Initially treating fading puppies and kittens - Veterinary Medicine
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Initially treating fading puppies and kittens
Providing adequate warmth, hydration, and nutrition are the priorities in treating puppies and kittens with this fading syndrome. Additional initial therapy is indicated when the cause of the illness is evident.


Lay sources often advocate administering bovine or caprine colostrum to neonatal kittens and puppies. While this colostrum will not provide any passive antibody protection, it may supply important nutritional components to the enterocytes.13 Further evaluation of such therapy is needed, but it likely does no harm.

At 3 weeks of age in puppies and 4 weeks of age in kittens, offer puppy or kitten food mush four times a day. Most healthy neonates will start to eat within a few days of this age. Mush is made by combining growth formula canned or dry with warm water to make gruel. Some kittens will refuse gruel yet readily eat dry food from an early age.


Type A kittens that nurse from a type B dam are at great risk of death. They may be saved by a transfusion of washed type B red blood cells or by a transfusion from the dam or a cat successfully cross-matched with the dam.2,4 Three days after birth, additional transfusions can be given that consist of washed type A blood, as the kitten will be forming its own antibodies by that time.2 Wash red blood cells three times in 0.9% saline solution to remove all traces of plasma. Avoiding the problem is the best solution by selecting a compatible sire and dam or by removing kittens at birth and before any nursing for the first 24 hours.

Puppies and kittens with hookworm infestation may also require transfusion. Donors should be cross-matched, and a 10 to 20 ml/kg transfusion can be administered intraosseously over a four-hour period.4


Kittens and puppies with pneumonia, either infectious or aspiration, may require oxygen therapy. Indications include cyanosis, tachypnea, dyspnea, and abnormal lung sounds on auscultation.6 The fraction of inspired oxygen should not exceed 40% to 60% to avoid oxygen toxicity, which can cause retinal damage or acute respiratory distress syndrome.14 While oxygen cages, either commercial or home-built, are readily available, the frequency with which ill neonates need to be assessed makes it difficult to sustain useful oxygen concentrations.

Intranasal oxygen is an excellent way to oxygenate ill neonates, and the technique is well-described.15,16 I use a small French feeding tube with multiple holes placed.15 The largest tube size possible should be premeasured to the medial canthus.15 Topical proparacaine may be used on the nasal mucosa.15 Tilt the neonate's head with its muzzle upward, and then insert the tube, directing it ventromedially to the premeasured distance. Attach the tube with suture or tissue adhesive close to the nostril, on the muzzle, and on the forehead. Then attach the tube through an adapter to a humidified oxygen source.15 An Elizabethan collar is recommended in all but the most lethargic of patients. For patients less than 22 lb (10 kg), administering humidified oxygen at a flow rate of 40 ml/min/kg will result in a tracheal oxygen concentration of 40%.16


Particular physiologic differences affect drug use in neonatal patients. Drug absorption can be reduced when drugs are given intramuscularly because of decreased vascular supply and small muscle mass.17 Absorption from subcutaneous injections can also be quite variable in neonates—drugs can either be more rapidly absorbed or less so.18,19 A neonate's temperature can also affect the subcutaneous absorption rate.6,19 Oral absorption can be more rapid because of increased intestinal permeability for the first few weeks of life; however, decreased oral absorption of some drugs is also seen.20 Hypothermic puppies often have delayed intestinal absorption. Intraosseous drug administration is often used, and absorption is rapid by this route.19

The volume of distribution of drugs is also altered in neonates because of a higher percentage of body water compared with adults. Plasma protein is lower in neonates, and this affects drug distribution. In addition, neonatal albumin has a lower affinity to bind many drugs, often resulting in a higher free drug concentration in serum.19 Also, the blood-brain barrier is more permeable for the first several weeks of life.19


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