Young kittens are challenging to manage due to their small size, unfamiliar physiology, and their tendency to deteriorate quickly. Sick kittens should be evaluated as soon as possible with a systematic approach, including a complete history (including the queen and litter mates, if available), a thorough physical examination, and diagnostic tests. Interpretation of the physical examination and clinical signs requires knowledge of what is normal in this age group.

While the neonatal period is usually considered to be the first 4 weeks of life, it is useful to consider specific risk periods for young kittens:

This chapter is focused on the management of kittens from birth to about 12 weeks of age. Additional resources are found in e-Box 46.1.

One of the first challenges facing the clinician examining the neonatal kitten is determining the age and sex. Unless the kitten comes from a breeding program, the exact birth date is often unknown. Several developmental milestones and physical characteristics can be used to estimate the age of kittens (Box 46.1). A common guideline, especially in shelters, is 0.45 kg (1 pound) per month of age. This guideline was evaluated in a study of 246 healthy research colony kittens up to 8 weeks of age and 1310 healthy privately owned kittens from 6 to 20 weeks of age.¹ The study concluded that body weight was an effective means of predicting age to within 1 week of true age in most kittens up to 10 weeks of age although this weight/age guideline tended to underestimate the age of male kittens. The kitten’s body condition should be considered as over- or under-conditioning will influence body weight.

Weighing young kittens accurately requires the use of a scale (such as a food scale) that measures in grams or ounces (Fig. 46.1). The typical kitten birth weight is 90 to 110 g (range, 80 to 140 g), although there is considerable variation by breed (Table 46.1) and by sex (males typically weigh more than females).^2–5 Low birth weight is associated with an increased risk of mortality in humans, pigs, cows, and dogs.⁶ It seems likely this is true in cats as well, with kittens weighing less than 75 g at birth at highest risk. This is likely because these kittens have low energy reserves and are even more dependent on milk intake than their normal litter mates. Slight weight loss (<10%) can occur in the first 24 hours of life, but the kitten should then gain weight daily. Normal kittens gain 50 to 100 g per week (10 to 15 g/day) and should double their birth weight by 2 weeks of age. Breeders and other caretakers of newborn kittens should be instructed to weigh kittens twice daily for the first 2 weeks of life, and daily for at least the next 2 to 4 weeks. Steady weight gain is the single best indicator of good neonatal kitten health. Early detection of low-birth-weight kittens and kittens that fail to gain weight normally allows for increased monitoring efforts and earlier intervention.

Kittens should be examined for gross anatomic abnormalities, such as cleft palate or lip; umbilical hernia or infection (omphalophlebitis); open fontanelles; limb, spine, and chest wall deformities; and nonpatent urogenital or rectal openings. The normal umbilical cord is dry, with no redness, swelling, or discharge at the umbilicus (Fig. 46.2). Umbilical cords fall off at 3 or 4 days of age.

The eyes should be inspected for abnormalities of the globe or eyelids and for neonatal conjunctivitis (ophthalmia neonatorum). The eyelids typically open at about 10 days of age (Fig. 46.3), but occasionally kittens are born with eyes already open, or the eyes open in the first day or two of life. Because tear production is not normal at birth, a topical lubricating ophthalmic ointment should be applied for about the first week of life to prevent corneal damage when the eyelids open early. The menace reflex and pupillary light responses may not appear until 28 days of age or later. A divergent strabismus may be present and may be normal until about 8 weeks of age. Evaluation of the fundus is difficult until after 6 weeks of age.

Kittens have lower blood pressure than adults, as well as greater cardiac output, and a faster heart rate in the first 2 weeks of life. Functional murmurs may be present in neonates because of anemia, hypoproteinemia, fever, or sepsis. Innocent murmurs not associated with disease are more common in puppies than kittens; murmurs present after 4 months of age should be investigated. Congenital heart disease usually produces murmurs that are loud and accompanied by a precordial thrill. The normal neonatal heart rate can be >200 beats per minute in the first 2 weeks of life (range, 220 to 260). By 4 weeks of age, vagal tone has been established, and the heart rate decreases to the normal adult range. The normal respiratory rate is 15 to 35 breaths per minute. See Box 46.2 for normal physiologic values for neonatal kittens.

High-risk time points for kitten morbidity and mortality are at birth, in the first 2 weeks of life, and around the time of weaning. There is no specific disease entity attributable to “fading kitten syndrome,” but a variety of causes have been identified. The most common causes of morbidity and mortality in kittens include:

In free-roaming populations, kitten mortality may be as high as 75%, with trauma and infectious disease accounting for most deaths.7 The lowest mortality rates (<5%) are found in well-managed, specific–pathogen-free colonies, and most pedigreed breeding catteries fall somewhere in between these two extremes. Several studies have examined kitten morbidity and mortality in pedigreed breeding catteries in different countries (Table 46.2). The published data show variability not only among breeds but also among populations of the same breed, partly due to geographic differences and the research methods used.

Data from such studies are especially useful to help breeders evaluate their breeding programs and identify areas of poor performance. Breeders experiencing greater than expected losses should investigate the causes. However, caution must be exercised because even though breeds may have the same name and similar phenotype in different countries, the genetic constitution may be quite different. A good example is the Burmese breed. The definition of this breed varies by country and registering organization, leading to genetically distinct populations with different disease risks.

A home visit can gather valuable information when working with breeders. However, if a home visit is not possible, the breeder can supply a floor plan and photos or video to help identify management issues. Unfortunately, little information exists on the optimum design of breeding catteries. Recommendations are often adapted from those designed for laboratory animals or boarding facilities ( e-Box 46.2).

Animal shelters represent a unique challenge for the health of young kittens. Providing pre-adoption health care in the shelter exposes kittens to an increased risk of infectious disease. Although kitten mortality data from shelters is limited, one study in the United Kingdom found that shelter kittens <7 weeks of age were four times more likely to die than cats between 1 and 3 years of age.⁸ A retrospective study in the United Kingdom that analyzed histopathology reports found panleukopenia was an important cause of death with a higher prevalence in kittens from shelters than from pet homes.⁹ A study in a large municipal shelter in the United States found that 11% of 172 orphaned kittens with diarrhea died or were euthanized.¹⁰ Kittens ≥4 weeks of age were 25 times more likely to survive than younger kittens. Finally, a study of 1353 shelter kittens <8 weeks of age cared for in a dedicated nursery found risk factors for dying included panleukopenia infection, weight loss, upper respiratory tract disease, anorexia, low body condition score at intake, low body weight at intake (65 to 258 grams), and diarrhea.¹¹

Congenital defects are abnormalities of structure, function, or metabolism that are present at birth. A congenital defect may cause physical impairment, or it may cause the death of the kitten before or after birth. Congenital defects in stillborn kittens often go unrecognized because few stillborn kittens are submitted for necropsy. Many congenital defects are cosmetic or minor, but others may cause serious impairment of health (Box 46.3). Congenital defects may be of various types:

Congenital defects may be heritable, and the inheritance pattern or mutation(s) responsible may or may not be known (see Chapter 52: Genetics of Feline Diseases and Traits). A few congenital defects are due to chromosomal abnormalities (e.g., pseudohermaphroditism). Many congenital defects are not heritable but are caused by other factors (Box 46.4). In some cases, defects may be caused by interplay of environmental and genetic factors. When cat breeders encounter a congenital defect where no information is available on heritability, several factors can be considered. A defect is more likely to be heritable if there is evidence of a breed or familial predisposition and the problem has a consistent age of onset and clinical course. A defect is less likely to be heritable if more than one abnormality occurs in a kitten or a litter or if there has been potential exposure to teratogens.

As in other species, congenital defects are a significant contributor to neonatal mortality in the cat although prevalence data is hard to come by. In an analysis of data from 14 breeds in the United Kingdom, 15% of litters included one or more kittens with congenital defects, ranging from 6% of Devon Rex litters to 31% of Tonkinese litters.² Excellent reviews of congenital defects in cats have been published in the last 20 years, including neurologic,¹² ocular,^13,14 renal,¹⁵ cardiac,^16–18 and vertebral column defects.¹⁹ Few studies were done with large numbers of cats. An exception is a retrospective review of medical records from over 57,000 cats for congenital heart disease.¹⁸ The prevalence of congenital heart disease was 0.14%, similar to that in dogs (0.13%). The prevalence of innocent murmurs (including dynamic left or right ventricular outflow obstruction) was 0.2%, compared with 0.1% in dogs. Ventricular septal defects were the most common, followed by aortic stenosis and hypertrophic obstructive cardiomyopathy. There was no sex predilection. Other common congenital defects in cats include thoracic wall deformities (e.g., pectus excavatum [PE], flat chest defect), cleft palate, and umbilical hernia. A few of the poorly documented defects are worth describing in more detail.

Flat chest defect is one of the common thoracic wall deformities in kittens that are not well described in the literature. Although the defect may be seen in any kitten, it is most common in the Oriental, Burmese, and Bengal breeds. The defect is characterized by a dorsoventral flattening of the rib cage and sharp angulation at the costochondral junction (Fig. 46.6). Curvature of the cranial thoracic spine may also be present. The defect is not present at birth, but the mean age when it was detected was 9.5 days in one study.²⁰ The defect has a variable presentation and is even transient in some cases. Mildly affected individuals may be difficult to detect. Moderate to severely affected kittens show poor weight gain, increased respiratory rate and effort, exercise intolerance. Severely affected kittens may die. In one study of Burmese kittens in the United Kingdom, 8.7% of the kittens with flat chest defect also had PE, suggesting an association.²⁰ Although similar thoracic wall deformities have been reported in taurine-deficient kittens, affected Burmese kittens in that study had higher whole blood taurine levels than unaffected kittens. No investigation into the best treatment for kittens with life-threatening chest wall deformity has been published, but breeders and owners often apply temporary splints made of cardboard or plastic to shape the compliant thoracic wall and sternum into a more normal confirmation until the ribs and sternum mature (Fig. 46.7).

Pectus excavatum (sometimes called funnel chest) is characterized by dorsal deviation of the caudal part of the sternum (Fig. 46.8). The deviation may be midline or lateralized. The sternal abnormality is often noticed early in life, and the defect is usually progressive. The etiology in kittens and puppies is poorly understood. No sex predisposition has been identified and breed predispositions have not been well-investigated. In a study of thoracic wall deformities, PE was detected in 5 of 244 Bengal cats, leading the authors to suggest a breed predisposition.²¹ There may also be a breed predisposition in Burmese cats, where PE is often seen with the flat chest defect.²⁰ The disease may be classified as mild, moderate, or severe based on measurements from orthogonal radiographic views to calculate the vertebral and frontosagittal indices (Table 46.3).^22,23 However, one study suggested that while these indices are useful for determining an anatomic disease category, they are not useful for determining if cats with moderate to severe defects are likely to have severe clinical signs.²³ Mildly affected kittens may have no clinical signs and do not require intervention. Severely affected kittens may be dyspneic, exercise intolerant, and fail to thrive. Midline sternal deviations may impair diastolic filling and contribute to exercise intolerance.²³ Several surgical approaches, such as wedge ostectomy,²⁴ trans-sternebral pinning,²⁵ and sternal wedge chondrectomy with internal splinting²⁶ have been described, but the most common surgical procedure is placement of percutaneous circumsternal sutures with external splinting (Fig. 46.9).^22,23,27 This technique works well in kittens <4 months of age with a non-ossified sternum because the goal is to pull the sternum outward and maintain this position while the sternum matures. Potential complications of the technique include inadvertent lung puncture or laceration and development of pneumothorax, inadvertent heart puncture, re-expansion pulmonary edema,²⁴ dermatitis under the splint, sinus tracts around the sutures, and recurrence of the defect. The external splint or brace is created from moldable, radiolucent splinting material (e.g., isoprene) that can be softened with hot water or hot air for molding to the desired shape. In this case, it should be molded into a U-shape to fit the ventral thorax and should extend most of the way up the sides of the thorax. Holes are needed on the ventral surface of the splint for sutures. Cotton batting or another soft material can be used under the splint to prevent pressure sores. Under anesthesia, a series of percutaneous sutures are placed around the sternum and through the holes in the splint. The sutures are tightened so the sternum is pulled outward. The sutures can be tied in a bow in case there is a need to loosen or re-tighten them. At the completion of the procedure, a lateral thoracic radiograph should be taken to verify suture placement and assess the degree of improvement in the position of the sternum. The owner should be advised to limit the patient’s activity and keep it isolated from other pets. The patient should be re-evaluated weekly to ensure the split has not loosened and there is no evidence of infection. If the sutures must be tightened or loosened to elevate the split to examine the skin underneath, sedation and analgesia must be provided. Radiographs should be taken at least once before the splint is removed to ensure the defect has been satisfactorily reduced. Typically, the splint stays in place for up to 8 weeks.

Tarsal hyperextension (also known as “twisted legs,” limb contracture, tendon contracture) is a poorly described congenital defect in kittens.^28,29 The defect is obvious at birth and often affects only one kitten in a litter. There is no breed or sex predisposition. The abnormality is characterized by severe tarsal hyperextension and metatarsal rotation (Fig. 46.10). Typically, both hind limbs are affected, but the condition can also be unilateral. No bone abnormalities or neurologic deficits are present. The etiology is unknown, but the defect has similarities with clubfoot in human infants. In the author’s experience, the deformity completely resolves on its own in most cases as the kitten begins to crawl and bear weight on the affected limbs. Initially, kittens may bear weight on the cranial aspect of the tarsus. In some cases, delayed resolution has prompted the use of either soft molded splints or fiberglass casts for external coaptation. If external coaptation is required, it should be instituted earlier rather than later to take advantage of joint flexibility in young kittens. Splints and casts must be changed weekly as the kitten grows and may be required for 6 weeks or longer. Physical therapy to gently manipulate the tarsal joint into normal configuration may also be helpful. Other musculoskeletal defects may accompany or be caused by the tarsal hyperextension. A case report of a kitten successfully treated for bilateral hind limb tarsal hyperextension with splinting described the development of bilateral, medially luxating patellas at 4 months of age that required surgical correction.²⁹

Blood chemistry and hematology values for neonates differ from the adult; most values normalize to adult rangs by 3 to 4 months of age (Tables 46.4 and 46.5). For several analytes, reference ranges change rapidly within the first days and weeks of life so that using age-appropriate reference ranges is important. In one study of kittens up to 8 weeks of age, reference ranges for alkaline phosphatase (ALP), creatine kinase, triglycerides, calcium, and phosphorus were higher than for adults.³⁰ Reference ranges for aspartate aminotransferase (AST), bilirubin, urea nitrogen, and creatinine were higher in newborns, but similar to or lower than adults by 8 weeks of age. Reference ranges for albumin and total protein were lower than for adults for the entire 8 weeks, and values for calcium and phosphorus were higher.

Venipuncture can be challenging in the smallest kittens. In one method, the holder positions the kitten in dorsal recumbency with the forelegs drawn toward the abdomen and the head and neck extended. Blood is drawn from the jugular vein using a 1-mL or smaller syringe with a 25- or 26-gauge needle. A butterfly catheter can also be used. Slow aspiration of blood is essential to avoid collapsing the vein. A small volume (0.5 mL) of blood can be used for the most critical tests (Box 46.5). Use of 0.5-mL microsample blood collection tubes is recommended and has been validated for evaluation of biochemistry and hematology samples.^31,32 Repeated sampling should be done cautiously, because the circulating blood volume of kittens is only about 70 to 95 mL/kg.

In kittens up to 3 to 4 weeks of age, urine should be collected by stimulating the perineum to start micturition. In this age group, cystocentesis should be avoided because the bladder wall is easily lacerated. Urine specific gravity is 1.020 or less in the first few weeks of life; adult values are reached by about 8 weeks of age as the kidneys mature.33 A fecal sample should be examined for common intestinal parasites, such as Giardia spp., Isospora spp., and roundworms, using zinc sulfate centrifugation and a direct saline smear.

Radiography is a useful diagnostic tool but may be difficult to perform because of the small size and often uncooperative nature of kittens. Sedation may be required to obtain good quality images; a pre-anesthetic sedation protocol for pediatric neutering would be an appropriate choice. It may be difficult to interpret radiographic images of kittens because contrast is poor from lack of body fat and mineralization of the skeleton is incomplete. Quality thoracic images may be difficult to obtain because of a high respiratory rate and chest wall motion. Thoracic radiographs of kittens may show a generalized increase in pulmonary interstitial opacity because of the increased water content of the lung parenchyma. The thymus may appear as a sail sign in the cranial left hemithorax, and the cranial mediastinum will appear wider than in the adult.

Assessment of cardiac size on radiographs may be difficult as the heart appears proportionately larger in the thoracic cavity because of decreased alveolar volume. However, reference intervals for assessing cardiac size using vertebral heart score (VHS) and cardiac–­thoracic ratio have been established for kittens from 6 to 16 weeks of age (Table 46.6).³⁴ The normal median VHS for kittens (9.5) is larger than that reported for adult cats (7.9).³⁵ The same study found that plasma NT-proBNP concentrations in normal kittens are similar to those in normal adult cats. In addition, the study found that right-sided echocardiographic heart measurements (right atrial diameter, right ventricular internal dimension in diastole) are similar to adult cats while the left atrial diameter in the long axis view was smaller in kittens than in adult cats.

Interpretation of skeletal radiographs presents difficulties because of decreased mineralization, open physes, and secondary centers of ossification. Trauma and infection are the most common lesions and are often associated with soft tissue swelling. It can be helpful to radiograph the unaffected limb at the same time for comparison to aid in interpretation.

The usefulness of abdominal radiography in kittens is hampered by poor abdominal detail because of lack of intra-abdominal fat, a small amount of normal peritoneal fluid, and a higher proportion of total body water. The liver appears comparatively larger than in the adult. The most common radiographic diagnoses are radiopaque foreign bodies and intestinal obstruction.

Ultrasonography is an effective modality for pediatric patients, especially for imaging the abdomen. Machines with a curvilinear variable frequency scan head (6.0 to 8.0 MHz) have been recommended. Sedation is rarely required for the procedure, and the kitten is best ­positioned in dorsal recumbency in a padded trough. Techniques for examining the abdomen and the normal appearance of structures have been described.³⁶ Common indications for abdominal ultrasonography include suspected GI foreign body, intussusception, congenital hernia, congenital renal disease, and urolithiasis, among others.

Normal electrocardiographic values for kittens in the first 30 days of life have been described.³⁷ Changes from normal adult findings are present during the first month of life, such as shift of the electrical axis from right to left, a progressive increase in R wave amplitude, and a progressive decrease in S wave amplitude. Measurements for P wave, PR interval, duration of QRS complex, and the duration of the QT interval are similar to adult cats. Neonatal kittens should have a sinus heart rhythm.

Necropsy is underutilized as a diagnostic tool for multicat environments such as shelters or breeding catteries because it is not uncommon for kittens to die or be euthanized before a definitive diagnosis can be established. Necropsy results may provide information necessary to save remaining littermates, a future litter, or other kittens in the environment, especially in the case of infectious diseases. For the best results, the whole body should be submitted (refrigerated, not frozen) to a qualified pathologist. If refrigeration is not possible, freezing is preferable to allowing autolysis to occur because some information may still be obtained.