The cat is not a small dog in critical care! Cats and dogs in crisis share many of the same disease entities, but may not show the same clinical signs. Pancreatitis in the cat may cause anorexia, severe hypotension and hypothermia, without vomiting or obvious abdominal pain typically seen in the dog. Heart disease in the cat may be evidenced by rear limb paralysis rather than fulminate respiratory distress. Cats have diseases and viruses unique to their species such as hyperthyroidism, feline asthma, feline lower urinary tract disease, and feline leukemia virus and immunodeficiency virus related diseases.
There are many aspects of critical care that are unique for the cat. Their physiologic response to shock, the procedures required for resuscitation, and the parameters that require careful monitoring present specific challenges. Knowledge of the traits specific to the cat is mandatory to optimize their ability to recover from critical illness. It is often necessary to resuscitate, support and stabilize the cat for extended periods of time prior to or throughout the course of definitive therapy.
The Shock Triad in Cats
There appears to be a triad of clinical consequences of shock in the cat: hypotension-bradycardia-hypothermia. It becomes apparent that each point of the triangle will cause or contribute to the severity of the other.
The physiologic response to decreased cardiac output in most species is tachycardia due to central sympathetic stimulation mediated by the baroreceptors. In a series of 77 hypotensive cats (blood pressure by Doppler < 80 mmHg systolic) at the Animal Emergency Center, all cats were found to have normal or slow heart rates, even when rectal temperatures were above 100°F (Oncken and Kirby, in preparation). Schwartz, in 1973, reported that when the baroreceptors have detected inadequate arterial stretch in the cat, vagal fibers are stimulated simultaneously with sympathetic fibers. It is possible that this reported mechanism blunts the typical tachycardic response. Since cardiac output is a function of heart rate and contractility, the compensatory response to shock is blunted. Perfusion to the periphery is impaired and contributes to hypothermia. As the core temperature falls, the heart rate will fall.
Heat is lost when there is a transfer of core heat into the skin with subsequent loss into the environment. Mild to moderate secondary hypothermia is often endogenously triggered in severe metabolic disease as a protective mechanism to decrease energy expenditure and oxygen utilization. Short periods of hypothermia may be advantageous in some cases of trauma-induced hemorrhage by protecting the heart and brain against ischemia until blood volume can be restored.
Although hypothermia can have protective effects during low-flow states, it can also have many deleterious effects. As hypothermia progresses below 34°C (94°F), thermoregulation becomes impaired. Animals with this degree of hypothermia will cease to shiver or seek heat. Peripheral vasoconstriction is replaced by vasodilation, and core heat continues to be lost. Heat production decreases, because the rate of chemical heat production in cells is depressed due to the decreased metabolic rate. Severe hypothermia also depresses the central nervous system, causing the hypothalamus to become less responsive to hypothermia. When the core temperature drops below 31°C (88°F), thermoregulation is completely lost. The increase blood viscosity and metabolic acidosis that accompanies hypothermia can also decrease myocardial function.
Two separate studies were performed in dogs and cats evaluating the effects of cooling on adrenergic receptor responsiveness. They both demonstrated that α1-adrenergic responsiveness decreases with cooling. Initially, there is a temperature-dependent increase in α1-receptor binding to norepinephrine. This is followed by a decreased receptor affinity for norepinephrine at lower temperatures, accompanied by a subsequent decrease in contractile response. This may indicate a temperature dependent change in receptor conformation, leading to decreased arterial responsiveness to catecholamines. Therefore, normal thermoregulatory induced vasoconstriction is lost at lower temperatures, and arterial vasodilation occurs. The vasodilation with the bradycardia will result in hypotension. The hypotension will compound the hypothermia and bradycardia.
From these studies it appears that there is both decreased receptor responsiveness as well as decreased catecholamine release responsible for the cardiovascular changes seen with hypothermia. The decreased catecholamine release may occur with more severe temperature decreases, due to a decreased baroreceptor response. This will affect the approach to fluid resuscitation in the cat (also see Shock and Resuscitation Parts I and II).
Chemical restraint and analgesia
Chemical restraint and analgesics should be utilized early in the course of therapy in cats that are fractious, distressed, hyperactive, aggressive, and/or painful. Pain can manifest in the cat by mental depression, tachycardia (rare), restlessness, and/or and irritable attitude.. In the critically ill cat, it is best to titrate analgesics and sedatives to effect, as responses are variable and can be affected by underlying renal and hepatic dysfunction. For mild to moderate restraint and pain control, butorphanol 0.4-0.8mg/kg IV q 2-6 hrs is given initially. For control of severe pain, the combination of injectable opioids oxymorphone (DuPont) 0.05-0.1mg/kg IV or morphine (Steris Labs) 0.1mg/kg IM with diazepam (Steris Labs) 0.2mg/kg IV is effective and reversible. Fentanyl patches (Duragesic, Janssen), 25mcg/hr patch per cat, provide therapeutic blood levels after approximately 12 hours lasting up to 72 hours.
The use of regional anesthesia (nerve blocks or infusion in body cavities), epidural analgesia, and/or pre-emptive analgesia with administration of injectable opioids given prior to surgical intervention are alternative approaches to consider. Lidocaine administered subcutaneously or intravenously can cause methemoglobinemia and Heinz body anemia in the cat and careful dosing is required.
Vascular access
Long term vascular access is best obtained from the medial saphenous vein in the cat. Long, flexible intravenous catheters are threaded anteriorly so that the tip of the catheter is resting in the abdominal vena cava. Central venous pressure (CVP) measured from this location have been found to be an adequate reflection of thoracic CVP measurements. (Machon, 1995) In addition, blood samples can be taken from the catheter, avoiding the stress of restraint for multiple venipuncture.
Fluid balance
Inadequate replacement and maintenance of intravascular and interstitial volume is the number one cause of patient decompensation and death in this author's experience. Animals with systemic inflammatory response syndromes (SIRS) or large third body fluid spaces will have massive loss of fluids from the intravascular compartment into the interstitial and third body fluid spaces.
The blood volume in the cat is 40-55 ml/kg in contrast to 90 ml/kg in the dog. When intravascular volume deficits result in poor perfusion, crystalloids can be administered as fast as 40-55 ml/kg/hr. However, resuscitation with crystalloids alone frequently results in significant pulmonary and pleural fluid accumulation. The resultant hypoxemia contributes to the shock pathophysiology.
Resuscitation from hypovolemic shock is best accomplished with a combination of crystalloids and colloids and rewarming procedures in the cat (see Figure 2 in "Shock and Resuscitation Parts I and II). Since rapid intravenous infusion of hetastarch results in vomiting and hypotension in the cat, hetastarch is administered at 5 ml/kg given over 5-10 minutes. Rapid infusion of stroma free hemoglobin (Oxyglobin®) can result in significant pulmonary edema, requiring its administration at 0.2-1.0 ml/kg over 5 minutes. The blood pressure is checked and once it is above 40 mmHg systolic, then only maintenance crystalloids are given while the cat is aggressively warmed.
Rewarming
Rewarming a hypothermic cat can be accomplished by several different methods: passive surface rewarming, active surface rewarming, and active core rewarming. During external heating, care must always be taken to prevent skin burns by controlling the temperature of the external heating devices or placing a barrier between the heat source and the patient. External heating devices can be constructed out of fabric filled with uncooked dried beans or rice. These packets are then warmed in the microwave. However, the temperature should be tested prior to placing these or any warming device in contact with the animal's hair coat or skin. Smaller animals can be placed inside heated pediatric incubators. A tent can be constructed out of blankets to trap heat and warm air from hot water bottles or warm air blowers near the animal. It is important to remove warm water bottles once they reach body temperature to prevent heat loss to the bottles by conduction.
When using aggressive surface rewarming in hypovolemic animals, the heat source should be applied to the thorax and abdomen, and the extremities should remain cool to prevent peripheral vasodilation. In addition, the warm periphery can decrease neuronal feedback to the thermoregulatory center, therefore decreasing the thermoregulatory response. Efforts to avoid rewarming complications should be made.
Restoring an adequate circulating volume is essential during the rewarming period. The author's recommendations are to only actively rewarm until a rectal temperature of 37°C (98°F) is reached. At these mildly hypothermic temperatures coagulation and cardiovascular functions are restored without overwhelming the circulatory system. This also may help prevent the "afterdrop" phenomenon by reducing the core to periphery temperature gradient. Once intravascular volume is replaced, and the major consequences of hypothermia are reversed, passive surface rewarming should be sufficient to allow slow return of normothermia as the patient's cardiovascular system recovers. It is vital to monitor the patient carefully for hypotension, arrhythmias, acid-base and electrolyte abnormalities, CNS depression, and pulmonary complications during rewarming and in the immediate period following. Any ongoing abnormalities should be treated aggressively.
After re-warming
Once the cat's rectal temperature has risen to 98°F, the blood pressure is rechecked. The hetastarch can then be repeated at 5 ml/kg increments over 15 minutes until the systolic blood pressure > 90 mmHg and the CVP is 6-8 cm of water (with adequate cardiac and renal function). The rectal temperature must be maintained as needed by hot water bottles and warm fluids. If the blood pressure does not remain increased, another 5 ml/kg of hetastarch may be required, followed by a CRI of hetastarch at 0.2-1.0 ml/kg/hr. Both colloids and crystalloids are administered at the minimum amount required to maintain pressure and volume.
The cat must be closely monitored for volume overload. Resuscitating to supranormal values in the cat is almost impossible without causing edema. This situation can be avoided by titrating down the amount of fluid being infused as soon as the rectal temperature, CVP and blood pressure are stable for 1-2 hours with the volume infused. Should volume overload occur, decreasing crystalloid rate of infusion, stopping colloid infusion, and administering furosemide at 2-7 mg/kg IV can help eliminate signs.
Blood pressure
Systolic pressure must be maintained above 90 mmHg, and more importantly, the mean arterial pressure is maintained above 60 mmHg. A comparison of indirect blood pressure measurement techniques in the cat has found the doppler to provide the most accurate information (McLeish, 1977). Poor perfusion that is non-responsive to adequate intravascular volume resuscitation necessitates a search for on-going fluid loss, hypoglycemia, hypoxemia, cardiac dysfunction, prolonged hypothermia and bradycardia, arrhythmias, electrolyte imbalances, cardiac tamponade, brain stem pathology, and hypertension. Persistent hypotension, not attributable to these complications, requires assessment of central volume, oxygen supplementation, pain control, evaluation of cardiac function (echocardiogram) with treatment as indicated. Blindly placing a hypotensive cat on dopamine or dobutamine may be a fatal mistake if the cat has an underlying hypertrophic cardiomyopathy.
When the intravascular volume and cardiac contractility are adequate, and hypotension persists, either stroma free hemoglobin (Oxyglobin®) at 0.2-1.0 ml/kg/hr or dopamine at 5-15 ug/kg/min is infused for their vasopressor effects. The dose of dopamine is initially 5 ug/kg/min and can be increased by 2 ug/kg/min intervals (up to 15 ug/kg/min) until the desired effect is seen. When blood pressures appear to be stable for 2-4 hours, the pressor drugs are gradually weaned to prevent volume overload and ischemic renal damage.
Cats with poor contractility and hypotension may required positive inotropic support. Serial echocardiograms done by the author on cats with persistent hypotension associated with a SIRS disease (e.g., pancreatitis, septic peritonitis) have shown dilation of the left ventricle and decreased contractility during their severe hypotensive stages of the syndrome. Though this improves as the disease resolves, positive inotropic support (dobutamine 1.0-5.0 ug/kg/min) can be required in the interim. A side effect of dobutamine in cats after 24 hours of infusion is seizures. Diazepam can be used to control them until the dobutamine is no longer required. It is ideal to monitor these patients by serial echocardiogram to evaluate contractility before, during and after therapy
Hypertension is suspected when systolic/ diastolic blood pressures are > 160/100 mmHg. (Kobayashi, 1990) Pulse quality is not a reliable indicator. Significant hypertension can lead to poor peripheral perfusion, retinal hemorrhage and detachment, renal damage, and myocardial wall thickening. The underlying cause is treated and a vasodilator chosen based on the cause; chronic renal disease: amlodipine at 0.625mg SID; hyperthyroidism: propranolol at 0.2-1.0mg/kg PO TID or atenolol at 0.2-0.5mg/kg SID; hypertrophic cardiomyopathy: diltiazem at 1-2mg/kg PO TID, or 10mg/kg PO SID of the CD formulation; and enalopril at 1/2 mg/kg sid.
Heart rate, rhythm and contractility
Careful auscultation of the heart is required to detect murmurs and gallop rhythms, suggestive of underlying cardiac disease. Murmurs are usually heard in one location in the cat, just left of the sternum between the 4th and 7th ribs. The gallop or murmur may be intermittent, requiring patience and concentration during auscultation. The author has a "Rule of 4" for cardiomyopathy in the cat. When any 1 of these 4 clinical signs are seen in the cat, cardiomyopathy must be ruled out: 1) murmur or gallop; 2) unexplained hypothermia; 3) unexplained bradycardia; and 4) louder than normal or moist lung sounds. It is not infrequent for a gallop or murmur to become noticeable after fluid resuscitation has occurred. The authors recommend that ketamine not be used in cats with a murmur or gallop since it can increase blood pressure and heart rate, causing decompensation of pre clinical cardiomyopathy.
Arrhythmias in cats most often have a definable and treatable underlying cause, such as hyperkalemia, hypokalemia, hypoxemia, hypercarbia, hypercalcemia, hypocalcemia, acidosis, hypomagnesemia, cardiomyopathy, or endogenous toxins from organ failure such as liver or kidney. It is always best to treat the underlying problem rather than give antiarrhythmics. Oxygen supplementation and antiarrhythmic agents can be required with careful attention given to drug dosage in the cat.
Glucose
The stress response in the cat frequently results in a transient hyperglycemia, requiring recheck to rule out diabetes mellitus. The blood glucose should be maintained between 100-200 mg/dl. Hypotensive cats must be closely monitored for hypoglycemia and glucose replacement can be accomplished by giving 0.25-0.5 gm/kg IV of a 50% glucose solution followed by a 2.5% concentration in the maintenance fluids. Initial volume resuscitation fluids should not contain glucose.
Electrolytes and acid-base balance
Alterations in potassium concentrations are to be expected in critical cats. Though ventroflexion of the neck and generalized weakness can occur with hypokalemia , these signs are rare. This requires that serum potassium levels be monitored and maintenance intravenous fluids supplemented (5-20 mEq/250ml of fluids). Cats with chronic renal disease can have profound potassium wasting, and require oral long term supplementation.
Heart rate is not a reliable predictor of hyperkalemia in the cat. Normal and rapid heart rates have been seen in male cats with urinary outflow obstruction and serum potassium concentrations greater than 10 mEq/L. When a cat has bradycardia (< 120 bpm) due to hyperkalemia, there may be only minutes to respond before circulatory collapse and death. Careful volume resuscitation and the administration of regular insulin (0.2-0.4 units/kg IV followed by 2 gms glucose per gram insulin) or calcium gluconate (0.2-1.5 ml/kg of 10% solution IV slowly) can be life-saving.
Hypophosphatemia can lead to red blood cell hemolysis and energy depletion. It is most commonly seen in the anorexic cat that is beginning to receive nutritional supplementation. Careful monitoring is required and replacement therapy given as required (potassium or sodium phosphate 0.01-0.06 mmol/kg/hr IV).
Oxygenation and ventilation
Cats with significant work of breathing must have their airway and breathing controlled with intubation and positive pressure ventilation on 100% oxygen early in the disease process. Do not wait until they are agonal--early intervention is the key!!! When rapid intubation is required, etomidate can be used at a dosage of 1.5-3.0 mg/kg IV (4-6 ml/5 kg cat when 2 mg/ml solution). Often etomidate is preceded by diazepam at 0.5 mg/kg IV to decrease muscle tone or spasms. Propofol can be used if the cat does not have hypotension at 4-6 mg/kg IV, titrated to effect.
Cats with SIRS commonly develop pulmonary edema and pleural fissure lines. There are no obvious signs until the edema is advanced. Initially, the cat will have an increase in respiratory rate and poor mucous membrane color. Auscultation finds louder than normal lung sounds and occasionally a pleural friction rub. When moist crackles are ausculted, pulmonary edema is severe.
Level of Consciousness and Mentation
A decline in the level of consciousness or mentation of the cat warrants immediate investigation for hypotension and hypoglycemia. Hypoxia, hypocarbia, hypercarbia, hypernatremia, hyponatremia, hyperglycemia, hypoglycemia, hepatic encephalopathy, hyperosmolality, severe fever, severe dehydration, shock, overwhelming sepsis, hypokalemia, hyperkalemia, tachyarrhythmias, bradyarrhythmias, and thiamin deficiency must be considered in the list of etiologies for changing consciousness.
Depressed mentation or level of consciousness requires that precautions be taken to protect the airway from aspiration of gastric or esophageal contents and the cat monitored for vasovagal reflex. The cause is aggressively pursued and therapy instituted to treat the underlying cause. Specific therapeutics may be required to reduce the intracranial pressure while the cause is being determined. The patients osmolality should be monitored, especially if the animal is being given parenteral nutrition. Glucose levels must be maintained, and appropriate nursing procedures employed (turn every 4 hours, lubricate eyes, elevate head, etc.)
Coagulation
Clotting times (ACT, PT, APTT) in the cat are normally shorter than in the dog, requiring their own set of normal coagulation values. Cats can become hypercoagulable with low flow states and SIRS diseases, requiring careful monitoring for declining platelet numbers and declining antithrombin levels. Profound hypothermia, as well as particular drugs, can interfere with platelet function. The most common clinical evidence of excessive bleeding from disseminated intravascular coagulation is failure of clot formation in a clot tube, and occasionally subcutaneous hemorrhage.
Cats with cardiomyopathy are prone to thromboemboli formation in their left atrium or in the peripheral vessels. Evidence of turbulent blood flow in the left atrium or presence of a clot is indication for anticoagulant therapy. Heparin is used initially at (200 IU/kg IV) and warfarin at (0.5mg/cat PO SID). The PT should be prolonged by 1.5 times normal. Thrombolytic therapy has had mixed results.
Red blood cell/hemoglobin concentration
Frequent blood sampling of critical cats can cause anemia severe enough to require blood transfusion by day 3 or 4 of hospitalization. The use of blood tubes and blood culture tubes designed for neonatal humans will minimize the quantities of blood withdrawn. Microhematocrit tubes can be used to harvest small aliquots of serum for in-house biochemical testing.
Cats have 3 major blood types: A, B, and AB. Cats with type B erythrocytes have strong, naturally occurring anti-A antibody. Less than 30% of type-A cats have anti-B antibodies, and type AB cats have no preformed antibodies to blood types. Because of the strong possibility of a significant transfusion reaction in type B cats receiving type A blood, a crossmatch is recommended prior to blood transfusion.
There are inherent differences in feline red blood cells (RBC). They have a life span of 72 days. Rouleaux formation is common and can be confused with red cell agglutination macroscopically. Normal feline RBC have Heinz bodies due to oxidative stress. There are 2 types of reticulocytes: punctate and aggregate. Aggregate reticulocytes mature into punctate reticulocytes with a longer life-span. This makes the corrected reticulocyte percentage a more accurate reflection of bone marrow response than the reticulocyte index in the cat. (Tvedten, 1989)
Macrocytic-normochromic RBCs are most common in FeLV-related myeloproliferative disorders, especially without reticulocytosis. Hemobartonella felis can be evident in cats stressed by illness and cause a hemolytic anemia. A normocytic-normochromic anemia commonly develops in critically ill cats. When a significant anemia is due to chronic renal failure, treatment with human recombinant erythropoietin is indicated.
Renal function
Impaired renal function is managed in the following order: assure intravascular volume is adequate; assure that MAP is greater than 60 mmHg; mannitol at 0.1 g/kg IV if animal is not volume overloaded and renal insufficiency is caught early; and furosemide 1mg/kg/hr for 4 hours. There is evidence that the cat may not have dopaminergic receptors in the afferent and efferent glomerular arterioles like the dog and humans, making the use of dopamine questionable in the cat for glomerular arteriolar dilation.
Geriatric cats have a high incidence of chronic renal insufficiency complicating the presenting disease. The inability to concentrate urine leads to volume depletion and potassium wasting. Hyperphosphatemia can cause hyperparathyroidism and hypocalcemia. Anorexia is significant and chronic anemia common. Renal hypertension can complicate resuscitation procedures.
Immune status, antibiotic dosage and selection, WBC count
The ability of the body to fight infection is assessed through white blood cell count and differential, fever response, and globulin levels. Immunocompromise can be the result of the underlying disease, FeLV or FIV viral infection, or the therapy. Cats that are on immunosuppressive drugs or have neutropenia require isolation and strict aseptic procedures and minimal invasive monitoring and therapeutic techniques.
Viral (feline leukemia virus, feline immunodeficiency virus, feline panleukopenia), protozoal (toxoplasmosis), and overwhelming bacterial (gram positive and negative) infections are common causes of immunosuppression. Feline leukemia virus can cause an immunodeficiency affecting lymphocyte function before myeloproliferative T-cell changes are manifested. (Olsen, 1984) Feline immunodeficiency virus generally requires the presence of intercurrent bacterial or other infectious agents to induce immunosuppressive syndromes. Feline panleukopenia produces an acute cell-mediated immunosuppression resulting in leukopenia. Testing for these viruses should occur when there are opportunistic infections, or persistent or reoccurring diseases in the cat. When these viruses are discovered in the critically ill cat, treatment of the illness can be difficult and prolonged.
Chronic illness associated with fevers and neutropenia may also suggest toxoplasmosis infection. Serum IgM titers may suggest active infection. A response is generally seen with administration of clindamycin HCl (Antirobe, Upjohn) at 25mg/kg PO q 12 hr for 2-3 weeks.
For bacterial infections, antibiotic selection is confirmed by microbiological culture and antibiotic sensitivity results. The capability of the critically ill cat to metabolize and eliminate the antibiotic, as well as potential untoward side-effects of the drug, are considered in the antibiotic selection process, as well. Most gram positive cocci and gram negative rods are susceptible to first generation cephalosporins. Cephazolin (loading dose: 40 mg/kg IV; then, 20 mg/kg IV qid) has few toxic side effects and can be given slowly intravenously. When a more aggressive approach is required, gentamicin (3-5 mg/kg IV sid) is given with the cephalosporin after hydration and renal function are determined adequate. Urine dipstick and sediment are monitored for proteins, glucose and casts daily as early signs of nephrotoxicity. The dose and milliliter amount administered should be double checked at each administration. Suspected anaerobic pathogens are treated with metronidazole (20-30 mg/kg/day divided into 3 doses) by intravenous slow infusion (reduce dose by 50% if cat has liver disease). In seemingly resistant bacterial infections, the considerations of mycobacterium, mycoplasma, and L-form bacteria should be investigated.
Bacterial L-forms and mycoplasma are cell wall-deficient forms of bacteria. Penetrating bite wounds or surgical incisions are common locations of L-form infection, often manifesting with dermal abscesses, cellulitis and polyarthritis. Mycoplasma is commonly associated with the development of secondary respiratory infections. The diagnosis of infections with L-forms and mycoplasma organisms is difficult because of the difficulty of isolating or identifying these bacterial by microbiological culture techniques and light microscopy. The treatment of these infections consists of administration of oral doxycycline (Lyphomed) at 5mg/kg PO q 12 hr until the discharges or respiratory signs have resolved for a week.
Atypical mycobacteriosis can occur and can manifest in the cat as multiple fistulous draining tracts in the skin and subcutaneous tissue following traumatic wounds. Microbiological confirmation is difficult with multiple sample submissions and acid-fast staining are often required to isolate the type. Treatment with high dose quinolones (enrofloxacin [Baytril,] 5mg/kg PO q 12 hr) can be tried for 6 week course.
Geriatric cats require added consideration of concomitant chronic diseases that may contribute to immunosuppression and longer recovery periods in the ICU. Other than chronic infectious diseases, hyperthyroidism, inflammatory bowel disease, renal insufficiency, diabetes mellitus, and dental disease need to be considered.
GI motility and mucosal integrity
Cats that are post-anesthetic, postoperative (especially abdominal surgery--and particularly gastrointestinal), hypokalemic, suffering from gastrointestinal, reticuloendothelial, or neuromuscular diseases, or on narcotic analgesics has a probability of having gastrointestinal paresis. Ileus predisposes the patient to bacterial and endotoxin translocation, poor intestinal nutrient digestion and absorption, gastrointestinal ulceration and vomition. The patient should be ausculted at least three times daily for bowel sounds. Ileus is best treated by nasogastric tube suctioning and relief of fluid and gas accumulation. This reduces vomiting and subsequent aspiration pneumonia. In nonpancreatic patients, metoclopramide (1mg/kg/ day IV by CRI) is utilized to promote gastric and duodenal motility. The dosage of metoclopramide should be reduced by 50% if there is liver disease present in the cat.
Drug dosages and metabolism
Many drug dosages in the cat have been extrapolated from studies done in the dog. Cats have a greater body surface area per unit of body weight when compared to the dog and dosage extrapolation between these species can be inaccurate.
The liver plays a key role in the unique metabolism of many drugs in the cat. Lipid soluble drugs (e.g., morphine, chloramphenicol, aspirin, primidone, acetaminophen, phenols, barbiturates, benzodiazepines, propofol) must be converted to water soluble by-products before excretion. Cats lack many of the hepatic glucuronyl transferases that normally enable conjugation and excretion of these drugs. Toxic levels of these drugs or metabolites can accumulate.
Enterohepatic recycling can also occur in cats and this can affect cumulative plasma concentration of certain drugs such as digoxin. Hepatic acetylation is well developed in the cat, causing faster clearance of drugs such as hydralazine and diltiazem. Procainamide requires acetylation prior to elimination, making its activity more predictable in the cat when compared to the dog.
Many of the published dosage recommendations by manufacturers are based on drug blood levels and clinical signs of toxicity. Unfortunately, there is scant information on the metabolic responses required for drug conversion and elimination by cats. The dosage recommendations for cats in the veterinary medical literature are often based on clinical experience and anecdotal information. When administering any drug to the cat, the proper dosage, route of administration, and dosing interval should be confirmed. In addition, based on the route of elimination, dosage and dosing intervals must be altered in cats with renal or hepatic disease.
Nutrition
Being carnivores by nature, cats require no carbohydrates but need high levels of meat-based protein. The cat's protein requirement is 50% higher for growth and over 100% for maintenance as compared to the dog. This is due to the presence of comparatively persistent, increased activity of hepatic proteolytic enzymes (transaminases and deaminases). (Rogers, 1977)
Cats require dietary sources of arginine. Arginine is required for normal protein synthesis and ammonia detoxification. Domestic cats lack intestinal pyrroline-5-carboxylate synthase, which is required for the production of an arginine precursor, ornithine. A urea cycle intermediate, arginine converts ammonia to urea. Cats can develop severe hyperammonemia from anorexia or ingestion of an arginine free meal (Morris, 1978). Arginine has other important roles that include: increasing endocrine secretagogue activity, improving nitrogen retention, acting as a substrate for nitric oxide production, reducing nitrogen loss in post-operative patients, enhancing collagen deposition in wounds, enhancing T-cell function, and the growth of lymphocytes. (Babul, 1994)
Cats also require a dietary source of taurine. Cats cannot synthesize enough from dietary precursors to meet obligate intestinal loss. The cat uses only taurine for bile salt synthesis (in comparison to dogs that can substitute glycine), causing an ongoing obligate loss of taurine with excreted bile salts. Taurine deficiency has been proven to cause dilated cardiomyopathy and retinal degeneration.
Cats do not have the ability to convert beta-carotene to active vitamin A (retinol). Cats lack dioxygenase enzymes in the intestinal mucosa that splits the beta-carotene molecule to vitamin A aldehyde (retinal). Preformed vitamin A must be ingested or administered as neither dietary nor intravenous betacarotene can prevent the development of vitamin A deficiency and its consequences of blindness. Since the cat cannot convert tryptophan to niacin, the niacin requirement in the cat is about four times that of the dog. Animal tissue is high in niacin and this requirement is normally met by ingestion of a high meat diet.
Arachidonic acid is needed in the feline diet, since cats cannot synthesize it from linoleic acid in comparison to the dog. Arachidonic acid is an essential fatty acid required for maintenance of cell wall integrity and can be found in diets containing animal source fats. Essential fatty acids should constitute 1% of the diet dry matter. Fatty acid deficiency results in poor hair coat quality and poor tissue integrity.
The nutritional requirements of the critically ill cat should be addressed early to minimize tissue catabolism and development of hepatic lipidosis. Meat-based diets should be selected that provide a good quality protein, vitamin A, thiamin and niacin. The diet should be adequately supplemented with taurine and arginine. When the food is warmed prior to feeding or highly aromatic foods are fed, the palatability of the food offered to stressed and ill cats is often increased.
Nursing care
The cat must be removed from the cage and thoroughly examined at least twice daily. Changes in their physical condition, even pulmonary function, may be very subtle and occur rapidly. Catheter sites must be checked daily, and each catheter labeled appropriately to avoid confusion of lines and misuse of the tubes. The paw distal to the peripheral catheter must be checked multiple times during the day for evidence of paw edema, requiring re-bandaging of the catheter. Elizabethan collars are often necessary for catheter security as well as an aid in handling aggressive cats.
Tender Loving Care
The mental health of the cat is often as important than the physical health. It must be remembered that these cats are pampered pets. Visits by the owners are to be encouraged when it benefits the pet and having familiar items in their cage will make the owner feel better, if not the cat. It is important for house cats to have fresh litter and a place for their food away from their litter box. Blankets or bedding makes them more comfortable. Providing a box for the cat to hide in or using other techniques of obstructing their view of strange animals, when their condition allows, reduces their level of fear and stress. Their biorhythms become disturbed when the ICU lights are on 24 hours per day. When possible, it is good to turn down the lights to stimulate night and promote sleep.
References
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2. Kohn CW, DiBartola SP: Composition and distribution of body fluids in dogs and cats, In: DiBartola SP, ed: Fluid Therapy In Small Animal Practice. Philadelphia: WB Saunders, 1989, p 1.
3. Chew D: Disorders of calcium and magnesium. In Rush JE, ed: IVECCS Proceedings 1994, p.175.
4. McLeish I: Doppler ultrasonic arterial pressure measurement in the cat. Vet Rec 100:290, 1977.
5. Kobayshi DL, Peterson ME, Graves TK, et al: Hypertension in cats with chronic renal failure or hyperthyroidism. J Vet Intern Med 4:58, 1990.
6. Tvedten H: Erythrocyte disorders. In Willard MD, Tvedten H, Turnwald GH, eds: Small Animal Clinical Diagnosis By Laboratory Methods. Philadelphia: WB Saunders, 1989, p36.
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8. Rogers QR, Morris JR, Freedland RA: Lack of hepatic enzymatic adaption at low and high levels of dietary protein in the adult cat, Enzyme 22: 348,1977.
9. Morris JG, Rogers QR: Ammonia intoxication in the near adult cat as a result of dietary deficiency of arginine. Science 199: 431, 1978.
10. Babul A, Hurson M: Arginine. In Gay S, ed: Nutrition in Critical Care. Missouri, Mosby Year Book Inc., 1994 p.107.