General Veterinary Medicine by KVASU PDF

KERALA VETERINARY & ANIMAL SCIENCES UNIVERSITY FOURTH PROFESSIONAL YEAR VETERINARY MEDICINE (4+1) UNIT I-GENERAL MEDICINE TEACHING NOTES Compiled By : ABHIJITH S P 1|Page...

KERALA VETERINARY & ANIMAL SCIENCES UNIVERSITY FOURTH PROFESSIONAL YEAR VETERINARY MEDICINE (4+1) UNIT I-GENERAL MEDICINE TEACHING NOTES Compiled By : ABHIJITH S P 1|Page 29 December 2020 HISTORY AND SCOPE OF VETERINARY MEDICINE HISTORY OF VETERINARY MEDICINE Origin of the term “veterinary” The etymology or origin of the word “veterinary” is less clear. It probably originated from the term "veheri" which means ‘to draw’ i.e., "any animal that works with a yoke." Other etymologists consider its origin from "vieh", which means ‘cattle’, and "terrin" which means ‘to be sick’. “Father of Veterinary Medicine” The concept of animal diseases and its management evolved thousands of years before A.D. and contributions came in from different persons and from different civilisations. Hence a controversy exist over who is the Father of veterinary medicine. Though the names of Hippocrates and Galen were discussed, Vegetius is generally considered the Father of Veterinary Medicine. He was the author of four books on diseases of horses and cattle in which he disregarded divine discipline as the cause of diseases. Shun Yang is regarded as the Father of Chinese veterinary medicine. Important personalities/ events First written record on veterinary medicine – Kahun Papyrus from ancient Egypt (1900 BC). Oldest well-documented evidence on veterinary practice was Code of Hammurabi (King Hammurabi; 1792 to 1750 BC). The Code mentions the type of surgery and the fees to be paid to the veterinarian. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India 2|Page 29 December 2020 In India during Vedic period, people were concerned about the management, diagnosis and treatment of diseases of animals. In ancient India, animals were treated on the principles of “Ayurveda”. Hippocrates (460-337 B.C.) described hydrothorax in oxen, sheep, and swine and mentioned the dislocation of the hip joint of cattle. Hippocrates is regarded as the Father of human medicine. Aristotle (384-326 B.C.) discovered some of the diseases of swine, dogs, cattle, horses, asses, and elephants, including rabies in dogs Gen. Xenophon (349-259 B.C.) wrote a treatise on horses and horsemanship in which was emphasized diseases and care of the feet. Shalihotra (about 3rd Century B.C.) was a pioneer of veterinary science in India. Shalihotra's principal work was a large treatise on the care and management of horses. The term ‘Shalihotra’ was used to refer horse doctors. Vaisampayana, Nakula and Palakapya were famous animal doctors who wrote Sanskrit treatise on animals. Mauryan Emperor, Asoka the Great (269 to 239 BC) established treatment centres for animals in his Kingdom. Galen (130-210 AD) - insisted ante mortem examination for food animals. The Hippiatrika is a compilation of veterinary writings (mainly on horses) of several different authors in the 5th and 6th century AD. An anonymous author compiled these texts in the 10th century. Among these early writers was Apsyrtus, a prominent army officer of the Byzantine era. This is regarded as the first comprehensive work in Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  3|Page 29 December 2020 veterinary medicine. In Greece, the term “Haippiathri” is used to refer horse doctors. Rufus in the 12th or 13th century wrote "De Medicina Equorum". The volume was a tabulation of original observations on equine diseases and its treatment with no reference to previous literature. Ruini Bologna, an Italian, wrote the first veterinary anatomy in 1598. About 200 years later, LaFosse, a Frenchman, published a second anatomy. LaFosse's book was the first one that had coloured plates. Establishment of Veterinary Schools/ Colleges The 18th century witnessed many plagues (diseases) among the domestic animals of Europe. These were: rinderpest (mainly), anthrax, blackleg, sheep pox, scabies, glanders, contagious pleuro-pneumonia, strangles, tetanus and wound infections. This paved the way for the establishment of first veterinary school at Lyons in France in 1762, followed by a second school at Alfort in 1765. 1791 - Veterinary college at London. 1853 - First veterinary school in North America (continent) at Mexico. 1857 – First veterinary college in USA at New York. Veterinary Colleges in India ▪ First Army veterinary school started at Poona in the year 1862. ▪ First Veterinary College - Babugarh in 1877 ▪ Second Veterinary College - at Lahore 1882 ▪ Third Veterinary College at Bombay 1886 ▪ Fourth Veterinary College at Calcutta 1893 ▪ Fifth Veterinary College at Madras 1903 ▪ First Veterinary College in Kerala at Mannuthy (Thrissur) in 1955, and second at Pookode (Thrissur) in 2004. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  4|Page 29 December 2020 ▪ First Veterinary University – Tamil Nadu Veterinary and Animal Sciences University (TANUVAS) in 1989. SCOPE OF VETERINARY MEDICINE The scope of veterinary medicine is very vast. It serves the society in a variety of ways which changes according to the changing needs of the society. The scope of veterinary medicine spreads over different areas/ sectors such as: - ✓ Food/ Farm animal medicine – Cattle, buffalo, sheep, goat, pig, poultry etc. ✓ Pet/ companion animal medicine – dog, cat, pet birds, horses etc. ✓ Laboratory animal medicine ✓ Wild animal medicine/ Zoo animal medicine ✓ Aquatic medicine ✓ Exotic animal medicine ✓ Species: Equine medicine, Swine medicine Avian medicine etc. ✓ Specialisation in veterinary medicine – Dermatology, Cardiology etc. ✓ Teaching, Research and Extension in veterinary medicine ✓ Control of zoonotic diseases ✓ Military use of animals – Remount Veterinary Corps ✓ Rural development and poverty alleviation ✓ Animal welfare ✓ Veterinary forensics and Veterinary Jurisprudence ✓ Disaster management ***** Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India 5|Page 29 December 2020 REFERENCES 1) The History of Veterinary Medicine (1939). IOWA State University Veterinarian, Volume:2(1), p:6-9. 2) https://editions.covecollective.org/chronologies/hippiatrika. 3) History and scope of veterinary medicine by Samad and Ahmed (2003), Bangladesh Journal of Veterinary Medicine, p:1-8. QUESTIONS 1. Father of veterinary medicine. 2. First veterinary school with the year of establishment (i) World (ii) India (iii) Kerala. 3. First veterinary University in India. 4. Write in one or two sentences. (i) Hippiatrika (ii) Shalihotra (iii) Haippiathri 5. Write a brief note on the history of veterinary medicine. 6. List the important sectors/ areas that reflect the scope of veterinary medicine. ********** Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India 1|Page 31 December 2020 THE CONCEPT OF ANIMAL DISEASE, DIAGNOSIS, DIFFERENTIAL DIAGNOSIS, TREATMENT, AND PROGNOSIS DEFINITIONS Veterinary Medicine is the branch of science that deals with the diagnosis, treatment, prevention and general study of the diseases of animals, especially the domesticated ones. Veterinary Therapeutics is the subject that deals with the treatment of disease in the domesticated animals. It includes the administration of medicines, vaccines and sera etc. and ancillaries such as hygiene, dietetics, management and nursing of sick animals. Farm Animal Medicine is a part of veterinary medicine that deals with the diseases of the farm animals. Pet/ Companion Animal Medicine is a part of veterinary medicine that deals with the diseases of the pet/ companion animals. Food Animal Medicine is a part of veterinary medicine that deals with the diseases of the animals reared for food. Clinical Veterinary Medicine (bed side medicine, internal medicine, curative medicine) is the branch of veterinary medicine that deals with the art of making a correct diagnosis of diseases of animals and its related remedial and curative measures. Preventive Veterinary Medicine deals with all the measures to control and prevent animal diseases. Health is a state of complete physical, mental and social well- being and not merely the absence of disease or infirmity (World Health Organisation) Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  2|Page 31 December 2020 Disease is any deviation from health is disease, that is any deviation from normal physical, mental or social well-being. It also indicates the inability to perform normal physiological functions or to maintain optimum production with adequate nutrition and optimum environmental conditions. MAJOR CLASSIFICATION OF DISEASES I. Classification on the basis of etiological factor(s) involved Specific disease: Disease caused by a specific etiological agent. Eg. FMD, Tetanus etc. Non-specific disease: Diseases caused by multiple etiological agents/ factors. Eg. Vomiting results from gastritis, intestinal parasites, renal failure etc. II. Classification on the basis of causative organism Infectious diseases - diseases caused by living organisms. Eg: Viral disease, bacterial disease, protozoal disease, mycotic disease etc. Non-infectious diseases – Diseases caused by factors other than living organism. Eg Vitamin deficiency, hereditary diseases, nutritional diseases, production diseases etc. Contagious disease - Disease spread by the intimate contact with the diseased animal. Eg: - Canine parvo viral enteritis, FMD etc. All contagious diseases are infectious diseases (ie., caused by an organism), but all infectious diseases are NOT contagious. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  3|Page 31 December 2020 III. Classification on the basis of onset of clinical signs Per-acute disease: sudden onset of signs, within 24-48 hours of entry of organisms into the body. Eg. Peracute HS, peracute mastitis etc. Acute disease: Signs develop over 3 to 7 days of acquiring infection. Eg. Bacterial enteritis Sub-acute disease: Clinical signs develop over 8 to 14 days (one to two weeks). Eg. Less pathogenic bacterial infections. Chronic disease: Disease that develop over more than two weeks of time period. Eg. Blood parasites, intestinal parasites Carriers: Animals that harbour the pathogenic organism in the body without showing any clinical signs. Snap shot diagnosis - diagnosis which is declared at the very approach of a patient at a glance. This may be biased and liable to be erroneous. Differential diagnosis - this is the ART of differentiation of disease by comparison and contrast with similar diseases. For example, the differentials for red/ coffee-coloured urine in cattle is cystitis, enzootic haematuria, bovine babesiosis, bovine theileriosis, leptospirosis, pyelonephritis, urinary calculi etc. Tentative diagnosis (presumptive diagnosis) - diagnosis based on clinical/ physical examination findings, until a precise diagnosis (confirmatory diagnosis) is made on the basis of laboratory or special investigations. Sign - outward manifestation of the disease observed through objective evidence. Eg. Vomiting in renal failure, rough hair coat in chronic protein malnutrition etc. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  4|Page 31 December 2020 Subjective symptoms - indicates the feelings expressed by the patient. Mainly applicable in human medicine, because they can narrate what they feel. Objective symptoms - symptoms observed by the clinician through various methods of examination. Eg. Ascites, limb oedema etc. Premonitory or precursory symptoms - At the initial phase of a forthcoming disease, some symptoms may appear and serve as a warning of the approach of a disease. Eg. Prodrome period before a seizure activity in dogs. Syndrome - denotes a group of different symptoms or clinical signs due to disease affecting a particular body system. Eg. Nephrotic syndrome. MAKING A DIAGNOSIS Diagnosis is the ART of recognition and determination of the nature of the disease. Correct diagnosis of diseases is the crux of veterinary medicine. We learn clinical signs of diseases and its physical examination changes to come to a reliable diagnosis. Diagnosis is further confirmed by making use of laboratory or imaging tests. DIAGNOSIS IS AN ART (not a science ???). A clinician enjoys veterinary practice, only if he/ she develop the skill to make a good diagnosis of diseases. The five methods of making a diagnosis are: - 1. The syndrome or pattern recognition In the syndrome/ pattern recognition method the clinician makes a diagnosis instantaneously on the basis of past experience. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  5|Page 31 December 2020 The present case is FIVE METHODS OF MAKING A DIAGNOSIS compared with the previous 1. The syndrome or pattern recognition cases in the clinician’s 2. Hypothetico-deductive reasoning memory. There is no need to 3. The algorithm method seek further supporting 4. The key abnormality method advice, and the diagnosis is 5. The database method made then and there. This method is good in the hands of experienced or well-trained clinicians because it is quick and reasonably accurate. Examples: - o The behaviour of a horse with abdominal pain – Colic. o Wart-like proliferative lesions on the skin and udder of a cow – Papilloma. o Sudden onset of weakness immediately following parturition – Parturient paresis. o Swollen, painful udder with changes in milk – mastitis o All local inflammatory lesions – laminitis, dermatitis, rhinitis, otitis externa etc. 2. Hypothetico-deductive reasoning In this method, the clinician listens to the owner’s complaint and draw up a short list (usually three or four) of diagnostic possibilities (differential diagnosis/ differentials). That is, the clinician generates multiple hypotheses from the initial cues. He/ she then ask questions and conduct clinical examinations that test the hypotheses. The questions and examinations should be directed at supporting or discounting the diagnoses (the Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  6|Page 31 December 2020 confirm/exclude technique). The original list of hypotheses is finally reduced to two or three. This is the tentative diagnosis and therapy is directed at managing all these diseases together. For example: - Fever with red/ coffee coloured urine – Theileria/ Babesia/ post- parturient haemoglobinuria/ cystitis in bovines Stomatitis in a cow – local bacterial stomatitis/ FMD Fever with anaemia – Theileria/ Anaplasma in cows Because memory is unreliable, the hypothetico-deductive method is subject to error by omission. 3. The Algorithm method The algorithm method is an extension of Method 2, in which the clinician remembers all the diagnostic possibilities of the case under consideration. This method works well if the list of possible diagnoses is complete and is frequently updated. Error by omission is not a risk in this method, because the algorithms have all the recorded diagnostic possibilities. This method is good for developing a software program. 4. The Key abnormality method This is a more time-consuming method. The key abnormality or clinical cue is identified from the history and clinical signs and the confirmatory diagnosis is made in five steps. i. Determine the abnormality of function present in the animal. ii. Determine whether a particular body system or systems is involved or whether the entire body as a whole is affected. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  7|Page 31 December 2020 iii. Determine the location of the lesion within the body system or the organ affected. iv. Determine the type of lesion. v. Determine the specific cause of the lesion. 5. The database method In the database method (also referred to as the problem-oriented method) the clinician conducts a complete clinical and clinicopathologic examination of the animal to acquire a comprehensive animal database. The problems (key signs) in this database are then identified and matched with the diagnostic database. The clinical and laboratory data are recorded in an orderly, systematic, and consistent manner. This system is now used widely in well-equipped veterinary teaching hospitals with hospital disease management software. TREAMENT AND PROGNOSIS Treatment a. Symptomatic treatment: based on symptoms b. Specific treatment c. Palliative treatment - type of treatment in case of incurable diseases to prolong the life span of the patient. d. Empirical treatment - treating patient by experience gained though a long-time trial and error methods. It is not always possible to explain the specific action of the therapy or exact pathology of the disease. Usually the pharmacological action of the agents used are unknown. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  8|Page 31 December 2020 e. Rational treatment - it is the scientific method of administration of the drugs based on precise diagnosis, knowledge of the etiology and action of the drug employed. Prognosis - forecast or foretelling the probable course and termination of a disease. Prognosis may be graded as favourable, doubtful, poor or grave. Sequelae - it denotes the affections which may arise after the apparent recovery of a primary disease. Eg. Nervous abnormalities after recovery from canine distemper infection ***** REFERENCES 1) Veterinary Medicine- A textbook of the diseases of cattle, horses, sheep, pigs and Goats by Peter Constable, Kenneth Hinchcliff, Stanley John, and Walter Grunberg, 2017, 11th edition, Elsevier. 2) Small Animal Internal Medicine by Richard Nelson and Guillermo Couto, 5th edition, Elsevier. QUESTIONS 1. Differentiate. (i) Health Vs Disease (ii) Diagnosis Vs Differential diagnosis (iii) Clinical veterinary medicine Vs Preventive veterinary medicine (iv) Prognosis Vs Sequelae (v) Rational treatment Vs Empirical treatment (vi) Specific Vs Non-specific diseases (vii) Infectious Vs Non- infectious Vs Contagious diseases (viii) Subjective Vs Objective symptoms. 2. List the five methods of making a diagnosis. 3. Prepare a tabular statement to differentiate the different methods of diagnosis. ********** Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India 1|Page 04 JANUARY 2021 HYPOTHERMIA, HYPERTHERMIA, FEVER Mammals and birds maintain a relatively constant body core temperature, even when the external thermal environment shows extreme variation. Such animals are called homoeothermic animals. This homoeothermic state is achieved by modifying the rate of heat loss from the body or the rate at which heat is produced. So, the body temperature is an indication/reflection of the balance between heat gain and heat loss. The four heat generating mechanisms in the body are (i) Metabolic activity (ii) Digestion of feed (iii) Muscular movement and (iv) Maintenance of muscle tone. Heat dissipating mechanisms include (i) conduction, convection & radiation; (ii) Evaporation of sweat, insensible perspiration; (iii) Through body secretions and excretions; (iv) Profuse salivation; (v) Exaggerated respiration, open mouth breathing and moisture vaporised by respiratory tract. Heat conserving mechanisms: (i) Peripheral vaso-constriction; (ii) Postural changes; and (iii) Pilo-erection. Shivering thermogenesis Vs Non-shivering thermogenesis Shivering thermogenesis consists of involuntary, periodic contraction of skeletal muscle. This is mainly seen in adult animals which are hypothermic. Non-shivering thermogenesis: In neonates, large amounts of brown adipose tissue are present in the abdominal cavity especially peri-renal areas, around large blood vessels and at the inguinal and prescapular areas. In non–shivering thermogenesis, heat is produced by the metabolism of brown adipose tissues. Brown adipose tissues get Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  2|Page 04 JANUARY 2021 converted to white adipose tissue by about 10 days after birth and consequently non-shivering thermo genesis decreases. NOTE: Horses sweat profusely and is an effective mechanism of heat loss. Sweating is a less effective mechanism of heat loss in pigs, sheep and European cattle. Increased density of sweat glands on Zebu cattle makes it more heat tolerant than European cattle. HYPOTHERMIA Hypothermia is a fall in body temperature (or lower than normal temperature) that occurs when excess heat is lost or insufficient heat is produced in the body. ETIOLOGY ▪ Excessive loss of heat due to cold atmospheric temperature, rainfall and speedy winds. ▪ Insufficient heat production - Insufficient body reserves, low birth weight, Insufficient feed intake. ▪ A combination of both. ▪ Secondary to many diseases such as parturient paresis, anaesthesia and sedation, profuse diarrhoea, shock, terminal stage of many diseases, shearing in sheep etc. EPIDEMIOLOGY New-born farm animals are prone to hypothermia in cool environments. PATHOGENESIS Hypothermia leads to a decrease in heart rate, cardiac output and blood pressure. Subnormal body temperature results in muscular weakness, respiratory failure, recumbency, collapse, coma and death. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  3|Page 04 JANUARY 2021 Vasoconstriction of cutaneous vessels during cold exposure occurs first in the ears, followed by the lower extremities and then in the skin surrounding the trunk. CLINICAL FINDINGS Cold extremities, shivering/ trembling, and subnormal temperature. Weakness, decreased activity. Bradycarida, weak pulse and collapse of major veins are characteristic. Death is common when body temperature falls below 35-degree C. In hypothermia secondary to other diseases, the decrease in temperature is not marked. Clinical findings are more related to the underlying illness. Eg. Milk fever in cattle. DIAGNOSIS ▪ History, Clinical and physical examination findings ▪ Clinical pathology – no characteristic changes ▪ Necropsy findings – no specific lesions DIFFERENTIAL DIAGNOSIS Prolonged exposure to cold environment Septicaemia/ Septic shock/endotoxemia Enteric diseases Hypocalcaemia Hypoglycaemia from simple starvation TREATMENT & CONTROL ❖ If the animal is wet quickly dry off and place in a warming pen. Provide heat using heat lamps/ ordinary lamps/ infrared lamps/ rugs. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  4|Page 04 JANUARY 2021 ❖ In neonates, if suckling reflex is present, give colostrum @ 50ml/kg body weight. ❖ Give 20% glucose parenterally or intraperitoneally @10ml/kg body weight (at a temperature of 39 degree C). ❖ Provide supportive therapy (Fluids, B-complex vitamins, antibiotics etc.), and treat for other concurrent ailments. ❖ Hypothermic animals can be immersed in water at 38-degree C. But this is labour intensive and require close monitoring. ❖ Control: (i) Provide a dry, wind-free environment for animals nearing parturition and for sick and weak animals. (ii) Ensure intake of colostrum immediately after birth. (iii) Monitor rectal temperature of weak neonates. HYPERTHERMIA Hyperthermia is the elevation of body temperature due to excessive heat production or excessive heat absorption or due to deficient heat loss, and the causes of these abnormalities are purely PHYSICAL. The best example is heat stroke. ETIOLOGY High environmental temperature or exposure to sunlight and poor ventilation. Severe muscular exertion especially when the humidity is high, animals are fat, have a heavy hair coat. Other causes - Dehydration, Excessive muscular activity as in Strychnine poisoning and Neurogenic hyperthermia due to damage of hypothalamus. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India 5|Page 04 JANUARY 2021 PATHOGENESIS A rise in temperature increases heart rate and decreases blood pressure due to peripheral vasodilatation. Respiration increases in rate and depth. At higher temperature, there is depression of nervous system and death is by respiratory failure. CLINICAL FINDINGS Initially there is an increase in thirst and the animal seeks cool places. Heart rate and respiratory rate increases. The initial sweating and salivation are followed by a marked absence of sweating. The animal becomes restless, dull, stumbles while walking and tends to lie down. When the body temperature reaches 41 degree C or 106 F, respiration becomes laboured. This is followed by shallow and irregular respiration, rapid and weak pulse, collapse, convulsions and terminal coma. Death occurs when temperature reaches 106 -108 F or 41.5 – 42.5 C. Abortion, embryonic morality and infertility occur in prolonged periods of hyperthermia. DIAGNOSIS History, clinical signs and examination of the environment. Clinical pathology – no characteristic changes Necropsy findings varies with severity of exposure. In severe heat stroke haemorrhages are seen in internal organs viz. kidney, heart, GI tract, testicles etc. DIFFERENTIAL DIAGNOSIS ▪ Simple hyperthermia Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  6|Page 04 JANUARY 2021 ▪ Toxaemia/ Septicaemia/ Viraemia – seldom exceeds 41 degree C or 106 F TREATMENT o Provide shade and adequate water to drink o Treat weak animals with IV fluids – 5% Dextrose or Normal Saline o Wipe the body with a towel/ cotton soaked in thermo-neutral water. Alternatively apply slightly cool water by spraying/ immersion. Cold water enema is also useful. o Supportive therapy – fluids, B-vitamins, antibiotics, antiemetics etc. o Tranquilising drugs such as chlorpromazine can be used when animals are to be confined under hot and humid conditions. FEVER Fever is an elevation of core body temperature above the level that is normally maintained by an animal and is independent to the effects of ambient conditions on body temperature. ETIOLOGY Septic fever ▪ Include infection due to bacteria, viruses, protozoa or fungi as localised or generalized infection, septicaemia etc. Aseptic fever ▪ Chemical fever – injection of foreign protein ▪ Surgical fever – due to break down of tissue & blood ▪ Tissue necrosis or infarction ▪ Severe haemolysis & hemoglobinemia ▪ Neoplasms – due to necrosis Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India 7|Page 04 JANUARY 2021 ▪ Immune reactions – anaphylaxis, angio-neurotic oedema PATHOGENESIS Fever is caused by pyrogens. Pyrogens are exogenous or endogenous. Exogenous pyrogens include pathogens such as bacteria, viruses, bacterial endotoxins, antigen-antibody complexes, severe hemoglobinemia and many inorganic substances. One of the most potent exogenous pyrogens is the lipopolysaccharide of gram-negative bacteria. Endogenous pyrogens are proteins released from granulocytes, monocytes and lymphocytes due to stimulation of exogenous pyrogens. These proteins are generally referred to as cytokines. One of the important cytokines is interleukin-1. Interleukin-1 initiates fever by inducing an abrupt increase in the synthesis of prostaglandins (from arachidonic acid) in the anterior hypothalamus. The elevated prostaglandin levels in the hypothalamus raise the thermostatic set point and induce the mechanisms of heat conservation and heat production. The three stages of fever are i. The period of increment and chill ii. The period of fastigium or constant temperature iii. The period of decrement or fever defervescence In response to the raised ‘set point’ at the thermo-regularity centre of hypothalamus, the body tries to conserve heat/ produce more heat. This is the period of increment. The period of increment is manifested by Cutaneous vasoconstriction, cold extremities, absence of sweating, reduced respiration and reduced urine output; Muscular shivering. Consequently, the rectal temperature rises. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India 8|Page 04 JANUARY 2021 Once the thermogenic mechanisms of the body raise the body temperature to the new ‘set point’ (elevated) the period of fastigium begins. The period of fastigium is characterized by mechanisms of heat dissipation and heat production returns to normal. This stage is characterized by cutaneous vasodilatation, sweating, diuresis, and absence of muscular shivering. When the causative pyrogens are removed from the body the period of decrement begins and the excess stored heat is dissipated. This stage is manifested as vasodilatation, sweating, muscle flaccidity and a decrease in temperature to normal. Advantages of fever - Increased phagocytic activity Adverse effects of fever – Anorexia, tissue wasting, DIC, convulsions. CLINICAL FINDINGS Depression, anorexia, muscle weakness, increased thirst Increased heart rate with a decrease in amplitude and strength of arterial pulse Hyperpnoea Oliguria & scant faeces Elevated body temperature FORMS OF FEVER Transient Sustained: without significant diurnal variation. Remittent: with exaggerated diurnal variation. Intermittent-fever: Fever last for 2-3 days and are interspersed with normal periods. Eg: Equine Infectious Anaemia (EIA). Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  9|Page 04 JANUARY 2021 Atypical: Temperature variations are regular. Biphasic-consists of an initial rise, a fall to normal, followed by a secondary rise. Eg. Strangles in horses, erysipelas in swine. DIAGNOSIS Fever is determined by recording the core body temperature or the rectal temperature. There are no laboratory tests that are specific for fever. However, tests to differentiate diseases include: CBC and serum biochemistry Microbiological testing and cytological analysis of body fluids - blood samples, CSF, synovial fluid, aqueous humor, vitreous humor, respiratory/ reproductive tract secretions, fluids collected from body cavities etc. Exploratory cytology and biopsy TREATMENT The main objective is to identify and treat the prime disease. In mild cases of fever in which the animal is apparently healthy and active with moderate food intake, antipyretics are not necessary. To control fever which cause discomfort and inappetence, use antipyretics. Eg. Meloxicam, Flunixin meglumine, Phenyl butasone, Acetyl salicylic acid, Paracetamol, Carprofen etc. ***** REFERENCES 1) Veterinary Medicine by Peter Constable, Kenneth Hinchcliff, Stanely Done and Walter Grunburg, 2017, 11th edition, Elsevier. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  10 | P a g e 04 JANUARY 2021 2) Small Animal Internal Medicine by Richard Nelson and Guillermo Couto, 5th edition, Elsevier. QUESTIONS 1. A lack of shivering does not indicate an absence of cold stress in neonates. Substantiate. 2. Differentiate (i) Shivering thermogenesis Vs Non-shivering thermogenesis (ii) Hyperthermia Vs Fever. 3. Increased density of sweat glands on ……………… makes it more heat tolerant. 4. Sweating is an effective method of heat dissipation in ……………. 5. List the differentials of hypothermia and hyperthermia. 6. Write the treatment for hypothermia and hyperthermia. 7. List the three stages of fever. 8. Write the etiology of fever. 9. Write the different forms of fever. ********** Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India 1|Page 7 January 2021 SEPTICAEMIA and VIRAEMIA Septicaemia is the acute invasion of the systemic circulation by pathogenic bacteria, which may cause sepsis or septic shock. If the infection is not adequately controlled, the bacteria localize in various organs. (Sepsis is a potentially life-threatening condition caused by the body's response to an infection). Bacteraemia is different from septicaemia. No. Bacteraemia Septicaemia 1 Bacteraemia is NOT Septicaemia is accompanied by accompanied by sepsis. sepsis. 2 Bacteria are present in blood Bacteria are present in blood only for transient periods and for longer periods and are do NOT produce clinical signs. accompanied by clinical signs. 3 Eg. After per-rectal Eg. Colisepticemia, Anthrax, examination, a clinically Pasteurellosis, Salmonellosis. unimportant bacteraemia Bacteria are present occurs, if the mucosal throughout the course of the integrity is disturbed. disease. Presence of a superficial or a deep abscess is not a septicaemic condition and do not produce septicaemia as long as the lesion is localised. Pathological change is seen only in the local area or tissues that are affected and bacteria are not present in the systemic circulation. Viremia is the invasion of the systemic circulation by pathogenic viruses with subsequent localization in various body tissues. The lesions produced are characteristic of the specific virus. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  2|Page 7 January 2021 Many infections associated with rickettsias, protozoa and fungi are also spread haematogenously throughout the body but do not initiate a systemic inflammatory response syndrome. ETIOLOGY ▪ Gram negative bacterial organisms – Mannheimia hemolytica, Salmonella spp., E. coli, Klebsiella spp. etc. ▪ Gram positive bacterial organisms – Bacillus antracis, α-haemolytic Streptococcus, Streptococcus suis Type-I, Actinobacillus equuli, Erysipelothrix insidiosa ▪ Viral organisms - Bovine Viral Diarrhoea (BVD) and Bovine Malignant Catarrh, Classical swine fever etc. ▪ Secondary Septicemia: Defects in immune system or immune- suppression due to various causes can lead to secondary septicaemia. EPIDEMIOLOGY Animals of all ages are affected. Young animals are more susceptible to neonatal septicaemia. PATHOGENESIS Pathogenesis is due to toxins and disseminated intravascular coagulation (DIC). Bacteria produce exotoxins or endotoxins. These toxins initiate an inflammatory response (through several biochemical mediators) and fever in the host body. Rapid multiplication and spread of pathogens to different body tissues can lead to widespread inflammatory response called SIRS or systemic inflammatory response syndrome. (The same general principles apply to viremia, except that toxins are not produced by viruses). Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  3|Page 7 January 2021 Disseminated intravascular coagulation (DIC) is the coagulation of blood within blood vessels. It is seen in severe septicaemia. Bacterial cell walls, antigen-antibody complexes and endotoxin circulating in the blood injure vascular intima. This initiates platelet adhesion and the formation of platelet thrombi. Widespread coagulation within the vessels deplete platelets as well as coagulation factors and result in haemorrhagic diathesis. Other pathogenic effects are localisation in organs/ development of a carrier status; and transplacental infections (abortion, foetal death & mummification). CLINICAL FINDINGS In septicaemia, animal becomes dull and weak. Other important signs are a rise in body temperature, respiratory distress, tachycardia, tachypnoea, hypotension, cold extremities and dehydration. Submucosal haemorrhages under the conjunctiva and in the mucosae of the mouth and vulva and subepidermal haemorrhages are seen. When the bacteria localise in organs such as joints, heart valves, meninges etc. the animal shows specific signs of the organ involved. In severe cases of septicaemia, animals become laterally recumbent and die. LABORATORY FINDINGS/ CLINICAL PATHOLOGY ▪ Hemogram: In general, leucocytosis with neutrophilia is seen in bacterial infections and leucopoenia in the initial phase of viral infections. Falling platelet counts, prothrombin and fibrinogen values indicates consumption coagulopathy. ▪ Blood culture Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  4|Page 7 January 2021 ▪ Examination of other body fluids, if required. Eg. Ascitic fluid, synovial fluid etc. DIAGNOSIS Diagnosis is based on history, clinical signs and laboratory findings. PM lesions include submucous and subserous haemorrhages may be seen in internal organs. DIFFERENTIALS o Toxaemia o Hyperthermia o All diseases characterised by fever TREATMENT ✓ Fluids ✓ Antimicrobials ✓ B-complex vitamins ✓ Other supportive therapy o NSAIDs are used with CAUTION, because it aggravate bleeding tendency. ***** TOXAEMIA/ ENDOTOXAEMIA Toxaemia is a clinical systemic state caused by widespread activation of host defence mechanisms to the presence of toxins produced by bacteria or injury to tissue cells. Toxaemia does not include the diseases caused by toxic substances produced by plants or insects or ingested organic or inorganic poisons. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India 5|Page 7 January 2021 ETIOLOGY Toxins are of two types: antigenic toxins and metabolic toxins. Antigenic toxins: These are produced by bacteria and to a lesser extent by helminthes. Antigenic toxins stimulate the production of antibody in the host animal. Antigenic toxins are divided into exotoxins and endotoxins. Exotoxins are protein substances produced by bacteria which diffuse into surrounding medium. They are specific in their pharmacological effects and in the antibodies they induce. Eg. Exotoxin produced by Clostridium spp., enterotoxins released by enterotoxigenic E. coli etc. Endotoxins are lipopolysacharides found in the outer cell wall of the bacteria. They are released into the immediate surroundings when the bacteria undergo rapid proliferation or, when the bacterial cell wall breaks. Eg. Coliform mastitis Metabolic toxins: Metabolic toxins are toxic chemical substances that accumulate in the body as a result of incomplete elimination of toxic materials normally produced by body metabolism or by abnormal metabolism. Normally these toxins are excreted in the urine and faces or detoxified in plasma and liver. Eg. ▲ In hepatic dysfunction, toxins that are normally detoxified by the liver, accumulate in the system. ▲ In obstruction of the lower alimentary tract, toxic phenols, cresols and amines are increasingly absorbed from the intestinal lumen, leading to a condition called autointoxication. ▲ Ketonemia due to abnormal fat metabolism. ▲ Lactic acidemia due to acute ruminal acidosis. PATHOGENESIS OF ENDOTOXAEMIA The toxic moiety of the lipopolysacharide molecule of all the bacteria is generally similar. Endotoxemia results in an extra ordinary sequence of pathophysiologic effects, involving all body systems. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  6|Page 7 January 2021 Endotoxins induce the release of biochemical mediators (such as platelet-activating factor, prostaglandins etc.) resulting in vasoconstriction, systemic hypotension, shock, disseminated coagulopathy, organ dysfunction, and death. CLINICAL FINDINGS OF ENDOTOXAEMIA Depression, muscle weakness Fever and congested mucous membrane In the early stages, heart rate and cardiac output increases. This is known as the hyperdynamic phase of endotoxemia. The animals have decreased CRT and red congested mucous membrane due to microcirculatory shunting in capillaries. With uncontrolled endotoxemia, the hyper dynamic phase progress to the hypodynamic phase of shock. Cardiac output decreases and CRT increases, skin and extremities become cool and animal become hypotensive and hypothermic. Other findings include diarrhoea, decreased urine output, DIC and petechial/ ecchymotic haemorrhages on mucous membranes and sclera. In chronic toxaemia, clinical signs include lethargy, inappetence, failure to grow or produce, anaemia and emaciation. LABORATORY FINDINGS/ CLINICAL PATHOLOGY Hematology: Leukocytosis and neutrophilia is seen in mild endotoxemia. In severe cases, leucopenia develops due to neutropenia and lymphopenia. Serum biochemistry: There is no diagnostically important alteration. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India 7|Page 7 January 2021 DIAGNOSIS History, clinical signs and laboratory findings. PM lesions: Gross findings depend on the location of lesion – Eg. Peritonitis, myositis, mastitis, metritis etc. TREATMENT OF ENDOTOXEMIA The principles of treatment of endotoxemia or septic shock include: (1) Remove the foci of infection. (2) Administer broad-spectrum antimicrobial agents with a Gram- negative spectrum or a combination of antibiotics depending on severity. Eg. Fluroquinolones, aminoglycosides etc. (3) Aggressive fluid and electrolyte therapy to correct hypovolemia, hypoglycaemia and electrolyte & acid-base disturbances. Isotonic fluids (NS or DNS) are given to correct hypovolemia and a balanced electrolyte solution (RL) to correct acid-base and electrolyte imbalances. Glucose must be included to correct/ prevent hypoglycaemia. Hypertonic saline (7.5% NaCl) enhances tissue perfusion and decrease the volume of fluid to be administered. Fluid therapy also aids in the dilution and excretion of toxin from the host body. (4) NSAIDs or Glucocorticoids to inhibit products of the cyclooxygenase pathway (inflammation). Flunixin meglumine (1.1 to 2.2 mg/kg q12-24h) is the most commonly used NSAID in horses and ruminants. NSAID is rarely used or used with caution in dogs and cats. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  8|Page 7 January 2021 The most commonly used glucocorticoid is dexamethasone (1.0 mg/kg q24h). Give dexamethasone as a CRI or slow IV mixed with fluids. (5) Other supportive therapy depending on the condition of the animal. Eg. B-complex vitamins, inotropic agents, vasopressor agents, hyperimmune serum, anticoagulants etc. Inotropic agents increase cardiac output and oxygen delivery. Eg. Dobutamine is the drug of choice. Vasopressor agents increase systemic arterial blood pressure. Nor-epinephrine is the drug of choice in hypotensive animals that have not responded to intravenous fluids or dobutamine injections. Other therapies: hyperimmune serum for endotoxaemia in horses, anticoagulants like heparin to counteract DIC. PROGNOSIS Prognosis is good in early stages of endotoxaemia. Persistence of severe neutropenia, high lactate in blood and hypotension are poor prognostic indicators. ***** REFERENCES 1) Veterinary Medicine by Peter Constable, Kenneth Hinchcliff, Stanely Done and Walter Grunburg, 2017, 11th edition, Elsevier. 2) Small Animal Internal Medicine by Richard Nelson and Guillermo Couto, 5th edition, Elsevier. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  9|Page 7 January 2021 QUESTIONS 1. Write in two or three sentences. (i) Septicaemia Vs Viraemia Vs Sepsis (ii) Antigenic toxins Vs Metabolic toxins 2. Differentiate bacteraemia and septicaemia. 3. Write the clinical features of endotoxaemia. 4. List the principles of treatment of endotoxaemia. 5. How can we make use of the total and differential leucocyte counts to diagnose bacterial/ viral infections? ********** Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  1|Page 13 January 2021 SHOCK, ALLERGY AND ANAPHYLAXIS SHOCK Shock is a life-threatening condition associated with reduced blood supply to vital organs in the body. Inadequate blood supply deprives cells and organs of oxygen and nutrients required to maintain normal function. Circulation of blood in an animal is maintained by a healthy heart and vasculature. Pathologic conditions that affect either of heart or vasculature or both decreases venous return back to the right atrium. This can lead to a condition called circulatory shock. (Other types of shock are anaphylactic shock, neurogenic shock and septic shock). Circulatory shock is of two types. When heart (pump) is affected, it is called pump failure or heart failure and it leads to a condition called cardiogenic shock. Heart failure can be classified as acute heart failure and chronic heart failure. When the functioning of circuit is affected it is called circuit failure and it leads to a condition called circuit shock. It is clinically very important to differentiate heart failure from circuit failure, because the diagnosis and treatment of cardiogenic shock is different from that of circuit shock. Cardiogenic shock will be discussed with the diseases of cardio- vascular system. Circuit failure/ shock is discussed in this lecture. Circuit shock results from hypovolemia, haemorrhage, maldistribution of blood or an obstruction to venous return. ETIOLOGY The common causes of circuit shock (failure) are:- 1) Hypovolemic shock: Hypovolemic shock occurs due to a reduction in the circulating volume of blood as a result of loss of plasma or free water. Eg. Fluid loss and dehydration due to diarrhoea, vomiting, burn etc. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India  2|Page 13 January 2021 2) Haemorrhagic shock: Haemorrhagic shock occurs when there is a reduction in circulating blood volume due to rapid loss of blood. Eg. Traumatic injury, umbilical haemorrhages in neonates, abomasal ulcer, pulmonary haemorrhage, parvo viral enteritis in dogs, blood sucking intestinal parasites, internal bleeding due to rupture of liver, uterus, splenic haematoma etc. 3) Maldistributive shock: Maldistributive shock occurs when there is a reduction in circulating blood volume due to increased capillary permeability, pooling of blood in capacitance vessels (such as the veins in the splanchnic circulation), or pooling of plasma in thoracic or abdominal cavities. Eg. Endotoxemia in neonatal septicaemia, salmonellosis, coliform mastitis, toxic metritis, septic shock, sudden withdrawal of ascitic or thoracic fluid etc. 4) Obstructive shock: Obstructive shock occurs when venous return of blood back to heart is reduced or prevented by a mechanical obstruction. Eg. Pericardial tamponade, pulmonary artery thrombosis etc. Obstructive shock is less common in large animals. PATHOGENESIS Hypovolemia, haemorrhage and maldistribution result in hypovolaemia, hypotension and decreased organ perfusion. A decrease in the perfusion of organs result in tissue hypoxia, anaerobic metabolism, L-lactate acidaemia, metabolic acidosis and multiple organ failure. The major effects of haemorrhagic shock are (i) loss of blood volume (hypovolemic shock) (ii) Loss of plasma protein (decreased oncotic pressure) and (iii) Loss of erythrocyte (anaemic anoxia). In obstructive shock, hypotension is due to decreased cardiac output. CLINICAL FINDINGS Clinical findings in the early stages include: - Depression, weakness, lethargy Inability to maintain normal gait and body posture, recumbency or collapse Pale grey to white and dry mucous membranes, Low body temperature, Cold skin and extremities, and a prolonged CRT (> 3-4 seconds). However, Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India 3|Page 13 January 2021 in the early hyperdynamic stage of maldistributive shock mucous membrane is injected and brick red in colour, temperature is normal or elevated, and CRT is normal or increased. Skin turgor is decreased Heart rate is increased, Pulse is small and weak – ‘thready pulse’, it is difficult to raise veins Anuria or oliguria Anorexia is usual, thirst may be evident. Terminal stages are characterised by profound depression, very low blood pressure, inability to raise veins, cardiac arrhythmia, extreme coolness of the body and death. Clinical parameters monitored in shock are heart rate, pulse character, mucous membrane colour and temperature of extremities. The single most valuable index is the heart rate. Clinical Samples: CBC, electrolyte and blood gas analysis, liver function, kidney function Imaging: Ultrasound, X-rays Special procedures: Abdominocentesis, Thoracocentesis DIAGNOSIS History, clinical and physical examination findings. Ultrasound/ X-ray/ Abdominocentesis/ Thoracocentesis: to identify internal bleeding. Clinical pathology: Clinical pathological findings helps to determine the cause and severity of shock and to monitor the effectiveness of therapy. Plasma L-lactate: 4 mmol/L indicates widespread anaerobic respiration and >10 mmol/L indicates a very poor prognosis. Normal venous blood oxygen tension, PO2 is 35-44 mm of Hg and the arterial blood oxygen tension, PO2: is 90 mm of Hg. In shock, oxygen tension decreases. Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India 4|Page 13 January 2021 Necropsy findings: Pallor of tissues in haemorrhagic shock. In obstructive shock there is increased pericardial fluid. Findings in hypovolaemic and maldistributive shock depends on the etiology. DIFFERENTIAL DIAGNOSIS ❖ Septicaemia ❖ Acute intestinal accidents ❖ Severe trauma ❖ Severe fluid loss for any reason ❖ Rapid removal of fluid from a body cavity TREATMENT I. Hypovolemic/ Maldistributive shock (i) Isotonic crystalloid fluids ▪ A MAXIMUM of 50 ml/kg to 90 ml/ kg of isotonic crystalloids is given as rapid IV infusion over 15 to 30 minutes for dogs and large animals to counter hypovolaemia and hypotension. For cats the maximum level of fluid infusion is 40 to 50 ml/ kg only. During rapid IV infusion closely monitor pulse quality, CRT and blood pressure to avoid overhydration, pulmonary oedema and death. A moderate speed of fluid administration is always advisable in practical setting. (NOTE: 50 to 90 ml/ kg can lead to pulmonary oedema. So, in my opinion give fluids @ 20 ml/kg body weight monitoring pulse quality and CRT; if possible, BP too. IV fluid administration above 20 ml/kg should be done with utmost care). ▪ Ringer’s Lactate is a balanced electrolyte solution ideal in shock conditions. (NOTE: In clinical practice, if history & diagnosis is less clear or if electrolyte levels and blood gas analysis are not available better to start with 0.9% normal saline). ▪ Fluids for restoration of extracellular volume (ECF) must contain Na and hence glucose/ dextrose solution are NOT indicated in the treatment of shock. Glucose/ dextrose after metabolism provide only free water without any ions. (ii) Hypertonic Saline solutions Dr. Arun George, Assistant Professor, Dept. of Veterinary Clinical Medicine, CVAS, KVASU, Thrissur, Kerala, India 5|Page 13 January 2021 ▪ 4-5 ml/ Kg of 7.2% NaCl solution infused IV over 4-5 minutes. ▪ Results in shift of fluid from interstitial to intravascular space. Hypertonic saline must be followed by IV isotonic crystalloid fluids. (iii) Colloidal solutions ▪ Colloids induce a more sustained increase in plasma volume than crystalloid solutions. General dose is 5 ml/ kg IV. ▪ Hypertonic solutions in combination with colloids give a more sustained response. II. Haemorrhagic shock ▪ Control haemorrhage. ▪ If haemorrhage is under control, hypertonic saline is recommended for initial treatment. If haemorrhage is not controlled the use of hypertonic saline is CONTRAINDICATED because increased blood pressure results in more protracted bleeding. ▪ Or give isotonic crystalloids sufficient to maintain vital functions. Eg. 0.9 % NS. Excess fluid therapy can aggravate haemorrhage. ▪ Haemostats o Ethamsylate – IM, IV, PO o Botropase – Inj. o Inj. Adrenaline is diluted and applied locally to prevent capillary haemorrhage. o 10-30 ml of buffered neutral formalin in 500 ml saline IV (to control post-parturient haemorrhage in horses) o Aminocaproic acid 10g in 1 litre of saline for an adult horse or @ 20 mg/ kg SD, IV o Ergonovine maleate, 1-3 mg IM every 3 hours (to control post- parturient hemorrhage in mares) Blood transfusion: PCV < 12% is indicative of blood transfusion in large animals. A PCV of