Owner documentation of a life saving treatment that worked for one nine-year-old cat with megacolon, written for owners who have been told euthanasia or surgery are the only sensible options and who may not know that another one exists.

Domestic shorthair, neutered male, 9 years · 9 kg → 7 kg · Status: stable, at home

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What this document is

Cake had megacolon that kept coming back. The standard fix is surgery, and by the time it was needed he was too unwell — and too heavy — to come through it safely. Enemas, a full manual clear-out, laxatives and a wet-food diet all failed to hold. At that point the realistic option given to me was putting him to sleep.

We found another option – my favorite vet suggested we try neostigmine, a drug that makes a weak colon push harder. He is still here – eating, grooming, using his litter tray, and happier than he was before this nightmarish adventure began. He just needs an injection every few weeks, and probably always will.

Neostigmine is not an established treatment for megacolon in cats. There is no trial behind it, no licensed indication, nothing in the standard textbooks. It is a folklore treatment — known to some vets, used quietly, never formally written up. That is exactly why it may not have been offered to you, and it is the first thing section 01 explains.

This is not a claim that it works for every cat, and it is not a protocol to follow at home. It is a written account of one cat’s treatment, detailed enough that you can take it to your own vet and ask whether it is worth considering.

I am raising money to cover the exorbitant treatment costs involved in saving Cake’s life (keeping him alive until we found the treatment recorded in this article) you can donate here.

Diagnosis	Dilated megacolon, recurrent obstipation
Complicating factor	Spinal spondylosis, painful defecation
Surgery	Ruled out — too unwell and too heavy for safe anaesthesia
Current regime	Neostigmine as needed, daily lactulose, Solensia every 6 weeks

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01 · A folklore treatment, not an established one

When Cake’s vet suggested the neostigmine she used to treat baby horses, she was clear about what she was proposing: this is not a scientifically established treatment for megacolon in cats. It is not licensed for it. There is no clinical trial. It does not appear in the textbook chapters or the treatment guidelines on feline constipation.¹ A vet who says they have never heard of using it this way is not being careless — there is very little for them to have heard.

What does exist is elsewhere. Neostigmine is well established in horses for large colon impaction, where it is the most commonly chosen drug of its kind.²³ It is used in human medicine for a condition in which the colon dilates and stops moving.⁴ The principle — restore the push to a bowel that has stopped pushing — is old and well understood. It is the specific application to cats that nobody has written down.

Mathematicians have a name for a result that specialists know, pass around and rely on, but which nobody ever formally published: a folklore theorem. It is true, it is used, and you will not find it by looking it up. Neostigmine for feline megacolon sits in roughly that position. Some vets know of it. Some have used it and seen it work. But because it was never written up, knowledge of it spreads by word of mouth between practitioners rather than through the literature — which means whether it gets offered to your cat depends largely on who you happen to be standing in front of.

That is the gap this document is trying to close, and it cuts both ways. A folklore treatment is not a secret good one that the profession has ignored. It is a treatment nobody has tested properly, which is a real reason for caution and a legitimate reason for a vet to decline. Your vet may have grounds you are not aware of, specific to your cat. The point is only that the conversation should be possible.

⚠ An honest caveat

Sometimes euthanasia genuinely is the right decision. A cat in unrelieved pain, with a colon that has stopped responding, or with other serious illness alongside, may be at the end of what medicine can reasonably offer. This document is not an argument that nobody should ever make that choice.

It is an argument that you should get to make the choice knowing what the alternatives were.

For biologists and medicine workers: Go looking for feline data on this and you find nothing. No pharmacokinetics, no efficacy trial, no safety series. Not a thin literature — an absent one.

Everything supporting it comes from other species. In horses, neostigmine is the prokinetic most often reached for in large colon impaction.² A CRI at 0.008 mg/kg/h raises faecal output and makes pelvic flexure smooth muscle contract in the organ bath.⁵ At 0.044 mg/kg IM it improves caecal and colonic contractility on ultrasound in Arabians — though those authors preferred metoclopramide, which they judged safer and longer-acting in that breed.² Foals with meconium impaction get 0.005–0.01 mg/kg IM or SC.⁶ Humans get it for acute colonic pseudo-obstruction.⁴

The same literature contains the awkward finding too: give 0.022 mg/kg four times at half-hour intervals and gastric emptying slows.⁵ Whatever neostigmine does to the horse gut, it doesn’t do it uniformly — useful distally, possibly counterproductive proximally.

Then there’s the species problem. The classical account of feline megacolon puts the lesion in the smooth muscle rather than the nerves,¹⁷ which is uncomfortable, because a drug that works by making neuronal acetylcholine linger needs a myocyte still capable of answering it. That picture has since gotten murkier — section 02.

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02 · What megacolon actually is

The colon is the last stretch of bowel. It draws water out of waste and pushes what is left towards the exit in waves of muscular contraction.

In megacolon the colon stretches wide and loses much of its ability to push.¹ Waste sits there. The longer it sits, the more water is drawn out of it, and the harder it becomes. Harder waste is harder to move, so it sits longer still.

Almost everything that follows in this document is an attempt to break that loop at one point or another. It is worth holding onto, because it explains why single treatments keep failing: an approach that softens the waste but does nothing for the pushing, or improves the pushing while the waste is already concrete, addresses half a problem.

In most cats no cause is ever identified. This is called idiopathic megacolon.¹ When a cat can no longer empty the bowel at all, the word used is obstipation.

⚠ The single most important number in this document

In a 2022 study, cats whose signs had lasted less than six months responded to medical management in 66.7% of cases. Cats whose signs had lasted six months or more responded in 5.6% — the rest needed surgery.⁸

If your cat is early in this, that is the window. It is the strongest argument in the literature for pushing hard on diagnosis and treatment now rather than managing conservatively and seeing how it goes.

For biologists and medicine workers: The breakdown of feline obstipation runs roughly 62% idiopathic megacolon, 23% pelvic canal stenosis, 6% nerve injury and 5% Manx sacral cord deformity — those four covering 96% of cases.¹ Keep dilated megacolon separate from hypertrophic: the first is the end stage of idiopathic colonic dysfunction, diffusely wide and hypomotile; the second is driven by something obstructing. They don’t behave alike and they don’t carry the same prognosis.⁹ On radiographs, take the widest colonic diameter over the length of L5. ≥1.48 is the feline cutoff; dogs are ≥1.5.¹⁰

Now the part that actually changed my mind about something. The older literature holds that cats don’t show the enteric neuronal loss seen in human megacolon.⁹ A 2022 histologic study makes that harder to maintain. In cats whose signs had run six months or more, the descending colon had a thickened muscularis mucosa (54.1 μm against 22.33 μm in controls), a fatter inner circular layer (743.65 vs 482.67 μm) and a thicker outer longitudinal layer (570.68 vs 330.33 μm) — but also fewer ganglion cells, 0.93 against 2.87, with necrotic myocytes up from 0.07 to 2.25.⁸ Myopathic, then, but neuropathic as well, and apparently more so the longer it goes on.

I’d rather spell out what that means for the drug in this document than leave it for a reader to spot. An acetylcholinesterase inhibitor doesn’t manufacture acetylcholine; it stops what the neurons release from being cleared. Lose the neurons and you lose the substrate. So ganglion cell attrition predicts a therapeutic window that closes over time — which fits those duration-dependent response rates rather too neatly for comfort.

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03 · The part that was missed: pain

Cake’s X-rays showed spondylosis — small bony spurs growing along the vertebrae of his lower spine. It is common in older cats and often causes no trouble at all, which is exactly why it is easy to dismiss.¹¹

But consider what a cat has to do to pass a stool: crouch, curl the lower back, hold that position, and strain. If that hurts, the cat puts it off. And putting it off is precisely what dries the waste out and hardens it. Pain and constipation feed each other.

This is not merely a plausible story. In a radiographic study of 1,365 cats, those with abnormal lumbosacral vertebrae were significantly more likely to have large bowel problems (p=0.0057, OR 1.73), and for acquired abnormalities specifically — the category spondylosis falls into — the odds ratio was 4.11 (p<0.0001).¹²

How we knew it was real

In my entire acquaintance with Cake, he had never washed the back half of his body. His front half was immaculate. This was put down to his size — he was 11 kg when I adopted him, and was around 9 kg by the time the symptoms of megacolon began. Even a 9 kg cat may simply not be able to bend that far.

He started grooming his back end again shortly after beginning pain relief every 6 weeks, before he had lost any meaningful weight. That timing is the whole argument. If bulk had been the obstacle, the behaviour would have returned gradually as the weight came off. It did not. It returned when the pain was treated.

Worth checking on your own cat

A scruffy or matted coat over the lower back, dandruff you only see behind the ribs, or a dirty bottom on a cat who used to be fastidious. Grooming is one of four validated behavioural domains used to assess musculoskeletal pain in cats — alongside mobility, activity and temperament — and all four improve measurably after analgesia.¹³ It is easy for everyone in the room to attribute to age or weight. It is worth saying out loud at the appointment.

For biologists and medicine workers: Spondylosis deformans is a ventral process sitting outside the vertebral canal — new bone laid down where the annulus fibrosus attaches, in response to disc degeneration. It isn’t facet osteoarthrosis and it isn’t degenerative lumbosacral stenosis, and it shouldn’t be discussed as though it were. Absent imaging that shows foraminal encroachment, don’t reach for a neurogenic explanation. What I’m proposing is behavioural avoidance.

The finding turns up incidentally in older cats often enough¹¹ that seeing it on a film proves nothing by itself. You have to build the case. There are two ways in.

Population level: across 1,365 cats, acquired lumbosacral abnormalities carried an odds ratio of 4.11 for distal GI dysfunction.¹² That is not a subtle effect.

Patient level: run a therapeutic trial against a behaviour that pain specifically limits, and caudal grooming is close to ideal for the purpose. It requires flexion and rotation, so it’s mechanically specific. Cranial grooming survives in a cat who is merely sore rather than systemically ill, which hands you an internal control. And it’s a validated pain domain that responds to analgesia in cats with musculoskeletal disease.¹³ Here it returned when the anti-NGF started, not as the weight came off.

The obvious objection is that all of this is unblinded and owner-reported, and caregiver placebo effect in veterinary analgesia is real and well documented. It’s worth noting that in Bennett and Morton’s cohort the veterinary surgeons’ scores fell significantly as well as the owners’.¹³ That helps. It doesn’t settle it. Supporting evidence, not proof.

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04 · What was tried, in order

Stage 1 — failed · A superficial enema

It cleared only the waste nearest the exit. Some stool came out, which looked like progress. The bulk of the blockage sat further forward, in the widened part of the colon, and fluid introduced from the rectum never reached it.

This is a common and instructive failure. If your cat has an enema and still seems wrong afterwards, or the belly still feels full, say so — partial output is easily mistaken for resolution.

For biologists and medicine workers: Whatever you infuse ends up in the descending colon and rectum. If the dehydrated mass is sitting in an ascending or transverse colon that has dilated to accommodate it, a conventional enema never gets near — and the stool that does come out reads as success to everyone in the room, which is the part that costs you time. I should be clear that this is me reasoning from where the fluid goes rather than citing a measured endpoint. I haven’t found anyone who has quantified it.

Stage 2 — worked, did not hold · Full manual deobstipation under anaesthetic

The vet emptied the entire colon by hand under general anaesthetic. At the same time she confirmed that nothing was physically blocking the way — no narrowed pelvis, no growth, nothing swallowed.

That check turns out to be the single most important event in this whole account, for reasons that become clear in section 05.

For biologists and medicine workers: Mechanical GI obstruction is a listed contraindication to neostigmine,¹⁴ so the moment someone documents a normal pelvic canal and the absence of stricture, mass or foreign body is the moment everything downstream becomes defensible. Write it down. It’s the difference between a considered off-label decision and a reckless one, and the only thing separating them in the record is whether anybody bothered to note it.

Stage 3 — failed · Daily lactulose and exclusively wet food

Lactulose is a sweet liquid laxative that draws water into the bowel and keeps stool soft. Cake had 5 ml daily in his food, and ate wet food only. Dietary modification and hyperosmotic laxatives are the standard first-line components of multimodal management.¹

The blockage rebuilt anyway. This is the pivotal observation: his colon had been completely emptied, his stool was softened, his water intake was good, and waste still accumulated. The failure was therefore not one of hydration and not a one-off mechanical event. His colon was not pushing.

For biologists and medicine workers: When a colon that has been emptied completely refills despite adequate osmotic laxative and good water intake, the failure isn’t consistency — it’s propulsion. That squares with what’s documented about contractile dysfunction in this disease.⁷ It’s also the observation that makes reaching for a prokinetic reasonable rather than speculative, which is a good argument for producing it deliberately rather than stumbling into it after the fact.

Stage 4 — unavailable · Subtotal colectomy

Where megacolon keeps recurring, the definitive treatment is an operation removing most of the colon. Cats generally do well afterwards — 72.2% favourable outcomes in the 2022 cohort,⁸ and a high rate of owner satisfaction across 18 hospitals in a 2021 series¹⁵ — and if it is genuinely available to your cat it is usually the better long-term answer.¹¹⁶

It was not available to Cake. By the time the question was live he was both markedly obese at 9 kg and unwell from the obstipation itself, and the combination made a long abdominal surgery an unacceptable risk. This is worth being precise about, because “not a surgical candidate” covers two very different situations: a cat who is too well to need it yet, and a cat who has become too unwell to survive it. Cake was the second.

There is a bitter logic in that which is worth naming. The disease that makes surgery necessary is the same disease that makes surgery dangerous, and the longer it runs the more true that gets.⁸ Waiting is not neutral.

On not having the surgery

For most of this document the non-surgical route reads as a consolation prize, and I want to correct that, because it isn’t only one.

Subtotal colectomy is major abdominal surgery, and the recovery is not nothing. Soft stools and sometimes frank diarrhoea are expected for the first few months afterwards, stools become firmer with time but rarely return fully to normal, and some cats have occasional soft-stool leakage.¹⁷ Outcomes are good and most cats end up with an excellent quality of life¹⁵¹⁷ — I am not arguing against the operation. But a cat who never has it also never has the anaesthetic, never has the laparotomy, never has the months of loose stool, and never carries the small risk of the anastomosis failing.

Cake has none of that. He has a dose every few weeks, a spoonful of syrup in his dinner, and an otherwise ordinary life. Measured against a cat who sailed through colectomy, that is second best. Measured against what was actually on the table for him — which was repeated anaesthetics or euthanasia — it is a good outcome by any standard, and it is allowed to be one.

For biologists and medicine workers: Cats with chronic obstipation or megacolon are normally considered colectomy candidates,¹⁶ so any record ought to say exactly why this one wasn’t — and ought to distinguish a risk-based exclusion from a staging one, because only the first can be undone. Cake’s was both at once: the anaesthetic and perioperative risk of marked obesity, compounded by what established obstipation had already done to him systemically.

Reassessing surgical candidacy after weight reduction belongs in the written plan rather than left to occur to somebody, particularly for a patient facing years of intermittent cholinergic therapy that nobody has safety data for.

That said, the comparison is less lopsided than it first looks. Median follow-up in the largest recent outcomes series was 64 days, and removing the ileocolic junction was associated with worse outcomes¹⁵ — so what becomes of these cats years later isn’t well described either. Add the expected morbidity: soft stool or diarrhoea through the first months, rarely normalising completely.¹⁷

Which leaves the real choice as one between a surgical option whose long-term course is thinly characterised and a pharmacological one whose long-term course isn’t characterised at all. Neither arm has the data you would want. I’d rather say that plainly than pretend the decision was obvious in either direction.

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05 · Neostigmine, and why the timing is everything

Nerves in the bowel wall release a chemical messenger that tells the muscle to contract. Neostigmine slows the breakdown of that messenger, so the signal persists and the contraction is stronger.¹⁴ In plain terms: it helps a weak colon push. It is given by injection, because it is not absorbed if swallowed.¹⁸

⚠ The critical point

A drug that makes the bowel contract harder is dangerous if the bowel is genuinely blocked. Mechanical obstruction of the gastrointestinal tract is a listed contraindication to neostigmine.¹⁴ Contracting against a hard mass that will not move does not expel it. It raises pressure inside a colon that is already stretched and thin-walled. That is painful, and at worst the bowel can be damaged or perforated. The same objection is made explicitly in the equine literature: a prokinetic given in the presence of a physical obstruction pushes against an impassable point and increases pain.¹⁹

This is why the order of Cake’s treatment matters more than any individual element of it. The same drug is either useful or harmful depending entirely on the state of the colon when it is given.

Neostigmine was used only:

• after the colon had been completely emptied by hand;
• after mechanical obstruction had been excluded;
• and thereafter early, while the contents were still soft enough to move.

For biologists and medicine workers: Neostigmine is a quaternary ammonium reversible acetylcholinesterase inhibitor. It doesn’t stimulate anything directly — it stops acetylcholine being cleared, so whatever the enteric neurons release hangs around and acts on both nicotinic and muscarinic receptors.⁴¹⁴ The contraction you’re after is the muscarinic one: M2 and M3, G-protein-coupled rather than ion channels, with M3 running PLC → IP₃ → calcium release → myosin light chain phosphorylation. The nicotinic side of it is ganglionic. Being quaternary keeps it largely out of the CNS,¹⁴ and also means it doesn’t survive the gut — hence the injection.¹⁸

Contraindications: mechanical obstruction of the gastrointestinal or urinary tract, and peritonitis. Adverse effects: bradycardia, hypersalivation, bronchoconstriction, and — the irony is not lost on me — increased gastrointestinal motility.¹⁴ Veterinary sources add asthma, pneumonia, epilepsy, peptic ulceration and arrhythmias.¹⁸ Overdose gives a cholinergic crisis, at which point you stop immediately;¹⁴ have atropine and the rest of the anti-shock drawer within reach.²⁰

The mechanical danger is where I’m reasoning rather than citing, so take it as physics rather than evidence.

Laplace: wall tension scales with pressure and with radius, and inversely with wall thickness. A colon that has been chronically dilated and thinned is therefore precisely the geometry that turns a given pressure into maximal wall tension — meaning the cats most likely to be handed a prokinetic for impaction are the cats least able to tolerate one. Well short of perforation you get vascular compression within the wall, mucosal ischaemia, and ulceration against something abrasive that isn’t going anywhere, with translocation to follow. And the stimulus isn’t evenly distributed either: the less-affected proximal segments still contract perfectly well, and what they generate is transmitted straight into the segment that is widest, thinnest and least able to push back. I haven’t found anyone who has modelled this for the feline colon specifically.

Why the human comparison only partly holds

Neostigmine is used in people for acute colonic pseudo-obstruction, which is defined as marked colonic dilatation in the absence of mechanical obstruction.⁴ But in that condition the distended colon is full of gas, which compresses and vents the moment motility returns. A megacolonic cat’s colon contains a solid mass whose deformability decreases by the day. Same drug, same organ, different mechanics — and the difference is the entire reason timing governs the outcome.

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06 · Cake’s regime

Neostigmine, intermittently

• We started with a small test dose, under observation, to check he did not react badly to the drug itself.
• Then, proceeded to an induction course: twice daily for three to four days, started after the manual clear-out.
• Ongoing Maintenance: I feel his abdoment around twice a week to check if waste has built up. If it has built up, he gets a dose. If not, no dose. His current dosing rate is one dose every few weeks (recorded how much and when administered), two at the absolute maximum.
• As his weight fell from 9 kg to 7 kg, the dose was reduced — proportionally more than the weight loss alone would require, and it still works.

⚠ The stop rule

Now that he is in ongoing treatment: If two doses do not produce a bowel movement, he does not get a third. He goes in for imaging and manual clearance instead. So far this has not occured. However, failure to respond to dosing is the signal that the contents have already hardened past the point where more contraction helps — and at that point further dosing is pushing against something that will not move. This rule is not a formality. It is what keeps the treatment on the safe side of the contraindication.¹⁴¹⁹

No doses are given in this document

Deliberately. Neostigmine is supplied at several different concentrations, and a volume that is correct for one cat and one product can be a significant overdose with another. Dosing is calculated per kilogram by a vet who knows which vial is in their hand. This document exists to start a conversation, not to replace one.

For biologists and medicine workers: Call the test dose what it actually is — a screen for idiosyncratic cholinergic sensitivity. It does not establish tolerance of the therapeutic dose, because cholinergic effects are dose-dependent¹⁴ and an escalation of that size isn’t covered by having survived the smaller one. I’d rather say so than let the sequence imply a safety argument it can’t carry.

The one thing here that might be worth something to somebody else: per-kilogram exposure ended up below the induction dose and still worked. Several explanations, none exclusive. Induction may simply have overshot — it was arrived at by climbing from a cautious start, not by coming down from a known ceiling. The biomechanics improved as he lost weight. Intervening earlier meant smaller and more deformable masses. And there’s a distribution argument: neostigmine is hydrophilic and quaternary,¹⁴ so it goes into lean tissue and extracellular fluid rather than fat, which means dosing an obese cat on total body weight delivers more per kilogram of the tissue that actually receives it than the number on the syringe suggests. That last one is inference from physicochemistry, not a feline measurement.

Lactulose, daily

5 ml once daily, mixed into wet food. This is not an optional extra alongside the neostigmine — the two are co-essential, and this is the mechanistic heart of why the combination works where either alone did not:

• Lactulose keeps the stool soft enough to be moved.
• Neostigmine supplies the force to move it.

Soft stool with no propulsion simply sits there — that is what the months on lactulose alone demonstrated. Strong propulsion against a hardened mass only builds pressure — that is the danger in section 05. Neither element is sufficient. The aim is soft but formed stool; watery diarrhoea means the dose needs revisiting with the vet rather than adjusting yourself.

For biologists and medicine workers: Lactulose is a synthetic disaccharide that mammalian intestinal enzymes can’t touch, so it reaches the colon intact, pulls water in osmotically, and is then fermented to short-chain organic acids which drop luminal pH and add further osmotic load. Hyperosmotic laxatives sit squarely in the standard multimodal package for this disease.¹ 5 ml q24h is on the cautious side for a 7–9 kg cat by conventional titration, and whether giving it more often would stretch the interval between neostigmine episodes is genuinely unknown here. If you do escalate, watch potassium — hypokalaemia worsens colonic motility, which rather defeats the object.

One wrinkle in the tidy two-factor story above: short-chain fatty acids themselves make feline colonic smooth muscle contract in vitro.²¹ So the laxative and the prokinetic may be less mechanistically independent than I’ve made them sound.

Solensia, monthly

An injection for pain every 6 weeks. It is a felinised monoclonal antibody that binds nerve growth factor, a substance that sensitises nerves to pain.²² It is licensed for osteoarthritis pain in cats;²³ using it for spinal pain is a slightly different application.

Its role here is not only comfort. If defecation stops hurting, the cat stops deferring it — which breaks the pain–avoidance loop from section 03 at the other end from the laxative and the prokinetic.

For biologists and medicine workers: Frunevetmab, a felinised anti-NGF monoclonal at 7 mg/ml, dosed by weight band — one 1 ml vial for 2.5–7 kg, two for 7.1–14 kg, aiming at a minimum of 1 mg/kg;²³ the EU SPC quotes 1–2.8 mg/kg monthly.¹⁶ Efficacy in osteoarthritis pain came out of a randomised placebo-controlled field study,²² and the pharmacokinetics and immunogenicity after IV and SC dosing have been worked out separately.²⁴

Keep an eye on the vial count when a patient is crossing that band boundary on the way down. Underdose at the heavier end and you have inadequate analgesia quietly sustaining the very pain–avoidance loop the drug was brought in to break — which is a particularly irritating failure mode, because from the outside it looks like the drug simply not working. Clearance is by protein catabolism, not hepatic or renal. Anti-drug antibodies can develop and cost you the effect, and nobody has established whether it’s safe alongside NSAIDs in cats.²³

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07 · Feeling the abdomen

Cake’s re-dosing is triggered by palpation — feeling the abdomen for waste building up, and treating before a hard mass has formed rather than after. That is what keeps the drug on the right side of the line described in section 05.

⚠ Read this before you try it

Ask your vet to show you on your own cat first, with their hands over yours. A description on a page is not a substitute for being taught, and the two structures you are distinguishing between feel more alike than this illustration suggests.

Never press hard, and never squeeze. A distended bladder can be ruptured by firm pressure. If your cat tenses, cries, or resists, stop.

The colon sits high and towards the cat’s left, running backwards through the rear half of the abdomen. The bladder sits low, central and further back. Both can feel firm. Telling them apart is the reason to be taught this in person rather than from a diagram.

How it is done

• Cat standing, or relaxed on your lap. Never when agitated.
• Fingers flat, using the pads rather than the tips. One hand each side, or one hand spanning the belly.
• Start behind the last rib, in the rear half of the abdomen, and work gently backwards until you are directly under the spine.
• Press slowly and lightly — enough to feel through the body wall, no more. The pressure is closer to resting your hand than to gripping.

What you are feeling for

• Normal: soft and yielding. Nothing firm that holds its shape.
• Filling up: a firm, sausage-shaped tube high on the cat’s left, running front to back. It may feel lumpy, like a row of hard beads through a sleeve.
• Not what you want: a hard, round, distinct ball sitting low and well back. That is more likely the bladder. Leave it alone.

⚠ A cat straining may not be constipated

A cat straining in the litter tray may be unable to urinate rather than defecate. From the outside the two look almost identical.

In a male cat, a urinary blockage is life-threatening within hours, not days. If you feel a tense, firm, round structure low and far back in a cat who is straining, do not press on it — phone the vet immediately and say you cannot tell which it is.

For biologists and medicine workers: The descending colon runs dorsally and to the left through the caudal abdomen towards the pelvic inlet, and a faecal column palpates as a firm tube, often segmented enough to feel like beads under the fingers. The bladder sits ventral and caudal and goes spherical as it fills. An owner can absolutely confuse the two, which is what makes the differential here more than academic: a straining cat with a tense round caudoventral structure may be urethrally obstructed — and urinary obstruction is itself a contraindication to neostigmine.¹⁴

The palpation-triggered, pre-emptive dosing is the part of this I’d actually want someone to take away. It shifts the intervention point from established obstipation to detected early accumulation, and that shift is the whole reason cholinergic stimulation stays on the right side of its own contraindication here. Where an owner is doing the palpating, document what they were taught and where their threshold for escalating sits.

And track two numbers rather than one: the interval between doses, and the days without defecation preceding each. If the trigger point drifts quietly later over time, the second number shows it and the first doesn’t — and a drifting trigger erodes the entire safety argument with nothing on the surface looking wrong.

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08 · Weight

Cake went from 9 kg to 7 kg. For an overweight cat this helps in several directions at once: less load on a painful spine, an easier crouch to pass stool, and better odds if surgery is ever reconsidered.

⚠ Do not do this quickly

Overweight cats must lose weight slowly and under veterinary supervision. Obesity and a period of reduced food intake are the classic setup for hepatic lipidosis, a serious and potentially fatal liver condition in cats.²⁵ No crash diets. If your cat stops eating, phone your vet. Weight loss that happens without you trying is also a reason to be seen, not reassured.

For biologists and medicine workers: The classic setup for hepatic lipidosis is an obese cat that stops eating, and the mortality without aggressive nutritional support is not trivial.²⁵ That deserves rather more attention than usual in a cat on intermittent cholinergic dosing, where nausea and a day or two of poor intake around each dose are entirely plausible.¹⁴ It is an unglamorous way to lose a patient you were otherwise managing well.

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09 · Day to day, and what to watch

• Lactulose in wet food, daily. Aiming for soft but formed.
• Wet food only. Water always available.
• A written note of when he goes, what it looks like, and whether he strained. This is the single most useful thing to bring to an appointment.
• Regular abdominal palpation, to catch accumulation early rather than late.

The number that matters most

How often the injection is needed. If the gaps between doses stay roughly constant, the regime is holding. If they start shortening, the colon is likely deteriorating — and that is the moment for a fresh conversation about what comes next, including whether surgery has become possible again at a lower weight.

Writing that down honestly is uncomfortable, and it is the reason this document is a record rather than a recommendation. A treatment that is working is not the same as a cat that is cured. The duration data in section 02 make clear that this disease has a direction of travel.⁸

⚠ Phone the vet now if

• Straining in the tray with nothing coming out
• Nothing passed for more than a couple of days
• Vomiting, especially with a tight or swollen belly
• Not eating, or gone quiet and withdrawn
• Crying or yowling in the tray
• After a neostigmine dose: weakness, collapse, or difficulty breathing

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10 · Taking this to your own vet

If your cat is where Cake was, these are the questions that opened up the useful parts of the conversation:

1. Has anything physical been ruled out — a narrowed pelvis, a stricture, a growth?
2. Could pain be part of why my cat avoids the tray? Has the spine, hips and pelvis been assessed, and would a trial of pain relief be reasonable?
3. If the colon has been fully emptied and it still rebuilds on laxatives, does that point to a propulsion problem rather than a hydration one?
4. Is my cat a surgical candidate — and if not, what specifically rules it out, and could that change?
5. If surgery is off the table, are there prokinetic options worth trying, including ones that are not standard?

For biologists and medicine workers: Before anyone reaches for neostigmine on the strength of this account, the established comparators deserve a hearing. Cisapride is the reference feline colonic prokinetic; it makes idiopathic megacolonic smooth muscle contract in vitro, and interestingly those contractions are only partly dependent on enteric cholinergic nerves²⁶ — which is a point in its favour, given the ganglion cell attrition in section 02. Compounding pharmacies will supply it.⁹

The comparator that really wants answering, though, is ranitidine (1–2 mg/kg PO q12h) and nizatidine (2.5–5.0 mg/kg PO q12h). Both stimulate feline colonic smooth muscle, apparently by inhibiting acetylcholinesterase — the same mechanism as neostigmine, orally available, and already described in this disease. Cimetidine and famotidine don’t do it.¹⁶⁹ Prucalopride at 0.64 mg/kg has cats defecating within the hour without changing consistency; misoprostol contracts feline colonic smooth muscle in vitro. Metoclopramide, domperidone and erythromycin act too far proximally to help here, and bethanechol’s side effects have kept it out of use.¹⁶¹¹

If you can achieve acetylcholinesterase inhibition by mouth, the injection has to justify itself. In Cake’s case it wasn’t tried first. I’d rather flag that as a hole in the record than dress it up as a considered choice.

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