M Shivkumar PDF

HISTORY OF VETERINARY MEDICINE
Veterinary medicine is as old as recorded history. Veterinary practices of some sort are,
undoubtedly as old as civilization itself. Ancient India has supplied the most concrete
identification of veterinary art is antiquity. Hindu mythology attributed the origin of medicine to
Brahma as Egyptian did to Imhotep and Greek to Appollow. In vedic period (1800-1200 BC),
Bramha via human mediator created the Vedas as an ethical guide to the world. Some of the
Vedas contain first treaties on the medicine of man and beasts.
Hippocrates (5th century BC), the father of medicine forwarded the theory that the disease is
a reflection of body humours. He thus profounded the theory of humoral pathology.
There are many old original and authentic authors on Indian veterinary science. Large
information is contained in their writings. Among such authors the names of Salihotra,
Palakapya, Rajaputra, Vaisampayana, Vyasa, Nakula , Sahadeva, Garga, Vatsya, Manu etc are
well recognized.
Among the authors of later stages come Jayadeva, king Indusena, Someswara, Vahada,
Basavamantri, poet Rudradeva, king Bhoja etc…. every one of them contributed a valuable book
on veterinary science but many of these works are now lost either in part or full. However,
portion of a few of these manuscripts are still available in libraries where old palm leaf
manuscripts are preserved.
Specialization was characteristic in ancient India and it is evident from the fact that author of
Veda on elephants is identified as Palakapya and that of horses as Salihotra is believed to be the
foremost of all Indian authors of veterinary science. His work on horses is very comprehensive.
It is presented in 8 parts (16,000 slokas in 120 chapters) dealing with their breeding, training,
feeding, watering, stabling, grooming and their effective treatment. Next in importance is
Palakapya, the first and the most ancient author on the sciences dealing with health and diseases
of elephants.
Nakula, one of the pandavas, is said to have written a book on horses called Asvachikitsa.
His brother Sahadeva, an authority on cattle and their disease, is understood to have written a
book called Goshastra .
Dr.M.Shivakumar Page 1
Systemic veterinary education
In France, the immense devastation caused by Rinderpest in 1710-1714 paved the way
for the establishment of the first modern veterinary school of the world in 1762 at Lyons. Its
graduates in turn became the nucleus of the faculty of the new veterinary schools, which were
established at Alford in 1766 and later on in Vienna, Berlin, Hanover, Munich, Copenhagen and
eventually in all countries. Dr.Benjamin Rush, the famous American physician was the pioneer
to augment the concept of veterinary education in USA in 1806.
In India, the first army veterinary school was set up in 1862 at Poona with a course of one
year duration. To produce efficient veterinarians, the first veterinary college was set up at
Babugarh in 1877. Later on, veterinary colleges were established at Lahore in 1882, Bombay in
1866, Madras and Calcutta in 1893 and so on.
Thereafter, with recommendation of the joint Indo-American team in 1955, a proposal for the
establishment of agricultural universities was made in 1958, clubbing Veterinary and Agriculture
sciences under one umbrella. The first agricultural university came into existence in Panthnagar
in U.P (now in Uttarakhand).
Following the establishment of agriculture Universities, veterinary and animal sciences

education got the boost through the assistance of ICAR. Today there are 37 veterinary colleges in
India. The first veterinary university known as TANUVAS was established on 20 September
1989 at Chennai. Next to be established were west Bengal University of animal and fisheries
sciences, Belgachia at Calcutta, Maharashtra Animal &Fisheries Sciences University at Nagpur,
and Pandit Deen Dayal Upadyay University of veterinary sciences at Mathura & KVAFSU
Bidar.
Veterinary medicine deals with the ailments of animals that do not, as a whole call for
manipulatory interference or employment of surgical methods. It has 2 aspects viz,
1. Theory of medicine: deals with principles on which a disease acts and produces various
effects. It also explains the therapeutics by which a disease can be cured, controlled &
prevented.
2. Practice of medicine: consist of adoption of these principles to the treatment and
prevention of diseases in order to relieve pain and suffering in animals.
Principles without practice are useless, whereas practice without principles would be
dangerous and would almost amount to quackery.
Therefore the main objective of veterinary medicine is to restore the health of the animal.
Diagnosis
The clinical diagnosis is a systematic way enables the vet to recognize an ailing animal
from a healthy animal. Obviously an important requisite is complete familiarity with states of
health and a sound knowledge of anatomy, Physiology, Pathology and behavior of all spp. The
presence of disease is revealed by certain changes in the structure of an organ or tissue and/or its
function, as well as in the behavior of whole living organism. Such changes are described as
clinical signs and the process of deducing the nature of disease from them is the diagnosis.
Thus, diagnosis is an art of recognizing a disease and of distinguishing it from other

diseases with help of externally visible or otherwise appreciable changes in the condition of an
animal or its organs. In other words diagnosis is the determination of the nature of the disease.
Diagnosis consist of 3 parts
1. Symptoms of disease – bloat -accumulation of gas, distended abdomen

2. Disease organ
3. Character of the disease and name
Terminologies: classification of diagnosis
Symptomatic diagnosis;
Based on the prominent clinical signs, but the site and course of the primary abnormality are
unknown, the diagnosis is said to be symptomatic.
E.g.; jaundice, colic or abdominal pain in horses and dogs
Tentative diagnosis
If a disease is not recognizable with certainty, the diagnosis is a tentative one. Often an
absolute diagnosis cannot be made at once. So, tentative diagnosis is made on the basis of
available information immediately but subject to change.
That is we have to write the name of the disease.
Direct diagnosis
When a disease is clearly recognized by observing structural lesions or pathognomonic

lesions directly, it is direct or definitive diagnosis. Direct diagnosis includes physical diagnosis,
that is, diagnosis through inspection, palpation, percussion & auscultation.
Confirmatory diagnosis
It denotes the actual disease condition of an animal, diagnosed through clinical, clinic-
pathological and immunological investigation.
Snapshot diagnosis
It is a diagnosis that is declared at the very approach of a patient at a glance. That is, just
by having a look at the case. Majority of the times this type of diagnosis depend on,
1. Experience of clinician
2. His skills and
3. Some important clinical signs of specific disease
Example:
a) Severe brisket oedema – suspected for TRP

b) Enlargement of parotid lymph nodes –Tropical Theileriasis
c) Snoring disease- nasal schistomiasis
d) Patella fixation- dragging disease
e) BQ- crepitation of heavy muscles
Snapshot diagnosis may be biased and liable to the erroneous.
E.g. A cow that is paretic shortly after calving may not have parturient paresis but septic
metritis resembling milk fever.
Test therapy diagnosis
When the diagnosis of the disease depends on the response of the animal to a particular
drug or medicine, it is said to be test therapy diagnosis.
E.g. polioencephalo malacia in calves or sheep can be diagnosed by the favorable response to
i.v administration of thiamin hydrochloride within few hours.
Exclusion diagnosis:
It is the determining of disease by excluding all other diseases.
Laboratory diagnosis;
It denotes the diagnosis of disease through clinical pathology on the basis of examination of
stool, urine, blood, milk etc….
Herd diagnosis;
In some cases a disease affects whole herd resulting in considerable loses.
Eg; loss of production, decreased work efficiency, death of the animals and inability to
attain/gain weight
The herd diagnosis is made by following principles
a) Complete clinical examination of affected animal showing pronounced/clinical signs.

b) Investigating the environment in which the animals are kept grazing, posture,
condition, feed offered and drinking water provided.
c) PM examination of dead animal
d) If dead animal is not available, then seriously ill animal is sacrificed and PM
examination is done for rapid diagnosis.
e) Dispatch of sample for specific laboratory investigation.
Difficulties faced by veterinarian in making confirmatory diagnosis when compared to humans
are,
 His animal patient unlike human patient cannot express its subjective feelings. He has to
depend on his own observation.
 Owners / attendants may not reveal the correct picture of illness. Very often they try to
mask the actual history; it makes the task of diagnosis more troublesome.
 Non co-operation of the animal patient. E.g.; ruminal motility has to be checked but if
animal is not cooperating then it is very difficult for diagnosis.
 Various species of animals with their different structures and functions of body systems
makes the process of diagnosis more complicated
 A wide variety of variation in normal physiology (temperature, pulse, respiration rate
etc…) in different species of animals with distinct behavior of them makes the task of
diagnosis more cumbersome than medical clinician.
Branches of veterinary medicine
1) Preventive veterinary medicine

Is that branch of veterinary medicine which ensures measures to maintain the
health when the disease is imminent. It deals with all measures to control and
prevent animal diseases.
2) Clinical veterinary medicine

Also called as bed side medicine/internal medicine/curative medicine
Definition; Clinical veterinary medicine is that branch which cover the art of making the
correct diagnosis and extends the remedial and curative measures against disease of
animals .
The veterinarian who deals with this branch is referred to as physician/internist
Veterinary clinical medicine can be sub classified as
 Cardiology
 Neurology
 Nephrology
 Gastro-enterology etc…
Internee:
Veterinary graduate undergoing 6 month internship
Disease:
Any deviation from normal physical, physiological and mental state of affairs.
Dis + ease (comfort)
It indicates the inability of person/ animal to perform normal physiological functions though
nutrition and environmental factors are maintained at optimum level.
Opportunity potentiality of pathogen X Virulence X Stress

Disease=
Resistance of the animal
CLASSIFICATION OF DISEASE
1) According to mode of origin or genesis
a) Hereditary/genetic: here genome is responsible for the disease. These are

transmitted by either sire or dam to the offspring because of genetic
predisposition.
Example:
 Haemophilia
 Diabetes mellitus
 Colour blindness
 Epilepsy
 Broken wind in horse – tracheal ring defect
b) Congenital: these are acquired during the intra uterine life. These occur during
organogenesis.
Example
 Atresia ani
 Cleft palate
 Congenital brucellosis
 Tuberculosis
c) Acquired; these are acquired after birth .these are contracted during entire life
span of the animal.
Example
 Senile cataract
 Acquired hydrocephalus
2) Based on system involved

I. Localized; clinical changes attributable to a disease is prominent and
confined to a particular spot or organ.
Eg; glossitis, abscess, stomatitis etc…
II. Generalized; whole system is involved; all parts of body may be
involved.
Eg; toxemia, septicemia etc….
3) According to changes in the organ

a) Structural / organic disease;
Disease which brings about pathological changes in the structure of any organ.
e.g.; pericarditis, nephritis, rickets, osteomalacia etc…
b) Functional disease;
Diseases which affects functional efficacy of any organ without altering
structural component of it.
Eg; idiopathic epilepsy, arrhythmia
4) According to specific cause;
a) Specific disease; diseases which have got definite identity and are produced by
specific pathogen or factor.
i. Contagious
ii. Infectious
Contagious; contagion – pollution by touching
Here the disease spread by intimate contact with the diseased animal
Eg; RP, FMD, fungal infections
Infectious; infecire – to put into
Disease is caused by living infecting organism
Eg: viral disease, bacterial disease, parasitic & mycotic disease.
5) According to The mode of infection;

Primary, secondary and intercurrent disease
A) Primary disease (principal disease)

It indicates those diseases which originates independently and are not influenced by another
disease
e.g. canine distemper, rabies, milk fever, ketosis …
B) Secondary disease
It indicates those diseases which supervene out of already prevailing primary disease.
Superimposed secondary bacterial diseases are very common outcome of primary viral diseases.
Secondary pneumonia is very common after viral diseases.
Eg: kennel cough due to B.bronchoseptica is a complication seen in canine distemper.
Secondary ketosis seen in abomasal displacement and TRP
C) Intercurrent disease
This occurs as a sequale to primary disease.
Eg: Chorea, a neurological complication of canine distemper, where there is continuous
twitching of some group of animals.
Panting (panters)- especially in exotic and cross breed cows after FMD
Hypertrichosis – overgrowth of hairs, hoof is noticed in FMD recovered Animals.
6) According To clinical manifestation (intensity )

Peracute, acute, subacute, chronic, carrier….
Peracute; duration of the disease is shorter than acute with a very severe course.
Illness lasts for few hours to 48 hours.
e.g. peracute mastitis, peracute HS, Anthrax etc…
a) Acute; this typeof disease is charecterised by a sudden onset and comparatively
short course with severe manifestations. Generally illness prevails for 3-14 days..
e.g.FMD, RP, Anthrax
b) Subacute; onset and seviarity is lesser than acute one. Usually it has a course of 2-
4 weeks
Eg: sub acute mastitis
c) Chronic; disease which has got a protracted course. Though the disease is not
severe in character but the long run may terminate fatally. Illness over 4 weeks is
considered as chronic disease.
Eg: TB, para TB, Brucellosis..
e) Carrier; it is a form of inter relationship between host and the agent without clinical
manifestation of the disease.
Eg ; Trypanosomiasis or surra in cattle, blue tongue in cattle, rabies in bats etc…..
7) Based on the spread of the disease;

a) Sporadic; disease which affects a single animal and shows no tendency to spread
within the herd.
Eg ; sporadic bovine encephalomyelitis
b) Enzootic; it denotes an outbreak of disease among animals in a definite area or
particular district.
Eg; enzootic haematuria in cattle, anthrax
c) Epizootic; disease which affects a large population of animals in large areas.
Eg ; RP, FMD
d) Endemic; disease which is normally maintained in animals.
e) Panzootic; when epidemic reaches on unusually large size in some country or spreads
over many countries.
Eg ; influenza
8) According to the place of origin;

a) Indigenous ; disease which are prevalent as native one
Eg; TB, filariosis
b) Exotic diseases; diseases which have been acquired from foreign countries.
Eg; African horse sickness
c) Emerging disease; disease which are not in existence but may be introduced at any
time.
Eg; louping ill in sheep, bird flu
9) According to the deficiency;

a) Defeciency diseases – eg; hypovitaminosis
b) Nutritional disease – eg; hypocalcemia
10) According to the physiological turnover

a) Metabolic diseases – eg; milk fever, hypomagnesemic tetany
b) Production diseases – eg; fatty cow syndrome
c) Endocrine diseases – eg; dibetes mellitus
Aetiology
Aetio – cause, logus- science
Cause of the disease is called aetiology. It refers to yhe knowledge regarding actual
precipitating factors responsible for eliciting the disease process.
Classification
1. Intrinsic
2. Extrinsic – a) infective agent b) Non infective agent
2. Psychosomatic
1) Intrinsic; self-generated
Eg ; hereditary diseases which are transmitted through genes
2) Extrinsic; which are derived from outside.

Infectious; bacteria, fungi, virus, protozoa, helminthes, rickettsia
Noninfectious; diet related nutritional deficiency, trauma, stress, radiation induced
hazards.
3) Psychosomatic; here the cause is psychosomatic which has got direct relationship with
psychological aptitude of the patient.
Eg; a) acral lick dermatitis/ boredom dermatitis; because of lack of attention from the
owner. Such dog create wound on plantar surface of forelimb due to constant licking.
b) Stereotypic behavior; in zoo animals due to prolonged confinement in cages which
limit the scope for movement.
Symptomatology
It is a science which deals with the symptoms of various diseases.
Symptom:
A symptom is any evidence that indicates the presence of the disease. It denotes adverse
feelings by the animals due to a diseased process. In human medicine the abnormal sensations or
feelings are expressed by the patient which is out of question veterinary medicine.
Sign:
It is outward manifestation of a disease observed through objective evidence. It is observed
by veterinary clinician, animal attendants or the others.
Eg; a) Bottle jaw condition – hypoproteinemia due to internal parasites
b) Red urine - haemoglobinuria
c) Loose stools – enteritis
d) Pale MM – anaemia due to nutritional deficiency/ infectious diseases.
Symptoms can be categorized into – a) subjective symptom

b) Objective symptoms
c) Premonitory or precautionary symptoms
Subjective symptoms: those that are perceptible to the patient only.

It indicates feelings expressed by the patient. This has got relevance in human medicine
where patient voluntarily express his difficulty to the clinician. Actual location of pain in any
organ can be obtained through interrogation of a human patient but this is beyond scope of
animal practice.
But in veterinary medicine also there are few examples of subjective symptoms.
Eg; a) horse kicks at the flank to express the abdominal pain
c) kicking at the belly is a sign of colic in cattle
Objective symptoms; Are those that are perceptible or obvious to the senses of the observer.
These objective symptoms are called clinical signs in veterinary practice.
Eg; a) fluid thrills in ascites
b) Doughy rumen in ruminal infection
Premonitory or precautionary symptoms:
These are observed before onset of the disease and serves as forewarning.
Eg; a) Epilepsy- sitting in a corner, not responding to the owner, these are premonitory signs/
prodromal stage of seizure.
d) Feeling of chill before onset of fever
Direct or idiopathic systems:
These indicate direct disease process and sometimes indicate the affection of a specific organ.
Eg: mucous and blood accompanied with tenesmus in dysentery.
Indirect or sympathetic symptom:
These are symptoms associated with any remote organs.
Eg: vomiting due to hepatitis in dogs.
Typical symptom:
Symptoms which are very much characteristics of a disease. Clinician may distinguish
the disease from its typical manifestation. This is also named as diagnostic symptom.
Eg:
 BQ – swelling with crepitation in heavy muscle.

 HS – swelling in throat region accompanied with dyspnea.
 Snoring – scistosomiasis.
 Whistling / roaring – recurrent laryngeal nerve paralysis.
 Athletic posture – marecks disease.
Atypical symptoms:
Symptoms which are irregular and bear any confirrmity of typical symptoms.
Eg: nervous manifestation of calf suffering from coccidiosis.
Periodical or remittent symptom:
Symptoms which entirely disappear and reappear after a short or long period.
Eg:
 Diphagic fever in canine distemper.

 Fever in surra (trypanosomiasis)
 Undulating fever –human brucellosis.
Diagnostic or pathogenic symptoms:
Symptoms which points directly and definitely to a particular disease and afford a distinct
basis for diagnosis. This may also be considered as characteristics symptom.
e.g.
 Lock jaw – in tetanus.

 Blood from natural orifices in anthrax.
Prognostic symptoms:
Those symptoms which frame a basis to the clinician to determine the course of termination
of a disease. The fate (prognosis) of a disease following a therapy may also be assessed.
Eg:
 High blood urea nitrogen in nephritis indicates ensuring death.

 Sudden relief of pain after sever colic in horse indicates symptoms of some organs
Prognosis:
Prognosis is the forecast of the probable duration and outcome of the disease. Prognosis
may be graded as favorable, doughtful, poor and grave.
Favourable: 100% surity of recovery.
Ex: uncomplicated traumatic peritonitis in cattle.
Doughtful:50% chance, which clinician cannot estimate or determine the extent of damage.
Ex: traumatic reticulo peritonitis with adhesion of diaphragm with abdomen.
Poor: 25% chance of recovery.
Ex: traumatic reticulo peritonitis complicated by absess in liver.
Grove: 100% surety of death/ fatality.
Ex: traumatic peritonitis following penetration of sharp foreign object.
Treatment or therapeutic measure:
In veterinary practice the economic aspect of treatment is very much important especially
in case of productive animal. It should always be borne in mind that cost of treatment does not
exceed the cost of animal.
Treatment means the knowledge of pharmacology/ adopting remedial measure for

treatment of disease. The aim of the treatment is to attain the sick animal and to bring it back to
its normal state of health. General care and nursing are very much important for rapid recovery
of a diseased animal.
Treatment may be classified as general and specific treatment.
General treatment:
Includes measures to be adopted to combat certain complications, during the course of a

disease and to resuscitate the vitality of the animal. It may be as follows.
a) Fluid replacement: fluid therapy

To counteract dehydration. It can be achieved by infusion of different types of fluid by
i/v or other routes.
b) Mechanical treatment:
Ex: exercise, massage, traction, etc. massage with various counter irritants is frequently
done in paraplegic dog.
c) Physical treatment:
Use of heat, electricity, different rays like x-ray, uv rays, infrared rays, etc. rays are
generally used in diseases of the musculoskeletal system.
d) Helio treatment:
Exposure to sunlight in case of rickets, hypopigmentation for synthesis of vitamin D.
e) Dietetic treatment:
May also be described as therapeutic nutrition. Here specific diet is required for certain
disorders and accordingly diet is modified.
Ex:
 Diabetic diet is low in carbohydrates but rich in amino acids.
 Renal disorders- rich carbohydrate diet and high biological value protein is
advised.
 In hepatic disorders- low fat diet and diet containing simple sugars.
f) Psychological treatment:
It includes symptomatic approach, training and psychiatric management to prevent
behavioral stress and various vices of animal.
g) Aerosol treatment:
This therapy is done for humidification of respiratory mucous membrane. Aerosol
drugs are used. By this acute and chronic respiratory disease can be treated.
Specific treatment:
It means administration of specific curative agents against certain diseases. It is only
possible when the etiology of the disease is diagnosed. The type of treatment aims at
removal or overcoming the offending agents causing harm.
Ex:
 For gram positive organisms - penicillin.

 For gram negative organisms- the choice of antibiotics are aminoglycosides,
fluroquinolones.
 Mixed infections – OTC, streptopenicillin.
Antibiotic toxicity are:
 HCN poisoning – sodium thiosulfate and sodium nitrite.

 Nitrite poisoning – methylene blue.
Symptomatic treatment:
It comprises institution of medical agents in order to get rid of certain symptoms which may be
causing diseases.
Ex:
 Antiemetic to relieve vomition

 Astringents preparation in gastroenteritis.
 Expectorent in respiratory diseases.
 Carminative mixtures in tympany.
Palliative treatment:
This type of treatment is extended in case of incurable diseases to prolong lifespan of individual.
Ex: insulin in diabetes mellitus, dialysis in CRF (to relieve uremia)
Emperical treatment:
It is the art of treating the patient by more experience gain through long time trial and error
methods.
Ex: inflation of udder with air in case of milk fever in cattle.
Rationale treatment:
It is the scientific method of administration of drugs based on patho physiology of disease
process and knowledge of pharmacotherapeutics of drugs.
Ex:
 Sodium bicarbonates in metabolic acidosis and ruminal lactic acidosis.

 Use of atropine sulphate to elevate spasmodic colic in horses.
Prophylactic treatment:
All the measures to prevent spread of diseases when it is likely to be contracted by animals.
Vaccination is part of prophylactic treatment and managemental aspects (quarantine, isolation,
disinfection) also a part of prophylactic treatment.
Disease Progression:
Disease progresses in four phases.
 Latent period/ incubation period

 Prodromal period (minor early signs)
 Period of manifestation (exact clinical signs)
 Outcome of disease
Latent period:
It is also termed as incubation period in infectious disease. It is the period from entry of the agent
into the animal till the manifestation of detectable clinical signs. Latent period ranges from
several minutes to several months.
Example:
 Ruminal lactic acidosis – 6 to 12 hours
 In most infectious diseases-7 to 10 days
 In diseases like BSE – 6to 8 years
Prodromal period:
It lasts from discovery of first sign of the disease to its complete manifestation
Example:
 On set of infectious diseases are invariably characterized by indefinite
manifestation such as general depression, chills, in appetence, rise of
temperature etc.
Period of manifestation:
It usually follows the prodromal period. It is the period of development of marked

clinical manifestations. These help the clinician to diagnose the disease through the very
characteristic features of the particular disease.
Example:
 Locked jaw in tetanus

 Prolapse of third eye lid – tetanus in equines
 Absence of barborygmi (normal gut sound) in colic
Outcome of the disease:
Once the disease is diagnosed, specific therapeutics regimen is inducted to arrest the
progress of the disease. This result in the outcome of the disease which depends on several
factors like state of disease, appropriate therapeutic regimen inducted virulence of the pathogen
and resistance of the host.
1. Recovery: may be complete or incomplete.
2. Relapse: It is the recurrence of a disease after a clinical cure. This usually

occurs due to under dosing. This can occur both in infectious and non
infectious diseases.
Example: in salmonellosis – course of the antibiotic treatment is for 7 to
10 days but animal shows signs of recovery at 5 days and client will nit
bring his animal to clinic. Now salmonella organisms take an upper hand
again causing the relapse of the disease. Due to resistance developed, and
this relapse will not respond to the same antibiotic.
In milk fever – if inappropriate dose of calcium is given , then there

will be relapse. Normally calcium at 8 to 12 gram per animal is required
but animal shows immediate response when ½ bottle (450ml) is given but
if remaining ½ is not given, then next day animal again becomes
recumbent.
3. Complications: in some cases, primary disease causes a weakness of the

body which then becomes susceptible to other diseases.
Example: secondary pneumonia due to Bordotella bronchiseptica

/Pseudomonas spp. in canine distemper.
4. Convalescence: it is the state through which a patient passes after a

prolonged illness till it regains normal health and optimum power of
production. After a period of prolonged illness it takes considerable time
to regain its vitality. For this reason, adequate nutrition fortified with
vitamins is required to sustain the loss of a patient following recovery
from an acute bacterial infection where it was under the regime of long
term antibiotic therapy.
5. Sequele: the clinical outcome which may arise after the recovery from the
disease.
Example: FMD - panting, hypertrichosis.
CD - chorea- repeated involuntary twitching of group of
muscles which is called as myoclonic jerks, this due to loss of some neural
impulse transfer.
6. Death: complete cessation of respiration without any response to the

external stimuli. Clinical death is characterized by depression of CNS
activity. This stage is called as somatic death but the molecular life in the
tissues is viable for about 5 to 6 minutes and these changes are reversible.
After this stage molecular stage ensures.
Signs of death:
 cessation of respiration
 cessation of circulation
 no response to external stimuli
 dilation of pupil and fixation eye ball
 fall of body temperature
 setting up of rigor mortis

GENERAL AND SYSTEMIC STATES
General and systemic states are involving multiple causative factors. Example:
temperature, shock, dehydration, etc.
Body temperature is measured by a clinical thermometer. It has got mercury containing

bulb which communicate with a thin capillary channel. Thermometer is calibrated from 97 –
108oF.
For human the mercury bulb is elongated and thin. The temperature is measured under
the tongue or the arm pit. But in animals, it is stumpy type of bulb and temperature is measured
by placing the bulb in rectum.
NORMAL TEMPERATURES:
Sl. No Species Temperature

01 Horse 99-101.50 F
02 Ox 100-1030 F
03 Sheep 102-1040 F
04 Goat 101.5-104.50 F
05 Dog 100.5-102.20 F
06 Pig 100-1040 F
07 Poultry 104.8-107.60 F
08 Cat 100.5-102.20 F
Usually a variation of 0.50 F allowance is given for very small and large animals.
Smaller the species - higher the temperature.
Female, pregnant, and young animals have a higher temperature than male, non-pregnant and old
animals.
There are disease conditions where in early morning temperature is higher than evening
temperature.
Ex: TB in horses.
Care to be taken:
 mercury column should be below the normal temperature
 thermometer should be sterilized by merging in Dettol solution prior to use
 bulb end should be lubricated with liquid paraffin or glycerin or soap especially in
case of small pup and kitten
 bulb of thermometer remains same contact with rectal mm
 should be kept inside for at least 1 – 2 min
Physiological rise in temperature can also take place up to 1o c. ex: after feeding, exercise,
parturition and when the animal is excited.
 1-1.5 0F more than normal- mild pyrexia.

 Up to 3 0F more than normal – moderate pyrexia
 > 3 0F than normal – high fever
 > 6 0F than normal – hyper pyrexia.
HYPOTHERMIA:
Hypothermia is a general systemic condition in which there is decrease in body

temperature below a critical level. Hypothermia results when heat loss exceeds heat production.
Low body temperature due to low BMR (Shock) or low environmental temperature, hypothermia
is due to failure of hypothalamus to maintain the body temperature.
Aetiology: due to Excessive heat loss or diminished heat production
Excessive heat loss:
1. Excessively cold air temperature will cause loss of heat if increased metabolic activity,
muscular tone and peripheral vasoconstriction fail to compensate.
2. Infusion of cold solution
3. Lying on cold, uninsulated surface or placing animal in cold room or environment
4. Induced vasodilation
5. Over aggressive treatment of hyperthermia
Diminished heat production:
1. Anaesthetic drug induced depression of hypothalamic thermostatic mechanism

2. Decreased muscle tone as in parturient paresis
3. Acute ruminal impaction
4. Sedation associated with profuse diarrhea in the cold cow syndrome and hypo-pitutarism
5. Hypoadrenalism myxedima
Sudden fall in temp in a previously febrile animal, the so called premortal fall is a bad
prognostic sign. Hypothermia may be a significant cause of post-shearing mortality in sheep,
especially where there has been a fall in body weight in the period immediately preceding
shearing.
Pathogenesis:
Drop in temperature
Stimulation of anterior pituitary
Release of thyrotropic hormone
Release of thyroxin
Increased BMR More heat
CLINICAL FINDINGS:
Prolonged severe hypothermia results in the occurrence of various disorders like

metabolic acidosis, atrial arrythmias, ventricular arrythmias, hypokalemia, hyponatremia,
increased blood viscosity, depressed myocardial function, coagulopathies, hyperglycemia,
insulin resistance, hepatic glycogen depletion and impaired gluconeogenesis which ultimately
leads to hypoglycemia and cold diuresis.
Cold induced ECG changes, viz., prolonged PR interval and widened QRS, increased
myocardial automaticity, inadequate oxygen delivery, lactic acidosis, absence of reflexes and
pain response and increased blood viscosity leading to microcirculatory sledging. Autonomiuc
and endocrine thermogenesis mechanism are inactivated, absence of spontaneous ventilation,
occurrence of ventricular fibrillation and oxygen regulation disorders.
Treatment:
1. Passive re-warming: effective in mild to moderate hypothermia when patient is capable

ofmetabolic or shivering thermogenesis. It is generally safe but is slow and exposes the
patient to the harmful effects of hypothermia for a long period.
a. Drying of the body surface
b. Wrapping of patients with blanket, towel, drapes etc
c. Insulation from cold table surface
2. Active surface rewarming: necessary in moderate to severe forms of hypothermia . it is

commonly used in hypothermic patients. Disadvantages of this technique are decreased
neuronal feed back to thermostatic centres and decrease in thermogenesis response.
a. Circulation of warm-water blanket
b. Infra red heat lamp
c. Surgical lamp
d. Warm water bath
e. Forced air dryers
f. Hot water bottle
g. Electric floor heater
3. Active core re-warming: minimize the potential for vascular collapse associated with
surface re-warming techniques.
a. Infusion of warmed IV fluids
b. Warmed humidified inspired air
c. Flushing the open body cavity with warm, sterile, isotonic poly-ionic fluids
d. Peritoneal dialysis
e. Flushing the stomach or rectumwith luke warm isotonic, poly-ionic fluids.
Hyperthermia: (over heating)
It results due to retention of excess heat as a consequence of disturbed thermo regulation

and impeded heat elimination into the surrounding environment.
This condition develops due to following reasons-

 High humidity of environment which limits heat loss
 Diminished air current which impairs cooling of body
 Inadequate sweating or no sweating
 Thick body coat of the animal
 Defects in thermoregulatory mechanism
 As a sequel to disease – ex: FMD
Hyperthermia is the term used to describe any elevation in case of body temperature above
accepted reference values for that species. Hyperthermia is a result of loss of equilibrium in heat
balance equation, such that heat is produced or stored. In the body at a rate is excess of heat lost
through radiation, convection, or evaporation. Hyperthermia is not a result of the body
attempting rise its temperature but is due to the physiologic, pathologic or pharmacologic
intervention where heat gain exceeds heat loss.
Sequence of hyperthermia:
1st stage:
Adoptive reaction to dissipate heat. Dilatation of peripheral vessel – accelerated blood
flow to peripheral organs – increased sweating – rapid respiration – loss of heat.
2nd stage:
Elevation of body temperature – excitement – restlessness – accelerated shallow

respiration – accelerated heart beat – accelerated pulse rate - increased metabolism – increased
nitrogenous wastes – convulsion and twitching of muscles.
3rd stage:
Excitement – diminished vital functions – shallow respiration – fall of BP –

unconsciousness – clonic spasms – respiratory failure – death.
Treatment:
- Large dose of crystalloid fluid infusion

- Oxygen therapy
- Surface cooling techniques- fan, water (preferably cool not cold), alcohol, ice packs
placed over large vessels areas (neck, axillas and inguinal region), whole body ice-water
baths
- Antipyretic drugs like antiprostaglandins, Dipyrone, Aminopyrone, Dantrolen.
- Internal cooling techniques- cold/ice isotonic, poly-ionic crystalloids by
intravenous/rectal/gastric lavage/peritoneal dialysis
Heat stroke:
(Heat stress, heat prostration, malignant hyperthermia)
This is special state of acute hyperthermia resulting from defects in the heat regulatory
mechanism against extreme environmental heat.
Susceptibility:
Dogs and cats have poor thermoregulatory mechanism and in dogs sweating is absent,
hence they are more susceptible.
In sheep – due to heavy wool it is also susceptible, hence summer shearing is done.
Pigs – limited lung capacity and heavy sub cut fat in sheep makes more susceptible.
During increased environmental temperature there is panting due to limited lung capacity
resulting in increased respiratory contraction causing increased body temperature. Pure breed
cattle like HF, jersey have poor thermoregulatory mechanism because of their adaptation to
temperate climate.
Factors responsible for heat stroke:
 Extreme environmental temperature

 High humidity in the environment
 Over crowding
 Transportation during high environmental temperature
 Limited supply of water
 Age – young ones and saline are less accommodative for heat regulation and so
susceptibility maximum
 Obese animals – less heat loss – increased body temperature
Pathogenesis:
Heat stroke - damage to CNS – tachycardia – dyspnea – convulsions – unconsciousness –

respiratory failure – death.
Exposure to high environmental temperature resulting in inability of hypothalamus to

cope up with the increased temperature hence cause increase in the set point.as a consequence of
which tachycardia develops, increased renal retention ( dyspnea), decreased filling time in heart
and low oxygenated blood in lungs which creates a state of hypoxia and hypoglycemia that is
more pronounced on the centers in brain – the outcome is convulsions(called as hyperpyrexic
convulsions most common in pups ) and sometimes unconsciousness and in extreme conditions
the respiratory center fails leading to death.
Clinical accounts of heat stroke:
 Dull and depression

 Rapid breathing
 Open mouth breathing – protrusion of tongue
 Frothy discharge from mouth and nostrils – congestion of mm
 Tachycardia – cardiac arrhythmia
 Temperature is high as 106 to 110 0 F – convulsions
 Paralysis of respiratory and motor centers
 Coma
 Death
Management and treatment:
a) Animal should be kept in well ventilated place and arrangement of fan / AC if

possible. Crowding around the animal should be avoided.
b) Sprinkling of cold water is advised. By this, temperature can be reduced by
20F. Sprinkling should be at highly vascular areas. It should be preferably on
head, rump, back and inguinal region.
c) Sometimes cold water enema may lead to increased dissipation of heat from
the body. i/v fluids based on electrolytes, CVP and hydration status.
d) Application of icepacks on back or rump, axillary and inguinal region
e) Provide cold water for drinking or ice cube for licking
f) Animal should be sedated by using tranquilizers resulting in decreased activity
of animal that in turn causes lowered BMR ending in decreased body
temperature.
Tranquilizers used in various animals are –
 triflupromazine – 0.2mg / kg b.wt for cattle
 xylazine – 1.1mg / kg b.wt for horse
 diazepam – 0.25 mg / kg b.wt for dogs
g) Corticosteroids can be administered to prevent hypothermic shock.
Ex:
 dexamethasone – 0.5 – 1.0 mg / kg b.wt ( long acting and more

potent)
 hydrocortisone – 5.0 – 10 mg /kg b.wt (short acting and less potent)
h) Antihistamines like pheneramine maleate / chlorpheneramine maleate can be
given; once the temperature comes with in manageable range antipyretics can
be given.
Ex:
 acetyl salicylic acid
 sodium salicylate
 analgin or paracetamol (tab or injection every 6 hrs)
Other options:
 phenyl butazone (50% antipyretic)

 diclofenac sodium
 nemusilide is another drug of choice (tablet or syrup or injection)
i) Broad spectrum antibiotics are given to avoid secondary bacterial infection

because in heat stroke there will be lowered immunity.
FEVER:Febris/pyrexia
Definition: Abnormal elevation of body temperature especially when the inflammation is

accompanied with infection. It is also defined as abnormal elevation of body temperature
resulting due to circulating toxins and exogenous pyrogens.
Heat regulation
Heat production due to BMR Heat loss due to
 Radiation
 Conduction
 Evaporation
 Pulmonary ventilation
(panting)
 Excretions from the body
(minor)
 Convection
 Secretion (milk)
Etiology:
Fever may be septic due to infection or aseptic due to inflammation or traumatic injury.
Generally pyrogens are the substances which elevate body temperature. They are of two types-
endogenous and exogenous.
Exogenous:
Infectious agents - bacteria, virus, fungi and protozoa.
Non-infectious agents – neoplasms/malignancies and tissue injuries.
Endogenous:
They include cytokines produced by macrophages like interleukins (IL-1) and tissue necrosis
factor (TNF). Exogenous pyrogens act through endogenous pyrogens.
Pathogenesis:
Exogenous pathogens enter into the body and cause release of lymphokines and
lymphocyte proliferation that stimulate the macrophages and monocytes to release cytokines like
IL-1 andTNF. The TNF cause membrane damage releasing phospholipids (arechidonic acid
precursor) thereby causing conversion of arechidonic acid via cyclo-oxigenase pathway resulting
in production of PGE2 which is further enhanced by the action of IL-1 especially in the
hypothalamus and this stimulates hypothalamus thereby elevating the thermo regularory set point
resulting in increase in the body temperature. Elevation of body temperature is also due to trhe
hypothalamus sending signal to vasomotor centre causing peripheral vasoconstriction thereby
preventing heat dessipiation.
Exogenous pyrogen Leukocytes Endogenous pyrogens
CNS (pre-optic anterior hypothalamus) fever
Endogenous pyrogens bacteria, virus, bacterial endotoxins etc.
Mononuclear phagocyte monokines, lymphokines
IL- 1 T – lymphocyte proliferation (immune response)
Prostaglandin (PGE2) endogenous pyrogen (arachdonic acid release)
Increase in thermal set point
Monoamines
Anterior hypothalamus
Vasoconstriction Piloerection Muscular contraction Heat production
Stages of fever:
1) Onset: stage of increment ie., rising phase of temperature.

Here the heat production is elevated because of the increase in the thermal set point and
peripheral vaso-constriction. In this stage, temperature goes on increasing and in few
cases the rise in temperature accompanied with chills and rigor. Though the body
temperature is rising, the extremities are cold.
2) Stage of fastidium: stage of maximum temperature.
Temperature reaches to maximum at this stage where heat production and dissipation are
at equilibrium and therefore temperature remains constant for a certain period of time.
3) Stage of decrement: decline of body temperature is noticed and heat dissipation

predominate heat production. Most of the time this stage is accompanied by profuse
sweating.
Beneficial effects of fever:

1. It is a body defense mechanism
2. It improves phagocytosis
3. It increase circulating polymorphs
4. Increases the velocity of blood (fever increase PR,HR,velocity of blood and cell
distribution to tissues)
5. Increase in temperature has a bacteriostatic effect
6. Improves Ag-Ab complex formation and activates complement system. But sometimes
micro-organisms overtake these mechanisms and take an upper hand and hence treatment
is required.
Types of fever:
1. Simple fever: Febris simlica
It is the type of fever where the temperature does not touch the normal limit in 24hr and
the variation of temperature does not exceed 2 0F in 24hr.this type of temperature is noted
in lobar pneumonia, enteric fever etc.
2. Remittent fever: Febrisremmittens

It is the type of feverwhere the temperature does not touch the normal limit in 24hrs and
tha variation of temperature is >2oF in 24hrs.
This type of temperature is observed in septicemia, bronchopneumonia, and urinary tract
infection.
3. Intermittent fever: Febris intermittens/Relapsing fever
It is that type of fever where the rise of temperature persists only for a few hours
of thye day. There is a regular brief attack of fever (pyroxysms) with a afebrile period
(apyrexia). In brief, there is high temperature for several hours followed by a drop to
normal temperature and again there is rise of temperature and so on.
This type of temperature is seen in human malaria, chronic surra in horse and
canine distemper (diphagic fever).
Based on febrile and afebrile period, intermittent fever can be divided into
a. Quotidian: There is daily rise and daily fall of temperature. This is seen in malaria in
human beings, E.coli infection or pyelitis etc.
b. Tertian: Temperature appears and disappears every alternate day ie., there is a gap of
one day. Ex: Malaria in humans.
c. Quartan: Here the temperature comes and goes every 4thday.
Ex: Malaria in African countries.
d. Hectic: There is sudden rise of temperature daily with chill or rigor, persistent for few
hours and falling equally suddenly with profuse sweating.
Ex:Malaria, empuema and E.coli infection.
4. Irregular fever: Atypical fever

Here fever has got no definite character. Daily fluctuation of temperature does not
follow a definite pattern. This type of temperature is most commonly observed in
veterinary practice.
Ex: Louping ill, CD, Swine erysephalus, strangle in horses.
5. Transient fever:
Fever subsides within about 24hrs after its development
Ex: Epimeral fever.
6. Continuous fever: Febris continua
The plateau of temperature remains for a longer period than the simple fever.
Ex: Tick borne fever.
7. Periodic fever:
Periodic attack of fever alternate with afebrile period.
Clinical classification of fever:

a. Acute fever: There is sudden sharp elevation of body temperature to the level of 1040F
or more. This type of fever is recorded in acute viral or bacterial diseases.
Ex: Acute pneumonitis, acute peritonitis etc.
b. Sub-acute fever:Temperature does not go too high and remains within the range of
1030F. this type of fever is recorded in mild inflammatory conditions like nephritis,
cystitis, metritis etc.
c. Chronic fever: Temperature does not exceed above1-20F beyond the normal range.
Course is usually prolonger. Temperature persists for a considerably prolonged period.
Ex: pulmonary TB, chronic pyometritis, surra in horse etc.
SHOCK: Syn: peripheral circulatory failure
Shock is a state of hypovolumia (decrease in the amount of circulatory volume) as a

result of disorganization of peripheral circulation.
Classification of shock:
a) Hypovolemic shock:Hypovolumic shock develops due to transitory reduction of

circulating blood volume either through loss of whole blood or its fluid components
following dehydration, hemorrhage, burn etc. dehydration due to acute gastro enteritis,
acute impaction and peritonitis may lead to shock syndrome. Adrenocortical
insufficiency or traumatised tissues may also produce transient hypovolumia.
b) Vasogenic shock: Vasogenic shock results because of release of vasoactive amines like
serotonin, histamine etc. cause peripheral vasodilation leading to shock.
c) Septic or endotoxic shock;septic shock occurs usually due to infection predominantly

with G-ve and occasionally due to G+ve organisms. The toxin of E.coli, klebsiella spp,
pseudomonas spp and staphylococcus spp are the most common precipitating factors to
induce shock.
d) Anaphylactic shock: this is an immune mediated/Type-1 hypersensitivity reaction,
wherein induviduals sensitized to a particular Ag and there is second exposure to the
same Ag. During first exposure, the animal gets sensitized and if second exposure is there
then it results in anaphylaxis.
Ex: Injection of drugs like penicillin or sulfa or blood or sera may produce this type of
shock.
e) Cardiogenic shock: Diseases of heart which reduces cardiac output may result in shock.
Myocardial infarction, acute myocarditis, cardiac arrhythmias, acute pericardial
tamponade, massive pulmonary embolism, mitral stenosis etc. are the causes which may
put the animal towards shock.
f) Neurogenic shock: Severe painful stimuli such as severe external trauma, extensive
burns, severe fracture concussion of brain etc. may cause shock in animals.
Pathogenesis:
In all forms of shock there is sharp fall in effective circulating blood volume with
lowered cardiac output and lowered BP along with impaired tissue perfusion. These changes lead
to tissue hypoxia in all the organs except in brain and heart where compensatory mechanisms
come into play by releasing catecholamines. In other tissues, due to hypoxia, anaerobic
metabolism develop which induces production of lactic acid resulting in acedaemia and
intracellular acidosis. If the animals are not treated at this stage, hypoxia will cause further
cellular damage which induces breakdown of lysosomal membranes, releasing intracellular
enzymes and K+ ions into the tissue fluids and the circulation.
-Hypotension
-Reduced blood flow to visceral organs
-tissue hypoxia S
-tissue ischemia H
O
-Less venous return
C
-Capillary stasis
K
-reduced cardiac output
-vasoconstriction
Clinical findings:
Most of the time animal is presented in recumbent position. In shock the skin becomes
cyanotic, moist, cold and clammy. Temperature remains subnormal, mucous membranes turn dry
andpale. There is shallow respiration; rapod thread pulse and low BP. The animal is dull, weak,
recumbent and restless. Oliguria and anuria is evident.
Treatment:
First aid: Animal should be wrapped with woolen blanket. Emergency oxygen supplementation
if availability of oxygen is there. Bleeding points, wounds should be checked for preventing
blood loss. Animal is sedated to avoid exaggerated response.
Generalized treatment:Antihistamines and analgesics can be given for vasogenic shock. Use of
corticosteroid is very much important as they are lifesaving drugs and form first line of treatment
in shock. Potent corticosteroids like dexamethasone, betamethasone @1-2mg/kg bwt are
indicated in the treatment of shock.
Corticosteroid role in shock:
 Enhances BP and cardiac output.

 Maintains tissue perfusion to vital organs especially to liver and kidney and due to this
functional integrity is maintained.
 Inhibits anaerobic metabolism and reduces lactic acidosis and subsequent metabolic
acidosis.
 Stabilization of cell membrane and prevent intracellular enzyme spillage.
 Helps to maintain the micro circulation by decreasing cell aggregation.
 Neutralize endotoxins.
Specific treatment:
If loss of whole blood – Blood transfusion.
If loss of fluid – Institute fluid and electrolyte therapy. Plasma expanders play important role in
case of burn.
For cardiogenic shock – Digitalis or digoxin can be given as cardiac tonic.
Septic shock – Broad spectrum antibiotic given parentrally.
For anaphylactic shock – Antihistamines and adrenaline are given.
Neurogenic shock – Potent analgesics and anti-inflammatory drugs are indicated.
DEHYDRATION
 Literal meaning-water loss

 Fluid and electrolyte imbalance or loss of fluid and electrolytes
 70% of body is made up of water and this water is composed of various solutes
(electrolytes). About 50% of this water remains intracellular and remaining 20% is
considered to be extracellular
 Extracellular component which is very vital which is again divided into
o Interstitial fluid volume/fluid – 15%
o Circulating fluid – 5%
 It is usually presumed that interstitial fluid : plasma is 3:1
 As per WHO, the dehydration is defined as loss of water and the dissolved solutes from
the body by physiological and pathological means
 Normally the water is lost from the body through various means like skin (sweating),
faeces, urinary output and to lesser extent through respiration.
Clinical dehydration can be an outcome of either of failure of water intake or excessive loss
of water.
Failure of water intake:
 Water deprivation
 Decreased activity of thirst center
 Due to ongoing toxemia and debility which causes lack of thirst
 Due to certain pathological conditions which affect deglutition process
Ex:-Enlargement of retropharyngeal lymph node
-Simple stomatitis
-Laryngitis
-Oesophagial paralysis
-Rabies (pharyngeal paralysis)
-Epimeral fever (transitory esophageal paralysis)
 Choke (esophagial obstruction)
 Phlegmon- inflammatory swelling of pharynx
Excessive loss of water:
 Any condition which results in gastritis or gastroenteritis resulting in a vomition or

diarrhea. Bacterial and viral diseases are responsible.
Ex: -BVD
-RP
-Winter dysentery large animals
-Salmonellosis
-Parasitic diarrhea
- CD, ICH Small animals
 Malabsorption syndrome – parvo viral gastroenteritis causes villous atrophy. In adult

dogs-exocrine pancreatic insufficiency wherein there is frequent passage of voluminous
feces is seen.
 Systemic conditions
-ruminal lactic acidosis
-abomasal displacement
-any condition which cause polyuria like CRF, DM, pyometra etc.
- Intestinal obstruction
- Excessive diuretics
Clinical dehydration is classified into three types
 Isotonic type of dehydration

 Hypertonic type of dehydration
 Hypotonic type of dehydration
Isotonic type of dehydration
In this type, there is an equivalent loss of water and solutes. Basically sodium being
important extracellular component reduces in ECF due to the following conditions
Ex: Acute gastro-intestinal disorders, fluid and food deprivation, repeated draining of fluid in
ascietis and profound sweating also results in this type of dehydration. There is no compensatory
transfer of water from ICF to ECF and usually such type of dehydration is treated with isotonic
fluid like NS/DNS. Depending upon the clinical manifestation other fluids like RL can also be
supplemented.
Hypotonic type of dehydration
Results due to sodium depletion. Here there is more loss of sodium along with water.
Usually it is severe type of dehydration and requires emergency treatment common clinical
condition which brings about this condition is acute gastroenteritis due to colibacillosis,
salmonellosis, acute gastric dilatation, acute intestinal obstruction and diabetic coma. Treatment
is preferably carried out by hypertonic NaCl solutions (2-5%).
Hypertonic type of dehydration
Water depletion type of dehydration. Excessive loss of water without much loss of sodium.Ex:
Diabetes insipidus. 5% dextrose as a parenteral fluid indicated.
1. Clinical assessment of dehydration:-
Degree of Total serum Changes in Skin turgor PCV % Fluid
dehydration solids(g/dL) eyeball test(retention of (haematocrit) required(ml
kin fold/sec) /kg b.wt)
Mild (4-6%) 7-8 No noticeable Not acceptable 40-45 >10-20
changes
Moderate (6- 9-10 Rarely visible 2-4 50 30-50
8%)
Severe (8-10%) 12 Sinking of eyeball 6-10 55 50-80
is prominent
Shock>10% >12 Pronounced 20-40 60 80-100
sinking of eyeball
 Camel can sustain 16-18% of dehydration which is an exception.
2. CVP: normal CVP is about 6-10cm level of water.
 <6cm indicates – HYPOVOLUMIA.

 >15cm indicate – HYPERVOLUMIA (or) fluid overland.
3. Electrolyte estimations:
This gives correct electrolyte imbalance occurred in the dehydrated patients. Plasma
bicarbonate estimation is very much important in case of enteritis. Normal level is 24-
30millimol/litre. In metabolic acidosis there is bicarbonate deficit & this metabolic acidosis can
be graded as mild, moderate & severe depending on charge in bicarbonate
concentration.(HCO3conc.)
 mild: 24-18mmol/litre
 moderate: 14-18mmol/litre
 severe: <10mmol/litre
CLINICAL SIGNS:-
1. Mild dehydration (4-6%)
Clinical signs are minimum but other compensatory mechanism counteracts dehydration.
Indicate hurried type of respiration, mild change in PCV/hematocrit value (mild increases) by
about 4-5%.
2. Moderate dehydration (6-8%)
Show mild signs of eyeball sinking, skin fold test remains elevated for about 2-4sec. &
haematocrit value are elevated by 5-10%. Body surface is warm but extremities are cold.
3. Severe dehydration (8-10%)
Animal is recumbent most of the time in the state of shock, mucosa congested, body
surface as well as extremities cold indicating the case is advancing towards peripheral circulatory
failure. Skin fold test remains elevated for about 10sec. Hematocrit value is increased by about
15-20%.
Electrolyte imbalances noticed in dehydration:
Major electrolytes which are lost creating electrolyte imbalance are Na, K, Cl& HCO3.
 Sodium:The loss of Na during dehydration is termed as hyponatraemia. The most

common cause of this is enterotoxigenic colibacillosis especially in case of young one.
 Chloride: Hypochloremia, loss of chloride ion which usually occurs as a result of net
loss of chloride in the intestinal tract. The common causes are acute gastric dilatation in
small animals, torsion & displacement of abomasums in large animals. In all these cases
large quantity of Hcl is secreted resulting in net loss of cl
 Potassium: The cause of hypocalcemia includes abomasal stasis, which is a sequel of

pyloric stenosis, upper intestinal obstruction & renal disorders.
PRINCIPLES OF FLUID & ELETROLYTE THERAPY
Fluid, electrolyte and acid-base therapy is symptomatic, supportive and should be used in
conjunction with and not substitute for more specific diagnostic and therapeutic procedure to
identify and correct the problem. Owing to lack of correct diagnostic techniques for the
measurement of fluid requirements, several guidelines experimental studies and clinical
experience have evolved to aid the veterinary clinician’s approach to fluid therapy. The use of
such guidelines or “rule of thumb” has become common practice in veterinary medicine today.
These guidelines in conjunction with proper patient evaluation (history, physical examination
and laboratory data) should be used to construct an objective therapeutic plan.
Most important principle is to minimize dehydration and prevent further loss of

electrolytes.
Calculation: body wt. (kg) x %of dehydration = litre of fluid required.
Electrolyte supplementation calculation-deficit is calculated using the formula-base deficit x 0.3 x body
wt.
Calculation of base deficit:
Calculating exact base deficit by estimating electrolytes. Rough estimation-when there is a mild
dehydration-10 meq, moderate-15meq & severe-20 meq.
ROUTES OF ADMINISTRATION
 Oral
 Per-rectal
 Intravenous- most satisfactory route for rapid means of rehydration. Demerits:- are fluids should be
very much sterile, exact composition should be there. Fluid to be administered should be of high
standard. In case of venous collapse, it is very difficult to give fluid by this route.
 Intra-peritoneal:-second choice of fluid administration. Fluid should be very much sterile, isotonic,
non-irritant & large volume of fluid can be administered by this route. Fluids should be warmed to
body temperature before administration.
 Sub cutaneous:-main limitation is loss volume of fluid can be administered. Fluid should be
sterile, non-irritant & isotonic.
Signs of overload:
Normal patients are quite tolerant of excessive volume of administration. It is excreted by
the kidney in the form of increased urine production. Signs of overhydration occur when fluid is
administered too rapidly. These include serous nasal discharge, restlessness, cough, dyspnoea,
pulmonary oedema, ascietis, polyurea, exaptholmosis, chemosis (edema of conjenctiva) diarrhea
and vomition.
Cvp=jugular filling will increase followed by an increase in respiratory rate effort (more
easily motivated in the cat than dog) before auscultable signs of pulmonary oedema develops. If
excessive crystalloids are advised, patients will typically develop signs of over hydration before
they develop signs of hypovolumia.
Estimate dehydration
Calculate body fluid deficit (% dehydration * kg b.wt)
Add estimated maintenance + ongoing losses
Patient at risk for fluid overload
YES No
Rehydrate over 12-24hrs Rehydrate over 4-12hrs
Composition of fluids to be administered
Fluids available for treatment can be divided into several categories including colloidal
solution, replacement and maintenance electrolyte solutions, and 5% dextrose in water. The
choice of fluids should be based on the degree of volume depletion and the nature of fluid loss.
When plasma volume depletion is secondary to haemorrhage, the best replacement fluid is cross-
matched whole blood. Provided the patient doesnot require treatment with a colloidal solution,
fluid defecit should be replaced with a fluid that most closely matches the type of fluid lost.
Generally replacement solutions can be used to replace normal urinary and insensible fluid losses
and sodium free solutions should be used to replace deficits in patients suffering from insensible
or pure water loss.
Animals dehydrating due to vomiting, diahrroea or burns tend to lose fluids that closely
match the composition of ECF, so replacement electrolyte solution closely resembling ECF
should be used to correct the deficit. Five percent dextrose in winter is relatively ineffective in
replacing balanced electrolyte losses because water distributes throughout total body fluids and
only about 30% remains within the ECF.
Further supplementation of replacement fluids may be required to correct avid base

imbalance and K+ defecits, depending on the cause of fluid loss. Vomitus is fairly high in Na+
and cl- but net hydrogen ion (H+) or HCo3- loss depends on the location of the lesion. Vomiting
due to pyloric outflow obstruction causes metabolic alkalosis due to H+ loss, leading to renal K+
wasting under the combined effect of dehydration and metabolic alkalosis. Ijn such
casesreplacement electrolyte solutions containing no bicarbonate or bicarbonate precursors such
as ringers solution and 0.9% Nacl should be used and K+ supplementation of replacement fuids
may be required to correct acid base imbalance and K+ deficits, depending on the cause of fluid
loss.Vomitus is fairly high in Na+ and Cl- but net hydrogen ion(H+) or HC03- loss depends on
the loacation of the lesion.Vomiting due to pyloric outflow obstruction causes metabolic
alkalosis due to H+ loss, leading to renal K+ wasting under the combined effect of dehydration
and metabolic alkalosis.In such cases replacement electrolyte solutions containing no
bicarbonate or bicarbonate precursors,such as Ringer’s solution and 0.9% Nacl should be used
and K+ supplementation may be required.However,most causes of vomiting in the dog other
than pyloric outflow obstrutction have a minimal effect on acid base imbalance except for a mild
metabolic acidosis.Thus,replacement electrolyte solution containing a bicarbonate precursor,such
as Ringer’s lactate can be used.Fluid losses due to diarrhoea are usually high in Na+,K+ and
HCO3-,so replacement fluids may need to be supplemented with K+ and HCO3-.
Maintenance fluids need not match ECF composition because urinary & normal faecal losses are
generally low in Na+ and insensible losses via the respiratory tract and through the skin are
virtually sodium free.Thus maintenance electrolyte solutions with reduced Na+ such as 2.5%
dextrose in half strength lactated Ringer’s solution or 2.5% dextrose in 0.45% NaCl are
recommended.
Animals with normal renal function that dehydrate due to insensible fluid losses and failure to
drink water because odf dementia have a pure water loss and should receive 5% dextrose in
water as the main replacement fluids.
Potential fluid, electrolyte,and acid-base disorders associated with

various abnormalities:
Abnormality Electrolyte balance Acid base status Fluid therapy

Simple - - Half strength or
dehydration,stress,exercise balanced electrolyte
solution,5% glucose
solution
Heat stroke K+ variable Metabolic acidosis Half strength
Na+ variable electrolyte solution
followed by balanced
electrolyte solution
Anorexia K+ loss Mild Metabolic Balanced electrolyte
acidosis solution;KCl
Starvation K+ loss Mild Metabolic Half strength or
acidosis balanced electrolyte
solution;KCl;calories
Vomiting Na+,K+, and Cl- Metabolic alkalosis Ringer’s
loss Metabolic acidosis solution,0.9% saline
chronically with KCl
supplementation
Diarrhoea Na+ loss,K+ loss Metabolic acidosis Balanced electrolyte
chronically solution;HCo3-;KCl
(if chronic)
Diabetes mellitus K+ loss Metabolic acidosis balanced electrolyte
solutions;KCl
Cushing’s disease K+loss occasionally mild balanced electrolyte
Metabolic alkalosis solutions;KCl
Addison’s disease Na+ loss Metabolic acidosis 0.9% saline followed
K+ retention by balanced
electrolyte solutions;
Urethral obstruction K+ Metabolic acidosis 0.9% saline followed
retention,Na+,Cl- by Balanced
variable electrolyte
solutions;KCl post
obstruction
Acute renal failure K+ Metabolic Balanced electrolyte
retention,Na+,Cl- acidosis(chronically) solutions
variable
Chronic renal failure Na+,K+,Cl- variable Metabolic acidosis Balanced electrolyte
solutions
Congestive heat failure Na+ retention Metabolic acidosis 5% glucose solution
Haemorrhagic shock Balanced electrolyte
solutions,blood
Endotoxic shock -- Metabolic Balanced electrolyte
acidosis solutions, 0.9% saline
Solutions for fluid therapy and their composition:
Solutions Electrolyte pH ENERGY kcal/L

concentration(mEq/L)
Na+ K+ Ca++ Mg++ Cl-
Colloidal solutions
Plasma(dog) 145 4.2 5 2.5 108 7.4 --
Electrolyte solution - - - - - - -
Replacement sol.
Lactated Ringer’s 130 4 3 - 109 6.5 9
solution
Ringer’s solution 147 4 5 - 156 5.8 -
Normal saline 154 - - - 154 5.4 -
Maintenance sol. -
2.5% 77 - - - 77 4.8 85
dextrose/0.45%
saline
2.5% dextrose ½ str 65 2 1 - 54 5 89
lactated ringer’s.
5% dextrose in - - - - - 5 170
water
World health organization solution for oral use only (1L)
Ingredients
Sodium chloride 3.5g
Sodium bicarbonate 2.5g
Potassium chloride 1.5g
Glucose 20g
Water qs add 1L
Procedure
1. Weigh sodium chloride, sodium bicarbonate and potassium chloride into a container
2. Add 100 ml of water
3. Place on air plate and stir well with magnetic stirrer
4. Slowly add glucose to stirring water and allow to dissolve
5. QS to desired volume (1L)
6. Store in refrigerator until used
7. Expiration of final product is 2 months from date of manufacture.
Final concentration (mM/L)

Na 90
K 20
Cl 80
HCO3 30
Glucose 111
Osmolality 333 (mOsmol/L)
DIGESTIVE SYSTEM
Pharynx:
Pharyngitis
It denotes inflammation of pharyngeal mucosa &sub mucosa.The inflammatory process

may extend to soft palate & tonsil leading to constriction of pharynx known as “angina” or
“cynanche”. It may be acute or chronic in nature.it is mostly observed in dog, horse & pig
characterized by purulent bilateral nasal discharge & regurgitation through nostrils while
drinking.
Aetiology:-
1. Physical cause:
 Injury from rough hard foods, dust, &foreign bodies.
 Irritation by smoke, gas, fumes through inhalation.
 Too hot or too cold food.
 Faulty use of instruments during exploration.
 Excess barking in dog.
2. Chemical cause:
Accidental ingestion of irritant chemicals or drugs.
3. Infective causes:
 Cattle:-IBR virus, Pasturella multocida, Mycobacterium tuberculosis, Spheropharus

necrophorus, B.lignieresi, Corynebacterium pyogens.
 Horse:-Strep. equi, Gastrophilus larvae, Para influenza virus, Rhino virus, Adeno virus.
 Pigs:-Streptococcus spp, Staphylococcus spp, B.anthracis, Aujesky’s disease.
 Dog:-Bordotella bronchoseptica (kennel cough), CD virus, ICH virus, Streptococcus
spp., Stapylococccus spp.
 Cat:-Streptococcus spp., Staphylococcus spp, Feline rhino-trachitis virus (feline flea),
Mycoplasma spp.
Pathogenesis:
The causative agents causes infection and causes swelling and pain resulting in painful
swallowing reflex leading to variable type of appetite. In severe cases extensive swelling of
mucosa causes partial obstruction leading to regurgitation of feed through nostrils .In some cases
infection may spread to retro-pharyngeal region causing swelling and occlusion of pharynx.
Clinical findings:
Dull and depression, off fed, stretching of head and non-inspiratory dyspnoea, mouth
breathing, protrusion of tongue, painful suppressed cough. Cough is more marked during feeding
and drinking .Regurgitation of food and water through nostrils .high rise in temperature in acute
case.
Purulent bilateral nasal discharge, oedema and congestion of soft palate, associated
lymph glands are swollen and painful. Cough reflex on deep palpation (induced cough)
Endoscopy reveals oedema of tonsil. Dog paws its head with fore feet accompanied with
salivation. Cat may show simultaneous laryngitis. Toxaemia may develop, prognosis is usually
favorable but death may be due to oedema of the pharynx with resultant asphyxia.
Diagnosis:
a) Characteristic clinical signs: bilateral nasal discharge, extension of head and neck,
cough on compression of pharynx, regurgitation of food through nostrils.
b) Endoscopic examination of pharyngeal mucosa.
c) Radiography and pharyngioscopy in small animals.
d) Culture and sensitivity of pharyngeal swab.
Differential diagnosis:
1) Pharyngeal paralysis: seen in rabies, bovine epimeral fever. Here drooling of

saliva - important clinical sign which may not be associated with inflammation.
Other accompanied signs in rabies are hyperaesthesia, ascending paralysis and
attacking complex. Shifting lameness, fever and enlarged superficial lymph nodes
are characteristics of epimeral fever.
2) Pharyngeal obstruction: signs are more severe, distress is much more and animal
make efforts to expel the foreign body like constant shaking of head, belching
type of movement. Obstruction can be found usually/manually.
Management:
1. Identify the cause.

2. Broad spectrum antibiotics depending on antibiotic sensitivity test to be
administered. If antibiotic sensitivity is not done
-Ampicilin + cloxacillin
- Sulfamethoprim
-2nd and 3rd generation cephalosporins
-streptopenicillin
3. Analgesics:
Anti-inflammatory drugs help to reduce inflammation and pain.
 Phenyl butazone.
 Nimesulide.
 Phenyl butazone+novalgin
Supportive treatment:
 Vitamin and mineral supplementation

 Animal should be offered soft palatable feed
 Soft bedding should be provided
 Vapour therapy –camphor or turpentine is added in warm water and the fumes
produced are inhaled which give a smoothening effect.
OESOPHAGIAL OBSTRUCTION: Also called as choke.
Definition
It is condition where there is obstruction of oesophagus. It could be complete or partial

with food mass, foreign bodies, inanimate object. Depending upon obstruction, various signs are
manifested-inability to swallow, regurgitation of food and water, continuous drooling of saliva,
severe distress and in ruminants bloat-called as secondary bloat or dependent bloat (cause is
away from rumen)
Aetiology:
Cattle: potatoes, cabbage, beat root, turnip, apple, onion, feed pellets, feed boluses, mineral
supplement bolus, anthelmitic bolus (sustained releasing bolus)
Horse: gelatin capsule, pieces of wood, dry food.
Canines: bones, vertebrae, soft toys, stones, pieces of wood, balls. Phosphorous deficiency
causes allotriophagia (pica) and is usually associated with choke
Cat: toys, food mass.
Pathogenesis:
Ingestion of object leads to physical obstruction hence peristalsis gets struck at the site
leading to inability to swallow. Followed by regurgitation through mouth or nostrils (but in
pharyngeal obstruction it is only through nostrils).
In horse both type of obstruction leads to regurgitation through nostrils (because of large
soft palate). If there is partial obstruction then liquid food is easily swallowed. Solid food gets
regurgitated. Local inflammation causes pain and animal will be in lot of distress.
Sequele:
If the case is not attended in time it may cause laceration and rupture of oesophagus,
stricture/stenosis. Oesophageal diverticulum-later on lumen enlarges which is called as mega-
oesophagus.
Extra luminal obstruction:
Obstruction of mediastinal region due to thymoma, cervical region due to enlargement of

retro-pharyngeal lymph node is possible.
Congenital defect-persistent aortic arch can also cause extra luminal blockage.
Clinical signs:
In cattle: Usually the obstruction is in cervical part and rarely at thoracic inlet. Animal suddenly
stops eating, shows anxiety and restlessness. Initially there is forceful attempt to swallow
followed by regurgitation. Continuous drooling of saliva, repeated chewing movement without
actually chewing feed. If obstruction is complete then bloat develops rapidly and adds to the
animals discomfort. Because of distension of abdomen, the respiratory distress and even systolic
murmur can be heard on auscultation on cardiac region.
In horse: Signs of restlessness are much more prominent and most of the times horses are
unmanageable. Horse makes forceful attempt to swallow followed by retching type of
movements. If the pain is severe at the site of obstruction the profuse sweating, stamping,
tachycardia and sometimes even rolling is seen. This is confused for colic for most of the times
and therefore immediate differentiation is required which can be done by passing of naso-gastric
tube.
In dogs: Here also dog is restless, constantly shakes head in order to expel obstructing mass.
Dog tries to swallow things followed by retching to regurgitate profuse salivation. Dog is excited
and is many a time nonresponsive to owner that is confused with rabies.
Diagnosis:
History: animal has tendency to ingest hard object or solid (potatoes, apple), habit of eating
inanimate objects due to pica.
Symptoms: forceful attempt to swallow, salivation, signs of distress, bloat in ruminants.
Palpation: palpation on the course of oesophagus is many times helpful for diagnosing
obstructing mass.
Passage of stomach tube / probe: done under sedation with xylazine or chloral hydrate.
Radiographic examination: barium meal x-ray.
Endoscopy: in animals gastro scope is used. It is a fibre-gastric endoscopy which reflexes in any
direction with light and magnified lens.
Oesophagitis: here is also there is pain and difficulty in swallowing but pharyngitis and
stomatitis will be accompanying.
Primary ruminal tympany: can be differentiated by passing stomach tube.
Treatment:
1) Sedation: animal is excited and in distress it may cause laceration. ex: chloral
hydrate- 10% solution, 0.5-1ml/kg
It has muscle relaxation effect, results in oesophageal dilation retrieval of
obstruction becomes easy.
2) Relieving of bloat: by abdominocentesis.
3) Location of obstruction: if near to the pharynx, then pressure is applied from
downwards, then by chital forceps foreign body is taken out. If it is in thoracic
inlet, attempts are made to push the obstruction using stomach tube.
4) Surgical intervention: obstruction in cervical part is relieved by oesophagotomy
whereas thoracic obstruction requires ruminotomy through oesophageal
opening forceps is passed and obstruction is taken out.
5) Antibiotics and analgesics for 3-5 days is given.
6) Animal is maintained on soft palatable diet.
RUMINAL DESORDERS
10-15% of the body weight is reticulo-rumen. Reticulo-rumen plays a very important role
in digestion and rumen microbial ecosystem is essentially designed to degrade ligno-cellulose
which is the most important component of feed. This ecosystem consists of bacteria, protozoa
and fungi. The rumen microbes basically are categorised into 4 different types depending on
their colonization.
1) Microbes which are freely suspended in the rumen.

2) Microbes which are loosely attached to the food particles.
3) Microbes which are tightly attached to the food particle.
4) Microbes which are attached to the rumen wall.
These microbes depending on their stain characters are grouped as gram negative
(predominant) and gram+ve.
Depending upon their substrate utilization, they can be classified as:-
Cellulose degrading microbe- rumenococcus albus, R.flavifaciance.
Hemi cellulose degrading – buferi vibro fibrisolvens.
Starch utilising-streptococcus bovis, bacteriodes aminophilus, and saccivomonas amylolytica.
Sugar fermenter- lactobacillus.
Acid utilizing- megasphaera elsedenii, oxalobacter foemigenus.
Protein degrading- bacteriodes rumenicola.
Urea degrading- streptococcus, staphylococcus, micrococcus.
Lipid utilizing- anaerovibrio lipolytica.
Methane producing/ generating- methanobravibacter vermenatiun.
Nitrogen fixing- clostridium pasteurinum.
Tannin degrading- streptococcus caprinus.
Protozoa:
The rumen contains both flagellates and ciliates, majority of them are ciliate. The ciliates
are broadly classified into two groups based on amount of cilia present on the body as
Holotrichus- Entire cell surface is covered with cilia.
Spirotrichus- there may be one or two patches.
Depending upon their nutritional requirements and their role in rumen, they are further divided
into-
Sugar fermenters- Isotricha spp, dasytricha spp.
Starch degraders- Entadinium, diplodinium.
DIGESTIVE DISORDERS
Simple indigestion:
`It may be defined as simple digestive disturbance which is clinically manifested by
inappetence, anorexia, complete or subclinical atony of rumen, infrequent defeacation and
constipation. There may be gradual reduction of ruminal motility resulting to retardation of
evacuation of food material.
Etiology:
 most common causes includes indigestible coarse type of feed offered to the animal
 Spoiled or moldy silage, mixing of soil, sand or bedding material in the feed.
 Sudden change in feed due to recent purchase of animal.
 Prolonged oral antibiotic therapy diminishes the micro flora resulting in indigestion.
 Inadequate supply of water – usually rumen contents should be semisolid, if it is a solid
due to lack of water mixing of feed will not occur.
Pathogenesis:
In simple indigestion, there is loss of motor function of reticulo rumen musculature. This
is either due to inhibition of normal stimulus of contraction or depression of the power of
contraction of ruminoreticular musculature. The rumen motility goes down both in frequency
and amplitude. This may be due to altered PH.
Heavy carbohydrate diet may lower the PH leading to an acidic environment and the PH
level may remain around 5, in this PH there is abnormal fermentation and over production of
lactic acid which causes further stasis of rumen.
On the other hand excessive intake of protein and NPN, there is excessive increase in the
rumen ammonia nitrogen and decrease of total volatile fatty acids and PH of ruminal fluid
becomes alkaline around 7.5. Due to this alkaline PH there is atony of rumen.
Ingestion of putrid toxic substances may lead to toxemia. Rumen contractions are absent
in toxemia. It may cause severe dehydration and hemoconcentration. There may be liberation of
histamine thus helps in inducing ruminal atony.
Clinical signs:
Depending on stage of indigestion signs are shown
a) Anorexia may be partial or complete
b) General attitude of animal is depressed
c) Decreased milk yield in lactating animal and decreased work efficiency in bullocks
d) Decreased ruminal contractions
There is no systemic reaction and other clinical parameters like pulse rate, heart rate,
temperature are usually in normal range. In some of the cases there may be passage of abnormal
feces which includes soft feces containing undigested feed particles.
Diagnosis:
a) History – recent purchase of animal, change in type of feed or environment.

b) Clinical signs- partial or complete anorexia, decreased ruminal contraction but all other
parameters are normal.
c) Physical and chemical examination of ruminal fluid – there will be decreased rumen
contractions and rumen may be doughy.
1. PH: there may be mild variation (0.2), normal 6.8 to 7.2
2. Concentration of microflora:
Concentration of protozoa under low field (LPF), is
+++ To++++ 20 to 30 (LPF)
++ 10 to 20
+ 1 to 10
In simple indigestion there is ++ or + but never nil.
3. Activity of protozoa : protozoa are large, medium and small. All the 3 types should have
normal activity / motility, non-motile and any one type of protozoa are suggestive of
change in the rumen PH.
All ruminal disorders
a) Acid indigestion / lactic acidosis :
Drastic PH decrease is less than 5.5 with absent of protozoa, history of access to high
carbohydrate diet. Animal will be totally dull. Splashing sound on ruminal palpation,
subacute type of microflora will be + but activity is nil.
b) Alkaline indigestion:
History of access to high protein diet, urea. In acute stage it may be life threatening
but animal is recumbent. Some animal shows CNS signs.
c) TRP – traumatic reticulo peritonitis:

Ruminal contractions are dependent on reticular contractions resulting in decreased
appetite. Presence of grunt upon pressing near xephoid region and recurrent tympani.
d) Displacement of abdomen :
Signs are typical bellowing just in front of paralumbar fossa in mid abdominal region.
This is common immediately after parturition due to involvement of uterus –
 Passing of scanty faeces

 Signs of abdominal pain
 If fluid is collected-PH =2, colour – ambor, no microflora
e) Vagus indigestion:
Chronic tympany/recurrent tympany
Treatement:
To improve ruminal contractions fallowing therapeutic regimen is adapted
Calcium supplementation – sub therapeautic dose of calcium boroglucanate @ 100-150ml,

prefarabaly given s/c so that the ruminal musle tone is maintained by slow release
Mgso4 supplementation – low dose carminative
-high dose-ruminotonic -100-150g
-at very high dose – laxative
Antimony potassium tartarate supplementation: antimony ions which are released induce
abomasal irritation and stimulate ruminal contraction
Eg: boviram (contains FeSO4 & Cobalt). Now it is added with trace minarals
External supplementation of yeast
Eg: Rumen bolus – Albendem, masticate
Ayurvedic preparations:
HB- Natural remidies-32 herbs are incorporated-40 – 60 gms
Herbostrong, Ruchamax- Dabar ayurvet
Herbosal- respal pharma
Anorexon forte – contains trace minarals which help as mineral supplement as well as activation
of microflora
Vit B complex & liver extract prepations – one of the causes for anorexia is suboptimal liver
effeciancy in lactic acidosis.
Eg: Belamyl – 10 ml for large animal
2 -3 ml for small animal
Cud transplantation – transplanting cud from healthy animal to affected animal
Dose – 5-10 ml /kg b.wt
ACID INDIGESTION OR ACUTE CHO ENGORGEMENT
Syn: rumen acidosis, grain engorgement, founder
*most common in goats

*main reason is ingestion of CHO rich diet
Definition:
A type of indigestion in ruminants due to ingestion of CHO rich diet which could by
severe toxiemia, change in ruminal ph towards acidic which inturn complicates as metabolic
acidosis, dehydration, complete ruminal stasis, recumbency fallowed suddenby death.
Etiology:
Sudden accidental ingestion of highly fermentable CHO diet. Most common source is
rich wheat floor, crushed grains, bakers dough, rotten fruits. It is observed that a mim. Of
60gm/kg b.wt is the required dose of fermentable CHO like crushed rice.
Pathogenesis
Access to crushed grains is more pathogenic than whole grains. The signs are exhibited
within 2-6 hrs of ingestion. Where in there is decrease in PH favoring the increase in population
of streptococcus bovis resulting in increased production of lactic acid there by reducing PH to
less than 5.5.This acidic PH activates the Lactobacillus species further reducing the PH up to 4.5
due to this there is increased osmolarity of ruminal fluid, due to this it withdraws fluid from
systemic circulation resulting in increased size of rumen.
The withdrawal of fluid from the blood causes dehydration and hemoconcentration.
The reduction in PH diminishes cellulolytic microbes and release of endotoxins and

histamine which causes ruminal stasis. There is increased absorption of lactate resulting in
metabolic acidosis, toxemia irreversible change in buffer system.
Clinical findinds
Clinical signs
Usually symptoms are visible 6 to 12 hrs after ingestion. Animal is dull showing signs of
abdominal pain (kicking at belly), increased situps, restlessness, distention of rumen leading to
distention paralumbar fossa (initially ) and in later stage there is bilateral distention of abdomen.
Absence of ruminal contractions, complete anorexia, grinding of teeth, elevated HR and RR,
subnormal temperature.Upon palpation of rumen bellotment – fluid flashing sound.
In some cases there is regurgitation of ruminal contents, usually diarreoa is the outcome
is about 24 hrs .the feces are semisolid, grey colored with foul smell. Advanced cases show CNS
signs like apparent blindness, staggering gait, head pressing and even laminitis.
It is categorized as(categorization helps in treatment):
 Peracute
 Acute
 Subacute
 Peracute :
 Recumbency
 More than 10% dehydration
 MM congested
 Pupils are dilated
 Typical fluid splashing sound from atonic rumen
 HR more then 120 / min
 Atonic rumen PH is 5.0 (4.5 – 5.0)
 Acute :
 Recumbecy / standing
 Shows ataxia
 Pupils dilated but response to light
 HR is 90 – 100 / min
 PH is 5.5 (5.0 – 6.0)
 Fluid splashing sound from rumen
 Atonic rumen
 Dehydration between 6 – 8 %
 Sub-acute:
 Doughy rumen
 HR is less than 90
 RR is 22 – 25 / min
 Decreased ruminal contractions
 Standing position
 No much signs of dehydration
 PH between 6 – 6.8
 No specific treatmet is required
 However NaHCO3 can be administered as precautionary measure
 Liver extracts also advised.
Diagnosis:
1) History
2) Clinical signs –
Acute, subacute or peracute- advanced cases show diarrhea, feces may contain
partially digested food grains with affensive small. In some of the per acute cases
there is regurgitation of ruminal contents through nose. Some animal show signs of
laminitis due to vitamin deficiency (Thiamin).
3) Lab investigations –
Examination ruminal fluid reveals
a) PH is 4.5 to 6.0
b) Absence of protozoa
c) Sub-acute type – less microflora but motility is sluggish
d) In acute cases microflora are totally absent and even traces
of microflora are not seen
Gram + organisms are more in stained smear of ruminal
fluid.
e) Color is milky grey ,
f) Smell is sour and acidic
4)MBRT: elevated to 10 - 15 min (normal value is 3-5 min)
5) SAT: is higher than normal of 7-9 min or absent
6) Biochemical tests:
 Blood lactate estimation > 25 mg / dl

 HCO3 is decreased because lactic acid is proton donor. The level falls to 20-
22m moles / ltr as against the normal value of 24/30 mmoles/ltr
 Hypocalcaemia is seen – sub clinical < 6.5 mg / dl
 Blood glucose is increased in initial stages followed by slight decreased or
normal glucose level
 Enzymeslike SGOT, LDH, serum arginase, gamma glutanyl transferase
(GGT) are elevated due to hepatic insufficiency.
1. Diffused peritonitis –
- Increased peritoneal fluid
- Pyrexia is seen which is not seen in lactic acidosis
- No specific change in ruminal fluid but change in peritoneal fluid whiah is turbid
with flakes and tends to clot
2. Coliform mastitis –
- Septicemia is very severe
- Animal is recumbent
- No change in ruminal parameters
3. Simple indigestion-
- decreased motility
- dull
- microflora + to ++
- ruminal PH is 6.6 – 7.4
Treatment:
First aid:
- withhold of water for 8 – 12 hrs though the animal is thirsty and dehydrated
- If apetite is present (usually anorectic), provide good quality hay, so that cellulytic
organisms get activated and suppress streptococcus bovis.
- If the animal is able to bear weight, little exercise should be provided. If diarrhea is
seen it is considered as good prognostic sign because it helps in evacuation of
toxic content of GIT.
Actual treatment:
1) Correction of PH and prevention of further productionof lactic acid by using

alkalizing agent like NaHCO3 and MgOH dose – 1gm/kg b.wt as 8 – 12 hrs
interval for 2 – 3 days.
Further production of lactic acid is stopped by administering oral or intraruminal
antibiotics to prevent lactic acid producing bacterial over growth.
Ex: amoxicillin – 20 mg / kg b.wt
Chloramphenicol- 50mg / kg b.wt
OTC – 20 mg / kg b.wt
2) Restoration of fluid and electrolyte balance:
NaHCO3 parentally to restore metabolic acidosis. Alternatively RL can be
administered as per the fluid requirement of the animal. Lactate is converted into
bicarbonate in liver and helps in reducing metabolic acidosis.
3) Rejuvenation of ruminal microflora and creating a positive ruminal ecosystem.
With above treatment, if the animal does not show any interest in ingestion for
about 10 days, we have to restore ruminal ecosystem. This done by oral
administration of Herbostrong, HB, motility inducing drugsare not indicated like
potassium antimony tartarate, where already ruminal mucosa is damaged and this
may cause exfoliation. But the best treatment is cud inoculation 5-10ml/kg b.wt.
Supportive treatment:
 Antihistamines like pheneramine maleate – 10 ml in large

animls and 3 ml in small animals.
 Corticosteroids (0.5mg/kg b.wt) in peracute cases to
prevent shock.
 Thiamine supplementation at the rate of 10 mg / kg b.wt
gives encouraging results.
 Parasympathomimetics like neostignin, calcium to attempt
restoration of ruminal motility.
Prevention:
 Education of formers not offer festival waste products.

 Increased roughage feeding.
 Avoiding grain rich feed.
RUMINAL TYMPANY/BLOAT
It is solely a disease of Ruminants. It results either due excessive gas production or

physical obstruction of the process of eructation of gas.
Classification:
1) Frothy/Primary/Leguminous/Dietary/Pasture Bloat
2) Free gas or Secondary bloat
Frothy Bloat
More life threatening. This is the primary bloat and is caused due to gas trapping off in
the form of stable froth.
Secondary Bloat
 Here there is obstruction in eructation

 Any obstruction in the 2 pathways (Oesophagus or GI Tract) leads to
accumulation of free gas.
Etiopathogenesis
The most common cause is grazing on lush green succulent pasture which is usually
immature and in pre-blooming stage. Leguminous pastures are more commonly associated with
frothy bloat.
Fallowing precipitating factors are associated with FROTHY BLOAT
 Animal factors
 Plant factors
 Microbial factors
Animal factors:
Incidence is common in some animals which are called as bloaters and is also common in
senile animals. The main cause is low production of saliva which is rich in mucinous anti-
frothing factor which reduces surface tension.
Draft animal- salivation is associated with feed intake, so in draft animals, less salivation
leading to bloat.
Senile animals- More wear and tear of teeth (table surface) leads to less chewing causing
less salivation resulting in bloat.
Plant factors:
Leguminous plants are more contributing factors, these contain-
 Cytoplasmic Proteins:- When these are released, they change to some structures
and coat on the top layer of rumen there by trapping gas.
 Large amounts of protein enzyme ESTERASE in leguminous plants acts on
peptic acid and N-acetyl glucouronide, which converts ruminal contents into more
viscous fluid
 Increased chloroplast particles, these adhere to outer surface of gas bubbles and
prevent coalesce and hence gas gets trapped in the form of small bubbles.
 Tannin has anti-frothy action is low in leguminous plants/succulent fodders.
Microbial factors:
 Slime producing bacteria-causes change in the surface tension trapping gas.

 Mucinolytic bacteria- Causes lysis / degeneration of mucin present in saliva which is an
frothy agent.
 Protozoa (Ophryoscolex spp)- Rupture of this leads to release of slime like material
which contributes for formation of stable froth
Effects
 Increased frothiness.
 Distension of abdomen called as capped para lumbar fossa, but later these change to
bilateral distension, which results in reduced lung capacity indicated by laboured
respiration.
 If not attended it leads to death due to hypoxia.
Clinical signs
Per acute bloat can cause death in animals. In acute form, signs are seen within 6-8 hrs.
Animal stops feeding, there is steady enlargement of left Para lumbar fossa also called as Capped
appearance of Para lumbar fossa. As the condition worsens there is restlessness, severe
dyspnoea, tachycardia, hurried respiration, and sometimes open mouth breathing with frothy
salivation, frequent defecation and micturation. In some animals signs of abdominal pain like
kicking at belly, frequent sit-ups are noticed followed by death.
Diagnosis
1) History of access to leguminous fodder.
2) Symptom- Gaseous distension of abdomen, Capped Para lumbar fossa, hurried breathing
and open mouth breathing.
3) Confirmatory differentiation: Paracentesis of Rumen is the best method. When left
paralumbar fossa is punctured, frothy & free gas keeps coming and animal feels
comfortable
Treatment
First aid
 Trocarisation to release gas

 Placing a stick in the mouth and tied behind the ear. This helps in eructation of gas. By
this animal moves its tongue thus salivation increases and help in reducing formation of
froth.
 Animal placed in well ventilated place.
 Application of coal tar to the tongue also increases the production of saliva which is rich
in mucin
Actual treatment
Use of non-ionic surfactants
a) Silica in dimethicone- Bloatosil Workhandt

available in both bottles of 100 ml and 250 ml
Dosage: Adults- 75-100 ml p/o, repeated every 8-12hrs.
It helps to coalesce air bubbles and free gas is released easily out, also reduces surface
tension.
b) Herbal preparations- Afanil- Dabun ayurvet
Equally competent with bloatosil and is also less costly
Dose is 50 ml for adult by oral or intra-ruminal
c) Synthetic polymers are also used
Poloxalene- (Pleuronic get- 64)
Ethyl cellulose gel- (Terric Get)
d) Dose- adults 25 gm-50 gm- orally
e) Other herbal preparations like Bloatospel- 50-60gm- mixed in water
f) Carminatives mixture
Supportive treatment
a) Anti-histamine
b) Gastric stimulants
c) Respiratory stimulants in life threatening cases
ALAKALINE INDIGESTION
It is a type of indigestion commonly seen in ruminants because of faulty feeding of

proteins or accidental ingestion of urea resulting in increased production of ammonia in the
rumen which is clinically manifested by signs of urea toxicity or ammonia toxicity
Etiology
1) Accidental ingestion of urea (fertilizer)-toxic doses 0.5 gm/Kg.

2) Exclusive paddy straw feeding.
3) Excessive ingestion of protein rich feed.
4) Placentophagia-contain high amount of protein.
5) Guar feed-highly fermentable in rumen-very common in goats.
6) Sewage water drinking-has high E.coli which changes pH towards alkalinity.
7) Eating of garden soil has microbes which changes the pH towards alkalinity.
Pathogenesis
Urea decomposed paddy straw or protein decomposition release lerge amount of ammonia
that makes the rumen pH highly alkaline to about 8-9.5, ammonia is absorbed into the rumen and
the animal exhibits signs of ammonia toxicity
Clinical signs
Sudden development of anorexia, salivation and lacrimation, there could be decreased
contraction or ruminal atony, signs of abdominal pain-groaning, constant sit-ups, kicking at the
belly. Faeces are usually pasty, pungent smelling. The vital parameters like HR, RR, PR are
increased there is no significant change in body temperature. In advanced cases nervous signs are
evident like convolutions, falling down on the ground, ophisthotonus, peddling. During
convulsive stage there is recurrent episode of bronchial spasms indicated clinically by interrupted
respiratory cycles and if not treated, most of animals die during this stage.
Diagnosis
1) History-Access to urea or exclusive feeding of straw.

2) Clinical signs-Atonic rumen, complete anorexia, signs of abdominal pain, passing of
pasty faeces, convulsions.
3) Lab: Ruminal fluid examination.
 Colour-Dark brown
 Consistency-Watery
 Smell-Putrefied/Fishy/Ammonical
 pH- >8.5/Up to 10
 Microscopically there is absence of micro flora
 MBRT, SAT time is elevated
4) Biochemistry-Increased BUN in blood and CSF to about 2-3 times
Differential diagnosis
1) Lead poisoning- Here also nervous signs are seen, but there is H/O licking point.
2) CHC poisoning-Which is applied as ecto-parasiticide or pesticide, here convulsive
episodes are more pronounced and response to calcium therapy along with history may
help in differentiation.
Treatment
1) Changing ruminal pH and stopping further ammonia production. This can be done by
administration of acetic acid- 4%, 100-500 ml (5-10 ml/kg body wt). Commonly vinegar
bottles are available as 1 litre, commercial lactic acid preparations are also used.
2) Preferably intra ruminal antibiotic is advised to check the growth of unwanted microbes,
Sterptopenicillin- 1 large dose.
3) Liver tonics- Play a vital role. B-complex preparation with liver extract is more effective
to improve to impaired liver function.
4) Cud transplantation for rejuvenation of micro flora.
TRUAMATIC RETICULO PERITINITIS (TRP) AND ALLIED DISORDERS /

SYNDROME
Synonyms: - Hardware disease-(means nails, parts of tense wire, metallic substance),

Traumatic reticulitis
Allied disorders are vagus indigestion (due to damage to vagus nerve), Diaphragmatic hernia
and aberrant injury to other vital organs. Also called as Hardware disease because 90 % of
conditions are due to ingestion of metallic foreign bodies. TRP is a common field condition
encountered in bovines which is clinically characterised by sudden onset of anorexia,
decreased milk yield in lactating animals, recurrent tympani, ruminal stasis and associated
signs if abdominal pain.
Etiology
Majority of the cases are caused by ingestion of metallic foreign bodies and as the
animals (bovines) are having indiscriminate feeding.
Pathogenesis
The ingested foreign body goes to the rumen. 1st to dorsal sac then to ventral sac, there
after by ruminal contraction it gets passed into Reticulum. Mucosa of Reticulum has got a
honey comb structure so it gets trapped in the reticulum (cranio-ventral location) there by
causes traumatic reticulitis. There after the foreign body keeps on piercing through the
reticulum wall that result in local peritonitis due to spillage of reticular contents. Initially it is
acute and if the foreign body gets adhered then results in chronic peritonitis. Extensive
spread of infection in peritoneal cavity causes diffused peritonitis which is always acute that
responsible for deaths in majority of cases
Sequalle of ingested foreign body
Ingestion causes Traumatic reticulitis
Acute localised peritonitis
Recovery if size of Chronic local peritonitis FB penetrates Acute diffused

FB is small. This is Diaphragm peritonitis
very rare
Diaphragmatic Vagus Leads to death Damage to

hernia indigestion pericardium
Traumatic pericarditis
CHF
Marked by jugular
palpation
Uncommon sequelae
1) Rupture of left gastro-epiploic artery causing massive internal haemorrhage leading to

instantaneous death.
2) Traumatic spleenitis, spleenic abscess, diaphragmatic abscess. If foreign body is
small lower anterior part of reticulum is the most common route of escape of foreign
body out of the rumen.
3) Aberrant passage of FB into thoracic cavity can cause lung abscess, traumatic
peritonitis, and mediastinal abscess.
4) Right axial abscess (right elbow)- here FB due to presence of rumen and reticulum on
left side, FB passes on right side and gets fixed in right intercoastal muscle leading to
abscess formation.
5) If FB is very sharp, results in heart rupture and haemorrhage called as cardiac
tempanode leading to cardiac arrest & death.
Clinical findings
Acute local peritonitis: Onset is quite sudden, complete anorexia, sharp decrease in milk
yield, animal shows signs of abdominal pain-kicking at belly, reluctant to move, cautious
gait, This is accompanied with grunt. This sign is more prominent when animal is
walking down the slope, due to gravity there will be pressure on foreign body by
abdominal organs.
Appearance: Tucked up appearance (kyphosis)- Dorsal curvature (arched back). All this
indicates some abnormality at xephoid region. The sign of pain and grunt are much more
pronounced during urination and defecation.
Systemic reaction:
Moderate fever- 103-104 0F, high pulse rate, RR is increased (due to ongoing toxaemia).
Usually ruminal contractions are decreased with suspended rumination and there is
always presence of moderate tympani which is called as recurrent tympani. Usually there
is constipation and passage of dry hard faeces (due to decreased intestinal motility
because of peritonitis and toxaemia-ingesta remains for longer period and there is
increased water absorption leading to dry hard faeces)
Pain:
Deep palpation with fist behind xiphoid cartilage-animal immediately shows grunt. This
is called as Fist test.
In chronic local peritonitis, the signs develop gradually.
Diffused peritonitis:- Always acute
Onset is sudden with prolonged toxaemia, and there is severe depression. If the
case is presented early, temperature is usually high but later it is subnormal. Most of the
times animal is recumbent indicating terminal stage and at this stage if treatment is not
initiated then animal enters into state of coma and death. But in terminal stage when the
animal is in lateral recumbency, bradycardia with arrhythmia is noticed, highly congested
cyanotic membrane.
Diagnosis
1) History- Pica
2) Clinical signs- Tucked up appearance, winged elbows, cautious gait, passage of hard
pelletted faeces with mucous.
3) Clinical examination of animal-

 Appearance/Posture- Tucked up appearance.
 Winged elbow
 Physical examination- BAMBOO TEST/PLOE TEST- Thick wooden pole is
passed behind the elbow and the animal is lifted. If animal makes loud grunt
sound it indicates pain on xiphoid.
 Either pinch/Spinal pinch-Here because of wither pinch animal makes
lardosis posture with loud grunting sound. If the grunt is mild then it can be
heard by keeping the diaphragm of stethoscope on the chest/trachea.
 Williams’s method of simultaneous palpation and auscultation (At 7-9th
intercostal space):- Reticulum approximates Diaphragm. The chest piece of
stethoscope is kept and by right hand 1st rumen is palpated/pushed. By this
some of the ruminal contents are moved to Reticulum which can be heard as
reticular splashing sound. If this with grunt it is indication of TRP.
4) Laboratory investigation:
a) TLC & DLC help to differentiate type of peritonitis. The typical picture of
acute peritonitis is neutrophilia with shift to left- This is considered as –ve
shift to left, since number of band cells does not exceed mature neutrophills
count.
 Normal: Neutrophills-30% and Leukocytes-60%
 But in TRP N=60% and L=38-40%
 TLC-Leukocytes nearly 10-12000/ µl is indicative.
 Leukocytes coupled with neutrophills which is negative shift to left
indicate acute localised peritonitis.
 Band cells are >6%.
 In chronic local peritonitis- Moderate leukocytosis <11000/ µl.
Neutrophilia is associated with monocytosis, i.e., >5% monocytes.
 Leucopenia is always suggestive of diffused peritonitis (<5000/ µl).
Immature neutrophills exceed the mature neutrophills which is called
degenerative shift to left (>40% band cells)
b) Peritoneal fluid analysis: Peritoneal fluid is collected by abdominal
paracentesis- 10 cm cranial and 10 cm to the right side of the umbilicus. In
adult cattle the tip of needle should not be too sharp to avoid injury to visceral
organs. (Needle bore- 16-18 gm). 10-20 ml fluid is collected and examined for
 Nucleated cell count: this is done by using WBC diluting fluid &
haematocytometer. The cells are >6000/ cu.mm indicate diffused
peritonitis.
 Protein estimation: Total protein-3g%- This indicates some exudates
accumulation and inflammation.
 Fibrinogen level- >10 gm/ Lt
5) Ferroscopy:
Magnets/metal detectors- to and fro movements are made at Xiphoid region.
6) Radiographic investigation:
500 mA x-ray machine is required for large animals. It not only helps in
indicating metallic FB but also help in identifying its location and integrity of
diaphragmatic line.
7) Laparoscopy:
Right flank laproscopy with semi-rigid fibre optic laproscope is also proving as a
reliable diagnosttic method.
8) Explratory laperatomy.
a) Bovine pyelonephritis: Signs of abdominal pain are seen but this is accompanied with
pus or blood in the urine.
b) Abdominal displacement: Here also ruminal stasis, passing pasty faeces and prolonged
inappetance are indicative but recurrent tympani, cautious walking, and kyphosis are
absent. Ballooning structure at mid flank region is seen in displaced abomasums. Here
faeces are scanty and pasty but in TRP faeces are hard, mucous coated.
c) Ephemeral fever: The illness only for 3 days, shifting lameness lymph node
enlargement & seasonal occurrence is common.
Treatment: 2 approaches.
1) Conservative medical therapy:
This is done when surgery can’t be taken due to debility of the animal, advanced
pregnancy. Here 1st priority is immobilisation of the animal. This is done by confining
the animal in a box-stall with a minimum space for movement immobilization facilities
formation of adhesions-restricts further passage of FB.
2) Surgical approach: “Rumenotomy”

In this usually left flank rumenotomy is done.
 If adhesions are there, they are removed to avoid complications like-Vagus indigestion.
 Presence of FB is cheeked.
 Extention of peritonitis is arrested.
 Then rumenotomy is advocated. 2/3rd contents are removed and then reticulum is
searched for FB.
 Recovery depends on time of surgery & complications.
 Failure of improvement is due to diffused peritonitis, escape of FB beyond diaphragm
and involvement of other organs.
Prevention & Control:
a) Chaffed feed should be passed over a magnetic field/belt to trap metallic objects.
b) Feeding of magnets –cylindrical/ bars with rounded edges.
(Size=7.5 long, which can be retrieved periodically.)
TAUMATIC PERICARDITIS
Inflammation of pericardium / pericardial sac by sharp foreign body and majority of the times it
is originating from reticulum subsequently leads to development of toxaemia & signs of
congestive heart failure (CHF)
Clinically it is manifested by fever, initial tachycardia followed by muffled heart sounds,

jugular pulsation followed by chording of jugular vein. A tendency to develop oedema at various
places is observed. Majority of the times, it is brisket but, even anasarca, ascietis and
hydrothorax can also be seen.
Etiology:
A sharp foreign body originating through reticulum (as a sequallae of TRP) is the main
cause. The incidence is more common in last trimester of pregnancy or immediately after
parturition.
Pathogenesis:
Penetrating foreign body causes inflammation of pericardial sac. Introduction of micro-

organisms sets in the infection. Initially there is net increase in pericardial fluid but later it
becomes thick. Adhesions formed between the pericardial fluid surfaces causes constructive
pericarditis which leads to decreased vital space for systole and diastole of the heart. Profound
toxaemia due to infection and pressure on the heart are responsible for majority of the clinical
signs.
Limited vital space in the heart leads to incomplete filling and retention of blood in
venous circuit which is manifested by signs of CHF. Ex: Jugular pulsation, complete anorexia
Clinical findings:
Profound depression, complete anorexia, persistent fever and rapid weight loss are
commonly observed. Initially there is tachycardia and increased respiratory rate (40-50/min), but
as the case advances increased pericardial adhesions make heart sounds less audible which are
called as muffled sound. Sometimes fluid splashing sound is audible on auscultation.
Pericardial frictional sound is very much evident on auscultation. Initially there is jugular
pulsation which in due course of time becomes engorged leading to chording of jugular vein.
There is a tendency to develop oedema due to passive venous congestion. Oedema is severe at
the brisket extending to ventral abdomen.
In few cases there could be development of ascietis-clinically ascertained by fluid thrill.

Other organ inefficiencies are clinically indicated by alternate diarrhoea and constipation,
complete anorexia, palpable enlargement of liver beyond 8th coastal arch and evidence of
proteinuria indicating renal insufficiency.
Diagnosis:
 History- Animal may be advance pregnant or recently parturated.

 Earlier signs like- Recumbancy, tympani, kyphosis, winged elbow are suggestive.
 Clinical signs- evidence of pain near xiphoid, jugular pulsation, persistant fever,
initially tachycardia followed by muffling, prolonged toxaemia and brisket
oedema.
 Lab investigation- It is done at 4-5th inter-coastal space with a special needle of 18
gauge and10 cm length. Fluid is watery in the initial stage of pericarditis, change
to thick, pasty and smelling in later stage.
 Radiography.
Bovine Leukaemia:- EBL/ Bovine lymphosarcoma- HF and their crosses are more
succeptible. Incidence is more common in Deoni cattle.
Especially cardiac form of EBL almost resembles TP. Here also low HR and brisket
oedema noticed.
But laboratory investigation indicates very high leukocyte count (>30,000/ µl) along with
lymphocytosis instead of neutrophilia, immature lymphoblasts are prominent in peripheral
smear/ lymph node biopsy.
Diaphragmatic Hernia (DH)
Herniation of reticulum through diaphragm into thoracic cavity. Majority of the times it is
consequence of TRP- it is clinically characterized by recurrent tympani which is frothy type,
prolonged anorexia, displacement of heart sound anteriorly.
Etiology:
a) Sequelae to TRP. Most of the cases are outcome of weakening of diaphragm due to the
lesions/ injury caused by TRP
b) DH is common in buffaloes, because there is inherent weakness at the centre of
diaphragm just opposing reticulum. Incidence is more in pregnant animals, due to gravid
uterus which causes increased intra-abdominal pressure facilitating herniation.
c) Sometimes severe straining during act of parturition also precipitates herniation.
Epidemiology:
The incidence is more common n buffaloes especially in pregnancy or immediately after

parturition.
Pathogenesis:
Lesions of TRP or FB weakens diaphragm and sometimes it may cause laceration leading
to herniation of the reticulum into the thoracic cavity. Possibility is more during advanced
pregnancy and immediately after parturition. Increased intra-abdominal pressure due to gravid
uterus, forceful contractions during calving facilitates herniation.
Outcome:
Reticulum causes adhesion with the diaphragm and thoracic organs leading to decreased
contractions. Fixation of reticulum causes closure of reticulo-omasal orifice, which interferes
with outflow of contents into omasum which this result in accumulation of contents. There by
forming of stable froth (frothy bloat). Intra-ruminal pressure in the advanced stage of DH
becomes so much that the contents sometimes are regurgitated through mouth and nostrils.
Clinical features:
Capricious type of appetite (variable type), there is loss of condition, persistent
abdominal distension/tympani, grinding of teeth, faeces usually are scanty and most of the times
it os pasty. Regurgitation of ruminal contents are noticed in the advance stage of DH. Most of
these cases carry history of earlier treatment for prolonged inappetite without success/
improvement. On auscultation, heart sounds are displaced anteriorly coupled with systolic
murmur. The reticular sounds are audible just behind the cardiac area (5-8th inter-coastal space).
Adhesions formed between reticulum and thoracic organs makes prognosis unfavourable
and most of the cases die in about 3-4 weeks of time after onset of bloat.
Diagnosis:
1) History- History of signs of TRP

 History of discomfort, pain at xiphoid, Recurrent tympani and arched back
 History of pregnancy or recent parturition.
2) Clinical signs- chronic recurrent tympani which is frothy type confirmed by paracentesis,
displaced heart sounds and reticular sounds, prolonged in appetite unresponsiveness to
treatment, regurgitation of ruminal contents are suggestive.
3) Radiography of thorax: 500 mA
 Barium meal contrast radiography reveals herniated reticulum.
 Plane radiograph reveals displaced heart and discontinuity in diaphragm.
4) Exploratory laprotomy
Differential Diagnosis:
Vagus indigestion- here also chronic recurrent bloat, hyper motility of rumen, but
displacement of heart & reticular sounds are absent.
Treatment:
Surgical intervention approaches are
1) Trans abdominal ventro-lateral laprotomy- on right side or left side is done in dorsal
recumbency.
 Surgical intervention is taken along with coastal arch.
 Adhesions are removed.
 Reticulum is pulled back.
 Herniarrhapy or Hernioplasty is done.
2) Thoaracotomy.
 Indicated when too much adhesions are found.
 1/3rd of ribs is resected and provision is made to approach hernial ring. Adhesions
are removed and reticulum is pushed back and herniorrhapy is done to close the
defect in diaphragm.
VAGUS INDIGESTION
Synonym: Hoflund Syndrome
It is chronic disease of fore stomach and abomasum which is clinically characterized by

prolonged anorexia, scanty patsy faeces, papple shaped abdomen due to gradual distension and
weight loss.
Etiology
1) Sequelae of TRP – In majority of cases, either FB or the lesions associated with FB cause
damage to vagus nerve especially ventral branch which ramifies ventral part of reticulum.
2) Abscess near reticulo-omasal junction.
3) Actinobacillosis of rumen and reticulum.
4) Lymphadenopathies- Due to EBL, TB adjoining the vagus nerve in thoracic cavity.
Pathogenesis
Vagus indigestion can be caused by two mechanisms depending on the part of vagus
nerve affected.
a) Achalasia- dysfunction of reticulo-omasal sphincter, this is called as anterior functional

stenosis. No outflow of reticular contents to omasum leading to accumulation of contents
in rumen & reticulum and results in ruminal hyper motility and develops into frothy bloat
leading to distension of abdomen. Similar pathogenesis is observed in diaphragmatic
hernia. Over a period of time because of this chronic vagus indigestion, there is typical
appearance of abdomen. If animal is observed from rear side – sagging on right side
which looks as pear shaped and capped prominence on left side. This is called as papple
abdomen- followed by uniform distension of abdomen in later stage.
b) Posterior functional stenosis which results because of pyloric stenosis. No out flow of
abomasal contents to duodenum and regurgitation of abomasal contents in anterior
chambers (internal vomition). Low pH in rumen due to hydrochloric acidosis called as
latent hydrochloric acidosis. This is called as abomasal reflux syndrome.
Varying degree of dehydration, metabolic alkalosis due to hypochloremia are major systemic
changes.
Clinical findings
Prolonged inappetence unresponsive to treatment, recurrent episodes of frothy bloat,

typical appearance of (papple shaped) abdomen, passing of scanty faeces. Initially hyper motility
of the rumen (4-5 contractions / 2 min) followed by hypomotility of rumen. Bradycardia with
systolic murmur audible during inspiration is characteristic.
Diagnosis
1) Clinical signs- papple shaped abdomen, unresponsive prolonged anorexia and recurrent
bloat.
2) Laboratory investigation- Reveals hypochloremia and hypokalemia, pH of the ruminal
fluid is acidic due to elevated chloride indicates abomasal reflux.
Differential Diagnosis
1) DH- most of the signs are similar except displaced heart sounds.
2) Omasal impaction- impacted firm mass can be palpated per rectally.
Treatment
Usually prognosis is unfavourable because the extent of damage to vagus nerve is unpredictable
1) Rumenotomy and lavage with warm water.

2) Nervine tonics- improve functioning ability of the nerves. Ex: B1, B6 and B12.
3) Administration of DOSS- Dioctile sodium sulfo-succinate acts as motility modifier,
dispense substances and causes segregation of contents and helps in evacuation. It is
administered as 120-130 ml in 5-6 L of mineral oil.
4) Efficacy of cisapride, also a motility modifier is not yet ascertained in large animal
practice.
ABOMASAL DISPLACEMENT
It is a displacement of abomasums from its normal anatomical position, it may be

towards the right side or left side, but clinical signs are same for both the types.
Normal position- Mid ventral line on the floor of abdomen slightly towards right side.
Left side-left displacement of abomasum-LDA
Right side-right displacement of abomasum-RDA
LDA is most common. This is an abomasal disorder where abomasum is displaced towards left
side and is trapped between rumen and left abdominal wall.
Etiology:
Atony of abomasum and accumulation of gas resulting in distension of abomasum is the primary
cause responsible for displacement and there is always link between high incidence of LDA and
low roughage high concentrate diet.
Precipitating factors:
 Immediately after parturition the incidence is more (3-4 days post partum)
 Immediately after parturition the animal is lifted from roughage to high concentrate diet
responsible for hypertonicity of abomasums (increased volatile fatty acids)
 During pregnancy rumen is shifted slightly by gravid uterus so abomasum is free to move
on abdominal floor so it moves to left side. But after parturition, involution of uterus
allows rumen to assume original shape on the abdominal floor, hence abomasums is
trapped between rumen and left abdominal wall.
 Rarely the condition is also noticed in heifers due to oestrus during mounting.
 In breeding bulls also during mounting displacement is seen but this is also rare.
 Post-partum hypo calcemia is also one of the precipitating factor for the occurrence of the
LDA which contributes for abomasal hypo motility.
Changes associated with displacement:
Compression of abomasums results in abstruction like syndrome. It is estimated that a

cow weighing about 400-450 kg can cause accumulation of 35 lit of fluid in trapped
abomasum. Biochemically there is a loss of chloride due to increased secretion of HCl,
resulting in hypochloremia and in due course of time, hypovolemia. Systemically there is
ongoing dehydration, metabolic alkalosis and in untreated cases there could be signs of
shock. In right side displacement, the dilated trapped abomasum can undergo about 180-2700
clock wise or anti clock wise twist resulting in abomasal volvulus which is life threatening.
Trapped abomasum stops further forward passage of ingesta indicating a true obstructive
episode.
Clinical findings:
Prolonged anorexia, drop in milk production, signs of ketosis (due to energy deficit) like
sweetish smell to urine, loss of condition. This is called as secondary ketosis. Distension of
the mid flank depending on the left or right displacement which resembles balloon like
enlargement.
The condition is further confirmed by simultaneous auscultation and percussion over the
distended organ or area between 9th -12th intercoastal spaces in an imaginary line drawn from
left midflank to elbow. Typical high pitched resonance sounds are heard and are called as
‘ping’ or ‘pebble in well’ sounds. Other signs are passing of scanty faeces, discomfort and
abdominal pain.
Abomasal volvulus in RDA reveals sudden onset of abdominal pain, crouching,

tachycardia followed by recumbency and death ensures within 36-48 hrs due to shock &
dehydration.
Diagnosis:
1) History of recent calving.
2) Clinical signs.
3) Simultaneous percussion & auscultation at 9-12th intercoastal space with evidence of
ping is characteristic.
4) Lab-Investigation--> Cl- & K+ estimation.
 Normal Cl- is 90 mEq/L. Hypochloremia <80 mEq/L.
 Haemoconcentration- increased PCV.
 Liptan test- paracentesis of displaced abomasum at 11th inertcoastal space and
contents investigated. Usually colour of the fluid is amber coloured, pH is 2-4
and protozoa absent.
5) Laparoscopy- highly torturous vascular and pink colour differentiates abomasum
from rumen.
6) Explanatory laparotomy.
Differential Diagnosis:
1) Primary ketosis- ketonuria is severe, response to glucose therapy without relapse.

2) TRP- winged elbows, grunt on palpation, fever are indicative.
Treatment:
1) Calcium supplementation improves tonicity of abomasum (calcium boro gluconate at

200-400 ml i/v or s/c). Tonicity causes flow of abomasal contents leading to decrease
in size of abomasum & the abomasum may come to normal site.
2) Concentrate diet is stopped & roughage feeding is advised.
3) Fluids & electrolytes- Ionic NaCl depending upon dehydration reduces metabolic
alkalosis.
4) Oral administration of mineral oil (3-5 L), mixed with Mg(OH)2 (500 gm).
5) Rolling of animal has been tried with good results.
LDA- animal is laid down on left lateral recumbency with forelimbs and hind limbs
tied separately, with a sudden jerk animal is brought in dorsal recumbency and with a
similar jerk it is rolled on to right lateral recumbency.
6) Surgical intervention
Right paramedian abomasopexy.
Right paralumbar omentopexy.
Abomasitis / Abomasal ulcer
Long standing Abomasitis leads to abomasal ulcer
Synonyms: Gastritis of Ruminants.
Definition: Inflammation of abomasal mucosa and clinically it is manifested by progressive

anorexia, loss of production and if damage to the mucosa is severe, then results into ulcers that is
clinically manifested by progressive anaemia and black tarry coloured pasty faeces.
Hemoglobin in stomach combines with HCl forming acid haematin which imparts
brownish colour to the faeces.
Etiology:
1) It is stress related disease, results in increased production of ACTH that stimulates the
release of gluco-corticoids which impairs mucosal turnover and the regeneration of
epithelium. As high yielding animals are more under stress and hence more susceptible.
2) Low quality feed leads to more irritation to gastric mucosa, especially in feed pellets if
course and rough particle is present.
3) Infection agents – Thielariasis – button shaped abomasal ulcers. Enzootic bovine leucosis
also associated with abomasitis and ulceration of abomasal mucosa. Worm infestation-
Haemochus spp.
Pathogenesis:
Stress leads to production of ACTH that stimulates the release of steroid hormones which
impairs mucosal turnover. There is diffusion of H+ and pepsin through the damaged mucosa
that accelerates deepening of ulcers, which may cause damage to the underlying blood
vessels leading to gastric haemorrhage.
Abomasal ulcers are categorized into 4 types based on the amount of erosion &
Haemorrhage associated with the ulcers (Smith et al., 1983)
Type I (Non-Perforating)
There is incomplete ulceration of abomasal wall. Usually such types of ulcers undergo
abomasal thickening and mild serositis with minimal haemorrhage.
Type II (Non-Perforating causing severe blood loss)
These ulcers while invading causes damage to major abomasal vessels in the sub mucosa
causing severe bold loss.
Type III (Perforating type with local peritonitis)
Ulcer has perforated abomasal wall but resulted in, local peritonitis. Here is also spread is
arrested, because of local adhesions to adjacent viscera.
Type IV (Perforating type with diffused peritonitis)
Diffused peritonitis due to widespread draining of abomasal contents.
Case fatality can reach up to
25 % - In Type I
50 % - In Type III and
100% - In Type II & IV
Clinical Signs:
Progressive development of inappetence, excessive thirst, signs of abdominal pain,

passing of soft pasty faeces. When abomasitis develops into ulcerative stage, the signs are
much more pronounced- Like progressive anaemia, passing of dark coloured pasty faeces
(melena), pronounced signs of abdominal pain, jugular pulsation, high pulse rate and
tachycardia are seen as compensatory mechanism for profound anaemia.
Ulcers associated with peritonitis are indicated by signs like fluctuating fever, atony of
rumen, progressive anorexia, passing of dark brown tarry coloured faeces, pain on palpation
on right costal arch nearing xiphoid.
Diffused peritonitis: Signs of toxaemia are much more pronounced. Initially, very high
temperature but in advanced cases, temperature is sub normal. Recumbency, shallow
respiration, cyanotic membrane indicate unfavourable prognosis.
Diagnosis:
a) History: - common in high yielding animals in urban origin, history of passing of dark
tarry coloured faeces.
b) Clinical signs: - Progressive anaemia, passage of dark tarry coloured faeces, signs of
abdominal pain, toxaemia.
c) Abomasocentesis: Paracentesis of abomasum.
Approach: From the middle of the 10th rib an imaginary line is drawn to meet a line between
umbilicus to xiphoid. Three cm from the point of intersection, towards the right, the needle is
inserted and fluid is collected for investigation (Venkataraman., et al 1989).
- pH
Normal abomasal fluid- light brown coloured
pH- 2-4 without any micro flora.
- In Abomasitis – dark brown is due to active lesions causing haemorrhage, pH is
increased due to HCl secretion
- Cl- content is high
In abomasal ulcers streaks of frank blood can be seen and it will be positive of
Benzidine test. It can also be done on faeces for the presence of occult blood
d) Plasma / Serum examination:
Chlorine and pepsinogen reveals hypochloremia along with hyperkalemia and
elevated pepsinogen
1) Abomasal impaction.
2) Omasal impaction.
3) Caecal dilatation.
Treatment:
a) Change in diet. Plane of nutrition should be changed with restriction on indigestible

component of food stuff with more nutritious component.
b) Antacids- Mg(OH)2 preferred for ruminants.
1 g/ Kg B. Wt, but when administered orally, some quantity get retained in rumen. Under
partial closure of oesophageal groove with a special tube the contents can be delivered
into Omaso-Abomasum. It also can be administered through a canula inserted at
abomasocentesis site.
c) Mineral oil like liquid paraffin, linseed oil can be administered at 8 ml/ Kg B. Wt by oral
route can smoothen gastric mucosa and decrease HCl secretion.
d) Supportive treatment: fluids and electrolytes like normal saline or DNS is administered
based on exact of dehydration. Depending on extent of abomasal damage, H2 blockers
can be used like Cimetidine, ranitidine at 1-2 mg/ Kg B.Wt by i/m route.
Gastric motility modifies in abomasitis are indicated as there is delayed gastric emptying,
Ex:-
 Metaclopramide- 0.3 mg/ Kg B.Wt by parentral route.

 Cisapride is used in monogastrics, but still not yet tried in ruminants.
 Surgical intervention in advanced cases.
 Blood transfusion to counteract anaemia.
 A course of parentral antibiotic to check ongoing peritonitis is advised.
Gastritis in Small Animals
Inflammation of gastric mucosa.
Classified as (1) Acute and (2) Chronic
Acute Gastritis: The cause may be either endogenous or exogenous.
1) Physical causes:
a) Ingestion of spoiled food, garbage.
b) Ingestion of foreign material- especially in puppies i.e., plastics, toys, ball etc.
c) Indiscriminate use of NSAIDs like aspirin, diclofenac, phenyl butazone,
Corticosteroids, antibiotics also cause gastritis.
2) Infectious agents:
a) Bacterial: most of them can’t sustain gastric pH but salmonella spp. can cause
gastritis.
b) Viral: CD, Parvo virus, Corona, Rota and even sometimes- ICH.
c) Parasites: Ascarids- Usual prediction site is upper gastro intestinal tract but
sometimes, if the worm load is high, then they may migrate to stomach.
d) Allergic food: Egg albumin, meat protein.
e) Other systemic disorder: Uraemia, chronic liver disorders, stress.
Pathogenesis:
The causative agents cause irritation to the gastric mucosa leading to inflammation of
mucosa resulting in recurrent vomition, loss of fluids and electrolytes, dehydration and
haemoconcentration. If irritant stays for prolonged time, there will be increased secretion of HCl
further causing irritation to the mucosa. Increased secretion of HCl results in loss of Cl - causing
metabolic alkalosis and hypochloremia. If irritation still persists, then ulceration of gastric
mucosa is likely to develop.
Clinical signs:
Persistent vomition. Vomitus is initially mucoid, later becomes frothy then bile starts
(since, sometimes duodenal contents are regurgitated and come in vomitus, hence yellow
coloured). Other signs include lethargy, signs of dehydration, sometimes haematemesis.
Tachycardia, hyperpnoea, crouched appearance of body, because of pain at xiphoid region.
When abdomen is palpated, then signs of pain are pronounced. This is called as tender abdomen
(sensitive to pain). In infectious diseases, along with these other associated signs are exhibited
specific to disease.
Diagnosis:
1) History: History of ingestion of foreign body, administration of aspirin, concurrent
diseases.
2) Clinical signs: persistent vomition, type of vomitus and tender abdomen.
3) Endoscopy: The best diagnostic tool in gastritis. Hyperaemic patches of mucosa can be
identified through gastroscope.
Treatment:
1) With hold the food for 8-12 hrs in order to provide rest to gastric mucosa. Because
induction of vomition is common in response to intake of food.
2) Providing ice cubes / Chilled water suppresses vomition.
3) Fluid and Electrolytes: DNS is the choice for fluid and depending on dehydration
administer fluid along with parentral antibiotics.
4) Antiemetics: Dopamine inhibitors like metaclopramide and domperidon. Given at rate of
0.1-0.5 mg/ Kg B.Wt- i/m or s/c or
0.01-0.02 mg / Kg B.Wt- i/v inj. or
0.2-0.5 mg /Kg B.Wt- p/o.
Domperidon is available only as oral preparation.
Phenothiazine compounds- Block CTZ and act as anticholinergic agents.
Chlorpromazine, prochlorperazine, acepromazine at 0.2-0.5 mg /Kg B.Wt- i/v, s/c, i/m.
5) H2 blockers: Decrease gastric secretions Ex: Cimetidine at 8-10 mg /Kg, Ranitidine at 2
mg /Kg, Famotidine at 0.5 mg /Kg by parentral or p/o.
6) Gastric sedatives protects gastric mucosa by forming a layer on gastric mucosa. Ex:
Preparatean containing Mg(OH)2 /Al(OH)3 ( Gelucil, Digene etc).
7) If foreign body is there- Surgical intervention or endoscopy guided retrieval is indicated.
8) Feeding soft palatable food like curd rice, baby foods.
CHRONIC GASTRITIS:
Chronic inflammation of gastric mucosa.
Etiology: Repeated exposure to irritants like allergic food, long standing foreign body in the
stomach, medicines.
Types: There are 4 types.
1. Chronic superficial gastritis

2. Chronic atrophic gastritis
3. Chronic hypertrophic gastritis
4. Chronic eosinophilic gastritis
Chronic superficial gastritis:
Inflammation is superficial and changes are seen up to lamina propria. Cellular infiltration of
lymphocytes.
Chronic atrophic gastritis:
Thin mucosa – histologically it is outcome of long standing chronic superficial gastritis. There is
decrease in the number of parietal cells.
Chronic hypertrophic gastritis:
Diffused or focal thickening of mucosa, glandular tissue shows both hypertrophy, hyperplasia –
common in senile dogs.
Chronic eosinophilic gastritis:
Usually it is immune mediated may be because of recurrent allergic food. Here

characteristic eosinophilic infiltration.
Clinical signs:
Recurrent vomition which is periodical, episodes are common in early morning, majority
of times vomitus is bile tinged, rarely blood tinged. Accompanying signs are loss of appetite,
abdominal pain, progressive anaemia, gradual loss of condition, pica and caprophagia.
Diagnosis:
Symptoms: always vomitus is bile tinged and periodical, anemia, weight loss etc..
Endoscopy: with gastric biopsy helps to differentiate the type of chronic gastritis.
Treatment:
1. Animal should be shifted to bland diet and multiple feeding of diet rich in carbohydrate is
preferred. Animal protein shall be avoided in the diet; instead of this protein supplements
with high biological value can be given.
2. Use of H2 blockers, oral antacids.
3. Short term corticosteroid therapy is indicated in eosinophilic gastritis.
4. Surgical intervention is required if any foreign body is detected in radiograph.
GASTRIC ULCERS/GASTRO INTESTINAL ULCERS
 Recent introduction of endoscopy in canine practice has revealed increased incidence of

this disorder.
 Incidence is more in adult dogs
 Females are more prone than males, there is no breed predilection
Etiology:
1. Indiscriminate use of non-steroidal anti inflammatory drugs like phenyl butazone,

ibuprofen, corticosteroids etc.
2. Renal or hepatic insufficiency, neoplasm, pancreatitis, hypo adrenocorticism and
stress are systemic causes.
3. Helicobacter pylori also have been reported as an isolate from canine gastric ulcer
(common isolate in human cases).
4. Inflammatory bowel disease.
Pathogenesis:
Gastric mucosal barrier consists of thick mucous layer and epithelial cells which
constitute important anatomic barrier to acid. Prostaglandins play an important role in
maintaining integrity of the gastric mucosa. Damage to the mucosal barrier by irritants increases
the mucosal permeability, allowing diffusion of acid back into the mucosa. Degradation of mast
cells in sub mucosa on contact with the acid results in release of histamine which stimulates
parietal cells to secrete more HCl which leads to mucosal erosion and ulceration.
Decreased cell turn over and mucous production in corticosteroid therapy, retention of
uremic toxins in renal failure, decreased mucosal blood flow leading to a loss of mucosal barrier
in liver failure or some other mechanism contributing for ulcer formation.
Clinical findings:
Vomition (recurrent) is chief sign. Vomitus contains frank or digested blood; melena may
be an associated clinical sign. Persistant weight loss, progressive anaemia, signs of abdominal
pain. Try to sit at the cooler places and inappetence is seen. Some of the dogs die instantaneously
due to perforation and internal haemorrhage.
Diagnosis:
a) History and clinical signs.

b) Endoscopy and abdominal ultrasound.
c) Continuous radiography with the barium meal.
d) Exploratory laparotomy.
Prognosis:
Depends on the stage
In simple case - good.
In later stage - poor.
Treatment:
a) Changing of the diet- Bland diet is introduced.

b) Oral antacid – magnesium hydroxide containing preparations are better.
c) H2 blockers are used.
d) Omeprazole – inhibits hydrogen ATPase and thereby preventing H+ ion production from
the parietal cells, given @ 0.7mg/kg b wt orally once a day (probably early morning on
empty stomach).
e) Cytoprotective – sucralfate @ 0.5 – 1g as a total dose 2-3 times by oral route, it forms a
complex with the proteinous exudate which is abundant in ulcers and provides a barrier
for the action of acids.
f) Prostaglandin analogues – misoprostol 2.5mcg/kg bwt 2-3 times daily by oral route also
reduces secretion and cytoprotective in action.
In general anti-ulcerative therapy should be continued for a minimum of 6-8 weeks with the
periodical review of the case.
PANCREATIC DISORDERS
Pancreatitis:
Inflammation of pancreas which is the chief exocrine gland responsible for secretion of
pancreatic juice that helps in the digestion of the food stuff.
Pancreatitis is of two types
1. Acute pancreatitis
2. Chronic pancreatitis
Etiology:
a) Obesity is one of the primary causes
Fat accumulation around pancreas and more of lipogenesis results in change in enzyme
structure and thereby enzyme cause auto-digestion (inflammation of gland).
b) Biliary tract disease:
As biliary tract is very much nearer to pancreas, any ongoing infectious agent is likely to
get transferred to pancreas leading to pancreatitis, as lymphatic supply to the biliary tract and
pancreas is same and this may lead to pancreatitis.
c) Prolonged corticosteroid therapy.
d) Systemic conditions like uremia.
e) Some of infectious diseases- CD virus can localize in pancreas and cause pancreatitis.
f) Immune mediated destruction due to auto antibodies may also lead to pancreatitis.
Clinical signs:
Lethargy, recurrent episodes of vomition and diarrhea, signs of abdominal pain are
indicated by typical posture. Ex: prayer like stance - giving extension to xyphoid, seeking cooler
surfaces. Signs of abdominal pain are more pronounced after a fatty meal. Bloated appearance,
going down in condition can also be seen.
Diagnosis:
It depends on typical symptoms/clinical signs and affected dogs are middle aged/senile.
Serum amylase is elevated. Abdominal radiograph reveals a ground glass appearance in the
duodenal loop which is characteristic of pancreatitis. Fasting hyperlipaemia is also an important
biochemical finding.
Treatment:
1. Resting the gland
Feed intake is restricted. Attempt should be made to reduce weight or obesity. Animal is
kept on analgesics. Morphine derivatives (potent analgesic) are given.
2. Course of antibiotic is advised to check the ongoing infection.
3. Few people suggest Heparin @ 150 IU/kg b.wt by i/v administration which decreases
possibility of clot formation in gland. Improves micro circulation and prevents ischemia and
helps in clearing lipoproteins (LDL and VLDL).
4. Dehydration is corrected by lactate ringers or normal saline.
5. Till the signs of recovery are shown, animal is supplemented with the pancreatic enzymes for
proper digestion.
Several preparations of pancreatic enzymes are available
• Festal tabs.
• Enzyme - Suspension / Syrup.
• Aristozyme.
EXOCRINE PANCREATIC INSUFFICIENCY (EPI)
Exocrine functioning of pancreas is affected which is clinically manifested by passing

voluminous glistening faeces, persistent weight loss in spite of good appetite, PICA, caprophagia
etc.
Etiology:
Rarely pancreatitis - fibrosis of gland leads to EPI. Idiopathic atrophy of pancreas and
adenocarcinoma of pancreas. Signs are evident when 80% of gland is destroyed. Treatment is
symptomatic and prognosis is guarded.
Pathogenesis:
Gland is destroyed leading to deficiency of pancreatic enzymes resulting in mal-digestion

and malabsorption causing osmotic diarrhea thus exhibiting symptoms of malabsorption.
Prolonged diarrhoea leads to loss of vital elements like fat and water, soluble vitamins and
micronutrients which is undigested and gives glistening appearance to the faeces. There is loss of
bicarbonate ions which leads to acidification of bowel leading to damage to intestinal mucosa. In
due course of time it may lead to inflammatory bowel disease (IBD)
Symptoms:
• Frequent passing of large voluminous faeces (glistening and foul smelling).
• Animal has got very good appetite but persistent weight loss is seen (polyphagia).
• Caprophagia, pica, dull, dry hair coat, polyuria.
Diagnosis:
•Clinical signs- Passage of voluminous faeces, weight loss in spite of good appetite.
•Fecal examination is the best tool- Stool samples tested for undigested starch, fat and presence
of trypsin.
•Sudan III staining- A fecal smear is stained with Sudan III or IV. Plenty of yellow fat globules
can be seen.
•Detection of trypsin in faeces- x-ray film is coated with gelatin, trypsin, being a proteolytic
enzyme, digests gelatin. A strip of exposed x-ray film is dipped in the fecal solution (1:10) and
kept in incubator for 1-2hours and then x-ray film is washed under tap water. If trypsin is present
in the faecal suspension the gelatin coat is cleared from that x-ray strip and it confirms the
presence of trypsin in the faecal suspension.
•Starch- Faecal smear is stained with 2% tincture iodine. Blue coloured starch granules indicate
positive test.
•Plasma turbidity test- A specified quantity of fat meal is fed to dog (corn meal is fed @
30gm/kg b.wt). Plasma is collected 2, 3 and 4 hrs post feeding and checked for lipemia. Absence
of lipemia indicate EPI.
EQUINE COLIC
Colic means pain originating from abdomen. Equines are highly susceptible due to lack
of threshold to pain. Diseases of the alimentary tract of horses that are characterized by
abdominal pain are generally referred to as equine colic.
Aetiology:
Accumulation of intestinal, caecal or colonic gas, hypermotility and intestinal spasms,

impaction of large intestine, gastric impaction, muconium impaction in new born animals, gastric
ulcer in foals, intestinal obstruction including intestinal accidents ( volvulus, intessusception and
strangulation). Luminal obstruction and luminal compression, sand colic, spasmodic colic,
verminous mesenteric arteritis, ascarid infection, massive strongyle infection, rupture of stomach
or intestine, enteritis and irritant cathartics are the common causes of colic in equines.
Epidemiology:
Incidence of colic is high in pastured horses. Colic due to volvulus, strangulation,

intussusception and hypermotility and spasmodic colic are more common in pastured horses at
times when strongyle larvae are more active. Colic due to impaction is more common in dry
months than in spring season.
Pathogenesis:
Horses suffer from colic frequently. Horses appear to have a low threshold to pain and is
frequently beset by minor digestive disturbances that result in a distended bowel. Distention of
the stomach or intestines may be static when there is accumulation of ingesta, gas or fluid, or
transient when local periodic distention occurs as a result of spasm and increased peristalysis of
intestinal segments. Static accumulations are classified as physical colic and transient distentions
as functional colic.
Physical colic:
Inability due to presence of physical cause
Impactive Flatulent colic AGD Intestinal Paralytic

Colic gas (lush green pasture) fluid in gastrium obstruction ileus
Sand low grade retention of Enterolith Peritonitis

roughagemeconium Volvulus Infection of
Torsion gut wall
Intessusception
Strsangulation
Distention
Functional colic:
Interferes with functions like motility, spasms/peristalsis
Verminous mesentricvirus BacteriaSpasmodic colic

arteritis (EVA) (Salmonella)
(strongylus vulgaris) -excitement
-Thunder storms
-cold water drinking
mesenteric vein
Impaired automatic balance
Pathogenesis:
Accumulation of food or gas causes GIT distention which produce stretching of nerve
fibres of intestinal muscles. This in turn stimulates the autonomic plexus causing violent
peristalysis. This is manifested as colic. In terminal stages, there will be degenerative changes of
autonomic plexus leading to atony of gut. There will be water and electrolyte imbalance.
Secondary cardiovascular effects will lead to shock. Systemic acidosis will be evident. Over
distention will interfere with circulation and respiration and cause death.
Clinical findings:
Pain is manifested by reatlessness, pawing or stamping, kicking at the belly, lying down
and getting up, laying on the back, groaning, grunting, rolling, sweating, protrusion of penis
without urinating or frequent urination of small amounts of urine and continuous playing with
drinking water without actually drinking any (sham drinking). The posture is often abnormal,
usually a saw horse attitude. Occasionally in horses with large bowel impactions a dog sitting
posture is observed for long periods, often on the way from recumbency to sitting up. Anorexia
and depression often accompany these signs.
In early stages the pain is usually intermittent and in most severe cases it is almost
continuous. Duration of pain may be for 10 min and it may repeat after an interval of 10min.
Projectile vomiting of intestinal contents through nostrils is very unusual in horses and is a
serious sign suggesting severe gastric distention and impeding nature. Horses also have increased
heart rate with weak pulse, and develop prolonged capillary refill time, cold extrimities, and
bright red (vasodilatory phase) followed by dark (vasoconstrictive phase) mucous membranes if
the problem is severe and affects cardiovascular integrity.
Evidence of shock is usually present only when the disease condition is severe and
involve impactive diseases (volbulus, torsion or thromboembolism) or advanced visceral
distention (extreme flatulence, impaction or dilation). FB such as sand or enteroliths in the large
colon may result in low grade recurrent colic. When an enterolith is passed into the transverse
colon where it obstructs the bowel, signs of complete obstruction and acute colic ensue. These
signs are manifestations of visceral pain, mediated by sympathetic nervous system. External
palpation and pushing on the abdomen usually do not elicit pain unless the affected inflammed or
dilated viscus is contacted.
In contrast, parietal pain associated with peritonitis usually is responsive to external

palpation. Animal with visceral pain show active signs of colic, and those with parietal pain are
usually reluctant to move and have a splinted abdomen. Acute peritonitis occurs with in minutes
following the rupture of the stomach or perforation of an ulcer as a result of immediate irritation
of serosal surfaces by acid contents. With rupture of colon or rectum it may take 12hr or more
before peritonitis is clinically apparent..
Diagnosis:
1) Based on clinical symptoms.
2) Based on rectal examination - difficult task due to compromised position of horse.
• Fluid filled intestine - flatulent colic.
• Absence of faeces in rectum - impactive colic.
• Hard pelleted faeces - obstruction.

3) Radiography and ultrasonography.
4) Laboratory investigation.
Several tests are indicated,
• Blood - Usually local peritonitis is indicated by leucocytosis and diffused peritonitis by

leucopenia.
• PCV is good indicator of signs of shock and dehydration.
45% and above - signs of severe dehydration and shock.
55% & above - Bad prognosis sign. Elevated plasma proteins are suggestive of
haemoconcentration.
Bio-chemical parameters:
• Elevated serum chloride.
• Low plasma bicarbonate(<20mEq/L).
• Elevated blood lactates(>25mg/dl) along with hyponitraemia are important biochemical

changes in colic.
• Peritoneal fluid analysis:
Total cell count- >5000 cells/mcl and 75% nucleated cells in peritoneal fluid is confirmatory of
advanced stages of colic.
Visual peritoneal fluid examination may reveal turbidity, foul smell and tendency to clot.
Pulse: <80 - favourable, >100 - unfavourable.
Capillary refill time: measured by pressing highly vascularised organ between thumb and fore
finger. Ex: tongue.
Blood lactate: >75mg/dl - poor prognosis.

Arterial blood pressure: Mean arterial pressure is measired, systolic pressure <80 mm Hg
indicates critical condition. (Normal systolic pressure - 100 mm Hg ).
Treatment:
•Analgesic drugs form first line of treatment, anyone of the following can be given.
- Detomidine 20mg/kg bwt i/m.
- Xylazine 0.5mg/kg bwt i/m or i/v.
- Pentazocine 1mg/kg bwt i/v or i/m.
- Flunixine meglumine 0.25-1.15mg/kg bwt i/v.
- Pethidine. 2mg/kg bwt i/v.
•Antispasmodics are to be given to relieve recurrent spasms.
- previously bromides were used , now not available.
- Valathamate bromide, epidosin is also alternate.
- Dicyclomine Hcl, antispasmodic+analgesic (spasmovet), can be given.
- Dipyrone @ 10mg/kg bwt i/v is used in western countries.
•In impactive colic gut lubricants play a vital role.
- Mineral oil/Linseed oil/Liquid paraffin are given to soothen and lubricate mucosa @ 3-5ltrs by
nasogastric tube.
- Doss (Dioctyle sodium sulfo succinate) is a good dispensing agent. It breaks the impacted
mass and helps in relieving the mass. Given @ 0.2g/kg mass of bwt, a maximum of 25-30gms.
•Cholinergic drugs like - Neostigmine 10-12mg(total dose) i/m or s/c.
•Fluids and electrolytes - Can be given to improve peristalysis in impactive colic. In majority of
cases, metabolic acidosis is seen and in such cases Ringers lactate/Isotonic solution of sodium
bicarbonate can be given depending on base deficit and state of dehydration.

•Corticosteroids are given to reverse the signs of shock. A dose rate as high as 250mg/kg
Dexamethasone has been given to save the life of horse.
•Surgical option.
- Rectal exmination indicating acute intestinal obstruction/strangulation/volvulus.
- Failure of efficient analgesic to provide analgesia in 20-30 min.
- Visible mucous membranes turning cyanotic.
- Inflammatory changes in peritoneal fluid.
OEDEMA
Oedema refers to excessive accumulation of fluid in tissue spaces and body cavities
involving the disturbance in the mechanism of fluid exchange between capillaries, tissue spaces
and lymphatic vessels. These are usually accompanied with endocrine, circulatory, hepatic and
renal changes. It is considered to be a clinical sign rather than a disease.
Aetiology:
From aetiological point of view
• Inflammatory oedema.
• Non - inflammatory oedema.
Inflammatory oedema:
Local inflammations, live boils, cellulitis, trauma, infection or chemical irritation result in
increased capillary permeability that may cause oedema. The main biochemical observation in
inflammatory oedema is low pH, accumulation of inflammatory cells and blockage of
lymphatics.
Noninflammatory oedema:

It occurs as a result of rise in hydrostatic pressure or fall in colloidal osmotic pressure.
- Increased hydrostati pressure: Usually mild type
Arterial end:
Hydrostatic pressure at arterial end is - 45mm of Hg.
Colloidal osmotic pressure at arterial end is - 30 mm of Hg.
Difference is ----- 15mm of Hg.
Oedema due to decreased colloidal osmotic pressure is most common type of oedema. Causes
are hypoproteinaemia which is the main biochemical finding.
Venule end:
Colloidal osmotic pressure is - 30 mm of Hg.
Hydrostatic pressure is - 15 mm of Hg.
Difference is - 15 mm of Hg.
Depending on the aetiological factor or involvement of tissue it may be of various types.
Cardiac oedema:
The venous congestion that occur in CHF increases permeability of vein leading to escape of
fluid in to tissue spaces and development of oedema. The CVP are elevated, capillary pressure
becomes higher and fluid is forced into tissue spaces.
As a result of low cardiac output, blood supply to the organs becomes inadequate and
metabolites are accumulated in the tissue spaces leading to higher solute concentration. To
overcome this more and more fluid flows into such spaces from the capilleries. Excretion of
sodium ions is greatly reduced and its concentration in extracellular fluid is elevated resulting in
water retention.

Retention of salts is the chief cause of oedema in CHF that ultimately enhances renal venous
pressure. Excessive aldosterone secretion increases tubular resorption while anoxia damages the
capillary endothelium with resultant increased capillary permeability.
Nephrogenic oedema:
In acute glomerular nephritis, there is capillary damage this results in retention of sodium ions
and excessive loss of plasma proteins. The development of oedema depends on kidney damage,
protein loss, capillery damage, retention of sodium ions or a combination of these effects.
As a result of renal damage, erytro poeitin production is reduced which may also help in
oedema development.
Allergic oedema:
As a result of contact with allergen, histamine like substances induce angio oedema, urticaria
and wheals develop on the body. Capillary permeability and hydrostatic pressure increase. These
forms passage of fluids and protein to interstitial space and oedema develops.
Pulmonary oedema:
Ciculatory volume is affected by haemodynamic factors and there is over loading of pulmonary
circulation. Physio - chemical factors that regulate fluid exchange in tissues along with the effect
of nervous system combine together to induce acute pulmonary oedema.
Hepatic oedema:
In hepatic fibrosis, fluid is accumulated in the dependent parts and ascietes is the chief
outcome. Due to fibrosis of cells portal circulation is obstructed, this helps in accimulation of
fluid in tissue spaces and peritoneal cavity. Hepatic damage also causes lowered protein
synthesis and hypoproteinemia which helps in further fluid accumulation.
Oedema of nutritional origin:
Plasma proteins help in maintaining osmotic pressure. A fall in colloidal osmotic pressure
induces oedema as a result of diffusion of fluid from vascular system into tissue spaces.

Since plasma albumin exerts a greater osmotic pressure, oedema is directly correlated with its
concentration.
Deficiency of protein in diet, its malabsorption or excessive excretion may lead to

hypoproteinemia. It can also occur in long standing diarrhoeal disorders and infestation of blood
sucking parasites or liver flukes.
Deficiency of vit - A in diet also causes generalised oedema.
Obstructive oedema:
In first calving of bovines or first foaling of mares, oedema of udder and ventral abdomen is
usually noticed. It is usually physiological or may be caused due to compression of venous
drainage by developing foetus. Such oedema is relieved with in a few days.
Tumours, fibrosis, vascular disease, lymphangitis, thrombo-phlebitis or periphlebitis impede

blood or lymphatic circulation and there is rise in hydrostatic pressure resulting in oedema.
In congenital genetic obstruction in calves and pigs, and sporadic ulcerative lymphangitis in
horse, obstructive oedema develops.
Pathogenesis:
when hydrostatic pressure increases or osmotic pressure is reduced, the fluid is leaked into the
tissue spaces since it cannot return to the capillaries. Accumulation of fluid in tissue spaces or
escape of fluid into serous cavities lead to development of oedema.
Clinical findings:
The fluid may accumulate in
S/c tissue - Anasarca
Peritoneal cavity - Ascietes
Pleural cavity - Hydrothorax
Pericardial space - Hydropericardium.

In bovines, fluid may accumulate in intermandibular space. In equines, it may be seen in limbs
if venous return is obstructed or there is lack of muscular movement. In African horse sickness,
local oedema of head is also noticed.
Oedematous swellings are soft, painless and pits on pressure.
If fluid is accumulated in abdominal cavity, there is abdominal distention and on tactile

percussion fluid thrills can be heard.
In hydrothorax and hydroperitoneum, respiratory and cardiac movements are restricted, and
ventral part of lungs collapses. Heart and respiratory sounds become dull. In cerebral oedema,
severe nervous signs are noticed.
Diagnosis:
• History and clinical signs: History of involvement of specific organ and swelling at the site
may reflect oedema.
• Palpation and percussion: Palpation and percussion of oedematous area may give an idea about
the disease.
• Exploratory puncture: Examination of fluid collected from the oedematous area reveals
transudate or exudate.
• Radiological examination: The oedematous swrlling present inside the body like hydrothorax
or hydropericardium may be diagnosed by the radiological examination.
• Blood examination: Oedema suspected to be caused due to lack of protein may be detected by
blood analysis as in such causes total protein and albumin levels are reduced. Liver function tests
are valuable in those cases, where hepatic oedema is suspected.
Uroperitoneum: Oedema should be differentiated from accumulation of urine in peritoneal

cavity. In such cases, rectal examination reveals empty bladder due to its rupture.

• Pericarditis: Besides pleyrasy and peritonitis, swelling is noticed but such swelling is usually
inflammatory and accompanied with toxaemia, pain and other signs of inflammation.
Examination of fluids helps in confirmation.
Treatment:
It is essential to treat the primary cause of the disease. Animals should be given rest, sodium
and water intake should be regulated.
- Usually animals are provided with sodium free diet.
- Use of diuretics like furesamide is valuable in relieving oedema.
- Since most of the affected animals have hypoproteinemia, they should be given high protein
diet.
- Cardiac oedema: Digitalis therapy is recommended.
- Renal oedema: Corticosteroids and aminoacids are beneficial.
- Hepatic oedema due to parasites : Specific anthelmenthic therapy in addition to liver tonics.
Such cases should be given excessive carbohydrate rich diet and aminoacids along with calcium
and oral antibiotics. Fat should be restricted.
- Nutritional origin: Whole blood or plasma expanders may be infused in addition to giving diet
rich in minerala, vitamins and aminoacids.
- Allergic oedema: Antihistamines and corticosteroids. If there is excessive fluid accumulation, it

may be removed slowly after exploratory puncture at the site. If fluid is not removed slowly, it
may cause acute dilatation of splanchnic vessels and peripheral circulatory failure.
ENTERITIS
Inflammation of intestinal mucosa resulting in diarrhea,dysentery(faeces mixed with

mucous and blood) and accompanying signs of dehydration and acid base imbalance
.occasionally signs of abdominal pain also seen.

Etiology
Bacteria:
E.Coli : commonly associated in calves below 1week of age.
Salmonellosis : S.typhimurium, S.Dublin-common in young animals but also seen in adults.
Cl.perfringens A, B,C,E-is associated with haemorrhagic enteritis.
M.paratuberculosis-Johnes disease-in adults.
Viruses:
Cattle-BVD,malignant catarrh,RP
Young ones-Rota,Corona.
Dogs-Corona,Parvo,CD,ICH
Piglets-TGE
Adult pigs-Hog cholera (swine fever)
Parasites:
Majority of nematodes and cestodes cause enteritis.
Nematodes-Toxocara vitullorum
Young calves-Strongyles-trichostrongyles, Bunostomum<Haemonchus,Trichuris spp.
Dogs and Cats –Toxocara canis, T.cati, Ancylostoma caninum, Toxocaris leonine.
Flukes/trematodes-Immature amphistomes are normally associated.
Cestodes:
Cattle and sheep-Monezia expansa,M.benedini
Equines-Anaplocephala magna

Dogs-Dipyllidium caninum,Diphylobothrium latum
Protozoa:
Coccidiosis-Eimeria and Isospora.
Cryptosporidia parvum-causes enteritis in young calves (1 month of age showing recurrent

diarrhea should be throroughly screened for cryptosporidiosis)
Chlamydial spp-Chlamydia psittacii
Fungi:
Candida, Aspergillus spp. Animals on prolonged oral antibiotic therapy are likely to develop
fungal enteritis.
Chemicals
Pb(lead),Mb(molybdenum),Nitrate ,Cu(copper),As(arsenic) and also Hg(mercury)
Managemental condition:
Poor nutrition, poor ventilation ,poor hygiene.
Pathogenesis: Inflammation of GI mucosa causing failure of absorption leading to diarrhea is

seen. mechanism of diarrhea is categorized in to 4 types.
a)Osmotic diarrhea:
Mainly because of decreased absorption from the gut leading to increased osmolarity of
intestinal content and there is over distention resulting in diarrhea.
Eg : osmotic diarrhea in lactose intolerance- lactose is not digested and this will be utilized by
some microflora and converts in to organic acid causing increase osmlarity leading to over
distention and diarrhea. This is also possible in other condition where absorptive surface
decreased. Eg-TGE in piglets , rota virus/corona viral enteritis in calves and dog where selective
destruction of villus surface of absorptive cells.
b)Secretary diarrhea:

Here mechanism stimulates intestinal mucous to secrete more fluid in the lumen and therefore
rate of secretion exceeds absorption.The best example for this is entero-toxigenic strains of
E.Coli.Increased secretion is due to stimulation of PG synthesis.
c) Exudative type of diarrhea:
The mucosal permeability is changed to such an extent that there is increased trans-mucosal
hydrostatic pressure resulting in net loss of protein which fluid in lumen. usually third degree
damage to gut mucosa result in this type and this is many times known as protein loosing
enteropathy. Eg: lymphatic enteritis, eosinophilic enteritis .
d) Diarrhea due to abnormal motility /decreased transit time:
hyper motility due to increased peristalsis results into recurrent evacuation of the bowel and here
there is ales time for digestion and assimilation.increased transit time favours bacterial over
growth.
SIBO_small intestinal bacterial over load /over growth is a common cause for this type of
diarrhea.
IBD-inflammatory bowel disease is also responsible for hyper motility.
In acute diarrhea –fluid and electrolyte loss is their-decreased absorption responsible for net loss
of weight .chronic episode results in debilitating type of diarrhea like Johnes disease.
Major biochemical changes:
a) metabolic acidosis due to net bicarbonate loss .
b) loss of fluid –dehydration .
c) hyponitramia and hypokalemia.
In chronic entropathies: Net loss of protein leading to hypoproteinemia and therefore animal
having chronic diarrhea shows signs of wasting. Eg:Johns disease and parasitic enteritis

hypoproteinamia leads to decreased colloidal osmotic pressure of plasma and fluid accumulates
in body spaces .eg: Bottle jaw .
Clinical signs:
 Depending on acute/chronic
 Diarrhea –it may be alone or with mucous and blood in dysentery.
 Depending on contributory factors other systemic signs are seen like fever ,anorexia,signs
of toxemia ,septicemia and signs of dehydration.
Following are few characteristics changes in feces:
I. Colibacillosis of young calves-chalky white type of diarrhea.

II. Parvo-viral &carona viral disease-foul smelling brown coloured faeces
,some times mucous shreads.
III. Pan cake like stools seen in CPV gastro-enteritis.
IV. Shooting type of diarrhea in RP.
Varying degrees of dehydration is common in acute diarrhea where as
cachexia, submandibular oedema is seen in chronic disease.
Diagnosis:
Criteria Small bowel diarrhea Large bowel diarrhea

Frequency Normal or slightly increased Very frequent episodes
Volume Faeces are bulky Small quantity
Urgency Absent Usually present
Tenesmus Absent Usually present
Mucous Absent/ present in little quantity Abundant
Blood It may be present and always dark brown colour The blood is frost or frank
blood
Steatorrhe Usually it is present Absent

a
General malaise Usually it is present Rare

Vomiting Present Absent
Examination of faeces:
Microscopic examination: parasitic ova/cyst are identified in parasitic enteritis when the faecal
smear is negative, then it may be due to bacterial or viral disease.
Bacterial enteritis –go for culture and sensitivity testing
Viral enteritis –go for serology (HA &HI are commonest)
Eg :distemper –ELISA,AGID.
Biochemical parameters
 Plasma protein estimation also helps in diagnosis of chronic enteritis(hypoprotenemia)

 Bicarbonate ,blood ph,sodium,potassium,PCV,total serum solid estimation are helpful to
conferm acid base disturbance and amount of dehydration.
 Usually leucopenia suggest viral involvement as primary agent or secondary
compication.
Treatment
The principles of treatment of enteritis are
1) Removal of the primary cause /identifying the causative agent and its removal
2) Replacement of the fluid and electrolyte
3) Stabilizing the GI motility
Helminthes –anthelminties are given
Cestodes –niclosemide 75-150 mg /kg.b.wt,praziquantel 5 mg/kg.b.wt by oral route.
Trematodes –closantel @7.5 mg/kg.b.wt,oxyclozanide 15-20 mg/kg po.

 Preferably antibiotic cource is practiced to prevent secondary infection in viral enteritis
parenteral route is preferred.
 Enroflaxacin , gentamicin , amoxicillin+cloxacillin and cefatoxin are used in canine
parvo viral GE.
 Protozoal/bacterial enteritis in bovines can be treated with gut acting antibacterials like
sulphanamides,furazolidone,combination of metranidazole &furazolidone.
 Supplements of electrolytes and fluids
 Stabilizing GI motility- GI protectant and antisecretory drugs are used.
 Loperamide tablets are used in dogs-1/2 to 1 tab tid it reduces peristalsis and
prevents recurrent evacuation of bowel but in acute diarrhea loperamide is not
advised.
 Gi protectant astringents and smoothening agents like kaolin, pectin have very
good effect.they inhibit secration from mucosa by coating to mucosa & increases
solids in feaces their by helping in forming the stool. for large animals
commercial antidiarrheal or astringents are available which helps in precipitation
of proteins and help in solidification of feaces and soothen the GIT.
Eg: neblon powder,diaspel,diaroak powder given at 40-60 gm ,bid po ,for ,3-5
days.
 Oral administration of probiotics helps in rejuvenation of intestinal
microflora.lactobacillus given orally(sporolac ).
INTESTINAL OBSTRUCTION
 It is an acute clinical emergency and can be caused by intestinal accidents like volvulus
,intusucception ,strangulation or due to intra or extra luminal blockage.
 Clinically characterized by signs of acute abdominal pain, absence of defecation followed
by shock .
 Many cases show high probability.

 Commonest causes are volvulus, intusucception, strangulation and intra luminal
blockade.
 Other causes like extra luminal masses causing pressure on intestinal wall may lead to
compression of lumen and block the intestine.
Etiology :
Intestinal accidents:
Volvulus-twisting of intestine on its own axis
Tortion –twisting of intestine along with its mesenteric axis .usually torsion is more common in
blind sacculated organs eg: caecum ,colon
Strangulation: constriction of a loop of intestine through a hernial ring. Eg :ventral hernia
Extra-luminal mesenteric lymphadenopathy ,hydatidosis or cysticercosis can cause luminal

compression and distruction .
Intraluminal blockage : due to foreign bodies and are classified as
Phytobezoars: originating from plant
trichobezoars :originating from animals-hair ball.
Enterolith is obstructing mass in the intestine .the effect of intestinal obstruction differs
from species to species due to ability to sustain associated pain and toxemia .
Eg: acute intestinal obstruction of small intestine can kill a horse in 24 hours
But similar situation do not result in to death of cattle for 6-7 days. possible explanation
to above situation is the succeptibility of spp to pain and presence/absence of bacteria in loop of
intestine.
Once there is obstruction, further flow of ingesta is inhibited at the same time,intestinal
secretion pouring fluid in the lumen, causing acute distention of the lumen. the unfavoured

organism colonize, releaseof endotoxin, absorption of toxic metabolites into the circulation result
in to profound shock, which has got direct effect on CVS and RESP system.
Over distention causes stretching of nerve endings to severe abdominal pain which is also
additional factor for onset of acute shock. As the condition advances dehydration leading to acid
base distrubation resulting in peripheral circulatory failure.
Biochemical changes:
Loss of bicarbonate, hypochloremia, hypokalemia, hyponatremia, in later stages hyper

kalemia and elevated BUN.
Clinical signs
Cattle kicking at belly,uneasy treading of hind legs and intermittent lordosis type
appearance with bellowing. The animal may show frequent situps. Pain is spasmodic and occurs
at regular interval and in some of the animal where pain is severe indicated by rolling on the
ground. usually there is accompanying anorexia. no defecation if feaces are present, palleted hard
and pass coated with mucous and blood. Animal makes severe straining course in order to
defecation. RR and HR are also elevated with varying degrees of dehydration. Per rectal
examination reveals empty rectum and inserted hand is coated with mucous and blood.
As the condition worsens , animals are recumbent showing signs of shock ,congested to
cyanotic mucous membrane,cold extrimities ,intermittent grunt,low papillary reflex.
If case is not treated majority of animal die within 24 -36 hrs after onset of shock
Horses :the signs of acute intestinal obstruction are always clear and almost resemble with colic
but episode is much shorter and signs of toxemia and shock appear much earlier.
High PR more than 80 /min,RR-60 to80/min, HR 100-120/min accompanied with other

signs with propuce sweating, panting type of respiration severe abdominal pain. Untreated cases
enter profound shock within 12-24hr.medical treatment of the case at this stage is almost in
effective indicating early surgical intervention.

Diagnosis
 Cl. signs-signs of abdominal pain and empty rectum

 Lab investigation –PCV >55-55% indicate haemoconcentration
 Biochemistry-decrease bicarbonate, sodium ,chloride. potassium initially
decreased but later hyperkalemia
 Leucopenia-usually indicate infarction of intestine, diffused peritonitis
 Leucocytosis indicates leaking of contents in the peritoneum ,peritonitis
 Increased BUN-indicates decreased kidney function due ongoing toxemia
and haemoconcentration .
 Perrectal examination
1. Gastric dilatation in horses: not accompanied with complete absence of feaces and presence of
blood and mucous stained faecal pallets. Nasogastric tube passing will specify the stomach
contents
2. Peritonitis
3. Renal colic-uroliths are similar picture but oliguria or anuria is the most prominent sign rather
than absence of defecation
Treatment:surgical correction supportive and symptomatic.
DISEASES OFRESPIRATORY SYSTEM
Respiratory system comprised of upper and lower respiratory tract, carries out the most
important function of gaseous exchange in which environmental oxygen is exchanged with
carbon dioxide .apart from this it also performs numerous other functions like entrapping emboli
and its destruction, activation of angiotensin, metabolization of bioactive substances.
e.g.serotonin,PG, steroids, sense of smell

Diseases of respiratory tract are commonly encountered in routine clinical practice and
therefore form important clinical entity for clinicians.
Principle manifestations of respiratory insufficiency :
The functional integrity of respiratory system depends on its ability to exchange oxygen
in place of carbondioxide from the venous circulation.Therefore,failure of adequate oxygenation
of tissues is sign of respiratory insufficiency and is termed as hypoxia.
Clinical hypoxia can be of 4 types:
a) Anaemic hypoxia:reduced oxygen carrying capacity of the blood seen in nitrite

poisoning and carbon monoxide poisoning.
b) Anoxic hypoxia: insufficient alveolar ventilation seen in strangulation, lung disease.
c) Stagnant hypoxia : reduced blood flow seen in CHF
d) Histotoxic hypoxia : inability of tissues to utilize oxygen encountered in cyanide
poisoning
NASAL DISCHARGE:
Serous,mucoid, mucopurulent nasal discharge is usual indications of respiratory tract diseases.
Mucoid and serous discharge: Indicate acute inflammatory diseases,
Mucopurulent- Always suggest secondary bacterial invasion.
Close inspection of nasal cavity helps in determining the origin of nasal discharge.
Unilateral discharge suggests a local problem where a bilateral indicates systemic involvement,
EPISTAXIS: Bleeding from nose, and if it is profused then called RHINNORHAGIA.
HAEMOPTYSIS: Is coughing of blood usually from lower respiratory tract.
Polypnoea: rapid breathing.
Tachypnoea: very rapid and shallow breathing.
Hyperpnoea: abnormal increase in rate and depth of breathing, but not up to the point of labored.

Dyspnoea: difficult or laboured breathing and can be of two types.
1. Exploratory dyspnoea: prolonged and forceful respiration associated with the chronic
obstructive lower airway disease(COPD).
2. Inspiratory dyspnoea: prolonged and forceful inspiratory effort associated with the
obstruction of upper respiratory tract (laryngeal paralysis, obstruction, collapse of
tracheal rings).
ABNORMAL RESPIRATORY SOUNDS:
Crackles - popping/bubbling sounds originating from lungs and suggestive of presence of

oedematous exudate in alveoli and bronchi.
Wheezes-continuous squeaking/ whistling sound caused by passing of air through narrowed

airway. These are suggestive of presence of tenacious exudates or narrowing of airways.
Pleuritic functional sounds- are produced due to rubbing of parietal and visceral surface
against each other which are more pronounced during expiration and are suggestive of
pleuracy or diffused pulmonary emphysema.
Absence of lung sounds or silent lung is suggestive of space occupying lesion in the thoracic
cavity or consolidation of lungs.
Coughing - It is an explosive expiration of air from lungs which is initiated by stimulation

of cough centre located in medulla oblongata due to irritation of sensory receptors of
airways.
Productive cough - suggestive of presence of exudative lesionand there is expulsion of

mucous and inflammatory debris.
Cyanosis - (Bluish discoloration) of visible mucosa in indicative of seriousrespiratory

insufficiency. Common causes of cyanosis include congenital heart diseases and all type of
hypoxia.
DIAGNOSTIC APPROACH TO RESPIRATORY TRACT DISORDERS :
Clinical examinations of the patients:

Clinical examination of patient suspected for disorder will definitely carry a history of
poor working performance, early exhaustion, abnormal breath sounds and presence of one or
the other clinical evidence like nasal discharge , respiratory distress at rest , coughing. A
thorough physical and clinical evaluation of the patient will help the clinician to pinpoint the
ongoing illness of which auscultation is the most important indispensable tool.
Special technique:
Nasopharyngeal swabs, percutaneous trans-tracheal aspiration, bronchoalveolar lavage

are used as special diagnostic techniques in the diagnosis of respiratory tract dysfunction.
Elevated absolute neutrophil count is bronchoalveolar lavage fluid (BALF) is considered

as diagnostic feature of COPD in horses. Similarly, presence of haemo - siderophages in the
BALF in thorough bred horses is suggestive of pulmonary hemorrhage.
Use of fibreoptic endoscope has improved the diagnostic skill of the physician and is
routinely being used in canine and equine practice. Flexible fibreoptic endoscope has clinical
advantage of non- invasiveness, visual inspection of airways and collection of sample with
minimal contamination.
Thoracic radiography is a valuable diagnostic tool for diseases of lungs and helps in
detecting atelectasis, consolidation of lung parenchyma, space occupying lesion and pleural
effusions. Ultrasonography has a limited use but can be used for guided thoracocentesis.
PULMONARY FUNCTION TESTS :
Caprography means measurement of carbon di oxide content of breath. Measurement of

respiratory volume, residual air and vital capacity of lungs is referred as spirography.
1 Selection of antibiotic: a course of antibiotic is essential to counteract bacterial

invasion.The choice of antibiotic depends on cost effective ratio,sensitivity of
microorganisms and effective penetration of the drug.Parenteral use of any one of the
following can be of choice under field condition.
 Combination of sulpha trimethoprim @20 mg/kg.b.wt

 Ampicillin ,amoxicillin or amoxicillin and cloxacillin combination at 10 mg/kg.b.wt
 Amikacin, azithrimycin, have promising role in small animal practice
2 Environmental alteration:
Provision of comfortable, well ventilated environment during convalescence brings
about early recovery
3 Use of antihistamines: is beneficial to antagonize the deleterious effect of histamine
and other substances.
4 Respiratory stimulants: like carbon di oxide ,nikethamide, leptazole, caffeine and
amphetamine are widely used. Doxopram hydrochloride, a centrally acting
respiratory stimulant is commonly used to antagonize respiratory depression in equine
practice.
5 mucokinetic drugs and bronchodialators: have effective muco ciliary clearance and
better penetration of antibiotic is the treatment of respiratory disease
Bromhexine, theophilline are drug of choice. Beta adrenergic agonist bronchodialator
eg: clenbuterol is used in the treatment of COPD .
6 Expectorants are indicated to expel mucous from the respiratory tract. Sedative
expectorants containing ammonium chloride are used in exhaustive, feracious cough-
whereas codeine or dextrametharphan containing expectorants are indicated In non-
productive cough to suppress cough centres .
DISEASES OF LUNG
Pulmonary congestion and oedema:
Engorgement of pulmonary vascular bed and subsequent increase in amt of blood in lung
parenchyma is called as pulm.congestion which later on leads to escape of fluid into interstitial
space and alveoli referred as pulm.oedema
Etiology:

Primary pulmonary congestion is due to inhalation of toxic fumes and smoke,
anaphylactic shock, hypostatic congestion of lungs(prolonged decumbency due to downer cow
syndrome,milk fever,fracture of long bone).
Secondary congestion occurs due to CHF
Pulmonary oedema can occur due to acute anaphylaxis,pneumonic pasturellosis,gram negative

sepis in pigs,CHF,inhalation of toxic gases and fumes,pulmonary form of african horse sickness
and bakers syndrome in foals.
Pathogenesis:
Reduced effective alveolar space,reduced vital capacity of lungs and impaired

oxygenation of blood are the hall marks of pulmonary congestion and oedema, the end effect is
anoxic hypoxia.
Clinical signs:
Increased depth of respiration to the point of extreme dyspnoea, open mouth breathing,
typical stance with front legs spread wide apart and abducted elbows , presence of crackles on
auscultation over lower parts of lungs is a characteristic.
Diagnosis:
 clinical findings
 lab investigation suggestive of bacterial isolation from nasal swabs,
eosinophilia on haematological examination
Treatment
1. epinephrine in anaphylactic shock

2. antihistamines like phenaramine maleate , promethazine
3. diuretics like furosemide @ 1-2 mg/kg. b.wt I/M
4. acetylsalicylic acid is more effective than antihistamines is providing symptomatic relief.
5. Corticosteroids like hydrocortisone@ 1mg/kg.b.wthave beneficial effect as anti-
inflammatory agents.

PULMONARY EMPHYSEMA
It is distention of lung caused by one distention of alveoli with rupture of alveolar wall
with or without escape of air into the interstitial space.
Etiology
Chronic obstructive pulmonary disease (COPD) in horses is the most important cause of
pulmonary emphysema moldy hay is linked with COPD in horse.In cattle acute interstitial
pneumonia, lung worm infestation (dictiocalus viviparous ),traumatic pneumonitis due to forgien
body and poisonous plants like serecio quadridentatus, perilla frufenses are attributing factors
for pulmonary emphysema.
Pathogenesis
Excessive dilation of alveoli due to narrowing of air ways lead to its rupture and escape
of air into interstitial space is most accepted hypothesis of pulmonary emphysema.
Other possible reason could be inherent weakness of alveolar wall and supporting tissue
unable to sustain the stress during forceful coughing or exertion .incomplete evacuation and
imperfect oxygenation of blood are the net result of pulmonary emphysema leading to hypoxia.
Clinical Findings
Increased rate of respiration at rest is the initial sign of pulmonary emphysema .as the
disease advances expiratory dyspnoea is evident which gets pronounced during exercise. It is
accompanied by expiratory grunt .on auscultation, presence of ‘paper crackling nahes ‘ and lung
parenchyma is sure indication of pulmonary emphysema .subcutaneous emphysema of wither is
considered as sequel of pulmonary emphysema .
Diagnosis
1.Based on clinical findings paper crackling rales on auscultation.
2.Narrowing of bronchioles and presence of abundant exudates in air ways during endoscopic
examination .

3. High absolute neutrophil count in BALF.
Treatment
Identification of primary lesion and its treatment is of para mount importance.Reduction

of inflammation of air ways with NSAID,beta-adrenergic bronchodialaters like clenbuterol
@0.8-3.2mg /kg body wt. and steroids are indicated .but prognosis is always guarded.
Inhalant corticosteroid in the form of spray (intranasal spray) have been found effective
in controlling the signs of respiratory distress.Sodium chromoglycate is also useful in the
treatment of COPD in horses as it prevent degranulation of mast cell.
PNEUMONIA:
Inflammation oflung parenchyma.It is usually accompanied with inflammation of

bronchioles and may get complicated with extention of infection to pleura leading to pleuritis.
Etiology:
Cattle: 1)pneumonic pasturellosis (pasturella.haemolytica)
1) Haemophilus somnus,Klebsiella pneumonia,Mycobacterium tuberculosis var

bovis,Mycoplasm mycoides var bovis,Fusobacterium necroporous otherMicro
organisms include Actinomyces pyogenus,Strepto cocci spp and Bedsomnia spp
2) Viral agents- like Rhino virus, Bovine herpes virus,Bovine respiratory syncytial
virus,Para influenza 3,Adeno virus 1,2,3,
3) Chlamidia andAspergillus fumigatous like fungal agent
Lung worm-dictyocalus viviparous
Horses
1) Streptococcus spp,pasturella spp,E.coli,actinobacillus equi,corynibacterium

equi,bacteroids spp
2) Virus like adino,equine herpis virus1,equine influenza,African horse sickness,
3) Lung worm –Dictyocallus arnfieldi
4) Pneumonia associated with pulmonary hydatidosis sequale of strangles.

Pig:
1) Pasturella spp,mycoplasma spp,actinobacillus pleuropneumoniae,

2) Lung worm metastrangyles apri
Sheep and goat:
1) Pasturella haemolytic ,strepto zooepidemicus,salmonella

abortus,salmonella ovis,pseudomonas pseudomallei
2) Maedi,visna and jaag siekte virus & PPR
3) Lung worm(dictyocalus filaria)
Pathogenesis:
Lungs are protected by pulmonary defense mechanism which constist of following ,
a) Mucociliary defence:mucous secreted by the respiratory mucosa acts to entrap the

particulate matter in the inhaled air. Ciliary mucosa is lining the respiratory tract is
unidirectional and thus does not allow particulate matter to move towards the lower
respiratory tract .It has been observed that particle more than 5 micro meter size are
removed by gravitational settling on mucous surface whereas smaller particle less than 2
micro meter settled down through diffusion and alveolar macrophages play important
role in clearing them.
b) Bronchus associated lymphoid tissue BALT
It play important role in cell mediated as well as humoral immune responce in the form of
activation of IG A,as mucosal antibody cover and macrophage activation for elimination
of invading pathogen
Pathophysiology of all types of pneumonia is based on interference with gaseous
exchange between alveolar air and blood which result in anoxia and hyperpnoea. This is
manifested clinically by polypnoea dyspnoea or tachypnoea later an consolidation of lung
brings about change in the quality of breath sounds. Depending on the type of
exudates,there will be a evidence of crackles and wheezes on auscultation, toxaemia in
bacterial pneumonia can be life threatening clinical emergency .
CLINICAL FINDINGS

Rapid shallow breathing is initial cardinal sign of pneumonia which changes to dyspnoea
in later stages suggestive of much of lung parenchyma as nonfunctional presence of moist ,soft
,but painful cough is suggestive of bacterial pneumonia .where as dry ,hacking and parxysomal
cough is indicative of viral etiology .bilateral muco purulent nasal discharge ,fever rough hair
coat ,presence of crackles or wheezes on auscultation are observed .
DIAGNOSIS
1) Clinical findings
2) Laboratory investigation
a. Isolation and identification of causative agent from nasal swab ,trans
tracheal aspirate or balt
b. Haematological investigation .
Leucopenia –suggestive of viral involvement
Leucocytosis –bacterial involvement
Prominent eosinophilia ->20% suggestive of parasitic infection
Detection of lung worm larve in fecal sediments suggests verminous
pneumonia .
Medical imaging technique
Thoracic radio graphy is helpfull in detecting opaque patechae suggestive
of consolidation of lungs .ultra sonography also has been proved useful in
diagnostic aid in detecting abscessation and anaerobic bacterial pleura
pneumonia .
TREATMENT
Bacterial: amphicilline, amoxicilline ,tetracycline,sulphonamide
Parasitic:levamisol,fenbendazole
Fungal: amphoteresine –b0.5 mg /kg bd wt and supportive treatment .
AFFECTION OF PLEURA
HYDROTHORAX: is accumilaion of transudate in pleural sac
Etiology:

1. Hypoproteinemia : is the most important cause of hydrothorax. Reduced osmolarity of
blood lead to escape of plasma into the body cavities .liver diseases ,parasitic
infestation,malnutrition,are few example of hypoproteinaemia .
2. Congestive heart failure and subsequent escape of plasma into tissue spaces
3. Few viral infection like African horse sickness and enzootic bovine leucosis
HEAMOTHORAX: It is accumulation of blood in the pleural sac
Etiology:
1. Traumatic injury to the chest wall and subsequent haemorrhage.

2. Haemangio-sarcoma of pleural surface
3. Aneurism the best example is spirocerca lupi infestation in cannines aortic aneurism
and exercise induced spontaneous rupture leading to haemothorax as been observed
in dogs
PNEUMOTHORAX: accumulation of air in the pleural cavity.
Etiology:
1) Injury to chest wall eg:fracture of rib ,stab injury to chest wall,perforation of pleural
membrane by foreign body.
2) Thoracotomy
3) Spontaneous rupture of nodules in lung eg:tuberculosis.
Pathogenesis:
Accumulation of fluid,blood results in collapse of natural portion of lungs and atelectasis.

The severity of dysponea depends on the degree of atelectasis.
In pneumothorax,air entered in pleural sac causes compression of lung of the affected

side. Pneumothorax is fatal in horses because the mediastinum is communicating where as it is
suitable in bovines as mediastinum is separate .collapse of lung causes alveolar
hypoventilation,hypoxia,and cyanosis can lead to compression and collapse of venacava.
Clinical findings:

In hydrothorax and haemothorax, gradual development of dyspnoea, percussion dullness
over ventral parts of lung, absence of breath sounds, rapidly developing anemia is observed.
In pneumothorax, acute inspiratory dyspnoea ,collapse of rib cage on affected side

and compensatory increase and bulging of unaffected side of chest wall, complete absence of
lung sound and tympanie sound on percussion (hyper resonance ) on affected side is observed
.displaced heart sounds can be characteristic.
Diagnosis:
Thoracocentesis in hydrothorax and haemothorax is useful.radiographic examination

shows collapsed lung and displacement of mediastinum.
Treatment:
Treatment of primary condition is hydrothorax and haemothorax is necessary .temparary

drainage for the fluid in pleural sac is helpful.Parenteral coagulants and blood transfusion can be
life saving measures in severe haemothorax.
Rest and preventing excitation are priorities in the treatment of pneumothorax.external

wound on chest wall should be sealed at the earliest. Emergency decompression of pleural cavity
with needle connected to rubber tube submerged in water/salive provides water seal drainage.
DISEASES OF URINARY SYSTEM
Urinary system comprised of paired kidney & ureters, one bladder which communicate to
the exterior by means of urethra.
Kidney consists of outer cortex & inner medulla. Nephron is functional unit of kidney.
There are about four lakhs nephrons in each kidney of dog. Each nephron is made up of
glomerulus(tufts of capillaries), surrounded by bowmanns capsules, proximal convoluted
tubules, descending & ascending loop of henle, distal convoluted tubule which joins the common
collecting duct.
Kidney performs several functions of which excretion of metabolic waste, maintainance

of fluid & electrolyte balance, production of erythropoietin & vitamin D3 & selective
reabsorption/excretion of certain matabolites are most important.
RENAL INSUFFICIENCY CAN OCCUR DUE TO:

1. Abnormalities in rate of renal blood flow.
2. The glomerular filtration rate.
3. Efficiency of tubular reabsorption.
PRINCIPAL MANIFESTATIONS OF URINARY TRACT DYSFUNCTIONS
1.Abnormal constituent in the urine.
Physical, chemical & microscopic evaluation of urine sample gives a fair idea about the urinary
tract disorders. Following list shows the abnormal constituent & tests to detect them.
A) Turbidity, pus, fowl smell to urine- Visual examination.

B) Protiens- Roberts test
C) Blood or Haemoglobin- OCCULT blood or benzidine test.
D) Myoglobin- Benzidine test
E) Glucose-Benedicts test
F) Ketone- Rotheras test
G) Crystals, cell, casts-Microscopic examination
2) Variation in the daily output of urine
A) POLYURIA-Increase in the volume of urine is called as polyuria. It is seen in excessive

intake of water, difficiency of ADH, diabetes mellitus & CRF.
B) OLIGUREA-Reduction in the daily output of urine. It is seen in dehydration, shock &

CHF. Urethral obstruction, cystitis & acute nephritis.
C) ANURIA- Complete absence of urine seen in acute renal failure. Glomerualr nephritis &
complete obstruction of urinary tract.
D) PALLAKURIA- it is a frequent painfull micturation in small quantities commonly seen in

cystitis.
E) Urinary incontinence- It is constant dribbling urine usually noticed in loss of tone of

urinary bladder sphincture.
F) DYSSURIA- Difficult & painfull urination
G) STRANGURIA – Slow & painfull urination associated with diseases of lower urinary tract
3) ABDOMINAL PAIN

It is manifested by constant sit ops, kicking at belly, constant groaning, over stretching
back and sometimes even rolling on the ground.
4) PALPABLE ABNORMALITIES OF KIDNEYS URETER, BLADDER & URETHRA
Enlargement of these structures on rectal palpation or by ultrasonography/ radiography

are suggestive of structural involvement of these organs.
The end stage renal failure are uraemia is exhibited by polysystemic signs like, uraemic
breathe, generalized oedematous tendencies, progressive anaemia & osteodystrophic changes
SPECIAL EXAMINATION & DIAGNOSTIC APPROACH FOR URINARY TRACT DYSFUNCTION
1) URINALYSIS
Urinalysis is a essential component of diagnosis of urinary tract dysfunction .
Detection of abnormal constituents of the urine gives an idea about the organ
involvement especially gravity of urine is also a simple test to detect the capacity of kidneys to
consereve the fluid and excrete the solids.
The normal specific gravities in most of the animal species ranges between
1.028-1.032. Increased specific gravity indicates acute renal diseases where as decreased specific
gravity suggests chronic renal failure.
2) RENAL FUNCTION TEST
Renal function test evaluate the amount of renal blood flow, rate of glomerular
filtration & effective tubular function. The blood urea & serum creatinine are sensitive indicators
of renal function. GFR is measured by the rate of disappearance of sodium sulphanilate given
intraveinously . Renal blood flow can be evaluated by measuring the clearance of certain dyes
like Bromo sulpha naphthalene ( BSP) offers IV administration. Elevated levels of GGT in blood
indicates the proximal renal tubular damage.
3) IMAGING TECHNIQUES
IV Pyelography using a contrast medium like iohexol gives anatomical structural

defects of the urinary tract. Ultra sonography is also being used in canine and equine practice.

ULTRA SOUND GUIDED PER CUTANEOUS RENAL BIOPSY has been tried in dogs & horses it
gives histological defects of renal parenchyma for confirmative diagnosis.
PRINCIPLES OF TREATMENT OF URINARY TRACT DISEASES
ANTIMICROBIAL DRUGS- Antibiotic sensitivity assay should be done before selection of

antibiotic. The ideal antimicrobial should have
1) selective excretion through kidneys.

2) Be active in varied pH of urine.
3) Low toxicity in case of administration.
4) broad spectrum activity.
In absence of sensitivity assay, strepto penicillin, sulpha trimethoprim combination,

ampicillin and cloxacillin, new cephalosporin like ceftriaxone, fluro quinolones like ciproflo,
norflox and recommend dose can be given.
FLUIDS AND ELECTROLYTES
Balanced electrolytes supplemented with calcium & potassium can be used to correct
the fluid and electrolyte deficits. In presence of oliguria or anuria, rate of fluid adminiatration
should be monitored to prevent over dehydration. After correction of fluid deficit, oliguria can be
treated with the help of diuretic like frusemide @1-2mg/kg BW non responding cases can be
treated with selective renal vaso dilators like dopamine @5mcg/kgBW/hr as infusion.
NON REGENERATIVE ANAEMIA
It is a major problem in CRF cases in dogs as there is inherent deficiency of

erythropoietin due to damage to the renal parenchyma, repeated blood transfusions can only be
alternative. Few reports suggests use of anabolic steroids @1-5 mg/kg to a maximum of 200 mg
to stimulate extra renal erythropoietin synthesis. Vit D3 should also be used in CRF in dogs to
counteract osteodystrophic changes .
DIALYSIS
Peritoneal and haemodialysis is considered as palliative but life saving measures in

CRF. However repeated peritoneal dialysis pose a risk of peritonitis and there is always cost has
inhibitory factor in haemodialysis.
CYSTITIS

It is inflammation of urinary bladder characterized by frequent painful micturation
with presence of inflammatory cells and bacteria.
ETIOLOGY
Introduction of infection due to repeated catheterization, stagnation of urine, ascending

and descending invasion and cystic caliculi are important cause of cystitis.
Corynebacterium renale in cattle, C.coli in dogs and pigs are common bacterial isolates from
the casts of cystitis. Female have high susceptibility due to shorter urethra.
PATHOGENISIS
Mucosal injury facilitate the invasion of bactiria, colonization and setting up of

infection,stagnation of urin and change in Ph act as predisposing facters .inflamatery changes in
bladder epithelium results in shedding of epithelial cells, RBCs,WBCs and pus cell.
CLINLCAL FINDINGS
Frequent pain full micturation with voiding of small quantity of urine, urine may be turbid with
presenc of RBCs, pus cells and transitional epithelial cells.
Acute case in cattle may signs of abdominal pain, love sniffing of tail, kicking at belly, treading
of hind limbs.
Male dog showing squatting urination posture urination is indication of cystitis.
DIAGNOSIS
1. clinical signs.
2. Urinalysis for proteins and microscopic examination of urine for the presence of pus cell,
RBC and epithelial cells.
3. Isolation, quantitative bacterial culture and antibiogram to provid guidline for choice of
antimicrobial.
4. Radiographic studies like cystogram or iv pyelography .
TREATMENT;
Antimicrobial preferabaly as antibiogram studies , forms the first line of treatment.
Sulfa-trimethoprim @ 30 mg /kg , cipro @3-5mg, cefalexin @11-17mg/kg can be given
7 to 14 days.
In alkaline Ph of urine, urinary acidifiers like ammonium chloride, sodium acid
phosphate can be given . as acidic urin has bacteriostatic effecte whereas in acidic urine
urinary alkalizers like NaHCO3.
UROLITHIASIS

Deposition of calculi/stone in any part of urinary tract is known as urolithiasis although
specific nomenclature like Nephrolith-kidney
Cystolith- for bladder are used.
The incidence is more common in males and specific geographical locations.
Composition of calculi varies from spp to spp .
DOGS; triple phosphate and calcium oxalate calculi are more common.
Dalmatian breed has special predilection for ammonium urate stones as they have
inherent defects in convertion of uric acid to allontoin .
In cattle, ca, Mg & ammonium phosphate containing calculi are more common.
ETIOLOGY;
1. Altered urinary pH.
2. Increased level of crystalloids than colloids.
3. Lack of water in draught like condition, dehydration .
4. Urinary tracte infection leading to desquamation of epithelial cells.
5. Excessive intake of ca, vit D or its increased level in water [hard water]
6. Vit A deficiency .
7. Ingestion of plants containing high oxalate estrogenic substance .
PATHOGENESIS;
Uroliths formation occure in 3 stages.
1. Stage of nidus formation
2. Stage of precipitation of solutes
3. Stage of concretion
Desquamated epithelial cells and necrotic tissue form the nidus .vit a deficiency and
plant estrogen contribute for desquamation of cells. Thogh urine is containing large
number solutes, it is having protective colloid. These colloids cannot ---------into a gel
that porevents precipitation of crystalloids. The mucopolysaccharide fraction of urine
acts as cementing substance whici favours the formation of caliculi which keeps on
increasing in size.
Urethral obstruction is most common at second curvature of sigmoid flexure in

bullocks & vermiform appendages in rams. Increased occurrence in castrated males is
due to relatively smaller diameter of urethra.
Urethral rupture & subsequent uroperitoniem is most important complication of

urethral obstruction. Partial obstruction of ureters can result in hydro nephrosis
syndrome.
CLINICAL FINDINGS
Signs of abdominal pain ;like kicking at belly, stretching of back, treading of hind
limbs can be observed. Strenous efforts to urinate accompanied by grunting &

grinding of teeth with passage of few drops of blood stained urine are the other signs.
Crystal deposits on preputial hairs are also observed.
Most of the times these signs are ignored, over looked or treated for some other
ailment, resulting in bladder rupture in about 48 hours. There is also possibility of
urethral rupture near the site of obstruction leading to escape of urine into connective
tissue of abdominal wall. This results in cellulitis & may causeloughing of skin &
toxaemia.
DIAGNOSIS
1) Clinical signs.
2) Radipographic examination.
3) Urinalysis of available urine.
4) Serum biochemistry indicating elevated BUN & creatinine.
5) Abdominocentesis to detect the uroperitoniem.
TREATMRNT
Surgical intervension is obvious in urethral obstruction, although
alternative medicine has treatment approach. Commercial preparation like
Cystone @ 10 tablets b.i.d. has been reported to be beneficial in early stages.
A course of antibiotic to check infection, urinary alkanizers/acidifiers & potent
analogue flunixin-meglumin/Pentazocine should be a part of treatment.
Pre scrotal urethrotomy is a common surgical approach to reach the site
ofobstruction in the sigmoid flexure.
ACUTE RENAL FAILURE :
ARF is a clinical syndrome associated with a rapid decline in renal function that occurs over a
period of hours to days. it is characterized by complication resulting from kidneys inability to
regulate fluid, electrolyte and acid base balance and excrete metabolic waste products.
Although ARF is not as common as CRF in dogs and cats, it causes significant morbidity and
mortality in veterinary patients.
There are many potential causes of ARF but only a few occur with any frequency most small
animals develops ARF as a result of nephrotoxicosis however disorders such as leptospirosis and
renal ischemia from use of NSAIDs are being recognized with increased frequency.

ARF
NEPHROSIS NEPHRITIS
Ischemic
Toxic Causes Infectious Causes
Causes
DRUGS MISCELLANEOUS
Leptospirosis
Aminoglycosides ENDOGENOUS Ethylene gylcol toxicity
Amphotericin B PIGMENTS Adm. of Methylene
NEPHROPATHY Blue
Tetracyclines
Hburia Adm. of radiographic
Cisplatin
contrast agents
Thiacetarsamide Mburia
Hypercalcaemia
Nsaids
ISCHAEMIC CAUSES:
Hypovolumia: dehydration, Hg, hypoalbuminemia, hypoadrenocorticism
Decreased cardiac output: CHF, pericardial disease cardiac arrhythmias
Renal vasoconstriction: myoglobinuria, haemoglobinuria, angiotensin converting enzyme

inhibitors, captopril, enalpril
NSAIDs: phenyl butazone, ibuprofen, naproxen, flunixin meglumine
Renal vascular thrombosis: bacterial endocarditis, DIC, nephrotic syndrome amyloidosis,

glomerulonephritis

Systemic vasodilatation: anaphylaxis, inhalation anesthesia administration, septic shock ,heat
stroke drugs(arteriolar dilators)
DIAGNOSTIC APPROACH:
Patients with ARF generally present with an acute onset of non specific clinical signs that may
include lethargy, in appetence, vomiting, diarrhea dehydration and in some case oral ulcerations.
One should suspect ARF on the basis of these historical and physical examination findings.
Additional diagnostic techniques include lab examinations (for CBC, serum chemistry profile,
urine analysis), Radiography, Ultrasonography, serology and in selected cases renal biopsy.
The results of diagnostic findings should be used
1) To determine the presence of life threatening complications.

2) Distinguish pre renal, renal and post renal azotaemia.
3) Determine urine volume (oliguria from non oliguria)
4) Differentiate from ARF from CRF.
5) Determine the specific causes of ARF.
Life threatening complications:
Before performing an extensive diagnostic evaluation, one should first evaluate patient for the
presence of life threatening abnormalities. This includes
1) Severe dehydration.
2) Hyperkalemia
3) Severe metabolic acidosis.
In some instances treatment of their problems may be necessary before the results of initial
laboratory tests are available. If at all possible, collect samples of blood and urine before
administrating and treatment. This will greatly facilitate the interpretation of results later,
especially urine analysis.
 Early detection and correction of dehydration help prevent additional renal injuries due to
hypo perfusion.

 Suspect hyperkalemia in patients with bradycardia or other cardiac arrhythmias ECG
changes associate with hyperkalemia may include prolonged PR interval, spiked T waves
absence of p wave, and prolonged QRS complex. Immediate treatment is indicated in
patients with >8 mEq/L to lower serum potassium concentration.
 Severe metabolic acidosis (pH <7.2 or total CO2 mEq/L) may also have detrimental
effects on cardiovascular system and should be treated to increase blood pH to above 7.2.
Localize azotaemia:
This can be done on the basis of physical examination finding and urine analysis results.
Dehydrated azotaemic patients with evidence of urinary concentrations (ie. urine specific Gravity
>1.030 in dogs and >1.040 in cats) most likely have pre renal azotaemia.
Hypoadrenocorticism, hypercalcaemia, diabetic ketoacidosis and diuretic or corticosteroid

administration may be associated with pre renal azotaemia and decreased urine sp. Gravity.
The response to treatment may help distinguish between pre renal and renal azotaemia.
Azotaemia that resolves rapidly after pre renal factors have been eliminated (e.g.: dehydration) is
most likely pre renal in origin, where as azotaemic that does not respond to the correction of pre
renal condition is probably due to renal failure.
Post renal azotaemia can usually be identified on the basis of the history, physical examination
and radiographic or ultrasonographic findings. Patients with lower urinary tract obstruction have
signs of dysuria, stranguria and pollakiuria. One should suspect post renal azotaemia due to
lower urinary tract obstruction in patients with anuria because pre renal and acute tubular
necrosis generally cause oliguria and anuria.
Determine urine volume:
Although ARF often causes oliguria, it may be associated with non oliguria (≥ 1.0 ml/kg/hr) in
some cases. Amino glycosides nephrotoxicosis is probably the most common cause of non
oliguria ARF in small animal patients. The presence of non oliguric indicated less severe renal
damage and a more favorable prognosis than does in presence of oliguria.
Management of ARF:

1) Identify treatable disorders and discontinuous administration of any potentially
nephrotoxic agents.
2) Correct fluid deficits and metabolic abnormalities.
3) Characterize urine production
 Oliguria
 Non oliguria
4) Provide fluid and metabolic needs for the maintenance phase of therapy.
Insensible losses – 13-20ml/kg/24hrs
40-60 ml/kg/24 hrs
Sensible losses – 27-40 ml/kg/24 hrs
5) Reduce nausea and vomiting
Cimetidine: 8 mg/kg SC or IV 6-8 hrs
Ranitidine: 2 mg/kg IV or SC 8-12 hrs
Famotidine: 0.5 mg/kg IV or SC
Metaclopromide:0.2-0.4 mg/kg SC 8 hrs or 1-2 mg/kg/day or continuous IV drip.
6) Provide nutritional support.
7) Monitor response to the therapy.
Treatment to hyperkalemia:
Approx. serum K+ ECG changes Therapeutic measures

conc.
Mild hyperkalemia 5.5 to 6.5 mEq/L None Volume replacement
with K+ free fluids
and initiation of
dieresis should be
sufficient
Moderate 6.6 to 7.5 mEq/L Bradycardia, Sodium bi carbonate
hyperkalemia prolonged T waves, (0.5 to 2.0 mEq/kg
prolonged PR IV)

intervals, widened OR Dextrose 5-10%
QRS complex infusion
OR Regular insulin
(o.25 to 0.65 U/KG
IV) and glucose (1.2 g
slowly IV per unit
insulin administration
Severe hyperkalemia >7.5 mEq/L Absent P waves, Calcium gluconate
Idioventricular 10% (0.5-1ml/kg IV)
rhythm, ventricular and initiate
tachycardia therapeutic measures
described for mild and
moderate
hyperkalemia
Strategies for reversing oliguria:
1) Ensure that volume deficits resulting from dehydration are corrected.

2) Consider mild volume expansion by administrating 3% body weight in replacement
fluids.
3) Administration loop diuretic frusemide at 2-3 mg/kg BW IV.
If successful, repeat every 6-8 hrs as needed. If unsuccessful administer 4-6 mg/kg IV at
one hr IV at 2 & 3 hours following initial dosage.
If frusemide alone is unsuccessful after several hours, administer vasodilator or osmotic
diuretics with frusemide like dopamine @ 1-5 mg/kg/hr.
OR
Mannitol 20-25% @ 0.25-0.5 g/kg IV over 5-10 minutes.
If successful, repeat every 6-8 hours as needed or administer as a 5-10% solution (diluted
in RL) at a constant rate of 2-5 ml per minute.
OR

Dextrose 10-20% at 0.5 ml/kg/min IV over 30 minutes or 25-50 ml per kg over 1 to 2
hours. If successful repeat every 8-12 hours to maintain dieresis.


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HISTORY OF VETERINARY MEDICINE

Following the establishment of agriculture Universities, veterinary and animal sciences

Thus, diagnosis is an art of recognizing a disease and of distinguishing it from other

Diagnosis consist of 3 parts

1. Symptoms of disease – bloat -accumulation of gas, distended abdomen

Terminologies: classification of diagnosis

E.g.; jaundice, colic or abdominal pain in horses and dogs

That is we have to write the name of the disease.

When a disease is clearly recognized by observing structural lesions or pathognomonic

a) Severe brisket oedema – suspected for TRP

Snapshot diagnosis may be biased and liable to the erroneous.

Test therapy diagnosis

It is the determining of disease by excluding all other diseases.

In some cases a disease affects whole herd resulting in considerable loses.

The herd diagnosis is made by following principles

a) Complete clinical examination of affected animal showing pronounced/clinical signs.

Branches of veterinary medicine

1) Preventive veterinary medicine

2) Clinical veterinary medicine

Veterinary graduate undergoing 6 month internship

Dis + ease (comfort)

Opportunity potentiality of pathogen X Virulence X Stress

1) According to mode of origin or genesis

a) Hereditary/genetic: here genome is responsible for the disease. These are

2) Based on system involved

3) According to changes in the organ

4) According to specific cause;

5) According to The mode of infection;

A) Primary disease (principal disease)

6) According To clinical manifestation (intensity )

7) Based on the spread of the disease;

8) According to the place of origin;

9) According to the deficiency;

10) According to the physiological turnover

2) Extrinsic; which are derived from outside.

Symptoms can be categorized into – a) subjective symptom

Subjective symptoms: those that are perceptible to the patient only.

Direct or idiopathic systems:

Eg: mucous and blood accompanied with tenesmus in dysentery.

Indirect or sympathetic symptom:

Eg: vomiting due to hepatitis in dogs.

 BQ – swelling with crepitation in heavy muscle.

Eg: nervous manifestation of calf suffering from coccidiosis.

Periodical or remittent symptom:

 Diphagic fever in canine distemper.

Diagnostic or pathogenic symptoms:

 Lock jaw – in tetanus.

 High blood urea nitrogen in nephritis indicates ensuring death.

Favourable: 100% surity of recovery.

Ex: uncomplicated traumatic peritonitis in cattle.

Ex: traumatic reticulo peritonitis with adhesion of diaphragm with abdomen.

Poor: 25% chance of recovery.

Ex: traumatic reticulo peritonitis complicated by absess in liver.

Grove: 100% surety of death/ fatality.

Ex: traumatic peritonitis following penetration of sharp foreign object.

Treatment or therapeutic measure:

Treatment means the knowledge of pharmacology/ adopting remedial measure for

Treatment may be classified as general and specific treatment.

Includes measures to be adopted to combat certain complications, during the course of a

a) Fluid replacement: fluid therapy

 For gram positive organisms - penicillin.

Antibiotic toxicity are: