Why all vets should hone their skills in animal behaviour

The gorgeous Poppy isn't entirely comfortable at the vet.

Why should every veterinarian in general practice hone their skills in behaviour? It’s a question posed by Dr Sarah Heath, RCVS and European Specialist in Veterinary Behavioural Medicine, at the Centre forVeterinary Education’s week-long behaviour conference.

There are plenty of vets who speak on different topics, but Dr Heath is a stand-out speaker. She spoke about situations and patients we deal with every day, but her angle gave me new ways to think about these. If you have not yet heard her speak and have the opportunity, take it.

Most of us find out the hard way that unwanted companion animals have implications. They may be local (house-soiling, aggression between animals in the household, aggression to people, behaviour stemming from anxiety that generates anxiety in others and so on). There are wider implications too – nuisance behaviour can damage neighbourly relations, or the media may portray behaviour in a certain way, leading to an unfounded or misdirected negative perspective, or there may be legislative consequences like laws banning certain breeds.

There are also implications in vet practice. Confrontational behaviour from our patients, or avoidance behaviour and fear, or problems between species in the clinic, can have all kinds of implications. For example, one of the key reasons that cat owners delay a veterinary visit is concern about their cat’s behaviour at the vet.

Dr Heath discussed why owners may not seek advice from veterinarians about behaviour problems. Many, she said, do not want the practice to think badly or negatively about their companion. They may be embarrassed and blame themselves, and society might blame them too. (For these people it can be reassuring to know the animal has a mental health issue). They may have erroneous information about behaviour and think certain behaviours are normal. They may not feel the vet has expertise in the area (the vet may feel the same way), or they may be worried that such a discussion will elicit a suggestion of euthanasia from the vet.

In her first talk, Dr Heath gave some practical tips that can be employed in practice to the benefit of our patients, their owners and vets.

• Consider the impact of coming to the vet on the mental/emotional health of our patients. If owners are aware that we are concerned about their animal’s affective state, they will be more likely to understand its importance. Dr Heath said that for cats, the vet visit can be challenging because they are control freaks who are suddenly withdrawn from their territory and subjected to fairly restrictive handling, which is fairly confronting; their ability to use some of their natural defence strategies (hiding, climbing up high) is limited; and there are scent challenges (which is a nice way of saying vet clinics reek of other animals, and their emotional cues like fear). For dogs, as well as scent challenges, there may be a perception of confrontation, and veterinary staff may lack understanding of appeasement behaviour and signalling. Animals are intelligent, sentient beings – they remember and worry about previous negative experiences.
• In discussions, be clear that owners do have mental and emotional health. If everyone is thinking in these terms, it is easier to talk about mental and emotional health problems.
• Emphasise that socialisation of puppies and kittens is NOT about exposing them to a tick-list of various stimuli (loud noises, slippery floors, other species, traffic noises). Rather, exposure should be about quality over quantity. Animals should only be exposed to these stimuli when they are in a positive emotional state – if they’re in a negative emotional state, they may become sensitised to and anxious/fearful/reactive to the stimulus.
• Cat owners need to be informed that cats socially mature between two and three years and the behaviour of their cat can change significantly at this time. We need owners to establish realistic expectations of feline compatibility in multi-cat households (more on this in a later post).

During her talk, Dr Heath referred to a range of excellent resources, including:

A course on developing emotional intelligence for puppies (very different from puppy training).

A book on training your cat. I have ordered this, it looks amazing (look out, Hero!).

Some fantastic posters drawn by Doggie Drawings artist Lili Chin, for the Association of Pet Behaviour Counsellors in the UK on 

“Hints for Managing the Stressed Cat” and “Hints for Managing the StressedDog.”

In other news, Dr Siobhan Mullan (Bristol University) and myself have been toiling away on a book about veterinary ethics for some years. It is the result of a huge team effort – contributors from around the world have provided some fantastic scenarios and responses to these, as well as some beautiful cartoons and illustrations. You can now pre-order the book through 5M, just click here.

Declaration: I attended three of the sessions at the CVE's conference at no charge as I put together a video presentation for a colleague who could not make it.

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What do cats and crocodiles have in common? Three things I learned about saltwater crocodiles

I came across this footprint from a saltwater crocodile on a beach in the Northern Territory.

Actually as soon as I asked that question I could think of multiple answers, such as the fact that they're both magnificent species, they are both partial to a seafood dinner, they can both suffer from fur balls - albeit from different sources), they can both surprise you with a little nip etc. etc., but one thing I wasn’t aware of until last week was this: they both get herpes. Actually most species have their own species-specific herpesviruses, but herpesvirus in crocodiles is a relatively recently described phenomenon.

I learned about it during a fantastic webinar presented by veterinary pathologist Dr Cathy Shilton and hosted by the World AquaticVeterinary Medical Association (WAVMA). The topic was diseases of farmed saltwater crocodiles in Australia.

Crocodiles are distributed in Australia’s tropical north. There are around 14 crocodile farms in Australia, approximately half of which are in the Northern Territory where Dr Shilton works. 

The largest farm holds around 40,000 animals. Around 70,000 eggs are harvested from the wild per year. (Back when I was a veterinary student I participated in one such harvest and was given the unpopular/hair-raising job of climbing onto the nest with an eski actually collecting the eggs from the nest while two big blokes kept lookout for mum).

Crocodiles are farmed primarily for their skins, which are sold into the luxury leather market. The majority of crocodiles are “harvested” from 2-4 years of age.

Saltwater crocodiles on a farm in the Northern Territory.

I learned a lot in the webinar, but if I had to pick three key points they were:

• Bacterial sepsis is the main cause of mortality, with gram negative pathogens mostly to blame. These include Providencia rettgeri, Morganella morganii, Edwardsiella tarda, and salmonella species (all of which sound like very exotic names for one’s offspring if nothing else). The majority (95 per cent) of mortalities occur in hatchlings. Bacterial sepsis likely occurs secondary to stress, which may be due to inappropriate temperatures (reptiles should always be kept in their preferred optimal temperature zone, and crocodiles like an ambient temperature of around 32 degrees) or other stressors like noise, disruption of the normal routine and so on. Interestingly, Dr Shilton observed that even if they present for sudden death, the stomachs of crocodiles with bacterial sepsis are always empty, i.e. they’ve been off their food for at very least one feed, possibly more. There may be some scope for further honing our skills on assessing the systemic health of reptiles.
• A herpesvirus is responsible for two distinct syndromes in Aussie salties. It usually affects 6-12 week old hatchlings. The first causes a conjunctivitis-pharyngitis which is a bit similar to the syndrome caused in cats, and apparently tortoises, although it sounds like it’s a bit more severe. That may be because there is a feline herpesvirus vaccine, or possibly because feline herpesvirus is endemic and maybe croc herpesvirus is rather new. Interestingly this syndrome was described in 2006. In 2009 another syndrome was described. This affects juveniles (6-10 months old) and is associated with systemic lymphoid proliferation and non-suppurative encephalitis. Clinically they fail to thrive. They may have splenomegaly or pulmonary oedema. This is more similar to Marek’s disease seen in poultry or bovine malignant catarrhal fever. There are currently no vaccines. Use of drugs such as famciclovir which are used in cats (and people) for herpesvirus signs have not been trialled, probably due to cost being prohibitive.
• Stress of some kind – possibly maternal stress – seems associated with “runting” or hatchling failure to thrive, which affects 10 to 15 per cent of stock each year. According to Dr Shilton farms have a vested interest in the welfare of animals as their aim is to produce blemish free skin, and stressed crocs tend to get diseases that cause skin lesions, or experience delayed wound healing. Stress is managed to an extent by managing stocking rates (not too low, as crocodiles get territorial, and keeping numbers of females higher than males, but also making stock numbers are excessive in pens). Hatchlings are also graded by size monthly to ensure that they are in pens with animals about their size. Even so, it seems as if welfare assessment of farmed crocodiles is an area where research is lacking.

This was a very well-presented, really informative webinar. WAVMA hosts some excellent webinars, so if you have any interest in creatures that swim, I'd encourage you to join up.

A few things I learned about rabbit desexing

Animal cakes at the AVA conference. I made sure I had my blood glucose checked at the wellness stand before sampling these carb-tastic beauties.

Have you ever desexed a rabbit? In some States in this country where rabbits are illegal to keep as pets (such as Queensland), it’s unlikely. But interestingly, between 150 and 200 vets rocked up to a session on rabbit desexing. It felt like everyone in the conference flocked to one room (which is a semi-accurate estimate, it was about 20 per cent). Some had over forty years’ experience. Which gives you an indication of how challenging it can be.

Exotics veterinarian Dr Brendan Carmel shared his techniques with the eager crowd. For males he recommends an open technique via a pre-scrotal incision. He doesn’t worry about subcutaneous sutures as there is barely any subcutaneous tissue, and uses tissue glue to close the wound.

He does advocate speying female rabbits because of the high incidence of uterine neoplasia. Depending on the study you read it’s between 40 and 80 per cent in rabbits over 3 years. Ovariectomy can be considered in rabbits at 2-3 months old.

Reassuringly, Dr Carmel advised that the mesometrium is a major fat storage area in rabbits. Thus speying an adult female rabbit who is a bit on the plus-size side is the lagomorph equivalent of desexing a bit fat Labrador. He advocates sending off any uterus that looks hyperaemic, lumpy or bumpy in case there is uterine neoplasia. Often in females with uterine adenocarcinoma, the fat has atrophied somewhat. If he palpates a very large uterus in an adult rabbit, run some bloods and do chest radiographs before you do surgery.

The risk of anaesthetic mortality remains high in rabbits (0.7-7.4% compared with 0.1-1.4% in cats and 0.05-1.3% in dogs). Owners need to be informed about this.

Airway control is challenging to achieve in rabbits but Dr Carmel uses a supraglottid device or V-gel, or uses a rigid endoscope to intubate. These are very nifty, I popped along to the V-gel stand to check them out and they’re really easy to place.

A V-gel used to maintain airway in a rabbit (nb this is a model).

A close up of the V-gel. You can autoclave and reuse these 40 times.

Dr Carmel advocates plenty of analgesia and higher than standard doses of non-steroidals in rabbits, up to twice per day. He does not discharge rabbits until they are eating. If they don’t eat, he assist-feeds them Critical Care formula. The details of course are in the proceedings, but it was an excellent talk.

Three things I learned: treatment of demodex in dogs

This is Jen. No, she doesn't suffer from demodex, but she does like to cool off in her shell pool.

As a companion animal veterinarian I see demodex mange (aka demodicosis) reasonably commonly in practice, so it was nice to hear an update on treatment and drug interactions by dermatologist Rob Hilton during another fantastic webinar this week.

He talked about demodex in dogs and cats but the key things I learned really relate to demodex in dogs.

It is caused by three species: D. canis, D. injai (much harder to diagnose and sometimes can only been seen on biopsy) and D. cornei which is probably a morphological variant of D. canis. 

The first thing I learned is that the juvenile form (localised or generalised) probably has a genetic basis but it is the mites and the bacteria associated with them via secondary infection which produce byproducts that induce immunosuppression. So the immunosuppression is reversed when you treat the bacterial infection and the mites.

Adult onset demodicosis is associated with an acquired immunodeficiency, but it can be difficult to identify an underlying cause in many cases.

The cornerstones of treatment are the macrocyclic lactones and amitraz, but no treatment is 100 per cent successful in clearing mites and no demodicosis can be considered cured unless it has been twelve months without relapse.

Adult cases where there is an uncontrolled, undiagnosed primary cause are very hard to treat.

The second thing I learned is the key reasons for treatment failure.

1. Not treating for long enough – dogs should be treated for three negative skin scrapes 3-4 weeks apart.
2. Resistance or refractory infestation – where 6 weeks after treatment commences, there are large numbers of mites, nymphs and eggs on skin scrapes/hair plucks
3. Poorly stored medications – especially the macrocyclic lactones, they don’t like being exposed to air or light
4. Not getting the treatment dose right
5. Not treating secondary infections (Dr Hilton recommends cephalexin 25mg/kg BID for a minimum of three weeks or 10-14 days from clinical resolution; or cefovecin fortnightly for two doses SC; as well as use of a chlorehexidine shampoo twice a week followed by a leave in conditioner).
6. Inability to treat the underlying cause
7. Immune system collapse

The third thing I learned is around minimising the risk of toxicity when treating dogs with the macrocyclic lactones.

Dr Hilton discussed the different drug doses he used, but the main point is that he uses a “build up protocol” in ALL animals, not just those with reported susceptibility to toxicity (usually commencing at 50micrograms/kg until the final dose is reached). The main reason for this is that while collies and shelties and select other breeds possess the MDR delta-1 gene defect (involved in the coding for P-glycoprotein), 1-2 per cent of any breed can have it…and some dogs WITHOUT the genetic defect will be susceptible to toxicity.

[P glycoprotein is present in lots of cells, and occurs in intestinal lining and the CNS vascular endothelium. It pumps out noxious agents from cells. Macrocyclic lactones are highly lipid soluble and readily enter the CNS, but P glycoprotein defects mean that these drugs can accumulate in the CNS].

Thus while genetic tests can prove that the drug is UNSAFE in a particular dog, they cannot prove that the drug is SAFE in that dog. He offers genetic tests for the gene in all patients where macrocyclic lactones may be used to treat demodicosis, but insists if there is any chance the animal may be related to a herding breed.

And he puts all animals through a build-up protocol even when the test is negative for the genetic defect.

There are a lot of drugs that should not be used in dogs on these medications and it all depends on whether they compete with P glycoprotein. These include antifungal azoles, some antibiotics and anti-emetics, numerous chemotherapeutic agents, anaesthetics and antihistamines.

Dr Hilton also talked about the use of amitraz in the treatment of demodicosis. Currently this is only available off label in Australia and there are some human safety issues that make its use rather challenging (e.g. potential health risks to diabetic pets and owners, ditto owners with asthma, owners and pets on MOAIs and SSRIs etc.)

Three things I learned: acute renal failure

My late cat Lily, with some FAKE lilies, to illustrate the point that lilies (the real ones) are a common cause of acute renal failure in cats. All parts of the plant are toxic, so if you want to buy a bunch of flowers for a cat owner, ask your florist for an arrangement that does not contain lilies. OR grab some fakies. They last forever.

Dr Graham Swinney gave a fantastic webinar on behalf of the ASAVA last night on acute renal failure (ARF) in dogs and cats. (If you're not a member of the ASAVA you are missing out, the webinar program this year is fantastic - you do need to be a member of the Australian Veterinary Association to join).

I like the way he broke it down. Kidneys are major players (I feel like I should be writing playas for the benefit of any younger readers) in body function, eliminating waste products, excreting drugs, regulating water and electrolyte balance and producing hormones like EPO. So kidney failure is kind of a big deal.

The good news is that we have two of them (kidneys that is). Renal disease can be structural or functional, but doesn’t tend to result in azotaemia until 75% of nephron function is lost (loss of urine concentration tends to occur earlier, i.e. when 2/3 of renal function is lost). (That's NOT a good reason to sell one on the internet. Incidentally, selling BOTH kidneys on the internet is a certified Dumb Way to Die).

Essentially there are three potential outcomes of ARF: 1) complete recovery; 2) chronic renal disease; 3) death. Best outcomes are achieved when ARF is detected early.

There are four stages of ARF.

1. Initiation – can last for hours to a day, the first injury to the kidney. We need to recognise this phase to maximise chances of recovery.  Trouble is that affected animals often do not illustrate clinical signs during this period, meaning that we can miss an option to intervene when our treatment is likely to be most effective.
2. Extension – hypoxia and inflammatory disease cause damage which may or may not be reversible. This phase can last days. (The proximal convoluted tubule and loop of Henle are particularly sensitive to hypoxic injury as these are very metabolically active).
3. Maintenance – renal changes are irreversible; at this stage removal of the underlying cause doesn’t necessarily improve the outcome. This stage can last days to weeks.
4. Recovery – repair and regeneration, may take months and may not be complete.

In many ways the distinction between ARF and chronic renal failure is one of time. ARF is caused by a sudden reduction in glomerular filtration rate (GFR) resulting in azotaemia.

Chronic kidney disease = reduction in GFR & azotaemia due to a renal disorder that has been present for at least 2 months. ARF is rapidly progressive although there is a chance of complete recovery if caught early. CRF is usually slowly progressive but its irreversible.

The two big categories of causes of ARF are

1. Ischaemic injury
2. Toxicity

Ischaemic injury can occur with hypotension, cardiac failure, thromboembolic disease etc.

Thousands of toxins can damage the kidneys. These include drugs that are commonly used therapeutically such as some antimicrobials, antifungals, chemotherapeutic agents, diuretics, ACE inhibitors, as well as diagnostic agents such as contrast.

Endogenous substances such as haemoglobin, myoglobin and even bilirubin can also be hard on the kidneys. Infectious agents (especially agents causing leptospirosis and bacterial pyelonephritis) and immune complexes can cause acute renal injury.

Other potential toxins include ethylene glycol and herbicides such as paraquat.

Clinical signs of acute renal failure vary from classic lethargy, inappetance, vomiting, polyuria and polydipsia to hyphema and/or blindness (secondary to hypertension), neurological signs (uraemic encephalopathy) and even respiratory signs (vasculitis leading to pulmonary oedema).

A detailed history is helpful in determining the potential underlying cause, e.g. access to a toxin such as lilies, grapes, ethylene glycol, medication prescribed for the owner or another animal.

It is important to assess the patient’s hydration status and body condition, the presence of a bladder (is there an obstruction?) and renal palpation, fundic examination and blood pressure measurement, rectal examination to rule out anal sac masses (which may be causing ARF due to profound hypercalcaemia) and in some cases palpate pelvic urethral obstruction, as this can help determine whether the patient has ARF or CRF and even the underlying cause.

The work up will help rule out treatable causes. Thus a CBC/MBA/UA, urine culture and sensitivity (even in the light of a bland sediment), cytology and even biopsy can help rule in/out pre and post renal causes and determine the presence of treatable disease (e.g. lymphoma, pyelonephritis). An ACTH stim can help rule out Addison's which can clinically look like ARF.

According to Dr Swinney, a patient with mild to moderate azotaemia and severe clinical signs is more likely to have ARF, while a patient with severe azotaemia and mild clinical signs is more likely to have CRF (the latter have more time to adapt).

And ARF doesn’t have a monopoly on renomegaly – you can also get enlarged kidneys from polycystic kidney disease, perinephric pseudocysts, haematomas, hydronephrosis, FIP, and compensatory hypertrophy. So don't be thinking that bilaterally big kidneys = acute renal failure.

A rather large polycystic human kidney. Note loads of cysts replacing most of the parenchyma. Not much room for functional nephrons there.

One of the most important points Dr Swinney made was the need to calculate the fluid deficit and replace it – often over 2-3 hours, as while that hypotension remains renal damage continues. As he said, these are not patients you simple put on 2x maintenance and leave for a day. So if you have a 50kg dog which is 10% dehydrated and you give 3 litres of fluids, the renal injury will continue.

Once the patient is better hydrated Dr Swinney considers using mannitol or frusemide to promote urine production where required. Other supportive care includes gastroprotectants such as H2 blockers or proton pump inhibitors, anti-emetics, oxygen support in hypoxaemic animals and nutritional support.

Three things I learned: dental radiology

There's a big artefact on this radiograph, but right beside it
is a nasty tooth root abscess.

Last week we were lucky to have Christine Hawke of Sydney Pet Dentistry visit the practice and host a workshop on dental radiology. Positioning small animal patients can be tricky, but she broke it down and I learned a few things in the process.

1. The root of the canine is usually over the second premolar (a trap for beginners is to aim for the crown, but we can see that - we really want to be aiming for the root).
2. If you want to split the roots on the radiograph (for example, the carnassial or fourth premolar), use a horizontal oblique view.
3. Anatomical structures such as the mandibular foramen can be superimposed over a mandibular tooth root giving the impression of a periapical abscess. If in doubt take a horizontal oblique view.

Three things I learned: fluoroquinolones

Microbiologists agree that love IS the best medicine...but the antimicrobial properties of fluoroquinolones are needed in some situations.

I've been sitting a little while on a webinar on the fluoroquinolone (FQ) class of antimicrobials (accessible on Bayer's Accelerate website).

Dr Darren Trott, senior lecturer in veterinary microbiology at the University of Adelaide, is an expert on antimicrobials and has spoken extensively about the issue of antimicrobial resistance. In fact, I've even stuck a swab up my nose in order to contribute to his research on MRSA carriage (my result returned negative, thank goodness).

The webinar was a nice review of FQ pharmacology, so in many ways it was a reminder of some important messages as much as anything else. I am sure others will take away different messages from the talk (so please watch it yourself - its 36 minutes).

So what did I learn?

1) If a pathogen becomes resistant to one FQ, it will typically be resistant to this whole class of drugs.

2) FQs are great because they are broad-spectrum, bactericidal, concentration dependent antimicrobials which allows their once a day dosing. But they do have some post-antibiotic activity which renders pathogens vulnerable to the host immune system even as the course is finished.

3) Prescribing veterinarians should opt for the higher end of the dose-range to minimise the risk of resistant pathogen emergence (in this regard pradofloxacin may be superior in that it has lower MICs (minimum inhibitory concentration) and lower MPCs (mutant prevention concentration) than other FQs.

I am going to cheat and add two more points as I think they are worth making. We all know that FQs at high doses are associated with retinal degeneration in cats. Risk factors include older patients, drug interactions, concurrent renal disease and possibly rapid intravenous injection so watch out for those.

Also, all FQs can inhibit cartilage growth which is why we avoid using them in young animals. 

It was a thought-provoking presentation as antimicrobial resistance is a major problem for the welfare of humans and animals. One barrier to prudent antimicrobial use, in real life, is the sheer cost of culturing every pathogen and determining sensitivity. At present, owners pay for this. But surely as a society we need to think about setting up systems where culture and sensitivity testing can be performed cheaply so that the appropriate antimicrobial could be used in every case. 

Three things I learned: snake envenomation in dogs and cats

This little snake doesn't intend any harm - and many don't, but snake envenomation
 is common in Australian dogs and cats.

The ASAVA hosted a webinar on snake bite envenomation, fortunately a condition very rarely seen in inner-Sydney. Dr Peter Best, a specialist based at South Tamworth Animal Hospital, clearly knows everything there is to know about snake bite envenomation right down to the molecular level.

Every year there are an estimated 6,000 snake bite envenomations of dogs and cats in Australia, with jack Russell terriers and Siamese cats overrepresented. (Am I alone in being surprised about Siamese cats?) – although Dr Best did point out that survival rates in cats were likely higher because cats are more agile and therefore may not get the full dose of venom. Of the humans affected, herpetologists and young, inebriated blokes are overrepresented (still more surprised about the Siamese cats).

More good news is that up to 50 per cent of bites did not result in envenomation – either because no venom was delivered or it didn’t penetrate skin.  But it’s impossible to be sure – even if you run diagnostics.

I could easily list 30 things I learned in this presentation, but the three main points I learned were:

a)      Onset of signs can range from minutes to 25 hours. That means that animals with suspected envenomation should be admitted for observation for 25 hours – and if they do deteriorate they can deteriorate rapidly.

b)      Dogs with pre-paralytic signs (i.e. vomiting, salivation, mydriasis and transient collapse) can recover – but the fact that they exhibit these signs mean they have had a potentially lethal dose. They need to be treated with anti-venom immediately. As with all things cats are a bit less obvious, being a bit weak and wobbly

c)       In human medicine the current trend is to give a fixed amount of anti-venom, but according to Best and his team this strategy does not work in dogs and cats. He recommends providing intermittent, positive pressure ventilation (IPPV) and administering anti-venom vials repeatedly (at intervals of around 10-30 minutes) until spontaneous ventilation occurs. (He pre-meds his patients with an IV antihistamine and a SQ dose of adrenalin).  One dog his team treated for brown snake envenomation required a staggering 13 vials of anti-venom (oh, and also two packs of whole blood, one of fresh frozen plasma and artificial ventilation for 36 hours). He survived.

It was an inspiring presentation,  based on a huge amount of clinical experience integrated with solid theory. 

Three things I learned: Peritonitis in cats and dogs

Dorsoventral radiograph of a shih tzu with a radioopaque gastric foreign body (in this case, a beer bottle top). This was an incidental finding in a dog which had been hit by a car (hence the thoracic imaging!). Foreign bodies can cause GIT obstruction, perforation and peritonitis.

The University of Sydney Veterinary Centre hosted a continuing education evening on the topic of peritonitis in the dog and cat. The presentations by Drs Alastair Franklin, Mark Newman, Heide Kloeppel and Chris Tan were fantastic.

So what did I learn?

·         The peritoneum is equivalent to 150 per cent of the body surface area, and the hypovolaemia and hypoproteinaemia that occur with peritonitis are similar to losses which occur with third degree burns.

·         Secondary peritonitis is the most common form, with 50 to 75 per cent of cases occurring due to loss of GIT integrity (and around 15 % of GIT resection and anastomoses break down – even those performed in referral facilities).

·         Aseptic peritonitis can be caused by endogenous chemicals (bile and urine – which I knew) but also exogenous chemicals (iodine and saline – yet we are required to flush with the latter! It does raise the question, in what circumstances is saline likely to cause peritonitis? I would expect it would be failure to suction all lavage fluid prior to wound closure, which might turn it into a medium for bacteria?)

·         It’s simple, but worth remembering: take rads before you perform your abdominocentesis, as even with careful technique you can introduce gas into the abdomen which complicates radiograph interpretation.

 The talk covered everything from abdominocentesis fluid analysis to anaesthetic considerations and ex-lap technique, emphasising the need for a multidisciplinary approach to a challenging problem.