factors

 Conditions leading to inability to posture or rectoanal pain

 Prior pelvic fractures
 Possible association with low physical activity and obesity
 Perineal hernias

PATHOPHYSIOLOGY

 Acquired megacolon results from chronic retention of fecal material that leads
to colonic absorption of fecal water and solidified fecal concretions.
 Prolonged distension of the colon results in irreversible changes in colonic
motility that leads to colonic inertia.

CLINICAL SIGNS

 Idiopathic megacolon—typically a chronic/recurrent problem; signs often

present for months to years.
 Constipation/obstipation
 Tenesmus with small or no fecal volume
 Hard, dry feces
 Infrequent defecation
 Small amount of diarrhea (often mucoid) may occur after prolonged
tenesmus.
 Weight loss
 Abdominal palpation reveals an enlarged colon with a hard fecal mass.
 Dehydration 

DIAGNOSIS
Differential diagnosis

 Lymphoma,
  Carcinoma,
 Intussusception
 Dysuria/stranguria
 Colitis

Laboratory  investigation

 Elevated packed cell volume, total protein and stress leukogram

 Electrolyte abnormalities
 Urinalysis—to confirm normal renal function in dehydrated animals and to
rule out lower urinary tract disease as a differential diagnosis

Imaging

 Abdominal/pelvic radiographs
 Enlarged, fecal-filled colon on plain abdominal radiographs
 Abdominal ultrasound
 Colonoscopy to rule out mural or intraluminal obstructive lesions

TREATMENT

 Manual evacuation of the colon using warm water enemas, water-soluble jelly,
and gentle extraction of feces with a gloved finger or sponge forceps;
 Most patients require parenteral fluid support to correct dehydration.
 Encourage activity and exercise.
 Many patients require a low-residue-producing diet; bulk-forming fiber diets
can worsen or lead to recurrence of colonic fecal distension.
 A high-fiber diet is occassionally helpful.
 Cisapride, a prokinetic GI drug (dogs, 0.1–0.5 mg/kg PO q8–12h; cats, 2.5–
10.0 mg/cat q8–12h)
 Stool softeners (e.g., lactulose, 1 mL/4.5 kg PO q8–12h to effect)
 Broad-spectrum prophylactic antibiotics

COLITIS AND PROCTITIS 

Definition

 Colitis—inflammation of the colon

 Proctitis—inflammation of the rectum
 ETIOLOGY
 Infectious—Trichuris vulpis, Ancylostoma caninum, Entamoeba histolytica,
Balantidium coli, Giardia spp., Trichomonas spp., Cryptosporidium spp.,
Salmonella spp, Clostridium spp., Campylobacter spp., Yersinia
enterocolitica, Escherichia coli, Prototheca, Histoplasma capsulatum, and
pythiosis/phycomycosis
 Traumatic—foreign body and abrasive material
 Uraemia
 Segmental—secondary to chronic pancreatitis (transverse colitis)
 Allergic—dietary protein and possibly bacterial protein
 Inflammatory/immune—lymphoplasmacytic, eosinophilic, granulomatous,
and histiocytic

PATHOPHYSIOLOGY

 Inflammation of the colon causes accumulation of inflammatory cytokines,

disrupts tight junctions between epithelial cells, stimulates colonic secretion,
stimulates goblet cell secretion of mucus, and disrupts motility.
 These mechanisms reduce the ability of the colon to absorb water and store
feces; which causes frequent diarrhea, often with mucus or blood.

CLINICAL SIGNS

Historical Findings

 Feces vary from semiformed to liquid

 High frequency of defaecation with small fecal volume
 Often demonstrate prolonged tenesmus after defecation
 Chronic diarrhea often with mucus or blood; cats may have formed feces with
hematochezia.
 Vomiting in dogs
 Weight loss is rare.

DIAGNOSIS
Differential diagnosis
  Neoplasia—lymphoma and adenocarcinoma
 Irritable bowel syndrome
 Rectocolonic polyps
 Cecal inversion
 Ileocecocolic intussusception

CBC/Biochemistry/Urinalysis

 Results usually normal; neutrophilia with a left shift is possible; eosinophilia

occasionally observed in eosinophilic colitis, parasitism, and
pythiosis/phycomycosis
 Mild microcytic, hypochromic anemia may occur in some patients with
persistent bleeding.
 Rare hyperglobulinemia in some patients (especially cats) with chronic
disease.

Other laboratory tests

 Examination of fecal floatation, direct fecal smear, bacterial culture, or fungal

culture (Pythium) may reveal an infectious cause.
 Feces may test positive for Clostridium perfringens toxin.

Imaging

 Abdominal radiographs—usually normal

 Barium enema—may reveal mucosal irregularities or filling defects in severely
affected patients, but this procedure is time-consuming and not cost-effective
 Abdominal ultrasonography—may reveal masses, diffuse thickening, or
altered architecture; can perform guided biopsies or fine-needle aspiration

Other diagnostic procedures

 Colonoscopy with biopsy—technique of choice for diagnosis; may see

disappearance of submucosal blood vessels, granular appearance of mucosa,
hyperemia, excessive mucus, ulceration, pinpoint hemorrhage (small
ulcerations), or mass
 Always take multiple biopsy specimens because the extent of mucosal change
does not necessarily reflect severity or absence of disease.

Pathologic findings

 Gross findings as described

 Histopathologic findings depend on the histologic type of colitis—
lymphoplasmacytic, eosinophilic, granulomatous, or histiocytic; hyperplastic
mucosa may be seen with irritable bowel syndrome; various infectious agents
may be seen with special stains.
 TREATMENT
Appropriate health care

 Outpatient medical management unless diarrhea is severe enough to cause

dehydration.

Nursing care

 Give dehydrated patients balanced electrolyte solution with potassium,

intravenously, subcutaneously, or orally.

Diet

 Patients with acute colitis can be fasted for 24–48 h.

 Try a hypoallergenic diet in patients with inflammatory colitis; use a
commercial or home-prepared diet that contains a protein to which the dog
or cat has not been exposed.
 Fiber supplementation with poorly fermented fiber (e.g., bran and a
-cellulose) is recommended to increase fecal bulk, improve colonic muscle
contractility, and bind fecal water to produce formed feces.
 Some fermentable fiber (e.g., psyllium or a diet containing beet pulp or
fructooligosaccharides) may be beneficial—short-chain fatty acids produced
by fermentation may help the colon heal and restore normal colonic bacterial
flora.

Client education

 Treatment may be intermittent and long-term in patients with

inflammatory/immune colitis, and repeated recurrence is seen in some cases,
especially those with the histiocytic and granulomatous forms.
 Granulomatous and histiocytic colitis, pythiosis/phycomycosis, and
protothecal colitis respond poorly to medical treatment; surgery may be
necessary.

Surgical considerations

 Segments of colon severely affected by fibrosis from chronic inflammation

and subsequent stricture formation may need surgical excision, especially in
patients with the granulomatous form of the disease; cecal inversion,
ileocecocolic intussusception require surgical intervention;
pythiosis/phycomycosis often requires surgical excision or debulking.

Medications - Drugs of choice

 Antimicrobial Drugs
o Trichuris, Ancylostoma , and Giardia—fenbendazole (50 mg/kg PO
q24h for 3 days, repeat in 3 months)
 o Entamoeba, Balantidium, Giardia , and Trichomonas—metronidazole
(25 mg/kg PO q12h for 5–7 days)
o Salmonella —treatment is controversial because a carrier state can be
induced; in patients with systemic involvement, choose the antibiotic
on the basis of bacterial culture and sensitivity testing (e.g.,
enrofloxacin, chloramphenicol, or trimethoprim-sulfa).
o Clostridium —metronidazole (10–15 mg/kg PO q12h for 5–14 days) or
tylosin (10–15 mg/kg PO q12h for 7 days)
o Campylobacter —erythromycin (30–40 mg/kg PO q24h for 5 days) or
tylosin (45 mg/kg PO q24h for 5 days)
o Yersinia and E. coli—choose the drug on the basis of bacterial culture
and sensitivity testing
o Prototheca —no known treatment
o Histoplasma —itraconazole (dogs, 5 mg/kg PO q24h; cats, 5 mg/kg PO
q12 h; several months of therapy is necessary); amphotericin B (0.25–
0.5 mg/kg slow IV q48h up to cumulative dose of 4–8 mg/kg) in
advanced cases
o Pythiosis/phycomycosis—ABLC (dilute in 5% dextrose to 1 mg/mL,
give 3 mg/kg IV Monday-Wednesday-Friday for 9 treatments)
 Antiinflammatory and Immunosuppressive Drugs for Inflammatory/Immune
Colitis
o Sulfasalazine (dogs, 25–40 mg/kg PO q8h for 2–4 weeks; cats, 20
mg/kg PO q12h for 2 weeks)
o Corticosteroids—prednisone (dogs, 1–2 mg/kg PO q24h; cats, 2–4
mg/kg PO q24h; taper dosage slowly over 4–6 months once clinical
remission is achieved)
o Azathioprine (dogs, 1 mg/kg PO q24h for 2 weeks followed by
alternate-day administration; cats, 0.3 mg/kg PO q24h for 3–4
months)
o Sulfasalazine—drug of choice for plasmacytic lymphocytic colitis
o Prednisone and azathioprine are indicated only in eosinophilic colitis
and severe plasmacytic lymphocytic colitis that does not respond to
sulfasalazine
o Reexamine the diagnosis carefully in dogs that do not respond to
sulfasalazine treatment in 4 weeks; the need for chronic maintenance
therapy means that an underlying cause (e.g., C. perfringens infection)
may have been missed.
 Motility Modifiers (Symptomatic Relief Only)
o Loperamide (0.1 mg/kg PO q8–12h)
o Diphenoxylate (0.1–0.2 mg/kg PO q8h)
o Paregoric (0.06 mg/kg PO q8–12h)
o Propantheline bromide (0.25–0.5 mg/kg PO q8h) if colonic spasm is
contributing to clinical signs