Veterinary · Clinical · also ECC
The first hour of an emergency: triage, shock, CPR, fluids and blood, poisoning and trauma, oxygen, and humane euthanasia.
In the exams: AVMA COE clinical competency on emergencies; EAEVE Day One competences on emergencies and euthanasia; NAVLE clinical practice
Emergency and critical care (ECC) is the medicine of the first hour and the days that follow it: deciding which animal is dying fastest, restoring oxygen delivery to tissues, restarting a heart that has stopped, stopping a poison from being absorbed, stabilising an animal hit by a car, and, when recovery is not possible or not kind, ending life humanely.
Every general practitioner is an emergency vet. What differs between countries is the equipment on the shelf, the blood products available, the drugs that are licensed, the law on who may euthanase and how carcasses are disposed of, and whether a referral ECC hospital exists within reach. This manual teaches the principles that hold everywhere and says where practice differs.
The subject is examined as a Day One competence by accreditation bodies (the AVMA Council on Education, EAEVE and the RCVS all require a new graduate to recognise and stabilise common emergencies and to perform euthanasia humanely), as clinical vignettes in the NAVLE, the RCVS Statutory Membership Examination, the Australasian Veterinary Examination and other licensing exams, and within the Medicine and Surgery units of Indian postgraduate entrance and state veterinary officer papers. Numerical work matters in every one of these: fluid deficits, drip rates, constant-rate infusions, transfusion volumes and toxic doses are calculated at the table, under pressure, and a decimal slip can kill.
Throughout, any drug dose given is a commonly cited textbook figure for teaching, not a prescription. Doses, licensed species and withdrawal periods vary by country and product; every dose is followed by the reminder to confirm against the product label and your national formulary.
Triage (from the French trier, to sort) is the rapid sorting of patients by how urgently they need treatment, not by the order in which they arrive. It begins on the telephone. A caller whose dog is struggling to breathe, has collapsed, is bleeding heavily, is having repeated seizures, has a distended abdomen and is retching unproductively, is a male cat straining without passing urine, has eaten a known toxin, or is in difficult labour should be told to come in immediately, with advice on safe transport. On arrival a trained nurse or technician performs a triage examination within the first minute or two, before paperwork. The category is reassessed, because a stable-looking trauma patient can deteriorate as it bleeds internally. Consent for emergency treatment and a realistic discussion of cost and prognosis should run in parallel with stabilisation, not delay it. In farm and equine practice triage often happens on a telephone call and then in a paddock or shed with limited equipment. The same ABC logic holds, but the most common immediately life-threatening presentations differ: colic with signs of endotoxaemia or uncontrollable pain in a horse; bloat, dystocia, uterine prolapse, hypocalcaemia or toxicity in ruminants; neonatal septicaemia, diarrhoea with severe acidosis or failure of passive transfer in calves and foals. In a herd outbreak with many sick animals, triage extends to deciding which animals to treat, which to slaughter for salvage where legally permitted, and which to euthanase on welfare grounds, and to recognising when a notifiable disease must be reported to the veterinary authority before anything else is done.
The primary survey follows the ABC order borrowed from human emergency medicine, with D for disability (neurological status) and sometimes E for exposure or external examination. Airway: is it patent, is there stridor or stertor (upper airway noise), is the animal cyanotic or unable to lie down? Breathing: rate, effort, pattern and auscultation; a short, shallow, restrictive pattern suggests pleural space disease, whereas loud inspiratory noise suggests upper airway obstruction and crackles suggest parenchymal disease. Circulation: heart rate and rhythm, pulse quality and synchrony with the heartbeat, mucous membrane colour, capillary refill time (normally under about two seconds) and extremity temperature. Disability: mentation (alert, obtunded, stuporous, comatose), posture, pupil size and response, and whether the animal can move all four limbs. The major body systems approach groups this as the respiratory, cardiovascular and neurological systems, with the urinary system added because urethral obstruction and uroabdomen are common killers. Life-threatening problems are treated as they are found: oxygen for a dyspnoeic animal, pressure on arterial bleeding, needle thoracocentesis for suspected tension pneumothorax, venous access and fluids for shock.
A minimum emergency database can be run from a few drops of blood: packed cell volume (PCV) and total solids (TS) by refractometer, blood glucose, blood lactate, and where available a blood gas with electrolytes, plus a blood smear and urine specific gravity. Reading PCV and TS together is useful: in a dog with acute haemorrhage the PCV may be normal at first because the spleen contracts and expels red cells, while total solids fall early, so a low TS with a normal PCV is a warning sign of blood loss. Lactate above the laboratory reference (commonly about 2.0 to 2.5 mmol/L) indicates hyperlactataemia, most often type A from tissue hypoperfusion; serial values that fall with treatment are more informative than a single value. Point-of-care ultrasound protocols such as abdominal and thoracic focused assessment with sonography for trauma, triage and tracking (AFAST and TFAST) look for free abdominal fluid, pleural and pericardial effusion and pneumothorax in a few minutes with the animal in lateral or sternal recumbency. Severity scores help to communicate and to research outcome: the Animal Trauma Triage score grades six categories (perfusion, cardiac, respiratory, eye/muscle/integument, skeletal and neurological) from 0 to 3, so higher totals mean worse injury; the modified Glasgow Coma Scale scores motor activity, brainstem reflexes and level of consciousness, each 1 to 6, so lower totals (3 to 18) mean a worse prognosis. Scores support, but never replace, clinical judgement about an individual.
Shock is a state in which oxygen delivery to the tissues is inadequate for their oxygen consumption, so cells switch to anaerobic metabolism, produce lactate and eventually die. Oxygen delivery (DO2) is the product of cardiac output and arterial oxygen content; cardiac output is heart rate times stroke volume, and oxygen content depends mostly on haemoglobin concentration and its saturation, with only a small dissolved fraction. Any failure in this chain can cause shock. The common classification has four circulatory types. Hypovolaemic shock follows loss of intravascular volume from haemorrhage, vomiting, diarrhoea, polyuria or third-space loss. Distributive shock follows inappropriate vasodilation and maldistribution of flow, as in sepsis, anaphylaxis and some neurological injuries. Cardiogenic shock follows pump failure, such as dilated cardiomyopathy, severe mitral valve disease or arrhythmias. Obstructive shock follows obstruction to flow, such as pericardial tamponade, gastric dilatation-volvulus compressing the caudal vena cava, tension pneumothorax or pulmonary thromboembolism.
Hypovolaemic shock in the dog is classically described in three stages. In compensated shock sympathetic activation produces tachycardia, pink or injected mucous membranes, a rapid capillary refill and normal or even raised blood pressure. In early decompensated shock the membranes become pale, capillary refill is prolonged, the pulses are weak, the extremities are cool and the animal is dull. In late decompensated shock there is bradycardia, hypotension, grey or cyanotic membranes, absent refill, stupor and oliguria, and death follows unless the cause is corrected quickly. Cats differ in an important way: a cat in shock is often bradycardic rather than tachycardic, hypothermic and hypotensive, and these three signs reinforce each other. Perfusion parameters are always read together: heart rate, pulse quality, mucous membrane colour, capillary refill, mentation, extremity temperature, blood pressure, urine output and lactate. The shock index, heart rate divided by systolic arterial pressure, has been studied in dogs as a quick screening number; a value above about 1 has been associated with shock, but it is a screen and not a diagnosis.
Anaphylaxis is an acute, severe hypersensitivity reaction in which mast cell and basophil mediators, especially histamine, cause vasodilation, increased vascular permeability and smooth muscle contraction. The organ that takes the brunt differs by species. In the dog the gastrointestinal tract and liver are the main shock organs: vomiting, diarrhoea (sometimes haemorrhagic), and hepatic venous congestion with raised liver enzymes and gallbladder wall oedema visible on ultrasound. In the cat, ruminants and horses the respiratory tract dominates, with bronchoconstriction, pulmonary oedema and dyspnoea. Epinephrine (adrenaline) is the drug of choice because its alpha effects reverse vasodilation and its beta effects bronchodilate and stabilise mast cells; intramuscular epinephrine at about 0.01 mg/kg is commonly cited in dogs, with intravenous titration in severe cases — confirm against the product label and your national formulary. Fluid resuscitation, oxygen and airway support follow, and antihistamines and glucocorticoids are adjuncts that act too slowly to replace epinephrine.
Resuscitation aims to restore perfusion quickly and then stop, because both too little and too much fluid harm. Isotonic crystalloids are given as boluses rather than as a single large volume: commonly 10 to 20 mL/kg over about 15 minutes in dogs and 5 to 10 mL/kg in cats, with reassessment of perfusion after each bolus — confirm against the product label and your national formulary. The older shock dose, one blood volume per hour (about 80 to 90 mL/kg in dogs and 50 to 60 mL/kg in cats), is now used as an upper reference for total volume rather than a target. Perfusion endpoints include normal heart rate, improving pulse quality and capillary refill, warmer extremities, improved mentation, a mean arterial pressure of at least about 65 mmHg or systolic pressure of at least about 90 mmHg, falling lactate and urine output of at least 1 to 2 mL/kg/h once the animal is resuscitated. Hypertonic saline (7 to 7.5 percent) draws interstitial and intracellular water into the vessels and allows small-volume resuscitation, useful in large dogs, horses and cattle, but its effect is brief and must be followed by isotonic crystalloid. In uncontrolled internal haemorrhage many clinicians use hypotensive (limited-volume) resuscitation, targeting a lower-than-normal pressure until the bleeding is controlled so as not to dislodge clots or dilute clotting factors; it is contraindicated in head trauma, where cerebral perfusion depends on adequate systemic pressure.
When hypotension persists despite adequate volume, vasopressors restore vascular tone. Norepinephrine, dopamine at higher rates, vasopressin and phenylephrine are used as constant-rate infusions; norepinephrine is widely regarded as the first-line vasopressor in septic shock, extrapolated from human guidelines. Dobutamine is a beta-1 agonist inotrope used when poor myocardial contractility, as in dilated cardiomyopathy or sepsis-associated myocardial depression, limits cardiac output. Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection. Veterinary definitions still often use systemic inflammatory response syndrome (SIRS) criteria: in dogs, the criteria of temperature below 38.1 or above 39.2 degrees Celsius, heart rate above 120 per minute, respiratory rate above 20 per minute, and white cell count below 6 or above 16 x 10^9/L or more than 3 percent band neutrophils are widely quoted, with two or more positive plus a documented or suspected infection suggesting sepsis. Feline criteria are different and include bradycardia. The pillars of management are rapid fluid resuscitation, intravenous broad-spectrum antimicrobials started as soon as possible after samples for culture (human data link each hour of delay to higher mortality), source control by surgery or drainage, vasopressor support and early nutrition.
Intensive care means frequent, structured reassessment. Kirby's Rule of 20 is a widely taught checklist of twenty parameters to review daily in every critical patient. Blood pressure is measured indirectly by Doppler (which reads close to systolic) or oscillometry, or directly by an arterial catheter, which is the gold standard. Mean arterial pressure can be estimated as diastolic plus one third of the pulse pressure. Body weight measured on the same scale twice daily is the simplest guide to fluid balance. Continuous electrocardiography detects arrhythmias such as the ventricular tachycardia common after gastric dilatation-volvulus and trauma. Urine output measured with a closed collection system is a direct window on renal perfusion; normal is about 1 to 2 mL/kg/h, and output persistently below about 0.5 mL/kg/h in a hydrated, normotensive patient indicates oliguria, though thresholds vary between texts. Nursing care, including turning recumbent animals, eye lubrication, catheter care, bladder management and early enteral feeding, prevents many complications that kill patients after the crisis has passed.
Cardiopulmonary arrest is the sudden cessation of effective circulation and ventilation. The Reassessment Campaign on Veterinary Resuscitation (RECOVER) published the first evidence-based consensus guidelines for canine and feline CPR in 2012, and updated them in 2024; they are the international reference in small-animal practice. Preparedness is therefore half the work: a stocked and checked crash trolley, drug dose charts by body weight, staff trained and regularly rehearsed, and a decision about resuscitation code status recorded on admission. An unresponsive, apnoeic animal should have CPR started without first spending time searching for a pulse, because the harm of compressing a heart that is beating is small compared with the harm of delay. Basic life support is chest compressions and ventilation. Compressions are delivered at 100 to 120 per minute, to one third to one half of the chest width, allowing full recoil between compressions, in uninterrupted two-minute cycles, with the compressor rotated each cycle to prevent fatigue. Most dogs are compressed in lateral recumbency over the widest part of the chest, using the thoracic pump mechanism. In keel-chested dogs such as greyhounds, and in cats and small dogs, compressions are placed directly over the heart to exploit the cardiac pump mechanism; in cats and very small dogs a one-handed circumferential technique may be used. Intubated animals are ventilated at about 10 breaths per minute with a short inspiratory time, simultaneously with compressions; overventilation reduces venous return.
Advanced life support adds monitoring, drugs and defibrillation. The electrocardiogram is checked briefly at the end of each two-minute cycle, during the compressor change, and the rhythm is classified as non-shockable (asystole or pulseless electrical activity, the commonest arrest rhythms in dogs and cats) or shockable (ventricular fibrillation or pulseless ventricular tachycardia). For non-shockable rhythms, low-dose epinephrine at about 0.01 mg/kg intravenously every other cycle (roughly every three to five minutes) is the standard vasopressor — confirm against the product label and your national formulary; high-dose epinephrine (about 0.1 mg/kg) is no longer recommended routinely because it has not improved survival to discharge. Atropine at about 0.04 mg/kg may be considered when the arrest is thought to be associated with high vagal tone — confirm against the product label and your national formulary. For ventricular fibrillation, electrical defibrillation is the only effective treatment and should be delivered as soon as a defibrillator is ready, with a single shock followed immediately by another full two-minute cycle of compressions; commonly cited external energies are about 4 to 6 J/kg for monophasic and 2 to 4 J/kg for biphasic devices — confirm against the product label and your national formulary. End-tidal carbon dioxide is the most useful monitor during CPR: values persistently below about 10 to 15 mmHg suggest poor compressions or a poor prognosis, and a sudden rise suggests return of spontaneous circulation (ROSC). Reversible causes are sought, often remembered as the Hs and Ts: hypovolaemia, hypoxaemia, hydrogen ion (acidosis), hyper- or hypokalaemia, hypothermia, hypoglycaemia; tension pneumothorax, tamponade, toxins and thrombosis.
Return of spontaneous circulation is the beginning, not the end. Most animals that achieve ROSC re-arrest or die before discharge, often because of the post-cardiac arrest syndrome: brain injury, myocardial dysfunction, systemic ischaemia-reperfusion injury and the persisting precipitating disease. Post-arrest care optimises blood pressure, avoids both hypoxaemia and excessive oxygen, keeps ventilation normal, controls glucose, prevents hyperthermia (mild therapeutic hypothermia is recommended in some protocols where it can be managed), treats seizures and supports organ function; referral to a 24-hour ICU is often the right decision. In large animals CPR is most practical in neonates. Foals and calves can be ventilated by nasotracheal or orotracheal tube or with a mask and self-inflating bag, and chest compressions are given in lateral recumbency over the heart behind the elbow; this is realistic in newborn foals and calves with birth asphyxia. Closed-chest CPR in adult horses and cattle is rarely effective because the thorax is too large to compress.
Total body water is about 60 percent of body weight in an adult animal, higher in neonates and lower in obese animals. About two thirds of it is intracellular and one third extracellular; of the extracellular fluid about three quarters is interstitial and one quarter is intravascular plasma. Water moves freely across cell membranes according to osmolality, which is set mostly by sodium outside cells and potassium inside. Across the capillary wall, the balance of hydrostatic pressure pushing fluid out and colloid oncotic pressure (mainly from albumin) holding it in determines filtration. This anatomy explains why an isotonic crystalloid infused intravenously distributes across the whole extracellular space: within about an hour only about a quarter of the infused volume remains intravascular. It also explains why 5 percent dextrose, once its glucose is metabolised, behaves as free water and distributes through total body water, leaving only a small fraction in the circulation, so it is useless for resuscitation. Three separate fluid problems must be distinguished: perfusion deficits (intravascular volume, treated fast), dehydration (interstitial deficit, replaced over hours) and ongoing losses plus maintenance.
Crystalloids are solutions of electrolytes and small molecules that cross the capillary wall. Replacement crystalloids resemble extracellular fluid. Lactated Ringer's solution (Hartmann's solution) contains roughly sodium 130, potassium 4, chloride 109 and lactate 28 mmol/L and some calcium; the lactate is metabolised by the liver to bicarbonate, giving an alkalinising effect, and the calcium means it should not run through the same line as citrate-anticoagulated blood. Balanced acetate- and gluconate-buffered multiple-electrolyte solutions commonly contain about sodium 140, potassium 5, magnesium 1.5 and chloride 98 mmol/L and no calcium. Sodium chloride 0.9 percent contains 154 mmol/L each of sodium and chloride; because its chloride is well above plasma chloride it tends to cause hyperchloraemic metabolic acidosis, but it is the fluid of choice in hypochloraemic metabolic alkalosis from pyloric obstruction or abomasal displacement, and in hyperkalaemia many clinicians use it or a balanced solution according to availability, since the potassium in balanced fluids is small. Hypertonic saline (7 to 7.5 percent) is a resuscitation fluid given in small volumes.
Colloids contain large molecules that stay mostly in the vessel and hold water there by oncotic pressure. Natural colloids are plasma, whole blood and albumin; synthetic colloids include hydroxyethyl starches (HES), dextrans and gelatins. Synthetic colloids were widely used in veterinary shock and hypoalbuminaemia for decades, but large human trials linked HES to acute kidney injury, coagulopathy and increased mortality in sepsis, and European regulators restricted and then moved to suspend HES products in human medicine. The practical position is that synthetic colloids should not be used routinely in septic or kidney-injured animals, and that where they are still used the clinician should weigh the benefit carefully and follow national guidance. Plasma is an inefficient way to raise albumin: about 45 mL/kg of plasma is needed to raise serum albumin by 1 g/dL, so plasma is given mainly for its clotting factors. Human serum albumin can cause immediate and delayed (type III) hypersensitivity reactions in dogs, so species-specific albumin is preferred where it exists.
A fluid plan has three parts added together: the deficit (dehydration), maintenance, and ongoing losses. Resuscitation of a perfusion deficit comes first and is not part of the 24-hour plan. Dehydration is estimated clinically as a percentage of body weight: below about 5 percent it is not detectable; at about 5 to 6 percent there is subtle loss of skin elasticity; at about 6 to 8 percent there is delayed skin return, slightly prolonged capillary refill and dry mucous membranes; at about 10 to 12 percent the tented skin stays up, the eyes are sunken and signs of shock may appear; at 12 to 15 percent the animal is in shock and death is imminent. The deficit in litres equals body weight in kilograms multiplied by the dehydration fraction; for example a 25 kg dog estimated 8 percent dehydrated has a deficit of 25 x 0.08 = 2 L, usually replaced over 12 to 24 hours. Maintenance for dogs is often calculated with the 2013 AAHA/AAFP fluid guideline formulae, 132 x body weight in kg to the power 0.75 mL per day for dogs and 80 x body weight to the power 0.75 for cats; a 20 kg dog therefore needs about 1,250 mL/day or about 52 mL/h. The plan is revised at least twice daily using body weight, perfusion, packed cell volume, total solids, urine output and electrolytes.
Without an infusion pump, rates are set by counting drops. The drops per minute equal the volume in mL multiplied by the drip factor of the giving set (drops per mL, printed on the packet: commonly 10, 15 or 20 for adult sets and 60 for paediatric microdrip sets), divided by the time in minutes. For example, 1,000 mL over 8 hours through a 20 drops/mL set is 1,000 x 20 / 480 = about 42 drops per minute. A constant-rate infusion (CRI) delivers a drug continuously at a dose expressed per kilogram per minute or per hour. The calculation always runs the same way: dose rate x body weight gives the amount per unit time; convert units (micrograms to milligrams, minutes to hours); then either set a syringe driver or add the right amount of drug to a fluid bag running at a known rate. For example, a dog of 25 kg prescribed dobutamine at 5 micrograms/kg/min (a teaching figure — confirm against the product label and your national formulary) needs 125 micrograms/min, which is 7.5 mg/h; if the drug is added to a 500 mL bag running at 50 mL/h, the bag lasts 10 hours, so 75 mg is added. Adding drug to a maintenance bag couples the drug dose to the fluid rate, so any change in fluid rate changes the drug dose; a separate syringe driver is safer for potent drugs such as vasopressors.
Hypokalaemia is common in anorexic, vomiting or polyuric animals and in cats with chronic kidney disease, causing weakness and, in cats, ventroflexion of the neck. Potassium is replaced by adding potassium chloride to fluids using a sliding scale, and the widely taught ceiling on the infusion rate is 0.5 mmol (mEq)/kg/h — confirm against the product label and your national formulary; faster infusion risks fatal cardiac arrhythmia, so bags containing potassium are never used for boluses. For a 20 kg dog the ceiling is 10 mmol/h, so fluid containing 40 mmol/L must not run faster than 250 mL/h. Hyperkalaemia occurs in urethral obstruction, uroabdomen, acute kidney injury, hypoadrenocorticism and massive tissue injury; the ECG shows tall peaked T waves, flattened or absent P waves, a widened QRS and bradycardia, progressing to a sine-wave pattern and arrest. Emergency treatment has three aims: protect the heart (calcium gluconate 10 percent by slow intravenous injection with ECG monitoring, which raises the threshold potential without lowering potassium), move potassium into cells (regular insulin with dextrose, or sodium bicarbonate, or a beta-2 agonist), and remove it from the body (fluids, relief of the obstruction, dialysis). Sodium disorders are really disorders of water. Chronic hypernatraemia or hyponatraemia must be corrected slowly, commonly no faster than about 0.5 mmol/L per hour (10 to 12 mmol/L per day), because the brain adapts to the abnormal osmolality: too-rapid correction of chronic hyponatraemia causes osmotic demyelination, and too-rapid correction of chronic hypernatraemia causes cerebral oedema.
Blood gas interpretation follows a fixed order. Look at the pH: acidaemia or alkalaemia. Find the primary process: if the carbon dioxide tension (PCO2) moves in the direction that explains the pH, the disorder is respiratory; if bicarbonate or base excess does, it is metabolic. Then ask whether compensation is appropriate. Commonly quoted canine rules (from DiBartola) are that in metabolic acidosis PCO2 falls by about 0.7 mmHg for each 1 mmol/L fall in bicarbonate, and in metabolic alkalosis it rises by about 0.7 mmHg for each 1 mmol/L rise; acute respiratory acidosis raises bicarbonate by about 0.15 mmol/L per mmHg rise in PCO2, and chronic by about 0.35. A value outside the expected range means a second, mixed disorder. Compensation never overcorrects the pH. The anion gap, calculated as (sodium + potassium) minus (chloride + bicarbonate), helps classify metabolic acidosis: a raised gap indicates unmeasured anions such as lactate, ketones, uraemic acids or the metabolites of ethylene glycol, and a normal gap with high chloride indicates bicarbonate loss (diarrhoea) or chloride gain (0.9 percent saline). Sodium bicarbonate is reserved for severe metabolic acidosis (commonly pH below about 7.1 or bicarbonate below about 12 mmol/L) that persists after correcting perfusion; the deficit is estimated as 0.3 x body weight (kg) x base deficit, of which a third to a half is given slowly — confirm against the product label and your national formulary, and more in neonatal calves, where a larger distribution factor (about 0.5 to 0.6) is used. Bicarbonate is not a treatment for lactic acidosis caused by hypoperfusion, which resolves with perfusion.
Blood is transfused to restore oxygen-carrying capacity, to replace clotting factors and, less efficiently, to supply albumin. The decision to give red cells rests on the clinical picture, not a single number: an animal with acute blood loss may need blood at a PCV that a dog with chronic anaemia tolerates quietly, because the chronic patient has adapted with increased 2,3-diphosphoglycerate and cardiac output. Products are fresh whole blood (all components, including functional platelets, if used within about 8 hours of collection), stored whole blood, packed red blood cells, fresh frozen plasma (all clotting factors, including the labile factors V and VIII), frozen or stored plasma (stable factors, useful for anticoagulant rodenticide toxicity), cryoprecipitate (fibrinogen, von Willebrand factor, factor VIII) and platelet products. Availability of commercial blood banks varies widely; many practices worldwide rely on a register of screened in-house donors, which should be healthy, vaccinated, of suitable temperament and weight, tested for regionally relevant blood-borne pathogens such as Babesia, Ehrlichia, Anaplasma, Leishmania, Mycoplasma haemofelis, feline leukaemia and immunodeficiency viruses, and typed.
Dogs have several dog erythrocyte antigen (DEA) systems, of which DEA 1 (formerly DEA 1.1) is the most immunogenic. Dogs do not have clinically important naturally occurring antibodies against DEA 1, so a first transfusion of mismatched blood rarely causes an acute haemolytic reaction, but it sensitises the recipient, and a second mismatched transfusion given days or more later can cause acute haemolysis. Typing donors and recipients for DEA 1 is recommended, and a crossmatch is required for any dog that has received blood before (commonly if more than about four days have passed since the first transfusion), and for dogs with an unknown history. Cats have the AB system with types A, B and the rare AB. Cats have naturally occurring alloantibodies: type B cats carry strong anti-A antibodies, so a single transfusion of type A blood into a type B cat can cause a fatal acute haemolytic reaction; type A cats carry weaker anti-B antibodies. The same antibodies cause neonatal isoerythrolysis when type A or AB kittens suckle colostrum from a type B queen. Every cat, donor and recipient, must therefore be typed or crossmatched before its first transfusion. Horses have many blood group systems, with the Aa and Qa factors most often implicated in neonatal isoerythrolysis in foals; donor horses are ideally Aa- and Qa-negative geldings that have never been transfused, and a crossmatch is recommended. Cattle have the J antigen and many others; a first transfusion is usually safe without crossmatching.
The volume of whole blood needed can be estimated as body weight (kg) x blood volume (about 90 mL/kg in dogs, about 60 mL/kg in cats) x (desired PCV minus recipient PCV) / donor PCV. For a 20 kg dog with a PCV of 12 percent, a target of 25 percent and a donor PCV of 45 percent, the volume is 20 x 90 x 13 / 45 = 520 mL. A rule of thumb gives similar results: about 2 mL/kg of whole blood, or about 1 mL/kg of packed red cells, raises the recipient's PCV by about 1 percentage point. Blood is collected into an anticoagulant such as citrate-phosphate-dextrose-adenine (CPDA-1) in a ratio of about 1 mL per 7 mL of blood, and is given through a filter (commonly 170 to 260 micrometres) to remove clots. It is started slowly (a commonly cited initial rate is about 0.25 to 0.5 mL/kg/h for the first 15 to 30 minutes) while temperature, heart rate, respiratory rate and demeanour are watched, then increased to complete the unit within about 4 hours to limit bacterial growth. Transfusion reactions are immunological or non-immunological, acute or delayed. Febrile non-haemolytic reactions are among the most common. Acute haemolytic reactions produce fever, tachycardia, haemoglobinaemia, haemoglobinuria and collapse, and require the transfusion to be stopped at once. Non-immunological reactions include transfusion-associated circulatory overload, citrate toxicity causing ionised hypocalcaemia (especially with massive transfusion or liver failure), bacterial contamination and sepsis, and transmission of infection.
Most poisoned animals are treated without a specific antidote, by stabilisation, decontamination and supportive care. The first step is the same as any emergency: the primary survey, with control of seizures, airway and temperature. The history gathers the substance, the product label and concentration, the amount, the time since exposure and the animal's weight, so that a dose in mg/kg can be calculated and compared with published toxic thresholds. Decontamination then prevents further absorption. Emesis is most useful soon after ingestion, typically within one to two hours for most substances, longer for some that form bezoars or delay gastric emptying. Apomorphine is commonly used in dogs, and alpha-2 agonists such as dexmedetomidine or xylazine are more effective in cats. Emesis is contraindicated after ingestion of caustics or hydrocarbons, in an animal that is seizuring, obtunded or has lost its gag reflex, and when the animal has already vomited. Rodents, rabbits, horses and ruminants cannot vomit effectively. Activated charcoal adsorbs many organic toxins and repeated doses interrupt enterohepatic circulation of some drugs, but it binds poorly to alcohols (including ethylene glycol and xylitol), heavy metals, iron, caustics and many salts, and can cause hypernatraemia and aspiration pneumonia. Intravenous lipid emulsion is used for some fat-soluble toxins such as permethrin.
Anticoagulant rodenticides (warfarin and the more potent second-generation compounds such as brodifacoum and bromadiolone) inhibit vitamin K epoxide reductase. Factor VII has the shortest half-life of the vitamin K-dependent factors, so the prothrombin time prolongs first, often within 36 to 72 hours, while bleeding (into the thorax, joints, lungs or body wall) usually appears 3 to 5 days after ingestion. Treatment is oral vitamin K1 for several weeks (commonly about 4 weeks for second-generation compounds), with the prothrombin time rechecked 48 to 72 hours after the last dose, and plasma for active bleeding; vitamin K3 is ineffective. Chocolate contains the methylxanthines theobromine and caffeine; commonly cited thresholds in dogs are mild signs from about 20 mg/kg, cardiotoxic signs from about 40 to 50 mg/kg and seizures from about 60 mg/kg of total methylxanthines. Xylitol stimulates insulin release in dogs: doses above about 0.1 g/kg can cause hypoglycaemia and above about 0.5 g/kg acute hepatic necrosis. Ethylene glycol (antifreeze) is metabolised by alcohol dehydrogenase to glycolic and oxalic acids, causing a high anion gap metabolic acidosis, a raised osmolal gap early, calcium oxalate monohydrate crystalluria and acute kidney injury; the minimum lethal dose of undiluted ethylene glycol is often quoted as about 4.4 to 6.6 mL/kg in dogs and about 1.4 mL/kg in cats. Fomepizole or ethanol blocks alcohol dehydrogenase and works only if given early, within a few hours in cats and within about 8 hours in dogs. Paracetamol (acetaminophen) is highly toxic to cats, which lack efficient glucuronidation, causing methaemoglobinaemia, Heinz body anaemia and facial and paw oedema; there is no safe dose for cats, and N-acetylcysteine is the antidote. Permethrin spot-on products for dogs cause tremors and seizures in cats; treatment is washing, methocarbamol or other muscle relaxants, and supportive care. Organophosphates and carbamates inhibit acetylcholinesterase, causing muscarinic signs (salivation, lacrimation, urination, defecation, bronchorrhoea and miosis), nicotinic signs (muscle fasciculation and weakness) and central signs; atropine controls muscarinic signs, and pralidoxime can reactivate the enzyme after organophosphate exposure only before the bond ages.
In ruminants and horses, poisonings more often affect groups of animals and arise from feed, plants and the environment. Nitrate accumulates in stressed forage crops and is reduced in the rumen to nitrite, which oxidises haemoglobin to methaemoglobin, giving chocolate-brown blood, cyanosis, dyspnoea and sudden death; methylene blue is the specific antidote, but its legal status in food-producing animals varies by country. Cyanogenic glycosides in plants such as sorghum and some grasses release hydrogen cyanide, which blocks cytochrome oxidase so that tissues cannot use oxygen: venous blood is bright cherry red, death is rapid, and sodium nitrite and sodium thiosulfate are the classic antidotes. Urea and other non-protein nitrogen fed in excess, or to unadapted animals, cause ammonia toxicity with tremors, bloat and death; cold water and dilute acetic acid given by stomach tube reduce absorption. Lead is among the most common poisonings of cattle worldwide, from batteries, old paint and ash; signs are blindness, head pressing and convulsions, and calcium disodium edetate with thiamine is used. Snake envenomation is a major emergency in dogs, horses and livestock in South Asia, Africa, Australia and the Americas; management is immobilisation, analgesia, fluids, monitoring for coagulopathy, neurotoxicity and rhabdomyolysis, and species-appropriate antivenom, and tourniquets and incision are not recommended.
Blunt trauma from road traffic accidents is the commonest serious injury in dogs and cats worldwide. Thoracic injury is present in a large proportion of animals hit by vehicles, even without external wounds. Pulmonary contusions (bruised, haemorrhagic lung) are the most common thoracic injury; they cause tachypnoea, hypoxaemia and crackles and often worsen over the first 24 to 48 hours before improving. Pneumothorax causes a rapid, shallow restrictive breathing pattern with quiet dorsal lung sounds. Suspected pneumothorax in a dyspnoeic animal is treated by needle thoracocentesis before radiography, typically in the seventh to ninth intercostal space in the dorsal third of the thorax, entering just cranial to a rib to avoid the intercostal vessels and nerve that run along its caudal border; fluid is sought more ventrally. Repeated rapid re-accumulation, or failure to achieve negative pressure, calls for a chest drain. Flail chest, two or more adjacent ribs each fractured in two places, produces a segment that moves paradoxically inwards on inspiration; the underlying lung contusion usually matters more than the flail itself.
In head trauma the aim is to protect the brain from secondary injury, which follows the primary impact and is driven by hypotension, hypoxaemia, hypercapnia, hyperthermia, hyperglycaemia and raised intracranial pressure. The brain is supported by restoring normal blood pressure and oxygenation first; hypotensive resuscitation is contraindicated. The head is kept elevated at about 15 to 30 degrees on a flat board, pressure on the jugular veins (from collars, jugular sampling or neck bandages) is avoided, and PCO2 is kept normal. Hyperosmolar therapy with mannitol or hypertonic saline reduces intracranial pressure in animals with deteriorating neurological status. Glucocorticoids are not recommended in head trauma: a large human trial found increased mortality. The Cushing reflex, systemic hypertension with reflex bradycardia, indicates dangerously raised intracranial pressure and possible impending brain herniation. In spinal trauma the animal is immobilised on a flat board until radiography or advanced imaging localises the lesion, and a neurological examination is performed carefully. The Schiff-Sherrington posture, extensor rigidity of the thoracic limbs with flaccid pelvic limbs, indicates an acute lesion between the second thoracic and fourth lumbar segments and is not itself a sign of poor prognosis. Absent deep pain perception caudal to a lesion after trauma carries a much poorer prognosis than when it is present.
Haemoabdomen after trauma commonly arises from the spleen, liver or kidneys and is detected by AFAST; most traumatic haemoabdomens are managed medically, with surgery reserved for continuing haemorrhage despite resuscitation. Rupture of the urinary tract, most commonly the bladder in dogs and the urethra in male cats and male ruminants, leads to uroabdomen with azotaemia, hyperkalaemia and dullness, often a day or more after the injury. The diagnosis is confirmed by comparing abdominal fluid with peripheral blood: in dogs, an abdominal fluid-to-serum creatinine ratio greater than about 2:1 and a potassium ratio greater than about 1.4:1 support uroabdomen; ratios for cats differ slightly. Urine is drained and hyperkalaemia treated before anaesthesia for repair. Septic peritonitis is suggested when abdominal fluid glucose is lower than blood glucose by more than about 20 mg/dL (about 1.1 mmol/L) and by intracellular bacteria on cytology; it needs surgery. Wounds are covered at once to prevent hospital contamination, then clipped, lavaged copiously with sterile isotonic fluid at moderate pressure, and debrided; the old teaching of a 6 to 8 hour 'golden period' for primary closure is a guide only, since contamination, tissue damage and blood supply matter more than time. Analgesia with full mu-opioid agonists is given early to every trauma patient; pain relief does not mask important signs and reduces stress-driven catecholamine release.
Respiratory distress is localised at the first examination by the breathing pattern and auscultation, before any radiograph, because handling and restraint can kill a severely dyspnoeic animal, especially a cat. Upper airway obstruction (brachycephalic obstructive airway syndrome, laryngeal paralysis, foreign body, tracheal collapse) produces a slow, noisy, predominantly inspiratory effort with stridor or stertor, and dogs with laryngeal paralysis commonly become hyperthermic. Lower airway disease such as feline asthma produces expiratory effort, sometimes an abdominal push and wheezes. Pulmonary parenchymal disease (cardiogenic or non-cardiogenic oedema, pneumonia, contusions, haemorrhage) produces a rapid rate with increased effort on both phases and crackles. Pleural space disease (effusion, pneumothorax, hernia) produces a rapid, shallow, restrictive pattern with quiet lung sounds, dull ventrally with fluid and dorsally with air. Cardiogenic pulmonary oedema in dogs typically shows a perihilar to caudodorsal distribution, while aspiration pneumonia is typically cranioventral. A cat breathing with its mouth open is in severe distress and needs oxygen before any handling.
Arterial oxygen tension (PaO2) at sea level on room air is normally about 80 to 110 mmHg; below 80 mmHg is hypoxaemia and below 60 mmHg is severe hypoxaemia, corresponding approximately to a pulse oximeter saturation (SpO2) below 95 percent and below 90 percent respectively. Hypoxaemia has five mechanisms: low inspired oxygen (altitude), hypoventilation, ventilation-perfusion mismatch (the commonest clinically), shunt and diffusion impairment. The alveolar-arterial (A-a) gradient separates hypoventilation from lung disease: alveolar oxygen tension is calculated from the alveolar gas equation, PAO2 = FiO2 x (barometric pressure - 47) - PaCO2 / 0.8. At sea level on room air with a PaCO2 of 40 mmHg, PAO2 is about 100 mmHg; a PaO2 of 70 mmHg therefore gives an A-a gradient of about 30 mmHg, well above the normal of about 10 to 15, indicating lung disease rather than pure hypoventilation. The PaO2/FiO2 ratio (normally above about 400 to 500) allows comparison of animals breathing different oxygen concentrations; values below 300 indicate significant impairment of oxygenation and below 200 severe impairment, the thresholds used in veterinary definitions of acute lung injury and acute respiratory distress syndrome. Ventilation is judged by PaCO2 (or end-tidal CO2 in intubated animals); a PaCO2 above about 60 mmHg indicates severe hypoventilation.
Oxygen is given to every animal in respiratory distress or shock while the cause is sought, by the least stressful effective method. Flow-by oxygen from a tube or mask held near the nose is quick and gives a modest increase in inspired oxygen, perhaps to about 25 to 40 percent at flows of a few litres per minute, and is ideal during the first examination. A face mask gives higher concentrations if tolerated. Nasal cannulae or nasal catheters inserted to the level of the medial canthus give about 30 to 50 percent at commonly cited flows of about 50 to 100 mL/kg/min for one catheter; a 20 kg dog at 100 mL/kg/min therefore needs 2 L/min. Oxygen hoods made from an Elizabethan collar and cling film, and oxygen cages, suit cats and small dogs; cages achieve 40 percent or more but need temperature, humidity and CO2 control, and every opening of the door loses oxygen. Prolonged exposure to high inspired oxygen, commonly above about 60 percent for more than 24 to 48 hours, risks oxygen toxicity, so the lowest inspired fraction that achieves an acceptable PaO2 or SpO2 is used. Mechanical ventilation is indicated for severe hypoxaemia despite oxygen supplementation (for example PaO2 below about 60 mmHg or SpO2 below about 90 percent), severe hypoventilation (PaCO2 above about 60 mmHg), or excessive work of breathing likely to lead to exhaustion and respiratory arrest. In horses and foals, intranasal oxygen insufflation through a tube placed in the ventral meatus is standard, and in adult ruminants oxygen is less often used but is practical in neonates.
Colic, meaning abdominal pain, is the commonest equine emergency, and the key decision is whether the horse needs surgery or referral. Indicators that favour a surgical lesion include pain that is severe or persists despite appropriate analgesia, a persistently high heart rate, large volumes of gastric reflux on nasogastric intubation, distended small intestine or displaced large colon on rectal palpation or ultrasound, abnormal peritoneal fluid (serosanguineous with raised protein and lactate) and absent gut sounds. Nasogastric intubation is both diagnostic and life-saving in horses, which cannot vomit and can suffer gastric rupture; net reflux of more than about 2 L is considered significant. Endotoxaemia, from absorption of lipopolysaccharide across damaged bowel, causes injected or toxic mucous membranes, tachycardia, fever and later laminitis. Maintenance fluid in adult horses is about 50 to 60 mL/kg/day, so a 500 kg horse needs roughly 25 to 30 L a day; resuscitation boluses are about 10 to 20 mL/kg, which is 5 to 10 L for the same horse, so large-bore catheters, coil sets and pressure bags are needed. In foals, failure of passive transfer of maternal antibodies is often defined as serum IgG below about 400 mg/dL, with 400 to 800 mg/dL as partial failure.
Neonatal calf diarrhoea is a leading cause of calf death worldwide. Affected calves develop dehydration, a metabolic acidosis often out of proportion to their dehydration (from D-lactate and faecal bicarbonate loss), hyperkalaemia and hypoglycaemia. A calf that is still standing with a good suckle reflex can often be treated with oral electrolyte solutions containing sodium, glucose and an alkalinising agent, while a recumbent calf without a suckle reflex needs intravenous fluids with sodium bicarbonate; the degree of depression and loss of suckle reflex correlate with the base deficit, and a larger distribution factor (about 0.5 to 0.6) is used for bicarbonate calculation in calves than in adults. For a 40 kg calf with a base deficit of 15 mmol/L, 0.6 x 40 x 15 gives about 360 mmol of bicarbonate — confirm against the product label and your national formulary. In adult cattle, small-volume hypertonic saline (7.2 percent, about 4 to 5 mL/kg intravenously over a few minutes) followed by free access to water or an oral drench of water is a practical field resuscitation for dehydrated cows — confirm against the product label and your national formulary; a 500 kg cow receives about 2 L. Periparturient hypocalcaemia (milk fever) presents as weakness, sternal recumbency with an S-bend of the neck, cold extremities and ruminal stasis, and is treated with slow intravenous calcium borogluconate while the heart is auscultated for arrhythmia; hypomagnesaemia (grass tetany) is a more urgent emergency with convulsions. Ruminal tympany (bloat) is either free-gas, relieved by passing a stomach tube and, in an emergency, by trocarisation or rumenotomy on the left flank, or frothy, treated with an antifoaming surfactant or oil given by tube.
Euthanasia (from the Greek for good death) is ending an animal's life with minimal pain, fear and distress, by a method that produces rapid loss of consciousness followed by cardiac or respiratory arrest and loss of brain function. The main reference guidelines are the AVMA Guidelines for the Euthanasia of Animals (2020 edition), which classify methods as acceptable, acceptable with conditions, or unacceptable, and, for slaughter and disease control, the WOAH Terrestrial Animal Health Code chapters on slaughter and on killing of animals for disease control purposes; national law, such as welfare acts and controlled-drug regulations, sets who may perform euthanasia and which drugs may be held. In many countries only a veterinarian may use barbiturates, whereas trained lay people may use approved physical methods on farms. The decision rests on quality of life and prognosis, weighed with the owner, who should be told what to expect (the eyes usually stay open, and agonal breaths or twitching may follow death); tools such as quality-of-life scales help structure the discussion. Informed, recorded consent is obtained from the owner or their authorised agent, except in narrowly defined legal circumstances such as an unowned animal in severe suffering, where national codes permit euthanasia to relieve pain.
The standard method in dogs and cats is an overdose of a barbiturate, most commonly pentobarbital, given intravenously; it causes rapid unconsciousness followed by respiratory and cardiac arrest. Sedation or anaesthesia beforehand reduces fear and struggling and is widely recommended, especially in fractious or distressed animals. An intravenous catheter makes the process smoother. When intravenous access is impossible, intraperitoneal barbiturate is acceptable in small animals such as cats and puppies, though onset is slower. Intracardiac injection is acceptable only in an animal that is already unconscious or anaesthetised, because it is painful and difficult to perform accurately in a conscious animal. Potassium chloride given intravenously stops the heart and is acceptable only in an animal under general anaesthesia. Neuromuscular blocking agents alone, strychnine, air embolism or drowning in a conscious animal, and exsanguination without prior loss of consciousness are unacceptable. Death is confirmed by the absence of heartbeat on auscultation for a sufficient time, absence of respiration, absent corneal reflex, fixed dilated pupils and loss of the eye's lustre; one sign alone is not enough. Barbiturate-containing carcasses are a hazard to scavenging wildlife and pets, which can be fatally poisoned, so they must be disposed of by cremation, deep burial or rendering according to local law.
In farm animals and horses, euthanasia methods must suit the species, the setting and the fate of the carcass. Barbiturate overdose is used in horses, usually after sedation and through an intravenous catheter, and the horse should be in a place where it can fall safely and where the carcass can be removed; the carcass must not enter the food chain or be left for scavengers. Physical methods are acceptable with conditions when performed by trained people with properly maintained equipment. A penetrating captive bolt causes concussion and brain damage; in most species it may not reliably kill on its own, so it is followed by a secondary step such as exsanguination or pithing. Correct placement is essential. For cattle, the commonly taught site is where imaginary lines from the lateral canthus of each eye to the base of the opposite horn (or horn position) cross on the forehead. For horses, it is on the midline where lines from each eye to the base of the opposite ear cross, directed along the line of the neck. For pigs, it is on the midline about 2 cm above the level of the eyes, aimed toward the tail. After any method, death is confirmed and a secondary method applied immediately if there is any sign of returning sensibility, such as rhythmic breathing, a corneal reflex or righting attempts.
In the clinics you will be the person who takes the telephone call, performs the first triage and places the catheter. Learn the primary survey until it is automatic, and practise the calculations until you can do them tired: maintenance by the AAHA formula, a deficit from percentage dehydration, drops per minute, a CRI, a transfusion volume and a toxic dose in mg/kg. Know the RECOVER compression and ventilation rates and the low-dose epinephrine figure, the difference between canine and feline blood groups, and the contraindications to emesis. For euthanasia, know the acceptable methods, the correct landmarks for physical methods in cattle and horses, and how to confirm death, and practise explaining the procedure to an owner.
At five years you run the emergency case load of a first-opinion practice. Your decisions: which calls come in now, how many boluses before you consider vasopressors or referral, whether a hypokalaemic cat's potassium rate is safe, when a dog with a known rodenticide ingestion needs vitamin K rather than just a prothrombin time at 48 hours, and whether the blocked cat's ECG needs calcium gluconate before sedation. You maintain the crash trolley, run CPR drills, keep a donor register and a typing kit, and write a written euthanasia protocol with sedation, consent and carcass disposal that meets your national law. In farm practice you decide on the spot between treatment, salvage and euthanasia for recumbent cows and colicking horses.
With twenty-five years' experience you set the emergency systems for a practice group or a region. You write triage protocols for reception staff, fluid and CRI charts that prevent decimal errors, blood product policies and donor programmes adapted to local pathogens, and standard operating procedures for euthanasia on farms, in shelters and during disease outbreaks, including human safety, biosecurity and carcass disposal. You audit outcomes (CPR survival to discharge, transfusion reactions, unplanned readmissions), mentor younger vets through difficult end-of-life conversations, and manage compassion fatigue in your team. You also judge when referral to a specialist ECC hospital serves the animal and the owner better than continuing locally.
At the research and policy level the open questions are many. Veterinary resuscitation still relies heavily on human and experimental data: the best fluid type and volume in canine sepsis, the place of colloids, the value of lactate-guided resuscitation, blood product storage lesions, the effect of RECOVER-based training on survival, and outcome prediction scores in species and regions where they were never validated. A senior researcher designs multicentre trials, builds registries of arrest and transfusion outcomes, studies toxicology in underserved regions (snake envenomation, pesticide poisoning), and contributes to guidelines on euthanasia and killing for disease control through AVMA, WOAH and national regulators. Reproducible calculation tools and decision support for low-resource practice are also research products with real welfare impact.
This manual does not yet cover: mechanical ventilation settings and modes in detail; extracorporeal therapies (haemodialysis, plasmapheresis); detailed antiarrhythmic protocols; paediatric and exotic-pet (rabbit, reptile, bird) emergency medicine; parenteral nutrition formulation; detailed antidote doses for each toxin (deliberately omitted, because doses and licensed products vary by country — use your national formulary and poison centre); species-by-species euthanasia drug doses (deliberately omitted for the same reason); and country-by-country law on who may perform euthanasia or hold controlled drugs. SIRS criteria, compensation formulae, toxic thresholds and transfusion rates are quoted as commonly taught figures and differ slightly between texts. The RECOVER 2024 update is summarised only where it confirms the 2012 principles; readers should consult the full 2024 documents for revised details.
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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