Veterinary · Clinical · also MSVE VMD-411, Veterinary Medicine
Clinical examination and special diagnostics, general systemic states, and the diseases of each body system, with fluid therapy and transfusion.
In the exams: NAVLE clinical practice 70%; BCSE medicine 50-55 items (its largest block); PRC Medicine 14%; Nepal NLEV 8; EGEL Plus diagnosis 17 and therapeutics 18; ICAR AICE-JRF core group 07; ICAR AIEEA-PG 13 (Medicine)
Veterinary clinical medicine is the discipline of finding out what is wrong with a sick animal without opening it, and treating it without surgery. This first medicine subject covers method and content. The method is history taking, clinical examination of each species, and the special tests that extend the senses: the electrocardiogram, paracentesis, rumen fluid, urinalysis, the ophthalmoscope, the endoscope and ultrasound. The content is the general states that cut across all disease (septicaemia, toxaemia, shock, dehydration, anaemia), the diseases of each body system, and fluid therapy and transfusion, the treatments used most often whatever the diagnosis.
The subject is taught across species because the same principle behaves differently in each. Dehydration in a scouring calf usually comes with metabolic acidosis; in a cow with abomasal volvulus it comes with metabolic alkalosis, and the right fluid differs. A horse's anaemia cannot be judged regenerative from a blood film, because horses do not release reticulocytes into the blood.
Every licensing and entrance exam treats this subject as core. Clinical Practice is 70 per cent of the NAVLE; medicine is the largest block of the BCSE; it is 14 per cent of the Philippine licensure exam and a named part of India's ICAR PG and PhD entrance exams and state Veterinary Officer exams. Questions are increasingly cases: history and signs, then "what is the diagnosis" or "what next". Each chapter here runs from mechanism to signs, to the test that separates look-alikes, to management by principle. Drug doses are given only where a standard value is certain; otherwise drugs are described by class, because doses, withdrawal periods and legal use in food animals differ by country and product.
Most diagnoses are suggested by the history before the animal is touched. Start with the signalment: species, breed, age, sex and reproductive status. A three-week-old calf with diarrhoea, a six-year-old Dobermann with exercise intolerance and a fresh Holstein cow off feed each narrow the list at once. Record the complaint in the owner's words, its duration and its course. Ask open questions first, then closed ones.
For herds the history is epidemiological. Morbidity rate is the number affected divided by the number at risk; mortality rate is deaths divided by the number at risk; case fatality rate is deaths divided by the number affected. High morbidity with low case fatality points to different causes from low morbidity with high case fatality. Record diet and recent feed changes, grazing, housing, water, purchases, vaccination and deworming, stage of lactation or pregnancy, and every drug already given. Prior treatment changes the findings, and a treated food animal may be inside a withdrawal period.
For companion animals also ask about travel (vector-borne diseases), toxin access (anticoagulant rodenticides, lilies in cats, grapes and raisins in dogs, ethylene glycol), thirst and urination, vomiting versus regurgitation, and cough. Polyuria and polydipsia, for example, open a list that includes chronic kidney disease, diabetes mellitus, hyperadrenocorticism, pyometra and hypercalcaemia.
Examine from a distance before handling, because restraint changes heart rate, respiration and behaviour. Note mentation (alert, dull, obtunded, stuporous, comatose), posture, gait, body condition, breathing pattern, abdominal contour, faeces and urine. In cattle, the abdomen viewed from behind shows whether the left or right side is distended, dorsally or ventrally: the first clue in bloat, vagal indigestion and abomasal disease.
Then examine closely in a fixed order. Record temperature, pulse and respiration; reference ranges differ between textbooks, laboratories and breeds, so use your school's table and judge values near the limits. Examine mucous membranes for colour (pale, icteric, cyanotic, congested, petechiae) and capillary refill time, normally under about two seconds. Assess hydration, palpate lymph nodes, then examine each system: heart and lungs, abdomen (auscultation, palpation, percussion, ballottement), urogenital tract, udder, skin, musculoskeletal and nervous systems.
For the heart note rate, rhythm, intensity and any murmur with its timing, point of maximal intensity and grade. For the lungs, crackles are discontinuous sounds from fluid or reopening airways; wheezes are continuous sounds from narrowed airways. Mainly inspiratory difficulty suggests upper airway obstruction; mainly expiratory difficulty suggests lower airway disease. Finish with a problem list and, for each problem, ask where the lesion is before asking what caused it. Special tests follow this reasoning; they do not replace it.
Ruminants. Count rumen contractions by auscultation or with a fist in the left paralumbar fossa; a feeding animal has roughly one to two primary cycles a minute, fewer at rest. Simultaneous percussion and auscultation finds gas-filled viscera, the "ping". Rectal examination is routine in adult cattle and horses. Tests for anterior abdominal pain are the withers pinch, the pole test (lifting the chest) and listening for a grunt during pressure over the xiphoid. Examine the udder and milk in every lactating cow off feed. In sheep and goats, conjunctival colour scored against a chart (FAMACHA) identifies animals anaemic from Haemonchus.
Horses. Pain behaviour, heart rate and gut sounds in four quadrants drive colic assessment, and nasogastric intubation is both diagnostic and therapeutic because horses rarely vomit. Pigs are examined largely as groups: pen observation, the thermometer and post-mortem of casualties. Dogs and cats need a body condition score (commonly a nine-point scale), lymph node check, abdominal palpation and basic neurological and ophthalmic screening. Cats hide illness, and low-stress handling gives more reliable findings.
Bacteraemia is viable bacteria in the blood, which may be transient and harmless. Septicaemia is bacteraemia with systemic illness caused by organisms multiplying in the blood and their toxins. Toxaemia is systemic illness from toxins absorbed from a local site while the organisms stay local, as in acute coliform mastitis or a decomposing retained placenta. Endotoxaemia is entry of lipopolysaccharide from Gram-negative bacteria into the circulation; it is common in horses with strangulating colic or colitis.
Illness comes from the host response. Microbial products activate macrophages to release cytokines and prostaglandins, causing fever (or late hypothermia), tachycardia, tachypnoea, white cell changes, vasodilation, leaky capillaries and activation of coagulation: the systemic inflammatory response syndrome (SIRS). SIRS caused by infection is sepsis; its end stages are septic shock, disseminated intravascular coagulation and multi-organ failure.
The toxaemic ruminant or horse is depressed and anorexic, with fever early and a normal or low temperature later, a fast weak pulse, congested membranes (a dark "toxic line" at the gum margin in horses), slow refill, cold extremities and gut stasis. A falling temperature with a rising heart rate is deterioration, not improvement. Acute Gram-negative sepsis typically causes leucopenia with a degenerative left shift; cattle, with a small marrow neutrophil reserve, show this sharply.
Neonatal septicaemia in calves, lambs, kids, piglets and foals is closely tied to failure of transfer of passive immunity (FTPI). Ruminant and equine placentas do not pass antibody, so the neonate depends on colostrum absorbed in the first hours; intestinal absorption of immunoglobulin is essentially over by about 24 hours. In dairy calves, serum IgG below 10 g/L at 24–48 hours is the classic definition of FTPI; in foals IgG below 400 mg/dL is failure and 400–800 mg/dL partial failure. E. coli and other Gram-negatives are common; watch for localisation in joints, umbilicus, meninges and eyes (hypopyon).
Haemorrhagic septicaemia of cattle and especially water buffalo is an acute pasteurellosis caused by Pasteurella multocida serotypes B:2 (Asia) and E:2 (Africa). Outbreaks follow the monsoon and stress: high fever, hot painful swelling of throat and brisket, respiratory distress and death within hours to a day or two. It is WOAH-listed and controlled by vaccination before the rains. In dogs and cats sepsis usually starts from a focus: pyometra, septic peritonitis, pyothorax or pneumonia. Parvoviral enteritis with neutropenia is a classic cause of Gram-negative sepsis from gut bacteria crossing the damaged mucosa.
Shock is inadequate oxygen delivery to tissues, so cells shift to anaerobic metabolism and produce lactate. It is classified by mechanism. Hypovolaemic shock follows loss of circulating volume (haemorrhage, diarrhoea, vomiting, sequestration in obstructed bowel). Distributive shock is loss of vascular tone: septic, anaphylactic or neurogenic. Cardiogenic shock is pump failure (dilated cardiomyopathy, severe arrhythmia). Obstructive shock is a physical block: cardiac tamponade, tension pneumothorax, or gastric dilatation-volvulus compressing the caudal vena cava.
In compensated shock, baroreceptor reflexes raise heart rate and constrict vessels: tachycardia, pale membranes, slow refill, cool extremities and a weak pulse with normal blood pressure. Dogs in early septic shock may be hyperdynamic, with red membranes and fast refill. Cats often present with bradycardia, hypothermia and hypotension together. When compensation fails, pressure falls, lactate rises, urine output drops and mentation worsens.
Bedside perfusion markers are heart rate, pulse quality, membrane colour and refill, extremity temperature, mentation, urine output, blood pressure and lactate; a falling lactate after treatment is more informative than one reading. Treatment follows mechanism: restore volume in hypovolaemia, add vasopressors in distributive shock once volume is restored, remove the obstruction in obstructive shock, and avoid loading fluid into cardiogenic shock.
Body water is about 60 per cent of body weight in adults and more in neonates; about two-thirds is intracellular. Dehydration is estimated as a percentage of body weight. Below about 5 per cent it is not clinically detectable. At about 6–8 per cent skin tent is slow, eyes slightly sunken and membranes tacky. At about 10–12 per cent the skin tent persists, eyes are clearly sunken, extremities cool and pulse weak. Beyond about 12 per cent the animal is in shock. In calves, the gap between the recessed eyeball and lower lid is a useful guide. Skin tent misleads in very young, old, emaciated or obese animals. Rising PCV and total protein support the estimate but anaemia or protein loss can mask them.
Each disease has its acid-base signature. Diarrhoea loses bicarbonate and sodium, and diarrhoeic calves develop metabolic acidosis, often with D-lactate that adds to their depression. Abomasal displacement or volvulus, vagal indigestion and pyloric obstruction trap hydrochloric acid in the abomasum, producing hypochloraemic, hypokalaemic metabolic alkalosis, sometimes with paradoxical aciduria; vomiting of gastric contents in dogs does the same. Grain overload causes lactic acidosis. Urethral obstruction in male cats causes acidosis with dangerous hyperkalaemia.
The anion gap, (sodium + potassium) − (chloride + bicarbonate), separates acidosis from unmeasured acids (lactate, ketones, uraemic acids, ethylene glycol metabolites), which raise the gap, from bicarbonate loss, where the gap stays normal and chloride rises.
Anaemia is a reduced red cell mass, measured as low PCV, haemoglobin or red cell count. It is a sign, not a diagnosis: pale membranes, weakness, exercise intolerance, tachycardia, tachypnoea and sometimes a soft haemic murmur, with jaundice and haemoglobinuria when haemolytic. Speed of onset matters as much as the PCV; an animal adapted over weeks tolerates values that would kill after acute haemorrhage.
Classify first by marrow response. Regenerative anaemia (polychromasia, reticulocytosis, often macrocytosis) points to blood loss or haemolysis; non-regenerative anaemia points to reduced production. The marrow needs about three to five days to respond, so every anaemia looks non-regenerative just after a bleed. Dogs respond most strongly. Cats produce aggregate and punctate reticulocytes, and only aggregates reflect recent regeneration. Cattle respond moderately. Horses do not release reticulocytes into the blood, so regeneration is judged from serial PCV, indices or marrow examination.
Mean corpuscular volume (MCV, fL) = PCV (%) × 10 ÷ red cell count (×10^6/µL). Mean corpuscular haemoglobin concentration (MCHC, g/dL) = haemoglobin ÷ PCV × 100. Macrocytic hypochromic cells suggest regeneration; microcytic hypochromic cells suggest iron deficiency from chronic external blood loss or, in piglets, milk-only diets; normocytic normochromic non-regenerative anaemia suggests chronic inflammation or kidney disease. In dogs, correct the reticulocyte percentage by multiplying it by the patient's PCV divided by a normal PCV.
Acute external blood loss follows trauma, surgery or coagulopathy such as anticoagulant rodenticide poisoning. Acute internal loss follows a ruptured splenic haemangiosarcoma in dogs, uterine artery rupture in periparturient mares, or bleeding abomasal ulcers in cattle (melaena). Chronic loss causes iron deficiency: Haemonchus contortus in sheep and goats, hookworms in puppies, heavy lice or ticks, bleeding ulcers or tumours. In grazing small ruminants, haemonchosis is the first diagnosis to exclude when anaemia comes with bottle jaw and weight loss.
Intravascular haemolysis produces haemoglobinaemia (pink plasma) and haemoglobinuria; extravascular haemolysis, in spleen and liver, produces jaundice without haemoglobinuria. High-yield causes are babesiosis (intravascular, "redwater"); bovine anaplasmosis (Anaplasma marginale, extravascular, worst in adults); tropical theileriosis of cattle and buffalo with prominent lymph node enlargement; leptospirosis in calves; bacillary haemoglobinuria (Clostridium haemolyticum, after liver fluke damage); postparturient haemoglobinuria of high-yielding cows and buffaloes, associated with hypophosphataemia; chronic copper poisoning in sheep with a sudden haemolytic crisis after stress; Heinz body anaemia from onions and other Allium species, brassicas in ruminants, wilted red maple leaves in horses, and zinc or paracetamol in dogs and cats; water intoxication in calves; immune-mediated haemolytic anaemia in dogs (spherocytes, autoagglutination, positive Coombs test); Mycoplasma haemofelis in cats; and neonatal isoerythrolysis in foals and kittens.
The commonest causes of non-regenerative anaemia are chronic inflammation and chronic kidney disease. In anaemia of inflammation, cytokines raise hepcidin, which locks iron in storage and blunts the marrow's response. In chronic kidney disease the main cause is reduced erythropoietin production. Feline leukaemia virus can suppress the marrow severely; chronic canine ehrlichiosis can cause pancytopenia. Oestrogen, some drugs and bracken fern cause aplastic anaemia; bracken in cattle also causes enzootic haematuria with long-term intake.
Deficiencies matter in production animals. Piglets are born with small iron stores, sow's milk is poor in iron and growth is fast, so indoor piglets not given iron in the first days of life develop microcytic hypochromic anaemia at about two to three weeks. Copper deficiency in grazing ruminants causes anaemia with poor growth, faded coat and, in lambs, swayback. Cobalt deficiency limits rumen synthesis of vitamin B12 and causes anaemia with wasting. When a non-regenerative anaemia has no obvious cause, a bone marrow aspirate or core biopsy shows hypoplasia, infiltration, fibrosis or ineffective erythropoiesis. Treat the cause; transfusion buys time when the anaemia itself threatens life.
The ECG is the test for rhythm; echocardiography assesses chamber size better. Dogs and cats are recorded in right lateral recumbency using lead II. Horses and cattle use a base-apex lead, because deep Purkinje penetration in their ventricles makes limb-lead amplitudes uninformative about chamber size. At 25 mm/s each 1 mm box is 0.04 s; at 50 mm/s it is 0.02 s. Heart rate is 1500 ÷ R-R interval (mm) at 25 mm/s, or 3000 ÷ R-R (mm) at 50 mm/s. For irregular rhythms, count QRS complexes over a known time and multiply to a minute.
Read rate, rhythm, P-QRS relationship, complex shape and intervals in that order. Sinus arrhythmia is normal in dogs. Second-degree atrioventricular block is common and usually physiological in fit horses at rest, disappearing with exercise. Atrial fibrillation is the most important arrhythmia of horses (poor performance): no P waves, fibrillation waves and an irregularly irregular R-R interval; it also occurs in large dogs with dilated cardiomyopathy and in cattle with gastrointestinal disease. Ventricular premature complexes are wide and bizarre without a preceding P wave; they accompany myocardial disease, gastric dilatation-volvulus, splenic masses, sepsis and electrolyte disturbance.
Hyperkalaemia progresses from tall peaked T waves to loss of P waves, widened QRS, bradycardia and finally ventricular fibrillation or asystole. A bradycardic blocked male cat, or a dog with hypoadrenocorticism, is hyperkalaemic until proven otherwise.
Paracentesis samples abdominal, pleural or pericardial fluid for colour, clarity, total protein, nucleated cell count, cytology and biochemistry. Effusions are classed as transudates (low protein and cells, from low oncotic pressure), modified transudates (raised hydrostatic pressure or leakage, as in heart failure) and exudates (high protein and cells, from inflammation or sepsis). Cut-offs differ between texts and species; use your laboratory's.
In horses, abdominocentesis is done at the lowest point of the ventral abdomen, slightly right of midline to avoid the spleen. Normal fluid is clear and pale yellow. A strangulating lesion makes it serosanguinous with rising protein, and peritoneal lactate above blood lactate supports ischaemia. Plant material or intracellular bacteria mean rupture, unless the needle entered distended bowel. In cattle, the peritonitis of reticular perforation is often walled off by fibrin, so ultrasound guidance improves yield.
In a foal with a suspected ruptured bladder, peritoneal creatinine at least twice serum creatinine confirms uroperitoneum. In dogs, abdominal fluid glucose well below blood glucose, or lactate well above blood lactate, supports septic peritonitis. Thoracocentesis is diagnostic and therapeutic in a dyspnoeic cat with effusion (chyle, pus, blood or heart-failure fluid). Pericardiocentesis relieves tamponade, commonly from haemangiosarcoma or idiopathic effusion in dogs.
Rumen fluid is collected by oro-ruminal tube or by rumenocentesis through the left ventral flank. Tube samples may contain saliva, which raises pH, so discard the first portion; rumenocentesis gives a truer pH and is used in herd investigations of subacute ruminal acidosis (SARA). Examine immediately.
Colour is olive to brownish-green on roughage, yellow-grey on concentrates, milky grey in grain overload and dark in putrefaction. Odour is aromatic normally, sour in lactic acidosis, putrid in putrefaction and ammoniacal in urea toxicity. Normal pH is about 6 to 7 on roughage and lower on concentrates; values below about 5.5 by rumenocentesis in a herd survey suggest SARA, and around 5 or below indicate acute lactic acidosis. Many active ciliate protozoa are normal; few or dead protozoa indicate an unhealthy rumen. In the sedimentation-activity test, active fluid shows floating gas-laden particles within minutes; inactive fluid simply settles. Methylene blue is reduced within a few minutes by active flora and slowly by inactive flora. Rumen chloride is normally low (below about 30 mmol/L); a raised value means abomasal reflux, as in abomasal outflow obstruction, volvulus or type II and III vagal indigestion.
Low pH, dead protozoa, Gram-positive flora (Streptococcus bovis, lactobacilli) and a milky sour sample mean grain overload. High pH, ammoniacal smell and absent protozoa after urea intake mean ammonia toxicity. High chloride with normal pH in a distended anorexic cow points to an outflow problem beyond the rumen.
A full urinalysis has physical examination, specific gravity (USG) by refractometer, dipstick chemistry and sediment. Dipstick SG pads are unreliable in animals. A USG above about 1.030 in dogs and 1.035 in cats shows adequate concentration; 1.008–1.012 is isosthenuria. In a dehydrated azotaemic animal, poorly concentrated urine points to renal azotaemia and concentrated urine to prerenal azotaemia, though hypoadrenocorticism and diuretics can also impair concentration.
Read dipstick protein against USG, and quantify persistent proteinuria with the urine protein:creatinine ratio (UPC) on an inactive sediment. Under IRIS, dogs are non-proteinuric below 0.2 and proteinuric above 0.5; cats are proteinuric above 0.4. The leucocyte pad is unreliable in dogs and cats. Ketones on urine or milk are the field test for bovine ketosis. In the sediment look for casts (tubular damage), cells, bacteria and crystals: struvite "coffin lids" in alkaline urine; calcium oxalate dihydrate "envelopes"; calcium oxalate monohydrate "picket fences", which with acute kidney injury suggest ethylene glycol; ammonium urate with portosystemic shunts (and normally in some Dalmatians); cystine hexagons.
Herbivore urine is normally alkaline and carnivore urine acid; horse urine is normally cloudy from calcium carbonate crystals and mucus. For red or brown urine, spin it: red cells settle. Then look at plasma: pink plasma means haemoglobin from intravascular haemolysis; clear plasma with dark urine suggests myoglobin, which is cleared quickly and does not colour plasma.
Direct ophthalmoscopy gives an upright, highly magnified view of a small fundic area; indirect ophthalmoscopy, with a condensing lens, gives a wider, inverted view better for surveying. Dogs and cats have a cellular tapetum, ruminants and horses a fibrous tapetum, and pigs none. Systemic disease shows in the fundus: retinal haemorrhage and detachment from hypertension in older cats with kidney disease or hyperthyroidism; papilloedema and blindness in young cattle with vitamin A deficiency; chorioretinitis in feline infectious peritonitis, toxoplasmosis and distemper; central retinal degeneration in taurine-deficient cats. Blindness with normal pupillary light reflexes means a cortical lesion, as in polioencephalomalacia and lead poisoning.
Endoscopy of the equine upper airway, at rest and during exercise, shows recurrent laryngeal neuropathy (almost always left-sided, "roaring"), dorsal displacement of the soft palate, guttural pouch empyema (Streptococcus equi) and guttural pouch mycosis, which can erode the internal carotid artery and cause fatal epistaxis. Gastroscopy after a fast diagnoses equine gastric ulcer syndrome, squamous or glandular. Endoscopy also guides tracheal wash and bronchoalveolar lavage, and in dogs finds foreign bodies and tracheal collapse.
In ultrasonography, higher frequency gives better resolution but less penetration. In cattle it shows fibrin, abscesses and reticular motility in reticuloperitonitis, abomasal position, liver abscesses, pericardial effusion and urinary tract disease; thoracic ultrasound scoring of calves is a practical herd tool. In small animals, FAST scans find free fluid in emergencies, and a left atrium to aorta ratio above about 1.6 on echocardiography is used as evidence of left atrial enlargement in dogs.
Simple indigestion is mild rumen dysfunction after a sudden diet change or poor feed: reduced appetite, motility and milk yield with near-normal vital signs, resolving in a day or two. Re-examine any "indigestion" not better in 48 hours; displacement, reticuloperitonitis or ketosis is often being missed.
Acute ruminal lactic acidosis (grain overload) follows sudden access to rapidly fermentable carbohydrate. Streptococcus bovis and then lactobacilli multiply, lactic acid drops rumen pH to 5 or below, protozoa die, rumen osmolality rises and draws water from the blood, and the animal becomes dehydrated, acidotic, ataxic and sometimes laminitic. Survivors may develop rumenitis and liver abscesses. Mild cases need grain removed and hay offered; severe cases need rumen lavage or rumenotomy, IV fluids with an alkalinising agent, and rumen fluid transfaunation. Subacute ruminal acidosis (SARA) is a herd problem of intensively fed dairy cows: variable intake, loose faeces, low milk fat and laminitis.
Vagal indigestion is failure of ingesta to pass normally through the forestomachs and abomasum, usually from vagal damage by adhesions or abscesses after reticuloperitonitis. The classic types are I, failure of eructation (free-gas bloat); II, failure of omasal transport; III, abomasal impaction; and IV, indigestion of late pregnancy. The cow develops slowly progressive distension with an "L-shaped" or "papple" silhouette from behind (left side distended throughout, right side ventrally), scant pasty faeces and sometimes bradycardia. Raised rumen chloride points to type II or III. Prognosis is guarded.
Bloat is overdistension of the rumen and reticulum with fermentation gas. The rumen presses on the diaphragm and venous return, and severe bloat can kill within an hour. Primary (frothy) bloat is caused by a stable foam that traps gas: on pasture after lush legumes such as lucerne and clovers, whose soluble leaf proteins act as foaming agents, especially pre-bloom and when wet; in feedlots after finely ground high-grain diets. Secondary (free-gas) bloat is failure to eructate normal gas: oesophageal obstruction ("choke"), mediastinal masses, vagal indigestion, tetanus, hypocalcaemia or abnormal posture.
Signs are distension of the left paralumbar fossa then the whole abdomen, distress, open-mouth breathing, tongue protrusion and collapse. A stomach tube separates the forms: gas rushes out in free-gas bloat, while the tube blocks with foam in frothy bloat. Treat free-gas bloat by releasing the gas and removing the cause. Treat frothy bloat with an antifoaming agent by tube (poloxalene, vegetable or mineral oil, or a surfactant such as dioctyl sodium sulfosuccinate); in a life-threatening emergency use a trocar and cannula or emergency rumenotomy. Prevent pasture bloat with grass-legume swards, hay before turnout, antifoaming agents in high-risk periods and ionophores where permitted; in feedlots, include enough coarse roughage.
Cattle and buffalo prehend feed with the tongue and swallow with little chewing, so wire and nails are swallowed and fall into the reticulum. Reticular contractions, and raised abdominal pressure in late pregnancy and at calving, push a sharp object through the wall, causing local peritonitis that fibrin usually walls off. It may migrate through the diaphragm into the pericardium, or into liver or spleen.
Acute cases show a sudden drop in milk and appetite, rumen stasis, mild fever, arched back, reluctance to move and abducted elbows, with a grunt on the withers pinch, pole test or xiphoid pressure. Neutrophilia with a left shift and raised fibrinogen and globulin support it. A metal detector shows metal is present, not that it has penetrated; radiography and ultrasound show fibrin, abscesses and reduced reticular motility.
Traumatic pericarditis carries the worst prognosis: tachycardia, jugular distension, brisket and submandibular oedema, and muffled heart sounds with splashing or friction sounds; humane culling is usual. Other sequelae are vagal indigestion, reticular and liver abscesses, and diaphragmatic hernia, well documented in buffalo in South Asia, with recurrent bloat and reticular sounds in the chest. Uncomplicated cases are treated with an oral magnet, systemic antimicrobials chosen by class, and confinement with forequarters raised, or by rumenotomy. Prevent it with magnets for incoming heifers and metal removal from feed.
Abomasal displacement is a disease of high-producing dairy cows, mostly within the first month after calving. A hypomotile, gas-filled abomasum floats to the left between rumen and body wall (LDA) or to the right (RDA); an RDA can twist into abomasal volvulus, a surgical emergency. Risk factors reduce abomasal tone or increase space: hypocalcaemia, ketosis and negative energy balance, metritis, retained placenta, twins, high-concentrate diets with little effective fibre, low dry-matter intake around calving and deep-bodied conformation. LDA is far more common than RDA.
The LDA cow has a reduced, often selective appetite, falling milk yield, ketonuria and scant faeces, with near-normal vital signs. The diagnostic sign is a high-pitched ping on simultaneous percussion and auscultation of the left upper abdomen over the last ribs. On the left, the alternatives are a rumen gas cap and pneumoperitoneum. On the right, pings come from RDA or volvulus, caecal dilatation or volvulus, spiral colon or rectal gas, and pneumoperitoneum. Ultrasound or a needle sample with acid pH confirms the abomasum. Abomasal volvulus causes marked dehydration, tachycardia, right-sided distension, scant dark faeces and a distended viscus on rectal examination, with hypochloraemic hypokalaemic metabolic alkalosis; high heart rate and severe dehydration before surgery predict a worse outcome.
LDA is corrected by rolling (cheap, frequent recurrence), rolling with toggle-pin or blind-stitch fixation, or surgery: right flank omentopexy or pyloro-omentopexy standing, right paramedian abomasopexy, left flank abomasopexy, or laparoscopy. Volvulus needs right flank laparotomy, decompression, derotation and fixation. Correct dehydration and alkalosis with chloride-rich fluids such as 0.9 per cent saline with potassium, IV when severe or orally when mild, and treat concurrent ketosis, hypocalcaemia and metritis. Prevention is transition-cow management; the herd displacement rate measures it.
Colic means abdominal pain, not a diagnosis. Horses are prone to it: they rarely vomit, have a long mobile large colon narrowing at the pelvic flexure and a long small-intestinal mesentery, and are often meal-fed and stabled. The key decision is medical or surgical. Assess pain severity and response to analgesia; heart rate, membranes, refill, PCV, total protein and lactate; gut sounds in four quadrants; rectal findings; nasogastric reflux (pass a tube in every colic: net reflux above about 2 litres is significant, and decompression prevents gastric rupture); abdominal ultrasound; and abdominocentesis.
Indicators for surgery are severe or persistent pain despite analgesia, progressive distension, persistent or rising tachycardia with worsening perfusion, distended small intestine on rectal or ultrasound examination, significant reflux, and serosanguinous peritoneal fluid with peritoneal lactate above blood lactate.
The main groups are spasmodic colic (commonest; loud gut sounds, intermittent pain), gas colic, simple obstructions (large-colon impaction, commonest at the pelvic flexure; sand and enteroliths regionally), displacements (left dorsal displacement with nephrosplenic entrapment, right dorsal displacement), strangulations (pedunculated lipoma in older horses, epiploic foramen entrapment, inguinal hernia in stallions, large-colon volvulus often in periparturient mares) and enteritis (duodenitis-proximal jejunitis, with large reflux but less pain after decompression). In cattle, colic comes with intussusception, caecal volvulus and urolithiasis; in dogs, gastric dilatation-volvulus in large deep-chested breeds presents with unproductive retching and cranial abdominal distension.
Analgesia comes first, for welfare and safe examination. Alpha-2 adrenergic agonists (xylazine, detomidine) give sedation and visceral analgesia but reduce gut motility and cause bradycardia and AV block. Non-steroidal anti-inflammatory drugs (flunixin meglumine) give analgesia and anti-endotoxic effects but can mask a surgical lesion for hours, so re-examine. Opioids (butorphanol) and spasmolytics (N-butylscopolammonium bromide, for spasmodic colic) complete the list. Doses and approvals differ by country, and many drugs exclude horses from the food chain; record them in the passport where that system applies.
Large-colon impaction is treated with oral fluids and electrolytes by nasogastric tube, laxatives such as mineral oil or magnesium sulphate, feed withdrawal, and IV fluids when severe. Enteritis needs gastric decompression, IV fluids and anti-endotoxic treatment. Chart pain, heart rate, reflux, rectal findings and peritoneal fluid over time. A strangulating lesion will not recover without surgery; when surgery is not possible, humane euthanasia is the professional decision and should be raised early. Prevention: forage-rich regular feeding, constant water, gradual diet change, faecal egg count-based parasite control, dental care, and not feeding off sandy ground.
Heart failure is inability of the heart to meet the body's needs at normal filling pressures. Left-sided congestive failure causes pulmonary oedema: tachypnoea, dyspnoea, crackles and, in dogs, cough. Right-sided failure raises systemic venous pressure: jugular distension and pulsation, hepatomegaly, ascites in dogs, pleural effusion in cats, and brisket and ventral oedema in cattle and horses. Low output causes weakness, exercise intolerance, syncope and prerenal azotaemia. The renin-angiotensin-aldosterone and sympathetic systems retain salt and water and constrict vessels, worsening congestion and remodelling. Chronic treatment therefore combines diuretics, drugs that improve contractility or dilate vessels, blockade of the renin-angiotensin-aldosterone system, and arrhythmia control.
Murmurs are graded 1 to 6: grade 1 is barely audible in a quiet room, grade 5 has a palpable thrill, grade 6 is heard with the stethoscope just off the chest. Describe timing, point of maximal intensity and quality. Soft flow murmurs are common in fit horses and must be separated from valvular regurgitation.
Myxomatous mitral valve disease (MMVD) is the most common acquired heart disease of dogs, mainly older small breeds, and earlier in Cavalier King Charles Spaniels. It causes a left apical systolic murmur, progressive left atrial enlargement and eventually left-sided congestive failure. The ACVIM consensus stages it: A at risk; B1 murmur without significant enlargement; B2 murmur with left atrial and ventricular enlargement meeting set criteria; C current or past congestive failure; D refractory failure. Stage B2 dogs benefit from starting an inodilator before failure, based on a large prospective trial. Stage C is treated with a loop diuretic, the inodilator, renin-angiotensin-aldosterone blockade and often a mineralocorticoid antagonist.
Dilated cardiomyopathy affects large and giant breeds such as the Dobermann and Great Dane, presenting with atrial fibrillation, ventricular arrhythmias, congestive failure or sudden death; Holter monitoring and echocardiography detect occult disease in Dobermanns. Hypertrophic cardiomyopathy (HCM) is the most common heart disease of cats. Many affected cats have no murmur and present with sudden dyspnoea from oedema or pleural effusion, or with arterial thromboembolism: a clot from the enlarged left atrium lodges at the aortic trifurcation, and the cat has sudden painful hind-limb paralysis with cold, pulseless limbs and pale pads. Check thyroid hormone and blood pressure in older cats, because hyperthyroidism and hypertension cause secondary hypertrophy. Heartworm (Dirofilaria immitis) causes pulmonary arterial disease and right-sided failure in dogs in endemic areas; caval syndrome with haemolysis needs surgical worm removal.
In cattle, traumatic pericarditis (chapter 5), bacterial endocarditis and brisket disease dominate. Endocarditis is usually secondary to a chronic septic focus such as a foot abscess, mastitis, metritis or liver abscess; Trueperella pyogenes and streptococci are common, and the right atrioventricular (tricuspid) valve is most often affected. Signs are recurrent fever, weight loss, tachycardia and a murmur, sometimes with right-sided failure, lameness and embolic pneumonia. Diagnosis is by echocardiography and repeated blood cultures; treatment is long and costly with long withdrawal periods. Brisket disease occurs at high altitude: chronic hypoxia constricts pulmonary arteries, causing pulmonary hypertension and right-sided failure with brisket oedema. Susceptibility is heritable, and early cases may improve at lower altitude. Selenium-vitamin E deficiency, cardiotoxic plants and ionophores also damage the myocardium.
In horses, atrial fibrillation often occurs in large athletic horses without underlying heart disease, causing poor performance at speed; after echocardiography excludes significant structural disease, conversion is attempted with drugs or transvenous electrical cardioversion. Valvular regurgitation is common in older horses and usually progresses slowly; safety to ride depends on chamber size and rhythm. Ionophores are highly toxic to the equine myocardium, so horses must never be fed cattle or poultry rations.
Locate the problem first: upper airway (inspiratory noise and effort), lower airway (expiratory effort, wheezes, cough), parenchyma (crackles), pleural space (rapid shallow breathing, muffled ventral sounds) or outside the respiratory tract (acidosis, anaemia, pain, abdominal distension). A heave line from chronic expiratory effort is typical of chronic obstructive or interstitial disease in horses and cattle. Tools are radiography, thoracic ultrasound, transtracheal wash for culture, bronchoalveolar lavage for cytology, nasopharyngeal swabs and paired serology, and post-mortem of casualties in herds. Stabilise a dyspnoeic cat with oxygen before imaging.
Bovine respiratory disease (BRD) is the most important disease of feedlot cattle and young dairy stock. Stress (weaning, transport, mixing, poor ventilation) and viruses (bovine respiratory syncytial virus, bovine herpesvirus 1, parainfluenza 3, bovine viral diarrhoea virus, bovine coronavirus) allow Mannheimia haemolytica, Pasteurella multocida, Histophilus somni and Mycoplasma bovis to colonise the lung; Mannheimia leukotoxin causes the fibrinous pleuropneumonia of "shipping fever". Cases show fever, depression, nasal discharge, cough, tachypnoea and cranioventral crackles. Early treatment with an appropriate antimicrobial class plus an NSAID improves outcome; prevention relies on colostrum, vaccination, less mixing and ventilation.
Acute interstitial pneumonia (fog fever) affects adult cattle one to two weeks after moving to lush pasture: rumen bacteria convert L-tryptophan to 3-methylindole, which damages the lung, causing sudden severe expiratory dyspnoea and emphysema with little cough and usually no fever. Dictyocaulus viviparus causes coughing in first-season grazing cattle. In goats, contagious caprine pleuropneumonia (Mycoplasma capricolum subsp. capripneumoniae) is WOAH-listed and highly fatal. Ovine pulmonary adenocarcinoma (jaagsiekte) is recognised by fluid running from the nose when the hindquarters are raised.
Severe equine asthma (formerly recurrent airway obstruction or "heaves") affects mature horses exposed to hay and bedding dust and moulds, or pollens at pasture in some regions. Neutrophilic airway inflammation, bronchospasm and mucus cause expiratory effort, a heave line, cough and exercise intolerance, with neutrophilia on lavage. Environmental control (turnout, soaked or steamed hay, low-dust bedding) is the basis of treatment; corticosteroids and bronchodilators relieve signs. Rhodococcus equi causes pyogranulomatous pneumonia with abscesses in foals of about one to six months, often found by ultrasound screening. Pleuropneumonia follows long transport with the head tied high.
In pigs, enzootic pneumonia (Mycoplasma hyopneumoniae) causes chronic dry cough and poor growth; porcine pleuropneumonia (Actinobacillus pleuropneumoniae) causes sudden death with dorsocaudal haemorrhagic necrotising lung lesions; atrophic rhinitis (Bordetella bronchiseptica with toxigenic Pasteurella multocida) distorts the snout.
In dogs, infectious respiratory disease complex ("kennel cough", including Bordetella bronchiseptica and canine parainfluenza virus) causes a harsh cough after dogs are housed together; tracheal collapse in toy breeds causes a "goose-honk" cough; brachycephalic obstructive airway syndrome combines stenotic nares, elongated soft palate, everted laryngeal saccules and hypoplastic trachea; aspiration pneumonia follows regurgitation, vomiting or anaesthesia and affects dependent lobes. Feline asthma causes episodic cough and wheeze with airway eosinophilia. Feline pleural effusion (pyothorax, chylothorax, heart failure, feline infectious peritonitis, neoplasia) is diagnosed and relieved by thoracocentesis.
Azotaemia is raised blood urea and creatinine; uraemia is the clinical syndrome of renal failure. Prerenal azotaemia comes from reduced renal perfusion, with concentrated urine; renal azotaemia from loss of nephrons, with poorly concentrated urine despite dehydration; postrenal azotaemia from obstruction or rupture. Types can coexist, and cattle and horses concentrate less than dogs and cats.
Acute kidney injury (AKI) is a sudden, often reversible loss of function. Causes include ethylene glycol, leptospirosis, grapes and raisins and NSAIDs in dogs; lilies (Lilium and Hemerocallis, including pollen) and ethylene glycol in cats; aminoglycosides and pigment nephropathy in many species; and oak and oxalate plants in ruminants. Stop the insult, restore perfusion, monitor urine output, and manage hyperkalaemia and acidosis.
The International Renal Interest Society (IRIS) stages chronic kidney disease in stable, hydrated patients by blood creatinine, substaged by proteinuria and blood pressure. For dogs: stage 1 below 1.4 mg/dL (125 µmol/L); stage 2 1.4–2.8 mg/dL (125–250 µmol/L); stage 3 2.9–5.0 mg/dL (251–440 µmol/L); stage 4 above 5.0 mg/dL. For cats stage 1 is below 1.6 mg/dL (140 µmol/L) and stage 2 starts at 1.6; higher stages match dogs. SDMA supports early staging. Management uses a phosphorus-restricted renal diet, phosphate binders, control of proteinuria and hypertension, fluids for dehydration, and treatment of anaemia and hypokalaemia.
Obstructive urolithiasis in ruminants affects males, especially castrates, with narrow urethras; stones lodge at the sigmoid flexure in cattle and at the urethral process in small ruminants. High-concentrate diets with high phosphorus, low calcium and high magnesium cause struvite and calcium phosphate stones; silica stones occur on some rangelands and calcium carbonate stones on clover pasture. Signs are straining, tail flagging, dribbling bloody urine and crystals on preputial hairs. Urethral rupture causes ventral subcutaneous urine accumulation; bladder rupture causes "water belly", sometimes with brief apparent relief. Amputation of the urethral process may relieve small ruminants; otherwise urethrostomy or tube cystostomy is needed. Prevent with a calcium to phosphorus ratio of about 2:1, salt to increase water intake, free water, and acidifiers such as ammonium chloride where appropriate.
Uroperitoneum in neonatal foals, usually colts, follows bladder rupture at birth. At two to four days the foal strains, distends and becomes depressed, with hyponatraemia, hypochloraemia, hyperkalaemia and peritoneal creatinine at least twice serum creatinine. Drain the abdomen and correct potassium before anaesthesia and repair.
In dogs, struvite stones are usually infection-induced (urease-producing staphylococci, Proteus), while calcium oxalate is common in small breeds; feline struvite is usually sterile and diet-dissolvable. Feline lower urinary tract disease (dysuria, haematuria, pollakiuria, periuria) is most often idiopathic cystitis linked with stress. A blocked male cat develops hyperkalaemia, acidosis and azotaemia and can die of arrhythmia within a day or two. In cattle, pyelonephritis (Corynebacterium renale group) causes haematuria and pyuria, and enzootic haematuria from long-term bracken intake causes bladder tumours.
Neurology asks where the lesion is, then what it is. Assess mentation and behaviour (forebrain and brainstem), posture and gait, cranial nerves, postural reactions, spinal reflexes and tone, and pain perception. Upper motor neuron (UMN) signs are paresis with normal or increased reflexes and tone; lower motor neuron (LMN) signs are paresis with reduced reflexes and tone and rapid atrophy. In dogs and cats: C1–C5 lesions give UMN signs in all limbs; C6–T2, LMN forelimbs and UMN hindlimbs; T3–L3, normal forelimbs and UMN hindlimbs; L4–S3, LMN hindlimbs, tail, anus and bladder.
The Schiff-Sherrington posture (rigid forelimbs, flaccid hindlimbs) localises an acute severe T3–L3 lesion but is not itself prognostic. Loss of deep pain perception caudal to a spinal lesion is the key poor prognostic sign in thoracolumbar disc herniation, common as Hansen type I extrusion in chondrodystrophic breeds such as the Dachshund. Peripheral vestibular disease gives head tilt and horizontal or rotatory nystagmus with the fast phase away from the lesion, sometimes with facial paralysis and Horner's syndrome from middle-ear involvement; central disease may give vertical or position-changing nystagmus with depression and postural deficits. Blindness with normal pupillary light reflexes indicates a cortical lesion. CSF analysis and MRI or CT move from localisation to diagnosis.
Polioencephalomalacia (cerebrocortical necrosis) is associated with altered thiamine status and with excess dietary sulphur. Young cattle, sheep and goats show cortical blindness with intact pupillary reflexes, head pressing, star-gazing, dorsomedial strabismus, opisthotonus and convulsions; early response to thiamine supports the diagnosis. Listeriosis (Listeria monocytogenes) follows poorly fermented silage: the organism ascends the trigeminal nerve to the brainstem, causing microabscesses, circling, head tilt and unilateral facial paralysis. Lead poisoning (batteries, paint) causes blindness, head pressing, jaw champing and convulsions. Rabies must be considered in every unexplained neurological case, with protection of people. Tetanus causes a sawhorse stance, third-eyelid prolapse, trismus and bloat; botulism causes flaccid paralysis with weak tongue and tail. Gid in sheep (Taenia multiceps cysts) causes circling; focal symmetrical encephalomalacia is a subacute enterotoxaemia of lambs; scrapie and BSE are notifiable prion diseases.
In pigs, salt poisoning after water deprivation causes intermittent convulsions with eosinophilic meningoencephalitis; Streptococcus suis meningitis in weaners causes paddling and opisthotonus and is zoonotic; Aujeszky's disease kills piglets with nervous signs; oedema disease (Shiga-toxin-producing E. coli) causes eyelid oedema and ataxia after weaning.
In horses, cervical vertebral stenotic myelopathy ("wobbler") causes symmetric ataxia worse in the hindlimbs in young fast-growing horses. Equine protozoal myeloencephalitis (Sarcocystis neurona, Americas) causes asymmetric multifocal signs with atrophy. Equine herpesvirus 1 myeloencephalopathy causes outbreaks of hindlimb ataxia, urinary incontinence and flaccid tail. West Nile virus matters where vectors occur. Hepatic encephalopathy from pyrrolizidine alkaloid plants causes head pressing and yawning. Equine grass sickness (dysautonomia) causes dysphagia, patchy sweating, tremors and ileus.
In dogs, idiopathic epilepsy usually begins between about six months and six years of age with normal interictal findings; seizures outside that range or with interictal deficits need investigation for structural and metabolic causes (hypoglycaemia, hepatic encephalopathy, hypocalcaemia, toxins). Status epilepticus is treated first with a benzodiazepine, then longer-acting anticonvulsants. Distemper causes multifocal disease with myoclonus. Fibrocartilaginous embolism causes sudden, non-painful, often asymmetric deficits. In cats, feline infectious peritonitis and toxoplasmosis cause CNS inflammation, and thiamine deficiency on all-fish diets causes neck ventroflexion and vestibular signs.
Creatine kinase (CK) rises within hours and falls within days; aspartate aminotransferase (AST) rises more slowly and persists. High CK with modest AST means recent or continuing damage; falling CK with raised AST means resolving damage. Nutritional myodegeneration (white muscle disease) from selenium and/or vitamin E deficiency affects calves, lambs, kids and foals on selenium-poor soils, with a skeletal form (stiffness, recumbency, weak sucking) and a cardiac form (sudden death); selenium has a narrow safety margin. Equine exertional rhabdomyolysis ("tying up") causes stiffness, sweating, firm painful muscles and myoglobinuria; chronic forms are recurrent exertional rhabdomyolysis in Thoroughbreds and polysaccharide storage myopathy type 1 (GYS1 mutation) in Quarter Horses and draught breeds, managed by low-starch, fat-added diets and daily exercise. Hyperkalaemic periodic paralysis affects Quarter Horse lines.
Nutritional secondary hyperparathyroidism follows low-calcium or high-phosphorus diets: bran-fed horses ("big head"), horses on oxalate-rich tropical grasses and carnivores fed all-meat diets. Laminitis in horses is associated with endocrine disease (insulin dysregulation, pituitary pars intermedia dysfunction), systemic inflammation and supporting-limb overload.
Septic arthritis of neonates spreads from the umbilicus in animals with poor passive transfer; synovial fluid has high neutrophil counts and protein. Bovine interdigital necrobacillosis (Fusobacterium necrophorum) causes sudden lameness with symmetrical interdigital swelling and a foul smell; digital dermatitis (Treponema spp.) causes raw strawberry-like lesions at the heel in housed herds; ovine foot rot (Dichelobacter nodosus) underruns the horn.
A dermatology case needs age at onset, season, pruritus, contagion to animals or people, lesion distribution and simple tests: deep scrapings for Demodex, superficial scrapings for Sarcoptes (often negative), coat brushing for fleas, tape cytology for bacteria and yeasts, trichogram, Wood's lamp (only some Microsporum canis fluoresces), fungal culture and biopsy.
In dogs, flea allergy dermatitis affects the lumbosacral area and tail base; atopic dermatitis affects face, ears, feet, axillae and ventrum, beginning in young adults; sarcoptic mange is intensely pruritic on ear margins and elbows, is zoonotic, and rubbing the ear margin often triggers a scratch reflex. Adult-onset generalised demodicosis calls for a search for underlying disease. Pyoderma (Staphylococcus pseudintermedius) is almost always secondary, and meticillin resistance makes culture important. In cats, miliary dermatitis and symmetrical alopecia are reaction patterns, often to fleas.
In livestock: calf ringworm (Trichophyton verrucosum, periocular grey crusts, zoonotic); dermatophilosis (Dermatophilus congolensis, "paintbrush" crusts after wetting); lumpy skin disease (capripoxvirus, WOAH-listed); sheep scab (Psoroptes ovis); greasy pig disease (Staphylococcus hyicus); the diamond skin lesions of swine erysipelas; zinc-responsive parakeratosis in pigs, worsened by high calcium; sweet itch (Culicoides hypersensitivity) and sarcoid (associated with bovine papillomavirus) in horses. Photosensitisation damages unpigmented skin: primary after photodynamic plants such as St John's wort, secondary (hepatogenous) when a damaged liver fails to excrete phylloerythrin, as with sporidesmin (facial eczema), Lantana and pyrrolizidine alkaloids. Liver enzymes separate the two.
A fluid plan answers: is fluid needed, how much, which fluid, and by which route and rate. Volume has three parts. The deficit in litres is percentage dehydration × body weight in kg: a 450 kg cow 8 per cent dehydrated has lost about 36 litres. Maintenance is commonly approximated at about 40–60 mL/kg/day for adult dogs and cats, more per kg in neonates; texts differ, so use your formulary's value. Ongoing losses (diarrhoea, vomiting, reflux) are measured or estimated. Replace the deficit quickly in shock and more slowly in chronic dehydration, cats and heart disease, and reassess.
Isotonic replacement crystalloids (lactated Ringer's, acetated polyionic solutions, 0.9 per cent sodium chloride) restore extracellular volume. Alkalinising balanced solutions suit the acidosis of diarrhoea; 0.9 per cent saline with potassium chloride suits the hypochloraemic hypokalaemic alkalosis of abomasal or pyloric outflow obstruction and gastric vomiting. Five per cent dextrose is effectively free water, not a resuscitation fluid. Hypertonic saline (about 7.2–7.5 per cent) given IV in small volume expands plasma volume rapidly and must be followed by isotonic fluid or, in ruminants, oral water. Colloids stay intravascular longer; concerns about kidney injury and coagulopathy limit synthetic starches. Bicarbonate for severe metabolic acidosis in mmol = base deficit × body weight × distribution factor, commonly 0.3 in adults and about 0.5–0.6 in neonatal calves.
IV routes (jugular, cephalic, ear vein, intraosseous in neonates) serve shock and moderate to severe dehydration. Subcutaneous fluids suit mild dehydration in small animals, isotonic only. Ruminants take large oral volumes by orogastric tube. A diarrhoeic calf that stands and sucks can usually be treated with oral electrolytes containing sodium, glucose (which drives sodium and water absorption by co-transport) and an alkalinising agent, while milk feeding continues; a calf that cannot stand or suck needs IV fluids.
Shock resuscitation in dogs and cats is based on the classic "shock volume" of crystalloid, roughly one blood volume: about 80–90 mL/kg for dogs and 50–60 mL/kg for cats, now given as fractions, commonly a quarter, as IV boluses over 15–20 minutes with reassessment after each — confirm against the product label and your national formulary. Cats and cardiac patients tolerate large volumes poorly.
Drops per minute = volume (mL) × drop factor (drops/mL) ÷ time (minutes). Macro-drip sets deliver about 10, 15 or 20 drops/mL and micro-drip sets 60; the value is printed on the set. A widely taught ceiling for IV potassium in dogs and cats is 0.5 mmol (mEq)/kg/hour — confirm against the product label and your national formulary. Never give concentrated potassium as a bolus; anorexic patients and those whose alkalosis is being corrected often need potassium.
Monitor body weight (1 kg approximates 1 litre), heart rate, pulse, mentation, membranes, PCV and total protein, lactate, urine output (about 1–2 mL/kg/hour expected in hydrated dogs and cats with healthy kidneys) and central venous pressure where available. Overload shows as tachypnoea, crackles, serous nasal discharge, chemosis, subcutaneous oedema and weight gain beyond the deficit; cats often develop pleural effusion. Stop and reassess.
Transfuse when anaemia or blood loss threatens oxygen delivery, judged by signs (tachycardia, tachypnoea, weakness, rising lactate) and by the speed of fall, not a single PCV. Whole blood replaces cells, proteins and clotting factors; packed red cells treat normovolaemic anaemia; fresh frozen plasma replaces clotting factors.
Dogs: DEA 1 is the most immunogenic antigen, and dogs lack clinically significant naturally occurring anti-DEA 1 antibodies, so a first mismatched transfusion rarely causes an immediate reaction but sensitises the dog; later transfusions need typing and cross-matching. Cats: type B cats carry strong natural anti-A antibodies, so a single type A transfusion can be fatal; always type cats, and type A or AB kittens nursing a type B queen develop neonatal isoerythrolysis. Horses: neonatal isoerythrolysis most often involves the Aa and Qa antigens. Cattle usually tolerate a first transfusion. A major cross-match tests donor cells against recipient plasma; a minor cross-match tests donor plasma against recipient cells.
Volume (mL) = body weight (kg) × blood volume (mL/kg) × (desired PCV − recipient PCV) ÷ donor PCV, taking blood volume as about 80–90 mL/kg in dogs and about 60 mL/kg in cats. As a rough rule, 2 mL/kg of whole blood raises a dog's PCV by about 1 percentage point. Collect into an anticoagulant-preservative such as citrate-phosphate-dextrose-adenine in a closed system, give through a filter, start slowly, and finish within about four hours. Stop for fever, urticaria, tachycardia, vomiting, haemoglobinuria or overload. In food animals record every drug given to donor and recipient.
Use this subject to build a fixed examination routine that you run on every patient, and a habit of writing a problem list before naming a diagnosis. Practise the calculations until they are automatic: dehydration deficit, drip rate, transfusion volume, bicarbonate, anion gap and heart rate from an ECG strip. Learn one case per unit well enough to explain it to a farmer or pet owner: a cow with LDA, a horse with colic, a blocked cat, a dog with MMVD, a calf with diarrhoea. Exams reward recognition of classic patterns. Build those patterns from real animals in the clinics, not only from lists, and check your findings against a clinician's before the animal leaves.
At five years, this subject is most of your working day. You decide quickly whether a colic can be treated in the field or must be referred, whether an off-feed cow needs a magnet, a roll or a surgeon, and which fluid a scouring calf needs without a blood gas. You run urinalysis and PCV/total protein in-house and read them correctly. You estimate dehydration and set up a fluid plan and a monitoring chart. You know the withdrawal-period consequences of every drug you give a food animal, and you record them. You also recognise when the owner's budget or the prognosis means the kindest outcome is euthanasia, and you have that conversation clearly.
A senior clinician uses this subject at herd and practice level. You read herd rates of displaced abomasum, BRD and lameness as measures of management and set targets with the farmer and nutritionist. You write practice protocols for colic triage, fluid therapy, transfusion and antimicrobial use that younger vets follow at night. You audit outcomes, such as colic survival, calf mortality and AKI cases, and teach from the failures. You advise on regulatory questions, including notifiable neurological and septicaemic diseases, residue control and prescribing law, and act as expert witness where a case is disputed.
For the researcher with long clinical experience, this subject raises open questions. Examples are better markers of sepsis and gut ischaemia in horses and cattle, the right fluid and the right volume for resuscitation across species, the evidence behind dehydration scores and transfusion triggers, and pathophysiology such as abomasal motility failure or the genetics of cardiomyopathy and myopathies. Design studies that answer questions practitioners actually face, report them honestly (including negative results), and help turn evidence into consensus statements. Many present rules, such as fluid rates and potassium ceilings, rest on limited data and deserve prospective testing.
This manual gives principles, classical signs and standard calculations. It gives almost no drug doses, and deliberately none for extralabel use in food animals, because doses, approvals and withdrawal periods vary by country and product: use your national formulary and the label. Reference ranges for vital signs and laboratory values are not tabulated, because they differ between textbooks and laboratories. Metabolic, production and deficiency diseases (milk fever, ketosis, hypomagnesaemia) are treated in Clinical Medicine II. Infectious diseases are treated in the preventive medicine subjects, and species-specific internal medicine (endocrinology, hepatology, gastroenterology of dogs and cats) in the companion-animal subject. Radiographic interpretation, detailed echocardiographic criteria, neonatal intensive care, exotic species and camelids are covered only in passing. Regional plant poisonings are named only where well documented.
Original practice questions written to the syllabus and pattern of the exams named in each question's examTags. They are not past papers and do not reproduce any board's questions.
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