Professional Documents
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SHRIKANT KULKARNI
The knowledge of basic physiology of alla the vital organs is very much
essential inorder to effecly achieve the therapeutic protocols and also to understand the
pathological changes that are taking place in body of the patient.The following
description is an attempt to revise the basic physiology of important vital organs in the
body.
BRAIN:
The brain is the center of the nervous system and is a highly complex organ. Enclosed
in the cranium. In spite of the fact that it is protected by the thick bones of the skull,
suspended in cerebrospinal fluid, and isolated from the bloodstream by the blood-brain
barrier, the delicate nature of the brain makes it susceptible to many types of damage
and disease. The most common forms of physical damage are closed head injuries such
as a blow to the head, a stroke, or poisoning by a wide variety of chemicals that can act
as neurotoxins. Infection of the brain is rare because of the barriers that protect it, but is
very serious when it occurs.
The most important biological function of the brain is to generate behaviors that
promote the welfare of an animal. Brains control behavior either by activating muscles,
or by causing secretion of chemicals such as hormones. Even single-celled organisms
may be capable of extracting information from the environment and acting in response
to it. However, sophisticated control of behavior on the basis of complex sensory input
requires the information-integrating
Several brain areas have maintained their identities across the whole range of
vertebrates, from hagfishes to humans.
• The medulla, along with the spinal cord, contains many small nuclei involved in
a wide variety of sensory and motor functions.
• The hypothalamus is a small region at the base of the forebrain, whose
complexity and importance belies its size. It is composed of numerous small
nuclei, each with distinct connections and distinct neurochemistry. The
hypothalamus is the central control station for sleep/wake cycles, control of
HEART:
The heart is a muscular organ in all vertebrates responsible for pumping blood through
the blood vessels by repeated, rhythmic contractions. The heart is composed of cardiac
muscle, an involuntary striated muscle tissue which is found only within this organ. In
mammals, the function of the right side of the heart (see right heart) is to collect de-
LUNGS:
Avian lungs do not have alveoli as mammalian lungs do. They contain millions of
tiny passages known as para-bronchi, connected at both ends by the dorsobronchi. The
airflow through the avian lung always travels in the same direction - posterior to
anterior. This is in contrast to the mammalian system, in which the direction of airflow
in the lung is tidal, reversing between inhalation and exhalation. By utilizing a
unidirectional flow of air, avian lungs are able to extract a greater concentration of
oxygen from inhaled air. Birds are thus equipped to fly at altitudes at which mammals
would succumb to hypoxia. This also allows them to sustain a higher metabolic rate
than an equivalent weight mammal.
LIVER:
The liver is the largest glandular organ of the body. This organ plays a major role in
metabolism and has a number of functions in the body, including glycogen storage,
decomposition of red blood cells, plasma protein synthesis, hormone production, and
detoxification. It lies below the diaphragm in the thoracic region of the abdomen. It
produces bile, an alkaline compound which aids in digestion, via the emulsification of
lipids. It also performs and regulates a wide variety of high-volume biochemical
reactions requiring highly specialized tissues, including the synthesis and breakdown of
small and complex molecules, many of which are necessary for normal vital The liver
is necessary for survival; there is currently no way to compensate for the absence of
liver function. The physiological functions of liver are:
KIDNEY:
The kidneys are paired organs, which have the production of urine as their primary
function. They are part of the urinary system, but have several secondary functions
concerned with homeostatic functions. These include the regulation of electrolytes,
acid-base balance, and blood pressure. In producing urine, the kidneys excrete wastes
such as urea and ammonium.
*****
This technique requires only topical anesthesia and a tuberculin syringe with a
25- or 27-gauge needle. Volumes should not exceed 0.25 ml in cats and Dogs and 1.0
ml in horses and cows. Subconjunctival medication reaches the cornea by slowly
leaking out of the injection site. Intraocular drug levels are attained by diffusion through
the cornea and sclera. Subconjunctival administration is used for diseases of the cornea,
anterior, uvea, anterior vitreous, and sclera. Subconjunctival or sub-Tenon’s therapy,
while not a true form of systemic medication, has potentially increased drug absorption
and contact time. Medications both leak on to the cornea from the entry hole of injection
and diffuse through the sclera into the globe. Drugs with low solubility such as
corticosteroids may provide a repository of drug lasting days to weeks. Appropriate
amounts must be used, as large amounts, especially of long-acting salts, can cause a
significant inflammatory reaction. For sub-Tenon’s injections, 0.5 ml/site is usually safe
and effective in small animals and ≤1 ml in large animals such as the horse and cow.
3.Retrobulbar medications:
They are used infrequently for therapeutics. In cattle, the retrobulbar tissues can
be anaesthetized with local anesthetic (lidocaine) for enucleations. Whenever any
medication is placed into the orbit, extreme care must be taken to ensure that the
medication is not inadvertently injected into a blood vessel, the optic nerve, or one of
the orbital foramen. Retrobulbar injection has a high risk of adverse effects and should
not be used unless the clinician is experienced and the animal is appropriately
restrained.
4. Intravitreal-used infrequently:
Topical antibiotics are indicated for the treatment of corneal ulcers, corneal
perforations, conjunctivitis and blepharitis. Ideal choice of appropriate therapy begins
with identification of the organism and its sensitivity. Culture or cytologic examination
of material from the affected area is necessary. Minor bacterial conjunctivitis infection
may not justify routine culture and may be amendable to initial therapy with broad
spectrum antibiotics. Normal ocular flora is predominantly gram positive; a
predominance of gram negative organisms is indicative of an abnormal condition.
2. Aminoglycosides:
c. Tobramycin.: Two to four times more effective against Pseudomonas spp. and
betalactamase producing staphylococci than gentamicin and effective against
gentamicin-resistant microbes.
3. Polypeptides:
4. Cephalosporins:
Antiviral agents are indicated for treatment of herpetic keratitis in cats. Corticosteriods
should never be used in the suspected ocular eye infections as they further aggravate the
condition. The topical antiviral agents are static in action and topically irritating, so
frequent administration is necessary and client compliance and patient tolerance are
issues.
1. Polyenes :
2. Imidazoles
a. Miconazole 1%: Drug of choice for most veterinary fungal keratitis cases, but no
longer readily available in IV preparation. Tolerated well as subconjunctival injection.
1 ml SID x 3-5 days if tolerated. Treatment frequency of a fungal keratitis may warrant
1 to 4hour treatment intervals. Lotions or sprays that contain ethyl alcohol should not be
applied to the eye.
2. Carprofen : Used in similar ways as aspirin. May have fewer side effects. Do not
use in Labrador retrievers - may cause liver disease. Dosages: 2.2mg/kg BID. Not
approved for use in cats.
3. Etodolac : Dosage: Dog-10 - 15 mg/kg, PO SID. Should not be used in Dogs < 5 kg
Drugs suitable for use as local anesthetics cause a reversible block of conduction
through nerve fibers by displacing calcium at binding sites in cell membranes. To be
effective, local anesthetics must have properties similar to drugs that penetrate the
cornea. They must be capable of existing in ionized (water-soluble) and nonionized
(lipid soluble) forms. Increased membrane permeability exists in an alkaline state. Local
anesthesia is less effective in inflamed tissue which has more acidic pH than normal.
a. Osmotic Agents (topical): 2-5% NaCl (hypertonic saline). Indicated primarily for
treatment of severe chronic corneal edema originating from superficial epithelial
disruption and for severe cornea bullae formation. Side effect-localized irritation.
b.Tear Film Supplements : All are indicated to control keratitis sicca. May provide
temporary comfort to corneal irritation resulting from distichia, entropion, or sutures,
and as a vehicle for delivery of medications. Tear supplements are available in solution
and ointment form and are intended to replace the aqueous or lipid layer of the tear film.
Preservative-free products generally recommended.
*****
Signalment:
History: most patients with cardiac diseases have exercise intolerance at some level of
excertion. In most instances cardiac diseases begins somewhat insidiously with slow
progression over a period of several months to years. With right sided failure, ascites,
hepatomagaly occur initially where as with left sided failure coughing, pulmonary
odema and dyspnoea are commonly observed. History of fainting, syncope or collapse
can also be observed in dogs with arrythmias. Functional ability of the other organs too
get affected like kidney and liver.
Physical examination: most of the dogs look apparently normal, but they
progressively go down in condition and may look thin to cachetic in later stages.
Affected animals stand with abducted elbows indicating respiratory distress or
pulmonary oedema. Cyanosis of the visible mucous membrane may result from right to
left shunting of blood as in case of tetralogy of fallot, atrial septal defect and ventricular
septal defect. Increased capillary refill time may be noticed in conditions of shock,
mitral valve insufficiency. Superficial veins, jugular vein distension can be observed in
right sided failure or pericardial effusion.
Ascultation: most important in assessing heart diseases. Both heart and lungs should
be asculted. 4 sounds are produced normally, but first 2 are heard frequently in dogs.
Murmers: are abnormal heart sounds as a result of vibration produced by the flow of
blood (turbulence in blood flow) in the heart or greater vessels.
Laboratory examination:
B. CONDUCTION ABNORMALITIES:
i)_Atrio-venticular heart block : occurs due to delay in transmission of impulses
from AVN to bundle of His
a) Ist degree AV Block: “PR” interval ≥ 0.13 sec.
b) II nd degree heart block: some “P” waves without “QRS” complex.
c) IIIrd degree heart block: more of “P” waves without ‘QRS” complex.
D. ECTOPIC ARRYTHMIAS
a) Atrial fibrillation: most common arrhythmias seen in small animal, depolarization
occurs randomly throughout atria, here “P’ waves are replaced by “F” waves (saw
toothed waves) i.e. fine irregular movement of the base line observed as a result of
atrial fibrillation.
ECG and radiography are the basic needs of the cardiac evaluation; the results
of these along with history and physical examination make clinician to arrive at a
definitive diagnosis. Although ECG is quite useful, it is not HIGHLY sensitive for
detecting hypertrophy of the heart chambers; it only supports a differential diagnosis
and should not be considered a definitive diagnostic test.
Subvalvular aortic stenosis : left ventricular out flow is obstructed below the arotic
valve and include incomplete fibrous ridges, discrete fibrous rings, such dogs usually
won’t bred, balloon catheter dilatation( like balloon angioplasty in humans) of the sub
aortic area is found to be helpful.
Pulmonic stenosis : right ventricular out flow obstructed along with pulmonic valve
dysplasia characterized by thickening of valves, various surgical procedures are
employed to correct this apart from the balloon catheter dilatation.
Patent ductus arteriosus : where in pulmonary artery gets fused with aorta, leading to
increased flow of blood from the aorta to pulmonary artery leading to increased
pulmonary flow, intern increased pulmonary venous return to ventricles resulting in
volume overload in ventricles ending up with left side congestive heart failure, surgical
ligation is the best method for clinical management though such animals are not used
for breeding purpose.
DILATED CARDIOMYOPATHY AND HYPERTROPIC CARDIOMYOPATHY
Most common disease in dogs and cats, initially anorexia, weakness, exercise
intolerence, coughing, pulmonary odema, syncope with progression to congestive heart
failure. Treatment should be directed towards (1) reducing the elevated ventricular
pressure in order to relieve congestion- i.e. oedema (2) increasing forward stroke
volume and (3) Optimizing heart rate and rhythm
Regardless of the underlying cause, decrease in filling pressure with alleviating
oedema is achived by administration of diuretics. Such animals should receive
furosemide parentrally at the rate of 2 – 3 mg/kg until it stabilizes.Refractory oedema
cases are most effectively controlled by adding a second diuretic that acts at different
site at kidney, i.e. spiranolactone at the dose rate of 1-2 mg/kg BID (PO) or thiazide
diuretic (hydrochlorothiazide) at the dose rate of 2-4 mg/kg BID (PO).
List of diuretics used in case of cardia ailments
Bendroflumethia Dog 0.2-0.4 mg/kg BID (PO) Hypovolemia, as for
zide Cat undetermined hydrochlorthiazide
Bumetanide Dog 0.01-0.5 mg/kg total (IV); Hypovolemia, hypokalemia,
0.03-0.06 mg/kg SID-BID (PO) metabolic alkalosis
Cat unknown
Chlorthiazide Dog 20-40 mg/kg BID-TID (PO) Hypovolemia, hypokalemia,
Cat 20-40 mg/kg BID (PO) metabolic acidosis
Furosemide Dog 2-4 mg/kg BID-TID (IV, IM, SQ, Hypovolemia, hypokalemia,
PO); metabolic alkalosis, deafness
2-8 mg/kg q 1h (IV) in severe
pulmonary edema
Cat 1-2 mg/kg BID-TID (PO, IM, IV),
do not exceed 2 mg/kg (IV)
This is common in certain breeds like GSD, bull terrier, Grate Dane. Seen most
commonly in older dogs and dogs over 13 years will exibit murmurs upon
ascultation.Diagnosis requires echocardiography. Surgical intervention, including valve
reconstruction, valve replacement and annuloplasty of the mitral valve has been
successful in associated clinical signs.
*****
a) Reduced oxygen carrying capacity of the blood (Anaemic hypoxia) seen in nitrite
c) Reduced blood flow (Stagnant hypoxia) seen in congestive heart failure and
Polypnea is rapid breathing, Tachypnea is very rapid and shallow breathing and
Hyperapnea is an abnormal increase in rate and depth of breathing but not up to the
point of labored. Dyspnea is difficult or labored breathing and can be of two types:
Pleuritic frictional sounds are produced due to rubbing of inflamed parietal and
visceral pleural surface against each other which are more pronounced during
expiration and are suggestive of pleurisy 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 :
Clinical examination of patient suspected for respiratory 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 techniques :
Use of fiber-optic endoscope has improved the diagnostic skill of the physician and is
routinely being used in canine and equine practice. Flexible fiber-optic 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.
6. Expectorants are indicated to expel the mucus from the respiratory tract. Sedative
expectorants containing ammonium chloride are used in exhaustive, tenacious
cough whereas; codeine or dextramethorphan containing expectorants are indicated
in non-productive cough to suppress the cough center.
DISEASES OF LUNG:
Pathogenesis: Reduced effective alveolar space, reduced vital capacity of lungs and
impaired oxygenation of blood are the hallmarks of pulmonary congestion and oedema.
The end effect is anoxic hypoxia.
Clinical signs: Increased depth of respiration to the point of extreme dyspnea, open
mouth breathing, typical stance with front legs spread wide apart and abducted elbows.
Presence of crackles (moist rales) on auscultation over lower parts of lungs is
characteristic.
Diagnosis:
• Clinical findings.
• Laboratory investigation like bacterial isolation from nasal swabs, eosinophilia on
haematological examination.
Treatment:
Diagnosis:
Pneumonia:
Etiology:
Clinical Findings: Rapid shallow breathing is initial cardinal sign of pneumonia which
changes to dyspnea in later stages loss of lung parenchyma functionas. Presence of
moist, soft but painful cough is suggestive of bacterial broncho-pneumonia. Whereas
dry, hacking and paroxysmal cough is indicative of viral etiology. Bilateral muco-
purulant nasal discharge, fever, rough hair coat, gaunt appearance, presence of crackles
or wheezes on auscultation are observed.
Diagnosis:
• Higher Antibiotics
• Antihistamines
• Potent anti-inflammatory agents or steroids
• Bronchodilators and other supportive therapy.
*****
The liver has very complicated functions and one of the most important
function is the detoxification of drugs such as antibiotics and its metabolites. Some
antibiotics can cause allergic reactions while others can cause direct damage to their
liver, which can be quite severe in patients with chronic liver disease. For patients with
a pre-existing liver disorder, the detoxification function of the liver is already
compromised and substances that would normally be metabolized could actually
accumulate in the liver or in the bloodstream.Liver disease may have a variable effect
on drug clearance. The effect is difficult to predict and almost impossible to quantify.
There are no tests for hepatic function that will reliably predict drug clearance. Changes
in hepatic function due to disease that may affect drug clearance are described by: :i)
decreased intrinsic clearance caused by loss of functional hepatic mass ii) Increased
fraction unbound of protein-bound drugs. Decreased drug protein binding caused by
decreased albumin; this may increase clearance of drugs that are highly protein bound
iii) decreased hepatic blood flow resulting in decreased drug clearance.
Antibiotics that accumulate in this manner could become toxic to the body and
its functions can change drastically from its original purpose. For the most part in
treating patients with preexisting liver disease who develop infections outside the liver,
one should use caution in prescribing drugs known to be dependent on liver for
inactivation or excretion. Usually a safer substitute drug can be found. One should also
take care to avoid use of hepatotoxic non-antibiotic drugs concomitantly. On the other
hand, drugs metabolized and/or excreted by the liver are theoretically ideal for
treatment of acute infections of liver and biliary tract.
Objectives
Specific therapies
Drugs
Antibiotics
Tetracyclines are concentrated in the liver and the bile but are only bacteriostatics
The following is a list of the most common antibiotics groups being used today. Each is
ordered according to their potential harmful effects on the liver, the top group being the
most potentially harmful and the last group being the least.
1.Tetracyclines: When used in larger doses, these can cause jaundice, fever, and fatty
liver. Metabolism by liver. All tetracyclines are concentrated in liver and excreted via
bile into intestine, where they are reabsorbed.
2.Macrolides :
A.Erythromycin: It causes damage to the liver via cholestasis (bile retention) and
jaundice. The harmful effects usually start to show after 10 to 14 days use and the
incidence rate is approximately 5 to 10%. Metabolism by liver,major excretory
pathway and it is excreted into bile in active form. Avoid estolate form in liver disease
and other forms in usual dosage.
B.Lincosamides:
Novobiocin: Metabolism by liver. Best to avoid in liver disease. This drug may induce
"jaundice" by five different methods, all generally uncommon.
Neomycin: Not metabolised by liver. Not more than 6 Gm PO in liver disease for gut
sterilization. If azotemia also present,kanamycin is preferred.
Chloramphenicol:
Metabolism by liver. Liver toxicity is rare. Use with caution in liver disease. If ascites
or jaundice is present, use under 25 mg/kg/ day or another drug.
Penicillins: These antibiotics cause the least liver damage. Generally, antibiotics in the
penicillin family are the most "liver friendly" and safe for chronic hepatitis patients to
use.
Advantages
• Appetite stimulation
• Anti – inflammatory
• Immunosuppression
• Anti- fibrotic
Disadvantages
• Predispose to infection
• Catabolic
Azathioprine
Ursodeoxycholic acid
• Alter bile composistion and stimulates bile flow in intra- hepatic cholestsais
Decoppering agents
Vitamin E
Diet
• Rationale= reduced blood NH3 and aromatic amino acids, yet permit
regeneration
• Protein sources
Carbohydrates
Fats
Vitamin/mineral supplementation
• Vitamin B complex
• Antibiotics
• Neomycin, metronidazole
• Artificial disaccharide
*****
Loss of these renal functions results in a narrowing of the physiologic range over which
the kidneys are able to adapt. For example, loss of urine concentrating ability
(regulatory failure) leads to obligatory increases in water intake. The failing kidneys
have impaired ability to adapt to extremes (high or low) in electrolyte intake. This
limited ability of the failing kidneys to adapt to variations in intake directly relates to
therapeutic plans.
• Trauma such as a physical injury that leads to rapid fall in blood pressure. An
accident that causes significant amount of blood loss.
• Consumption of rat poison, turpentine or external toxins such as antifreeze,
pesticides and certain plants.
• Illnesses related to heart result in lack of, or inadequate supply of blood to the
dog's kidneys, which in turn can lead to accumulation of toxins in the
bloodstream.
• Chemotherapy drugs, anti-fungal medicines, and certain antibiotics.
• Urinary tract infections
• Bladder or urinary tract obstructions due to kidney stones.
• Dehydration
• Pain around kidneys
• Arched back and stiff legged gait
• Difficulty in urinating
• Diabetes
• Physical trauma
• Abnormally developed kidneys.
• Cysts in kidneys.
• Autoimmune diseases
• An unbalanced or poor quality diet can cause chronic canine kidney disease.
Food that has high phosphorous content can be problematic for dogs. If the food
contains insufficient amount of calcium, then the kidneys are unable to remove
the phosphorous effectively. This leads to formation of kidney stones, which
eventually leads to kidney failure. Very high doses of vitamin D can also have
harmful effects on the dog's kidneys.
• Increased thirst (the dog consumes greater amount of water than normal).
• Frequent urination, that is pale in color.
• Nausea and fatigue
• Depression
• Constipation
• Weight loss
• Weakness and inability to tolerate exercises
• Tendency to bruise or bleed easily
• Bad breath (smells like ammonia)
LABORATORY EXAMINATION
The first part of a urinalysis is direct visual observation. Normal, fresh urine is pale to
dark yellow or amber in color and clear. Normal urine volume is 750 to 2000 ml/24hr.
A red or red-brown (abnormal) color could be from a food dye, eating fresh beets, a
drug, or the presence of either hemoglobin or myoglobin. If the sample contained many
red blood cells, it would be cloudy as well as red.
pH
The glomerular filtrate of blood plasma is usually acidified by renal tubules and
collecting ducts from a pH of 7.4 to about 6 in the final urine. However, depending on
the acid-base status, urinary pH may range from as low as 4.5 to as high as 8.0.
Protein
Normal total protein excretion does not usually exceed 150 mg/24 hours or 10 mg/100
ml in any single specimen. More than 150 mg/day is defined as proteinuria. Proteinuria
> 3.5 gm/24 hours is severe and known as nephrotic syndrome.
Glucose
Less than 0.1% of glucose normally filtered by the glomerulus appears in urine (< 130
mg/24 hr). Glycosuria (excess sugar in urine) generally means diabetes mellitus.
Nitrite
A positive nitrite test indicates that bacteria may be present in significant numbers in
urine. Gram negative rods such as E. coli are more likely to give a positive test.
Leukocyte Esterase
A positive leukocyte esterase test results from the presence of white blood cells either
as whole cells or as lysed cells. Pyuria can be detected even if the urine sample contains
damaged or lysed WBC's.
MICROSCOPIC URINALYSIS
Hematuria is the presence of abnormal numbers of red cells in urine due to: glomerular
damage, tumors which erode the urinary tract anywhere along its length, kidney
trauma, urinary tract stones, renal infarcts, acute tubular necrosis, upper and lower uri
urinary tract infections, nephrotoxins, and physical stress.
Pyuria refers to the presence of abnormal numbers of leukocytes that may appear with
infection in either the upper or lower urinary tract or with acute glomerulonephritis.
Usually, the WBC's are granulocytes. If two or more leukocytes per each high power
field appear in non-contaminated urine, the specimen is probably abnormal.
Casts
Urinary casts are formed only in the distal convoluted tubule (DCT) or the collecting
duct (distal nephron). The proximal convoluted tubule (PCT) and loop of Henle are not
locations for cast formation. The factors which favor protein cast formation are low
In end-stage kidney disease of any cause, the urinary sediment often becomes very
scant because few remaining nephrons produce dilute urine.
Bacteria
Crystals
Common crystals seen even in healthy patients include calcium oxalate, triple
phosphate crystals and amorphousphosphates
Evaluation Purpose
Blood urea nitrogen Assess degree of azotemia
Serum Creatinine To establish the diagnosis & measure intrinsic renal function
Urinalysis To establish diagnosis & identify renal complications
Urine culture To rule-out urinary tract infection
Complete blood count To detect anemia of renal failure & inflammatory
complications
Serum sodium To detect hyponatremia or hypernatremia
Serum potassium To detect hypokalemia or hyperkalemia
Serum total carbon dioxide To assess metabolic acid-base status
Serum chloride Useful in assessing serum tCO2 and Na concentrations
Serum phosphorus To detect hyperphosphatemia
Serum calcium To detect hypercalcemia or hypocalcemia
Serum albumin & total To assess nutritional status
protein concentrations
Body weight To assess nutritional status
Protein:creatinine ratio (if To assess magnitude of proteinuria
proteinuric)
Blood pressure To evaluate for hypertension
Fundic examination To evaluate for hypertensive retinopathy or other systemic
Changes in the diet: changes in the diet should be made gradually over a period of one
– two weeks.Warming of food improves palatability.warm water should be added to
dry feed.fresh aromatic feed should be offered.
Food aversion : occurs if nauseated patients are force fed.If painful sample collection
or drug administration is associated with feeding unpalatable drugs should not be
mixed with regular feed or water.
Modifying feeding patterns and environment: Animal should be fed frequently with
small quantities of food, placing palatable food in the patients mouth or paws may
stimulate a licking response
Modification of drug dosages: nephrotoxic drugs that require renal excretion should
be avoided in patients with renal failure
These render ingested phosphorous contained in the saliva , bile and intestinal juices
unabsorable. These agents are administered by mixing food or just before meal.
Aluminium containing intestinal phosphorous binding agent include aluminum
hydroxide, aluminum carbonate and aluminum oxide, Dose 30 to 90 mg/kg/day .
Available as antacid preparation in liquid, tablet or capsule forms, Sucralfate, a
complex polyaluminium hydroxide salt of sulfate used primarily for gastro intestinal
ulceration is also effective than aluminum based agents, excess usage may lead to
hypercalcaemia Calcium acetate is the most effective and given at a dose rate of 60 –
90 mg/kg/day. Calcium carbonate is given at a dose rate of 90-250mg/kg, calcium
based agents must be administred with feed both to enhance phosphorous binding and
to minimize absorption of calcium.
Potassium gluconate 2-6 mEq/cat/day as powder , tablet , gel or elixir .Patassium citrate
can also be given.
Dietary sodium restriction: Daily sodium intake should be reduced to 0.1 to 0.3
percent of the diet on a dry matter basis ( 10-40 mg/kg/day) without reduction of
sodium intake administration of some anti – hypertensive drugs such as beta adrenergic
receptor antagonists and arteriolar vasodilators ; may lead to sodium retention extra
cellular fluid volume expansion attenuation of anti hypertensive effects .
PHARMACOLOGIC CONSIDERATIONS
Renal insufficiency can markedly alter one or more of the pharmacokinetic parameters
of a drug including oral bioavailability, volume of distribution, drug binding to plasma
proteins, and most importantly the rates of metabolism and excretion, i.e., drug
clearance. To minimize drug toxicity and maximize therapeutic benefits, it is often
necessary to adjust drug dosage in proportion to the degree of renal efficiency
To maintain a therapeutic level and, at the same time, avoid drug accumulation and
toxicity in a patient with reduced renal function, the clinician must consider reducing
the size of the maintenance dose or the dosing frequency or both. In general, this
reduction should also be proportional to the degree of renal impairment but should also
take into account adaptive or compensatory changes in the metabolism and excretion of
the drug through non renal routes.
Protocol for Therapy and Follow-up of UTI: Therapy is successful only if the urine
does not contain any pathogenic organisms. Treatment is ineffective and relapse will
occur if the bacterial colony count has only been reduced. It is recommended that acute,
uncomplicated UTIs and some reinfections be treated for a period of 10 to 14 days
Aminoglycosides
5 Cefadroxil 0.5 g q 36 h
8 Cefotetan 1–3 g q 48 h
0.75 g IV q 24 h
11 Cefoperazone 1g q 12 h
2g q4h
12 Cefotaxime 1–2 g q 24 h
15 Ceftriaxone 1–2 g q 24 h
16 Cefepime 0.25–1 g q 24 h
β -lactams:penicillins
20 Ampicillin-sulbactum 1.5–3.0 g q 24 h
23 Sponsored
KVC Oxacillin
CVE training programme 1–2 gon “Clinical Pharmacology
q 4 h& Forensic
Toxicology” organized by the Dept.of Pharmacology &Toxicology,Veterinary
24 Penicillin 24
College,Bidar,from G th -29th August,2009
0.5–2 million units q 4-6 h
105
25 Penicillin G benzathine 1.2 million units IM x 1 dose
27 Piperacillin 3–4 g q 12 h
*****
Main use -
Substances Dose levels Form
Animals
Oestrogens alone: 10–20 mg/day feed additive steers, heifers
DES 30–60 mg/day implant steers
DES oil solution veal calves
steers, sheep,
DES 12–60 mg implant
calves, poultry
Hexoestrol 12–36 mg implant steers, sheep
Zeranol
Gestagens alone: 0.25–0.50 mg/day heifers
Melengestrol acetate
heifers, culled
Androgens alone: 300 mg implant
cows
TBA
Combined
25mg-120 mg
preparations: implant calves
DES+Testosterone feed additive swine
DES+Methyl-
30–45mg-300 mg
testosterone implant steers
Hexoestrol+TBA 36mg-300 mg
implant steers
bulls, steers
Zeranol+TBA 20mg-140 mg
implant calves, sheep
Oestradiol-17β+TBA 20mg-200 mg
implant heifers, calves
Oestradiol-17β benzoate
+ 20mg-200 mg
implant steers
Testosterone propionate
*****
Seizures are a clinical signs which occurs due to cerebral dysfunction, which
originates from structural (Trauma or Tumor) or functional (Physiological or
Metabolic) causes. Seizure, Convulsion, fits are all synonyms for abnormal electrical
discharge of brain cells which occurs all of a sudden and stops suddenly. Whereas,
epilepsy is somewhat confusing in the sense that, recurrent seizures will be there but
that occurs due to some other disease process or primarily it is unrelated to brain
disorder. Further epilepsy is classified into primary epilepsy also called as Idiopathic,
Genetic, True or inherited epilepsy where there is a genetic involvement is recognized.
Secondary epilepsy also called as acquired or symptomatic epilepsy, is due to residual
brain damage due to trauma, encephalitis, hydrocephalus...Etc.
STAGES OF SEIZURE:
A seizure has 4 stages, first prodrome stage which lasts for several hours to
days, second aura or preictal stage often it is not recognized in animals, Third actual
seizure or ictus stage which lasts for seconds to few minutes and Fourth postictal stage
which lasts for several minutes to hours or sometimes goes days together without
notice.
CLASSIFICATION OF SEIZURES:
During Partial seizure, only one portion of the cerebral cortex is spontaneously
discharge electrical activity, therefore clinical appearance of seizure vary depending on
the function of the involved area. If the focus of the seizure is on the left motor cortex,
then involuntary muscle jerking is observed in the right side of the body. Partial with
secondary generalized seizure; some of the signs include at the beginning pet exhibits
Neurological examination:
CBC (complete Blood count) for e.g.: in lead poisoning, one can see nucleated RBC’s,
low/normal PCV, Basophilic stippling. In chronic disorders or in fungal diseases,
monocytosis may be observed and leucocytosis with shift to left indicate inflammatory
response and perhaps the infectious cause of seizure.
SERUM CHEMISTRY:
Cerebrospinal fluid analysis (CSF) analysis, skull radiography, EEG, CT, and MRI may
provide more information regarding the type and extent of intracranial lesion. Analysis
of CSF should include, RBC, WBC count, cytology, protein estimation and culture for
aerobic, non aerobic and mycotic infection. CSF analysis also includes measuring titers
for CD, Toxoplasmosis, Cryptococcosis. Specialized imaging techniques like CT and
MRI are becoming widely used and offer best means of diagnosing and locating brain
tumors and infracts.
Phenytoin half life of this drug in cat is reported to be varying from 24 to 108
hours. Because of this kind of variation in half life, dasage has to calculated on an
individual basis.
• Felbamate: approved in human beings for use in US, as it has side effects of
causing aplastic anemia and hepatotoxicosis, its use is declined. The half life in
dogs is 5 to 8 hours, and recommended dosage is 15 to 60 mg/kg every 8 hours.
In combination with phenobarbitol it has potential to cause liver and kidney
damage, so such animals are to be routinely screened for liver enzyme activity
and kidney function tests.
• Gabapentin: The half life of the drug in dogs is 2 to 4 hours, so frequent
administration is must. It is primarily excreted by kidney in humans and dogs,
but in dogs it undergoes partial hepatic metabolism. Dosage is 10-15 mg/kg
t.i.d. liquid formulation is also available.
Therapy:
Initially it should be directed towards stopping the seizure and correcting the
systemic consequences of seizure. The underlying cause should then be determined so
that a more definitive therapy can be instituted.
CONCLUSION:
*****
Surgery in wide range of species and for different organ disorders are being
attempted more commonly by field veterinarians. Anaesthesia cannot be same for all
surgeries and for all species of animals. This topic aims at discussion and
demonstration of anaesthetic protocols for surgery.
Objective: To judge patient’s physical status and its ability to withstand stress of
anaesthesia and surgery.
Methods :
1. History
2. Physical examination
3. Palpation, percussion, auscultation
4. laboratory examination
The history and physical examination are the best determination of the presence
of disease.
Laboratory tests may be undertaken as per the history and signs of the patient.
Preanaesthetic history and signalment
B. Body weight
1. Vomition
2. Diarrhoea
3. Polyurea- Polydypsea
4. Seizures
5. Coughing
6. Exercise intolerance
7. Weight loss
F. Previous allergies and anaesthesia
A. Body weight
1. Obesity
2. Cachexia
3. Dehydration
B. Cardiopulmonary evaluation
1. Heart rate and rhythm
2. Auscultation
3. Capillary refill time
4. Mucus membrane colour
5. Pulse character
C. CNS evaluation
1. Temperament
2. Seizers, coma
3. Vision, hearing
D. Gastrointestinal evaluation
1. Parasites
2. Abdominal palpation
E. Hepatic evaluation
1. Icterus
2. Abnormal bleeding
F. Renal evaluation
1. Palpate kidney and bladder
G. Integument
1. Tumour
• Severe dehydration
• Pneumothorax
• Cyanosis
• Oliguria
1 Procedure to be performed
. <15 min
15 min to 1 hr
> 1hr
Major/minor surgery
2 Available equipments, assistance
.
3 Temperament of the patient
.
4 Physical status
.
5 Breed
.
Based on history, physical examination and lab examination, patient has to be classified
under any one of the following category recommended by American society of
anaesthesiologists and anaesthetic agent and procedure has to be selected.
1. Thiopental sodium
Disadvantage: Full recovery takes upto one hour.
I V route is difficult in ferocious dogs.
2. Propofol
3. Diazepam + Ketamine
4. Neurolept analgesia
15 minutes to one Hour (intermediate duration)
1. Thiopental sodium
2. Propofol
3. Diazepam + Ketamine
Above drugs can be used and redosed to effect by administering one third to
half of the original dose to prolong the effect more Halothane can also be used.
More than one hour (long duration): Inhalation anaesthesia – Best, Halothane,
Isoflurane: Rapid recovery, Even sick and debilitated dogs recover quickly.
Vaporizer settings :
Induction in circle
Intraoperative monitoring:
Recovery in dogs
1. Chloral hydrate was widely used before the advent of other anaesthetics
2. Phenothiazine tranquilizers
Acepromazine and Promazine are two commonly used drugs.
Because it is long acting, inexpensive and does not produce severe ataxia.
Recovery: Horses need extreme care during recovery due to fractures and injuries
during that period. Xylazine (0.2mg/kg) can be given to calm down the horse during
recovery. Head rope and tail rope may be applied and tied to the rings in the recovery
room.
Ruminants accept physical restraint well and can be operated under sedation and local
analgesia. General anaesthesia is used for thoracic surgery or for Diaphragmatic
hernia.
General anaesthesia: sedatives are not usually used before induction in cattle as they
may prolong recovery. IV anaesthetics recommended for ruminants are thiamylal (6-
10mg/kg), propofol (6mg/kg), guaifenesin. Propofol produces anaesthesia for 5-10
minutes, induction and recovery is smooth. Xylazine (0.05mg/kg) and ketamine
(2mg/kg) can also be used.
Local analgesia: Most of the operations in ruminants are done under local analgesia
with sedatives. Various local anaesthetic techniques such as linear infiltration, regional
nerve blocks are used. Lignocaine hydrochloride is the most commonly used agent. The
dose is 2mg/kg BW.
Conclusions
Necessity of anaesthetic combination and techniques are increasing
Not a single protocol is suitable for all species and for all surgeries
Dogs and horses are operated under general anaesthesia
Mostly cattle, sheep and goats are operated under local analgesia
Success of general anaesthesia depends on type of species, weather canine,
equine, ruminant or wildlife.
*****
The choice of antimicrobial agent in the clinical practice should be based upon
susceptibility of the infecting organism to the drug concentrations achieved in the tissue
and pharmacokinetic characteristics of the drug and its dosing protocol. Although,
several class of antimicrobials are readily available, the clinical cure may not be always
successful and its partially attributable to lack of culture and sensitivity tests under field
conditions. Therefore, atleast, one can bank upon certain pharmacokinetic principles in
the routine clinical practice as well as in serious infections like meningitis, endocarditis
and in immuno-compromised hosts.
Why Pharmacokinetics ?
Pharmacokinetics deals with absorption, distribution, metabolism and excretory pattern
of a given therapeutic agent. Selection of antimicrobial agent based on its
pharmacokinetic characteristics aid in achieving optimal concentration at the desired
site. For example, the location of infection can have a major influence on the drug
concentration achieved there, as some sites (eg: CNS) are protected by barriers to drug
penetration, while others (eg. mammary gland, urinary tract) local pH may favour drug
accumulation. Knowledge of pharmacokinetic data is also useful to avoid possible
toxicity in a given species as well to take necessary precautions during physiological
stress (eg. pregnancy, lactation) or pathological conditions (eg: hepatic failure, renal
dysfunction). The probable antimicrobial agent that can be employed in the clinical
practice should be selected after giving due considerations to following issues:
What organ/s is/are involved?
What pathogen is most likely?
What antibiotic in most likely to be effective?
What drug concentrations at the site of infection?
What drug/route are most likely to achieve that concentration?
PHARMACOKINETCS
Cephalosporins:
Wide variation in pharmacokinetic properties is observed among cephalosporins.
Generally cephalosporins possess widespread distribution in ECF in the body, but
their penetration across biological membranes/barriers varies with the compound.
Many cephalosporins (II & III generations) diffuse across biological
membranes/barriers and attain high concentration in synovial fluid, occular fluid,
prostate or CSF.
Group I (eg: cephalothin, cefaloridine) does not pass across blood : milk or
blood : CSF barrier. However, Group II (eg: cefataxime, cefamandole) can pass
across inflamed meningeal layers and therefore, drug of choice for meningitis
caused by enterobacteriaceae. Group III (eg: cefoperazone) and Group IV
(moxalactam) are highly active against P.aeruginosa. Third generation
Conclusion:
The antimicrobial chemotherapy particularly in the absence of antibiotic sensitivity
testing facility under field conditions is a difficult task. In the routine clinical
practice as well as in the absence of microbial sensitivity pattern, one can adopt
certain pharmacological principles discussed here so as to obtain clinical and/or
bacterological cure. To ensure this, the veterinarian must update their knowledge
pertaing toclinical pharmacology of newer antimicrobials released in to market.
*****
The veterinarian will be encountered with diagnosing and treating the animals
exposed to toxicant /poison which may be either accidental or malicious in origin.
History, clinical signs and necropsy of the animals will assist in rapid tentative
diagnosis which will help in the treatment of other affected animals in case of
accidental poisoning. In case of malicious poisoning, which may turn up into
veterolegal case, the identification of the toxin/poison is a must to establish the cause of
death. In all poisonous/toxicological cases, chemical analysis of the biological
specimens is essential to know the cause of death or illness., for which proper
collection and despatch of toxicological specimens to the laboratory is necessary.
Post-mortem examination
Necropsy by routine procedure is to be performed as soon as possible
after the death of animal. The animal should be examined externally for the presence
of any incisions (for sui poisoning, snake bite etc.,) on the skin or mucous membranes.
The oral cavity is examined for corrosive lesions (acids/alkali) or changes in colour of
mucous membrane (nitrate, co, cyanide poisoning). As most of the toxins gain entry
through gut, examination of gut mucosa, the contents, their smell, colour and pH (acids,
alkali, urea) is a valuable guide in diagnosing toxicoses. Poisoning by salts of heavy
metals results in significant post mortem lesions but poisoning by alkaloids like
strychnine produces very feeble lesions.
The natural orifices, sub-cutaneous fat tissue, muscles, bones and teeth (in
fluorine poisoning), body cavities, and internal organs should be examined. The
stomach should be punctured rather than cut open for examination to note the character
of smell. Puncture ensures greater accuracy and a longer time smell. Some of the
poisons emit characteristic smell like bitter almond in hydrogen cyanide poisoning,
The contents of the stomach ,small intestine and large intestine vary from
traces to flakes of paints or lead objects, grains or baits, seeds etc. Blood should be
examined for its colour and clotting characters. Cyanide poisoning imparts cherry red
colour, arsenic imparts rose red colour and nitrate poisoning turns the blood to brown
colour.
Collection of samples
A successful toxicological investigation requires appropriate specimens, history
and clinical signs, necropsy lesions and circumstantial evidences. Sample for analysis
should include a suspected source material; often gut contents, so that ingestion of
suspected material can be proved. Secondly, a sample of tissue (depending on tissue
affinity of the suspected poison) must be included, to prove that absorption of the
poison has occurred. It is always advisable to include a sample of liver to confirm
absorption of orally ingested poison. In survival cases the following materials may be
sent for analysis:
Sampling containers
Specimens for toxicological examination must be collected preferably in wide
mouth glass bottles of about 2L capacity having air tight stoppers. Alternatively,
plastic containers can be used in place of metallic containers or old cans to avoid
contamination by lead or other metals. The sampling bottles should be numbered,
labeled properly, indicating details of the case, nature of content, place and date of
preservation. Do not forget to put your signature (i.e. veterinarian who has conducted
necropsy). Specimens should be packed individually and necessary measures should
be taken to avoid loss of some poisons by escape of gas or by bacterial fermentation.
Preservation of materials
For visceral organs like pieces of liver, kidney, stomach, intestine, contents of a
stomach and intestine saturated solution of sodium chloride can be used.
Suspected plants or food can be sent to the laboratory without adding any
preservative
Ice pack/ waterproof frozen sachets, are used in case of the samples being
transported in refrigerated or frozen state
Rectified spirit (95% ethyl alcohol) 1 ml/g of tissue is the ideal preservative for
toxicological specimens. ( except in alcohol, phosphorous and carbolic acid
poisoning conditions)
Formaline should never be used for toxicological analysis of specimen samples as
it hardens the tissue without giving scope for scraping and interferes in with the the
analysis by making the extraction of poison much more difficult. .
Blood ,urine and serum should be refrigerated and never be frozen.
The materials for histopathological examination can be kept in a fixative preferably
10 percent formalin in a wide mouthed glass container with proper labelling and
well protected by cotton padding/ covering.
Adequate refrigeration is of special importance when submitting body fluids and
materials for nitrate/nitrite analysis
In case of small animals (poultry, small dogs, lab animals) the cadavers are sent as
it is, in case of large animals the gastrointestinal contents are collected from the
vicinity of changes in the gastric/intestinal mucosa. If there are no changes, a
representative sample is collected, but in medium sized animals the stomach tied at
oesophageal and duodenal end, intestine tied at both ends and bladder with tied
ends is sent separately.
Labelling information
The samples being sent to the laboratory must be accompanied by proper
protected labelling with all the details regarding the case, including the following
information
Name and address of the doctor and the owner of the animal
Animal identification characteristics-species, colour, age, sex, breed etc.
Number of animals affected and number of animals dead
Date of onset of symptoms and the death
Clinical signs recorded by the doctor and symptoms noticed by the owner
Type and the quantity of samples sending
Postmortem findings
Suspected poison/toxicant
Any other circumstantial fact or information which may assist the laboratory in
identifying the causative agent
In veterolegal cases , the label containing the details is placed inside the
specimen container and another label is pasted on the wooden box/cloth covering
the container. The sample is then sent to the forensic laboratory , with the
*****
For the majority of cases of poisoning treatment with an antidote is not possible,
instead prompt medical intervention to improve the condition of the animal can
ensure its survival. These practices focus on promoting the removal of the poison
or neutralizing it, whilst maintaining the vital functions of the animal.
Removal of the poison
1. Decontamination of the skin:
Some substance (hydrocarbons, acids, alkalis, agrochemicals, etc.) may,
as a result of an accident or a spillage, contaminate the feathers or fur of animals.
In general it is important that in such circumstances the following are undertaken:
• Epidermal structures (wings, nails, claws, feathers, fur) should all be cleaned with
the greatest care, paying particular attention to areas such as the ears, between toes,
etc.
• The cleaning should be undertaken quickly to avoid licking and ingestion of the
poison, and to limit cutaneous absorption.
• Use soapy water (preferably a soap with a low pH), rinsing with copious tap water;
repeat as often as necessary
• Dry carefully and thoroughly (e.g. with a hair dryer)
• The following must never be used: organic solvents (alcohol, white spirit, etc.) or
oily substances which may actually increase percutaneous absorption of the toxin.
• Do not rub the area vigorously; cleaning and drying must be gentle but thorough
• The animal could well be in a state of shock and must be handled accordingly.
• Move to a quiet place with additional heating (e.g. a heat pad, if necessary)
2. Gastric emptying:
a. Emetics:
Use emetics if ingestion has taken place within the preceding 2-3 hours. Never
induce vomiting in following circumstances:
*****
Critically ill patient is a special challenge to the clinician because the underline
problem is not evident for about 24 to 48 hrs after initial presentation. Expeditious
therapy in right time can be life saving, whereas delayed adequate therapy may be
ineffective therapeutic failure. Most common clinical conditions in ambulatory patients
are trauma with internal/ external hemorrhage, poisoning and post surgical
complication. In fact, specialized care of emergent patient begins with initial phone call
from the owner and instructions to be given regarding first aid and transport
procedures. Level of consciousness, breathing pattern and external hemorrhage should
be enquired on priority.
Triage is the art of assigning the priority to emergency patients and to their
problems by evaluating certain parameters. Three important assessment criterion are A,
B and C.
A – Airway:
B – Breathing:
C – Circulation:
• Dilatation of pupils
a) Positioning of animal:
b) Resuscitation:
2. Management of shock:
Assessment of shock:
Therapeutic management:
Fluid therapy:
The main aim of fluid therapy is to restore circulation and improve the
tissue perfusion. Choice between crystalloid and colloidal solutions
should be determined. Crystalloid supplements fluid along with
electrolytes, whereas colloidal solutions expand the plasma volume.
• Dextran 70
• Hexastarch
• Gelatin polymers
• Frozen plasma
• Normal Saline
Alpha Adrenergic agonist: These drugs help in improving cardiac output and
thereby improve tissue perfusion. Dopamine used @ 5 – 10 µg/kg/min as
*****
SOURCE OF POISONINGS
1. Insecticides:
Organochlorines: By virtue of their high lipid solubility these agents can enter the
neuronal membrane with ease and therefore interfere with normal functioning of the
nerve membrane sodium channel. The clinical signs of toxicity can be broadly
categorized in to:
2. Rodenticides:
Commonly used among farming community to control animal pests like rats,
mice and wild species. These include Warfarin and second generation warfarin like
compounds, Zinc-and aluminum phosphide, ANTU, Flouroacetate and outdated
methods like bait made up of Arsenicals or Strychnine (seed powder).
Anticoagulant rodenticides: These include warfarin (less used now a days) and second
generation anticoagulant rodenticides viz: Bromadiolone (Mortin), brodifucoum. The
main source of poisoning is the ingestion of residues of the rodenticides or baits
intended for killing rodents. These rodenticides interferes with normal function of
vitamin-K and causes coagulation defects by inhibiting clotting factors II,VII,IX and X.
The poor coagulation mechanism cause massive internal haemorrhages over aperiod of
time. Normally after period of about 2-5 days clinical signs appears and these include
anorexia, pulmonary coughing (epitaxis, dyspnoea),hypothermia, haematuria, stiffness
of hind quarters and sudden death. Internal haemorrhage, blood in the
GIT(gastroenteritis), haemopericardium and menigeal/cerebral bleeding and
haemorrhages in joints are the pathological lesions one can observe during necropsy.
The affected animals should be shifted to quiet and warm place and the line of
treatment include Vitamin-K1 in physiological saline (Vitamin-K3 not recommended)
and cardio-vascular support.
Zinc phosphide/ Aluminium phosphide: It is one of the cheapest and quite effective
rodenticide. Commonly used in fruit market, horticultural farming, and almost every
grocery shops/ APMC yard to destroy rats, mice, squirrels etc. Often it is also used in
malicious poisonings to kill dogs, cats and even wild animals. Monogastric species
are more sensitive rather than ruminants. Acute zinc phosphide toxicities is due to
conversion of Zinc-phosphide → phosphine (PH3) gas in the stomach following
hydrolytic reaction with water in the GIT under acidic pH. Absorption od phosphine is
responsible for wide spread cellular toxicity with necrosis of GIT and other vital organs
like liver and kidneys. Clinical signs include anorexia, lethargy, abdominal pain, bloat
(in ruminants), deep respiration, ataxia, prostration and dyspnoea, gasping, convulsions
and death. Post-mortum lesions include pulmonary congestion, edema, sub-pleural
haemorrhages, congestion of liver and kidneys. Acetylene odour may be detected in
stomach. No specific treatment is possible, however symptomatic and supportive care
maybe given. Gastric lavage with 5% Sodium bicarbonate, Calcium boro-gluconate
injection, anticonvulsants and measures to prevent shock can be undertaken as a life
saving measure.
The lethal effects of cyanide is due the its binding with Fe+3 component of
cytochrome oxidase a3, a key enzyme involved in cellular respiration. Thus,
hyperoxygention of blood would lead to cherry red/ bright red colour of venous blood .
Intoxicated animals shows salivation (frothy), bradypnoea, mydriasis, ataxia,tremors,
epileptiform scizure, cardiac arrhythmia and clonic-tonic convulsions. Invariably loss
5. Nitrate/Nitrite:
Atropine sulfate
Fluoride Calcium borogluconate 3-10 ml of 5-10% solution.
Pentobarbital May protect against lethal dose
(experimental) (Note: all
treatments are generally
unrewarding).
Heparin Protamine sulfate 1% solution give 1.0-1.5 mg by
slow IV injection to antagonize
each 1 mg of heparin. Reduce dose
as time increases between heparin
injection and start of treatment
(after 30 minutes give only 0.5 mg)
Iron salts (Iron Deferoxamine mesylate Dosage for animals not yet
tonics) (Desferal, Ciba) established. Dosage for humans is
5 g of 5% solution PO, then 20
mg/kg IM q4h-q6h. In case of
shock, the dosage is 40 mg/kg by
IV drip over 4-hour period. May be
repeated in 6 hours then 15 mg/kg
by drip q8h.
Lead Calcium disodium Maximum safe dosage is 75 mg/kg
EDTA (CaEDTA) per 24 hours (only for severe case);
EDTA is available in 20% solution
for IV drip, dilute in 5% glucose to
0.5%; For IM, add procaine to 20%
solution to give 0.5% concentration
of procaine.
EDTA and BAL BAL is given as 10% solution in
oil.
(a) In severe cases (CNS
involvement with > 100 µ g lead
per 100 µ g whole blood) give
4 mg/kg BAL only as initial dose:
follow after 4 hours and q4h for
3-4 days with BAL and EDTA
*****
3) Treatment with drugs or antibiotics has little effect on the course of the disease
4) Outbreaks are usually seasonal because particular climatic sequences may favor
fungal growth and toxin production
Classification:
Among these most common are aflatoxins. Aspergillus moulds grow rapidly
when the moisture is <15%and the temperature is 24-25ºC.They commonly affect
GNC, CSC, coconut cake, sunflower cake, wheat, sorghum, millets, soybean, peas and
almonds.
iii)Chronic - decreased feed efficiency, decreased productivity and weight gain, rough
hair coat, anaemia, enlarged abdomen, mild jaundice, depression and anorexia.
Abortions may occur.
Postmortem Lesions:
Wide spread heamorhages,Icterus,Gastroenteritis,Hepatic necrosis,Massive
centrilobular necrosis,fibrosis of bile duct,Enlarged liver,Hydrothorax,
Ascites,Oedema of Gall bladder wall,Pericellular cirrhosis
Microscopically
Typical hyperplasia of bile duct,Neoplastic growth of
hepatocytes,Hyperchromasia
Diagnosis: based on
History,Clinical signs,PM findings,Detection of Aflatoxin M1 in milk &
urine,liver, kidney,Serum liver enzymes SGOT,SGPT,ALP elevated,Reduced
prothrombin activity,Hyperbilerubinemia,Tlc,Hplc,RIA,ELISA
Differentiate diagnosis:
5. Activated charcoal 6.7 mg / Kg I/R as 30% W/V slurry in M/15, PH7 Phosphate
buffer
**Along with charcoal,stanzolol/oxytetracycline(any one)
Much of the error in detecting mycotoxins in feed results from sampling (or
subsampling) rather than from analytical methodology. Samples can be taken at various
stages—from growing crops or during transport or storage. Whenever possible,
samples should be taken after particulate size has been reduced (Ex: by shelling or
grinding) and soon after blending has occurred (as in harvesting, loading, or grinding).
Sampling is most effective if small samples are taken at periodic, predetermined
intervals from a moving stream of grain or feed. These individual stream samples
should be combined and mixed thoroughly, after which a subsample of 10 lb (4.5 kg)
should be taken.
Probe sampling is acceptable when grain has been recently blended but is less reliable
because different microenvironments within the storage facility may cause areas of
mold or mycotoxin concentration. A suggested method of probe sampling is to sample
at 5 locations, each 1 ft (30 cm) from the periphery of a bin, plus once in the center.
This should be done for each 6 ft (2 m) of bin depth. Thus, taller bins would require
more samples, and the total weight should be >10kg.
Dry samples are preferable for transport and storage. Samples should be dried at 176-
194°F (80-90°C) for > 3 hr to reduce moisture to 12-13%. If mold studies are to be
done, drying at 140°F (60°C) for 6-12 hr should preserve fungal activity.
Containers should be appropriate for the nature of the sample. For dried samples, paper
or cloth bags are recommended. Plastic bags should be avoided unless grain is dried
thoroughly. Plastic bags are useful for high-moisture samples only if refrigeration,
There are about 236 species of snakes in India but only 50 of these are
venomous, However, the common poisonous snakes of India that man and animal come
into contact, which are those we call the ‘Beg Four’: Cobra, Krait, Russel’s viper and
Sea scaled viper, Apart from these, the other venomous snakes found in India includes
Sea snakes, Pit viper and King cobra. However, Occurrence of venomous bite from
these snakes are less common. In animals, many a time incidence of snakes bite is near
leg region and nostrils.
Sensitivity: Horse>Man>Sheep>Cattle>Goat>Dog>Pig>Cat
Venom composition: The venom compositions vary significantly among various class
of poisonous snakes. Therefore, the course of toxicity as well as well as cause of death
will be different, and obviously therapeutic approach will also vary. On most occasions,
the identification of snake is not available or doubtful.
Krait 20 mg 6-8 mg
Cobra: Cobras are widespread group of snakes. In India, we have three kinds: the
monocled, spectacled and black. Cobras can be easily identified by their “defence
display” by spreading their long bones to their famous hood. Cobras are most active at
dust, having along the wedges of agricultural fields in search of rats/mice. For this
reason they live mostly in cultivated area. They lay eggs (10-30) between June &
August and female stays with them until they hatch two months later. The cobra venom
is rich in 10 or more macromolecular substances. These includes enzymes, cardiotoxic,
neurotoxic factors. The cobra venom is rich in enzyme acetylcholinesterase. Therefore,
rapid depletion of acetylcholine (ACh) at neuromuscular junction occurs following
envenomation. This leads to “muscular paralysis” (flacid paralysis). In addition to it,
the alpha-neurotoxin is a powerful cholinoceptor blocker (nicotinic receptors). These
factors hinder the function of muscles involved in respiration and consequently death
occurs due to “respiratory paralysis”. It is important to identify the “big four”
dangerous snakes. At first sight cobra looks like a non-venomous rat snake, but,
remember that the rat snake has a pointed head and larger eyes and it can run faster.
Krait: The common krait is easy to recognise. It has bluish-bluck body with white
cross bands and the head is short and blunt. Kraits venom is 10 times as powerful as
that of the cobra and of all the Asian snakes its venom is the most toxic (neurotoxic).
Kraits are noctoural. They are active at night and rest during the day. They are
found throughout India and live mostly in sandy soil in rat burrows. Their favarite
hiding places are piles of wood (on bricks which provide many pray to shelter in. They
are canibalistic- eat snakes, rats, lizards and birds. Famale lays eggs (10-15) and stays
with them until hatch. The krait is often confused with smaller harmless wolf-snake.
Russel viper: Is a fat and bulky snake, but it can move with surprising speed when in
danger. Its regular chain-like pattern and flat arrow shaped head make it easy to
recognise. Its fangs are along and curved. They give birth to youngones directly,
usually 20-40 at a time and equipped-with venom and fangs birth, viper venom is rich
in proteolytic enzymes, hemolytic and spreading factors.
Saw scaled viper: It is the smallest member of “big four” and usually confused with
long and thinner cat snake. In South India it grows to only 30 cm. length and it is the
causes of many bites as it is widely distributed. The body has brownish and white zig-
zag pattern and the head, as in all vipes, is flat, Usually they hide under rocks and
bouldersor/in low shrub bushes.Like kraits, saw scaled vipers are noctoral but
Pit vipers:These are forest snakes and feed on frogs and lizards. Commonly found in
coffee and tea plantations in India. Pit vipes have a small “pits” between nostrils and
eyes. They are heat sensitive and can detect change in temperature when warm blooded
animal comes near. There are 15 species of pit vipers and bites are fairly common.
Venon is not powerful and seldom results in death. Young pit vipers aften lift their
“colourful tail” to attract frogs.
First-Aid treatment:
The first and foremost aim, in case of cobra/krait bite is to retard the absorption
of venon from the site of bite. This can be done by applying a torniquet, provided site
of bite is suitable for that. Do not disturb/ or/excite the animal with little care incise the
area (1/4) and bleed. It is always better to avoid KMnO 4 solution for wound wash and
instead use 5% soap wash in 30 min. after bite. It is not advisible to apply torniquet in
case of vipers bite as this venom is rich in spreading factors (local tissue necrosis). In
such case, freezing of tissue is ideal to reduce enzyme activity.
Hospital treatment:
The nature of hospital treatment practically depends on identity of the poisonous snake.
Polyvalent antivenin (Haffkine Institute, Mumbai) is the drug of choce in the absence
of identity. It is better to avoid administration of anti-histaminic as they are found to
increase toxic potential of certain viper’s venom. Popularly, hopital treatment can be
remembered as “AAA”:
∗ A = Antivenin.
∗ A = Antibiotic (broad spectrum)
∗ A = Antitetanus / Gas gnagrene antitoxins.
The antivenin (monovalent/polyvalent) should be administered IV at the rate of
100 ml. (small animals) or 10-50ml. (large animals). Administer antivenom with 1:00
epinephrine (0.5-1 ml. s/c) to avoid shock. Apply 1-2ml. of antivenin over the wound
(site of bite in case of viper bite. Monitor the cardio vascular activity constantly.
Narcotic analeptic is recommended in case of cobra bite to counteract intense pain.
Epinephrine and corticosteroid to overcome hypotension and shock. Employ plasma
volume expander (6% dextran-40) and calcium gluconate to reduce hemolysis. In case
of viper bite, even if the patient survive, amputation may be performed to avoid spread
of local tissued necrosis or gangrene formation.
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