Flat-chested kitten syndrome (FCKS) is a disorder in cats wherein kittens develop a compression of the thorax (chest/ribcage) caused by lung collapse. This is a soft-tissue problem and is not caused by vertebral or bony malformation. However, lung collapse can be a secondary symptom caused by bony deformity affecting the thorax such as pectus excavatum. In mild cases, the underside of the chest becomes flattened (hence the name of the condition); in extreme cases the entire thorax is flattened, looking as if the kitten has been stepped on. The kitten will appear to go from normal to flat in the space of about two to three hours, and will usually then stabilise. FCKS is frequently misdiagnosed as pectus excavatum due to inadequate veterinary literature or lack of experience with the condition on the part of the clinician.
FCKS is most frequently caused by collapsed lungs (and not as formerly believed, by a muscle spasm in the intercostal muscles). There are numerous causes for lung collapse, and therefore numerous causes for FCKS. One possible cause for flat chestedness that develops soon after birth is atelectasis.
Causes of atelectasis include insufficient attempts at respiration by the newborn, bronchial obstruction, or absence of surfactant (a substance secreted by alveoli that coats the lungs and prevents the surfaces from sticking together). Lack of surfactant reduces the surface area available for effective gas exchange causing lung collapse if severe. There can be many reasons for atelectasis in kittens, but probably the most common cause is prematurity. Newborn atelectasis would not be unusual in a very large litter of kittens (such as 10), where the size of the litter may lead all the kittens to be small and mildly underdeveloped.
Unlike human babies, kittens are born very immature: blind, deaf, the intestinal tract not fully developed etc., so even slight prematurity may tip them over the edge from being viable to non viable. Many FCKS kittens may have fallen just the wrong side of this boundary in their development at the time of birth. Further, if a kitten does not scream or open its lungs well enough at birth, even if it is fully mature and has sufficient surfactant, it may end up with atelectasis. Patches of atelectasis in the lungs mean that part of a lung is not operating properly. If the kitten goes to sleep and its respiratory rate drops, the patches of atelectasis can slowly expand until large areas of the lung collapse and cannot be reinflated. Good advice to any breeder therefore would be to ensure that kittens cry loudly when they are born, to make sure that the airways are clear, but also that the lungs expand as fully as possible. (This was the reason newborn babies were always held upside down immediately after birth (so that any residual fluid drains downwards) and smacked to make them cry strongly.)
Some kittens suffer from congenital 'secondary' atelectasis, which presents shortly after birth. There have been no reports of kittens born flat (primary atelectasis). Hyaline membrane disease is a type of respiratory distress syndrome of the newborn in which there is formation of a hyaline-like membrane lining the terminal respiratory passages, and this may also be a (rarer) cause of FCKS. Pressure from outside the lung from fluid or air can cause atelectasis as well as obstruction of lung air passages by mucus resulting from various infections and lung diseases – which may explain the development of FCKS in older kittens (e.g. 10 days old) who are not strong enough to breathe through even a light mucus, or who may have inhaled milk during suckling.
Tumors and inhaled objects (possible if bedding contains loose fluff) can also cause obstruction or irritation of the airway, leading to lung collapse and secondary atelectasis. In an older cat the intercostal muscles are so well developed, and the ribs rigid enough that the ribcage will not flatten if the lung collapses: in kittens the bones are much more flexible, and the tendons and muscles more flaccid, allowing movement of the thorax into abnormal positions.
Other causes of lung collapse can include diaphragmatic hernia, or diaphragmatic spasm (breeders report the position of the gut and thorax as appearing to be like a 'stalled hiccup'). Diaphragmatic spasm is easily checked by pinching the phrenic nerve in the neck between the fingertips. Kittens with this type of FCKS will improve almost immediately, but may require repeated pinching to prevent the spasm from recurring.
Evidential basis and statistical analysis
Almost all reporting of FCKS is treated as anecdotal, since it comes from breeders and not from veterinary practitioners. However, in the absence of robust clinical studies breeder-reporting is the only source of information currently available. Reporting about type of FCKS is hampered by the lack of differentiation between one type and another by both breeders and vets. The data informing this article came from three sources: Analysis of emails reporting cases of FCKS sent to the owner of a website giving information about the condition and methods of treatment, 1999-2019 [87 of these kittens were examined in person by the author] Data gathered by the THINK project 2005-2015 who published an online questionnaire (the project is now defunct) Directly solicited reports requested from 27 individual breeders of Abyssinian (4 responded) and 35 breeders of British Shorthair (2 responded) in the UK The 20-year analysis was compared with the Governing Council of the Cat Fancy in the UK (GCCF) analysis of numbers of kittens registered during the same period. The full report is to be published during 2020.Reference will be provided when publication information is available.
Only direct reports from owners (362) about their own cats or vets examining kittens (2) were considered. Kittens exhibiting any other condition (including pectus excavatum) were excluded. The overwhelming majority of reports (76%) were of single FCKS cases in a litter, with the remainder whole or part litters. The data comprised 311 reports of litters of kittens in which one or more developed FCKS, for a total of 464 affected kittens (see table).
Reports in which the sex was specified showed breakdown by sex of male 56%/female 44%. 16 breeders reported that whereas they might have expected the smallest kitten in a litter (if any) to develop FCKS, it was the largest and strongest kittens that developed flat chests, and these were often males. The condition does not appear to be sex-linked, but the preponderance of male kittens in this reporting group may be due to the fact that males tend to be larger than females and these are the kittens getting most milk or suckling hardest because they are stronger, in which case the type of FCKS in these litters may have been due to colic caused by overfeeding (see Causes, below).
Reports originated from 21 countries (Australia (15), Austria (11), Belgium (2), Canada (8), Denmark (3), Finland (2), France (24), Germany (13), Hungary (1), Japan (2), Netherlands (14), New Zealand (6), Norway (5), Portugal (1), Singapore (1), Slovakia (1), South Africa (5), Sweden (11), Switzerland (1), UK (100), USA (85)) and covered 39 breeds (including non-pedigree domestic shorthair, non-pedigree domestic longhair, and some ‘unrecognised’ crosses between two pedigree breeds or pedigree breeds x DSH). 10 reports did not specify breed.
High numbers of reports in certain breeds has in the past been taken to imply that some breeds are more prone to the condition than others, but the data is skewed by various factors: a) the numbers of kittens bred; b) cluster-reporting in response to articles in breed club circulars or c) the work of a particular group of breeders (cf Burmese) in attempting to address a problem that they had seen in their own lines d) the culture within an individual breed of information-sharing or reporting problems. Breeders are generally not inclined to discuss health issues because of a culture of blame and gossip, having a dramatic effect on information-sharing. No ‘cluster’ triggers have been identified for the relatively high number of reports in the Maine Coon or Bengal breeds, while the Burmese cat club commissioned a study into the condition in 1997 by Sturgess et al, and the THINK project solicited reports from Burmese breeders specifically. However statistics on the registration of kittens provided by the GCCF show that Bengal, Burmese and Maine Coon are consistently in the top nine breeds by number of kittens registered (see table). The breeds showing highest numbers of kittens registered therefore broadly correlate demographically to reports of FCKS. More significant is perhaps the low number of reported cases in the British Shorthair (especially when compared with the Manx), but this seems to be attributable to the culture of breeders and level of diagnostic awareness in that group.
Mortality: of 195 cases where the outcome was notified, 88 died, or were euthanised due to distress; 107 recovered and survived beyond 3 months of age. Those that recovered fully did not appear to suffer any long-term respiratory effects (Interference of the development of the upper spine while the body was held in an incorrect position by the FCKS led to long-term kyphosis in some, but not all, cases), although reporting is patchy.
Mentions of FCKS in the veterinary literature (usually no more than a single sentence) include no descriptive information and have no evidential basis, in particular the claim in Saperstein, Harris & Leipold (1976) that the condition may be hereditary, which has been repeated in subsequent literature.
Onset and diagnosis FCKS develops usually in kittens around three days of age, and sometimes affects whole litters, sometimes only individuals or part of a litter. Kittens can go flat any time during early maturation, some flattening as late as 10 days of age or (in very rare cases) later. It is possible that the later-developing cases are due to Respiratory tract infection or pneumonia. Until 2010 FCKS was believed to be caused by a spasm in the intercostal muscles, but re-examination of old post-mortem data (i.e. that kittens remain flat even when they are dead and therefore cannot maintain a muscular spasm) and new data has led to the conclusion that flattening is caused by failure of the lungs to inflate normally or, when it occurs in older kittens, by lung collapse. This cause is now cited by the veterinary community (Sturgess 2016) but without any source acknowledgement.
Gross physical symptoms include flattening of the underside of the thorax in moderate cases (a ridge can usually be felt along the sides of the ribcage, running parallel to the spine); complete flattening of the upper body in extreme cases (the kitten looks as if it has been stepped on); moderate to extreme effort and/or gasping during breathing; the gut is drawn upwards during the in-breath. Breathing is not usually rapid (as in pneumonia or pyrexia) but at a normal rate when compared with unaffected kittens. The position of the thorax and activity of the abdomen is not unlike that seen during normal hiccups, but the sudden spasm in hiccups is slowed down or halted in FCKS: where a hiccup releases, returning the body to a normal position, FCKS breathing does not release. There may be involvement with digestive difficulty in FCKS kittens (see Colic, below).
Determining whether a kitten has FCKS or not can be difficult with only text descriptions: a mild case of FCKS causes the thorax to feel similar to the shape of a banana when held curve downward. The ribcage is not fixed in position, and the most noticeable effect in mild cases is the ridge along the side of the ribcage.