GIT Flashcards
Peritonitis?
Abdominal pain?
Unsure? Surgery until proven otherwise
** need to make sure the pain is abdominal– so must try to localize
Further assessment should be undertaken to
determine if the pain is definitely abdominal.
Beware
of referred pain especially from the
back including abdominal splinting from neck
pain or lumbar/sacral
pain
Pleuritis and Pneumonia can also manifest as
pain on abdominal palpation
How do more stoic animals show pain (examples)?
Abdominal problem– surgical v. medical?
What causes abdominal pain?
Acute abdomen GIT requiring surgical treatment
* severe Gastro-enteritis (viral/bacterial/parasites/toxin/HGE)
* Pancreatitis
* Obstipation
* Colitis
surgical or medical?
Surgical or medical?
Surgical or medical?
Top of the list for serious GIT problems
Stabilization
What would kill it first
* IV fluids for circulator support– try to restore or maintain tissue perfusion/ blood pressure
* Analgesics
* Oxygen
* Antibiotics
* Other symptomatic treatment
Analgesia for stabilisation
Start with a pure agonist unless biliary stasis
* If opioids are not rapidly reducing/ controlling the pain then add in other agents as CRIs
- ketamine, lignocaine, metetomidine, or intra-abdominal/intrathoracic/local blocks of lignocaine/bupivicaine
** Do not use NSAIDs in patients that are haemodynamically unstable or have GIT/ Renal involvement
Initial tests in an emergency patient
Peripheral blood PCV/TS in acute abdomen cases
Blood glucose in acute adomen– increased DDX?? Decreased??
Increased BUN in acute abdomen
Assessment of blood smear in emergency case
Look for signs of
- Regeneration- Anisocytosis, macrocytosis, polychromasia
- DIC- schistocytes, rbc fragments
- Leucocytosis with or without a left shift
- Leucopenia
Signalment impact on DDX
Information required to determine DDX
* exposure to potential toxins
* other animals affected?
* Vaccination history
* Worming history
* When does pain occur (constant v. fluctuating: more marked after eating)
Abdomen clinical assessment
What are we trying to achieve with imaging for abdomen?
* Do we need to go to surgery?
* Do we need to sample?
* What management is required?
Options for imaging abdomen
What views do you want from RG of the abdomen?
Increase in gas… suspicious of an obstruction
Reading the abdominal radiograph
Pacreatitis showing up on RG?
Transverse colon is displaced caudally often
Intraabdominal serosal detail
Where is the spleen?
young– poor serosal detail because of brown fat
Effusion secondary to lymphoma
Peritonitis
Peritonitis due to perforating foreign body
Thin patient will have loss of serosal detail
Evaluation for abdominal fluid
* AFAST: Abdominal Focused Assessment with Sonology for Trauma
diaphragmatio-hepatic (DH)
Spleno-renal (SR)
CC- cysto-colic
HR- hepato-renal
Not a ruptured bladder, an artefact
On U/S what does echogenecity tell us?
We have cells.. so we need to sample it– blood?
Fluid analysis of abdomen… what are we ruling in or out? How do we collect?
How to collect fluid from the abdomen
Diagnostic peritoneal lavage
Fluid analysis from the abdomen
Fluid classification
What are some specific findings from abdominal fluid that point towards specific disease processes?
What does glucose or lactate tell us?
Top differential if you find the following in abdominal fluid:
* bacteria?
* toxic neutrophils?
* plant fibres?
* GIT leakage?
DPL fluid analysis
Diagnostic peritoneal lavage (DPL)
* Amylase > serum– pancreatitis, trauma to pancreas or small bowel leakage
* Alkaline phosphatase > serum– significant intestinal trauma, ischaemia or leakage
* Bilirubin positive in a non icteric patient– leakage from biliary system or proximal bowel
* Creatinine > serum– uroabdomen but need contrast studies to confirm
Retroperitoneal haemorrhage
Free gas post sx for SI foreign body
Free abdominal gas (normal after a surgery– but after 2 weeks should be decreasing down to nothing)
Decreased serosal detail and BIPs (Barium Impregnated Polyethylene Spheres)
** Suspicious that there was free abdominal gas– lied them down on the side for 10 minutes.. then horizontal beam radiograph- you can see the free gas in the peritoneal gas… turns out to have a rupture of the duodenum
Hepatic mineralization
Free abdominal gas with no history of surgery?
Someone needs to go there!
How might you see an abdominal mass lesion?
Viscera displaced by mass lesion
* Assess location of stomach and SI
* Recall the normal position of the abdominal organs
When can you count with RG number of puppies?
58-60 days (starts at 45 days)
* U/S 21 days– but harder later on
Location of abdominal organs NEED TO KNOW!!!
Hepatic mass- displaces the stomach
Hepatomegaly– slightly rounded margins
and Splenic mass (mid ventral abdomen, heavy and flop down)
Splenic masss (displacement of intestines)
A mass that is more dorsal in the abdomen is in the retroperitoneal space like this adrenal mass
* A mass that is more ventral is in the peritoneal space
Look caudally– Lymphoma of the Medial Iliac LNs (MILs)
** ventral to L6 and L7– sublumbar LNs– if enlarged mass lesion
Large urinary bladder– due to poor management rather than pathological process
Bates body and hepatic mass
Right Renal Mass
Splenic mass (central)
Paraprostatic cyst– uncastrated male dogs are rare in the city v. rural
Imaging of the stomach– what are you looking for if diseased?
Gastric dilation
GDV- position of the pylorus, and the stomach twists into two bits– compartmentalization
** is it just big and distended or twisted as well??
GDV
GDV
GDV– often megaoesophagus and gas distended small intestines
Liver in the acute abdomen
Hepatomegaly
Liver abscess
Emphysematous cholecystitis
Gall bladder mucocoele
Splenic torsion– C shaped spleen
Key to good abdominal radiographs
General ideas of antibiotic usage with GIT
Broad spectrum choices of antibiotic for GIT
Regurgitation or vomiting?
Regurgitation
What does regurgitation usually mean?
Signs of regurgitation?
* Is there a yellow-green stain to it?
* Abdomen contract when vomiting?
* Abdominal radiograph- Bone stuck in oesophagus– staffies and westies can get big things in their mouths
Control of vomiting
Efferent pathways
- autonomic nervous system inhibits motility gastric body, oesophagus and sphincters
- somatic nervous system driving force
CNS and vomiting
Causes of vomiting
DDX of acute vomiting… GI
DDX of vomiting… not GI
What do you need to know when presented with an acutely vomiting animal?
History for a vomiting patient
Vomiting or regurgitating?
Does it seem to be primary GI?
Do I have a suspicion of what I am dealing with?
Is it a pretty sick animal?
Physical examination of vomiting patient
Should know– if needs further basic investigation, if needs treatment only or with diagnostics
* May know– underlying cause
When to treat a vomiting animal empirically (non-specifically)
When to investigate further with a vomiting patient as opposed to treating empirically
How do you rule out metabolic disease in a vomiting animal?
What infectious disease would you rule out in a vomiting dog?
Faecal parvovirus in at-risk dogs
How do you rule out a surgical emergency in a vomiting patient?
* No prior signs of illness, known scavenger, younger (usually), dogs > cats
Clinical signs of GI obstruction
What do we have left after basic investigation if they are still vomiting?
* Systemic infections: FeLV, FIV, leptospirosis, canine distemper
* Toxins: drugs, chemotherapy, heavy metals, organophosphates
*Metabolic disorders: uraemic, hypoadrenocorticism, liver disease, hypercalcaemia, DKA, Pyometra, peritonitis
Further investigations of vomiting patient
Linear foreign bodies
Clinical signs of intussusception
Diagnosis and treatment of intussusception
ANP is frequently associated with peri-pancreatic necrosis (and therefore hyperechogenicity surrounding the pancreas) and therefore easier to identify. However the changes in chronic pancreatitis are much more subtle and generally consist of patchy echogenicity, fluid accumulation within the parenchyma and sub-capsular area as well as a dilated pancreatic duct. Ultrasonic diagnosis is mild pancreatitis ie no peritonitis and just altered echogenicity of a slightly enlarged pancreas then generally there is only mild disease and a good pronosis.
** In this image we can see the hyperechoic areas on the fat surrounding the pancreas and an enlarged pancreas with hypoechoic and hypoechoic areas within it.
cPLI/Spec cPL– IDEXX test – Canine Pancreas specific lipase
Perforated intestinal tract– septic peritonitis– tennis ball in intestine and had to resect part of intestine. Plasma transfusions, vasopressors, etc.
Acute vomiting take aways
Feline PLI– pancreatic lipase immunoreactivity test
Acute vomiting.. exploratory laparotomy??
Haemoglobin– low
PCV– low
RCC- low
Cholesterol- low
Total protein- low
Albumin- low
** imaging unremarkable
** Should we scope or perform exploratory laporatomy now?
Third episode… something not right
* Fluids, analgesia
** no stress leukogram… no steroids!! Glucocorticoid deficiency (doesn’t have mineral corticoid deficiency because electrolytes are normal)
Don’t want loops of SI to be larger/ more distended than the LI
FB! Can’t really see on this view
Don’t want loops of SI to be larger/ more distended than the LI
FB! Corn cob
Linear FB in a cat
Linear FB with contrast that highlights the bunching
Common disturbances with GIT patients
* Treatment/ correction of these pre-op problems important to: optimise outcomes and prevent complications
* Fasting for elective procedures can minimize risk of spillage but decreases gastric fluid pH
* If gastro-oesophageal reflux anticipated– consider H2 antagonist or proton pump inhibitor
* Rapid induction and airway control if vomiting reflux likely (prevent aspiration)
Five regions of the stomach
Vascular anatomy of the GIT (arterial)
Vascular anatomy of the GIT (venous)
Halstead’s principles
Surgical approach to the abdomen
Isolation of the GIT for surgery
Contamination in abdominal surgery
Gross contamination in abdominal surgery
Peritoneal lavage
Gastrotomy/ Gastrectomy
Suture materials and patterns for the stomach
Use of stapling in GIT surgery
Types of staplers
Post op considerations gastrotomy
Post op therapy gastrotomy
Enterotomy indications
Enterotomy technique
Enterotomy closure
Taking an intestinal biopsy
Intestinal resection and anastomosis
Techniques of intestinal resection and anastomosis closure
Sutured end-to-end anastomosis
Managing luminal disparity sutured end-to-end anastomosis
Stapled anastomosis– side to side (aka functional end-to-end)
Stapled anastomosis– circular end-to-end staplers (EEA)
End-to-end anastomosis- skin staplers
Enteroplication/ Enteroenteropexy
Suture line reinforcement techniques
Gastro-oestophageal reflux- complication
Complications– septic peritonitis
Adhesions as a complication
Short bowel syndrome
Treatment of short bowel syndrome
Ileus as a complication
Four common sites of lodgement for FBs
Fish hook as an Oesophageal FB
Removal of oesophageal FBs
Oesophagotomy
Gastric FBs
Gastrotomy for FB removal
Gastrotomy closure
Solid Intestinal FBs
Linear intestinal foreign bodies
Intestinal foreign bodies considerations (if you leave it or how you remove it)
Delayed gastric emptying
Pyloroplasty procedures
Breed predisposition for GDV
Clinical signs of GDV
Pathophysiology of GDV
Pre-surgical management and stabilization of GDV
GDV pre-surg management and stabilization
When should you perform a GDV?
Gastric repositioning
Gastric wall necrosis/ partial gastrectomy
Gastropexy
Splenectomy and GDV
Post op management GDV
Prognosis for GDV
Prophylactic Gastropexy
Intestinal intussusception
Neoplasia of the GIT
Intestinal and colorectal neoplasia
Feline Idiopathic Megacolon
Feline Idiopathic Megacolon Medical Therapy
Subtotal colectomy with Feline Idiopathic Megacolon
Closure and prognosis of Feline Idiopathic megacolon
How would you know before surgery if you might need to do a partial gastrectomy?
Really high lactate levels & response to fluid therapy does not significantly alter the lactate levels
Recommended type of gastropexy
incisional gastropexy– match up two cuts
(longer acting absorbable– PDS)– eventually form a good fibrous union
When to use empirical treatment with acute vomiting and diarrhoea
Types of empirical treatment in acute vomiting and/or diarrhoea
Anti-emetics indications for use? C/I?
Phenothiazines as an anti-emetic
NK1 receptor antagonists and dopaminergic antagonists as anti-emetics
Narcotics, antihistamine, anticholinergics, butorphanol, and 3-HT3 antagonists– as anti-emetics?
Prokinetics indications for use
Metoclopramide and ranitidine as prokinetics?
Cisparide as a prokinetic?
Anatomy of the oesophagus
Function of the oesophagus
Regurgitation
Clinical signs of regurgitation
Obstructive causes of regurgitation
Non-obstructive causes of regurgitation
Diagnostics with regurgitation
Megaoesophagus
Vascular Ring Anamoly
Foreign body
Endoscopy
Ancillary diagnostics for regurgitation
Complications of regurgitation
Bronchopneumonia (can be a complication of regurgitation)
Treatment and prognosis of regurgitation with FB and vascular ring anamoly
Treatment and prognosis of regurgitation caused by neoplasia or oesophageal stricture
Treatment and prognosis of spirocercosis, pythium indisiosum, OR hiatal hernia?
Hiatal hernia in a dog–
Hiatal hernia is a genetic disease of dogs characterized by a hernia of the anterior stomach through the diaphragm.
Although this is usually a birth-related defect, it can occur in dogs secondary to diaphragmatic hernia[3], tetanus[4][5] and Duchenne muscular dystrophy (dystrophin-deficient muscular dystrophy)
** more common in dogs with brachycephalic syndrome
A hiatal hernia, which occurs more common in dogs with brachycephalic syndrome[7][8], is defined as any protrusion of abdominal contents through the oesophageal hiatus of the diaphragm into the thoracic cavity in the presence of an intact phrenico-oesophageal ligament
Treatment and prognosis of congenital, idiopathic, or neuromuscular regurgitation?
Treatment and prognosis of endocrinopathies or immune-mediated or neoplastic causes of regurgitation?
What kind of ongoing care is needed with regurgitation?
Take home points of regurgitation
“ARCHIE” 2 year old M(N) Labrador
Clinical signs:
-
Owner noticed that he has been vomiting more frequently for
the past 3 days
-
Has always brought up food for the past month
Physical examination:
-
BCS 3/9
-
RR: 40, with mild dyspnoea
-
Temperature: 39.6 degrees
celcius
o
WHAT QUESTIONS WOULD YOU ASK?
o
WHAT IS YOUR PROBLEM LIST?
o
WHAT ARE DIFFERENTIAL DIAGNOSIS?
What do you think of when you consider abodominal distension?
What to look for with fluid in abdominal distension?
Then determine the type of fluid
Exudate v. ascites
Causes of ascites
Causes of modified transudate with ascites
Causes of pure transudate in ascites
Pure transudate
* Decreased oncotic pressure
* Albumin < 15 g/L
What exudates are likely to be chronic?
* blood- a little bit sometimes with bleeding tumours of liver and spleen
* Chyle- can be but very rare
* Not urine
* Neoplastic- can be, but very rare
* Inflammatory- limited conditions
•
Te n
- year
- old German Shepherd(neutered
female)
•
Abdominal distension noted over past week,
and reduced appetite
•
Collapsed this morning
* Fluid filled abdomen- not painful
* RR 60 bpm
* Difficult to auscultate heart, but pulse rate 140 bpm
* Temperature 38C
* When standing, can’t hear lung sounds ventrally
* Jugular vein distended
* No cyanosis or pallor
* Evidence of Increased hydrostatic pressure– thorax and abdomen fluid and cranial (jugular)
* therefore increased diastolic pressure or increase RV pressure
* What can cause this? Right sided CHF (rt atrial mass, tricuspid valve disease, pulmonic stenosis, RV cardiomyopathy, pericardial effusion)
* Diagnostic plan
- thoracocentesis
Haemangiosarcoma
* Pitting oedema all limbs and ventrum
* RR 38
* Lung sounds muffled ventrally
* What does this suggest? What do you do next?
* Blood results: TP 30 g/L (60-80); Albumin 12 g/L (24-40), Globulin 18 g/L (36-56)
* Causes of low protein??
* Causes of low protein: Decreased production (liver disease), Increased loss (skin, urine, GIT)
** With liver disease–> low urea, glucose, bile acid stimulation
** With increased loss–> can usually tell!–> only albumin, confirm with urine via cystocentesis: if dilute then a urine protein- creatinine ratio–> albumin and globulin, can also have low lymphocytes or cholesterol
DDX: no signs of pleural fluid, fluid is an exudate
FIP
Basics of FIP
Wet FIP
Dry FIP
FIP Diagnosis
* Major cause of abdominal fluid in cats, especially young
* may have green- yellow appearance
* Often mucinous
* Rivalta’s test in clinic
* Immunohistochemistry of fluid confirms disease
* RT- PCR
Fat as a cause of abdominal distension DDX
* Hypothyroidism, hyperadrenocorticism, obesity
Feel a big mass– abdominal mass?
Floppy abdomen DDX?
* Loss of dorsal muscle mass
* Hyperadrenocorticism
Chronic abdominal pain
DDX for true abdominal pain
* Any distension, torsion, or compression:
- GDV, mesenteric volvulus, intussusception or FB, urethral obstruction and bladder distension, intestinal spasm, splenic torsion, neoplasia, acute renal failure
Abdominal pain not originating from abdominal disease
Approach to animals with pain
Analgesia is important- do not wait for full diagnostics!!
* Later: U/S if indicated… urine analysis/ culture, pancreatic lipase, endoscopy
Chronic pancreatitis
* Breed disposition
* Difficulties in diagnosis:
- no specific clinical signs, no specific clinical pathology changes, no reliable change in PLI, intermittent in nature
* DDX IBD
* Definitive diagnosis: Histopathology– when? How? Why? Target treatment, possible effect on diabetes control or development of exocrine pancreatic insufficiency
Treatment of chronic pancreatitis?
* history taking for vomiting patients: pair-think-share
Problem list and DDX:
- Acute abdomen with vomiting
- Dehydration
- Not eating today
- Quiet
Which procedures do you do first?
Rehydration fluid therapy– maintenance fluid therapy, PCV/TS/blood, gas/ electrolytes, blood pressure (MAP 80), SPO2 97%, Buprenorphine 10 mcg/kg
What are the 4 types of fluid therapy?
Deciding the kind of fluid therapy
shock rate– 90 ml/kg over 1 hour (dog); 60 ml/kg over 1 hour (cat)
* A– 0.07 x BW over 4-24 hour; Hartmann’s crystalloid
AFAST- looking for fluid– haemorrhage or perforation??
Pale MM you would also see. Septic peritonitis could also see.
Radiograph
Barium– used to be gold standard– should not be used to assess if suspect perforation (presence of gas or loss of serosal detail on the RG)
* Maropitant- anti emetic– why not give?? Could make them seem more comfortable (mask an obstruction), effects on GI motility around an obstruction to cut off blood supply to an intestinal loop further and cause more damage
If no to surgery
Clean contaminated (could go in and find pre-existing perforation, so then would be contaminated)
** so we will use AM prophylaxis– cephalosporins on board before and during– inhibitory concentrations in the serum
Before and during
3 Aborad (further down the GIT)– in the healthy part is where you want to make you incision
Start feeding about 12 hours after surgery
What are your goals for sending the dog home?
Antibiotics, abdominal U/S to see if any fluid– problems with U/S in this patient?? There will be gas and so it is hard to see things with gas around– also there will be post-op fluid, so have to decide if that is normal or too much. Abdominocentesis.
You will see loss of serosal detail too– from surgery? Or from the disease process??
** Cytology– looking for cells and bacteria– looking for neutrophils responding to inflammation acutely… and the number of neutrophils.. Spey= 5-10,000 healthy looking neutrophils vs. lots more and degenerative (or toxic in the blood) neutrophils
* Run paired fluid and serum
* Glucose/lactate (sepsis)
* Triglycerides (if chylous)
* Creatinine/ Potassium (uroabdomen)
* Bilirubin
* Amylase/ lipase (pancreatitis)
Post op support
Enteral feeding
Medical management of acute abdomen
Definition of acute pancreatitis
Pathophysiology of pancreatitis
Zymogens are catalytically inactive precursors of digestive enzymes. They are secreted from the
pancreas into the lumen of the small intestine in response to food.
Enterokinase, a peptide produced by small intestinal m
ucosal cells, activates trypsin. Trypsin
then activates an enzyme cascade, cleaving the activation peptides from other digestive
zymogens
Trypsin has been shown to initiate activation of all pancreatic enzymes.
Therefore trypsinogen
activation within the
pancreas results in subsequent activation of
all
pancreatic enzymes within
the pancreas.
The pancreas has a number of safeguards in place to protect it from this intra-
pancreatic activation of pancreatic enzymes and subsequent auto
-digestion.
These safeg
uards include:
•
Storage of the enzymes as inert zymogens separate from lysosomal enzymes within the
acinar cell
•
Secretion into the intestinal lumen, and activation within that lumen
•
Local pancreatic trypsin secretory inhibitor (PTSI) that ‘coverts’ activate
d trypsin back to
trypsinogen. This gets overwhelmed if >10% trypsin is activated.
•
Circulating anti-
proteases
PANCREATITIS
DEVELOPS
WHEN
THERE
IS
ACTIVATION
OF
THE
DIGESTIVE
ENZYMES
WITHIN
THE
PANCREAS
RATHER
THAN
WITHIN
THE
INTESTINAL
LUMEN,
RESULTING
IN
AUTO
-
DIGESTION
OF
THE
PANCREAS
AND
SURROUNDING
FAT
Aetiology of pancreatitis
* mainly high fat and low protein
* therefore urolithiasis diets
* Not for eating the wrong thing
Development of pancreatitis
Systemic inflammation
Potential clinical signs of pancreatitis
* Cats: associated with hepatic lipidosis and main sign anorexia or mild lethargy
Likelihood of clinical signs in acute pancreatitis
Diagnosis of acute pancreatitis
** Clinical signs and suscpicion
Clinical priorities in acute pancreatitis
U/S Diagnosis of Acute Pancreatitis?
Spec-Canine Pancreatitc Lipase
Canine pancreatic lipase measures lipase that originates solely in the pancreas. The canine pancreatic-lipase immunoreactivity (cPLI) assay was developed into a commercially available specific canine pancreatic lipase (spec-CPL) sandwich ELISA, with results < 200 µg/L expected in healthy dogs, and results > 400 µg/L considered consistent with a diagnosis of pancreatitis (7). A new in-clinic rapid semiquantitative assay (SNAP-cPL; Idexx Laboratories) has also been developed. The reported sensitivity of spec-cPL for diagnosing pancreatic inflammation in dogs ranges from 21 to 88% (8-12). The sensitivity of pancreatic lipase is greatly increased when more severely affected dogs are assessed. Specificity of pancreatic lipase has been reported to range from to 80% to 97.5% (9, 11-13). In summary, a negative result for SNAP-cPL or cPLI means it is likely that the dog has disease other than acute pancreatitis. A positive result still requires confirmation and elimination of other disease by some other modality.
Spec-canine pancreatic lipase interpretation of results?
Sensitivity & Specificity of Spec cPL
SPEC cPL–> a cageside sandwich ELISA??
SNAP in acute abdomen…. is it any good?
* a negative cPL means a dog is unlikely to have pancreatitis (<10% chance)
* A positive cPL means the dog is likely to have acute pancreatitis (>30% chance) but that pancreatitis may not be the reason for presentation
11/ 27 = 40%– not to say there wasn’t pancreatic inflammation but it wasn’t the reason for the animal presenting
Pancreatic lipase immunoreactivity for cats (PLI)
A species specific pancreatic lipase immunoreactivity (fPLI) radioimmunoassay has recently been developed with a reference range established of 1.2-3.8 μg/L12. One study showed a very high sensitivity (100%) in 5 cats with ANP, but 54% for the 13 cats with CP9. Overall the specificity of fPLI in that study (compared to 8 healthy cats and 3 symptomatic cats with normal pancreatic histopathology) was 91%, which shows there may be minimal effects from other diseases. Once larger studies have been published the true sensitivity and specificity of this test can be established. However, it does appear as if there may well be a difference in the diagnostic utility of this test in CP versus ANP, similarly to measurement of cPLI in dogs.
Feline PLI
Cytology in diagnosing acute pancreatitis?
Treatment of acute pancreatitis
* no to very little evidence in dogs or cats
* much extrapolation from human and experimental studies
PANCREATIC microcirculation
The artery often supplies islets first and therefore bathes the acinar cell in relevant hormones, or the so-called ‘insuloacinar’ portal system’.
The downstream supply to acinar cells makes them uniquely susceptible to poor perfusion and hypotension, an important factor in the development of pancreatitis,
* Current recommendations in people: early fluid resuscitation is essential– most effect in milder forms of disease; lactated ringers solution superior to normal saline– potentially due to reducing acinar acidosis and down-regulating NF-kB
Is rapid fluid resuscitation enough in cats and dogs??
Cats can develop pulmonary oedema rapidly (possible in dogs too!)
Cobalamin
Plasma in pancreatitis treatment??
Use of plasma in acute pancreatitis has been
shown to
not
be clinically effective at low or high
doses in people
•
Use of plasma for treating dogs with acute
pancreatitis has been declining recently
•
One retrospective study showed higher mortality
in dogs that received plasma (7/20) compared to
those that didn’t (6/57)
–
Significant bias in study
Analgesia with AP?
First step in analgesia:
assume pain is present, recognise and quantify level of pain
, re-assess frequently
* second step: start with maximal analgesia thought necessary, don’t start low and then work up
Mild to moderate pain treatment (AP)?
Moderate to severe pain (AP) treatment?
Pain meds to avoid in AP
When to start nutrition in AP
* In dogs (and especially in cats) as soon as stable start nutritional intervention if they are not eating voluntarily
Anti-emetic drugs
Anti-emetics tx of AP
* Goals of anti-emetic treatment
- unlikely to resolve ALL episodes vomiting
- concurrently control nausea
- allow feeding
- minimise continued fluid losses
** Therefore currently recommend maropitant initially– add in ondansetron if signs of nausea, poor emetic control (0.5 mg/kg slow IV then PO q 12-24 hours OR 0.5 mg/kg/h for 6h)
Other anti-emetics aside from Maropitant with AP
Gastric acid suppression in AP
Complications of AP
THEREFORE…. if not causing pain… benign neglect
If causing pain… percutaneous drainage
Corticosteroids in AP?
* possibly hydrocotisone; possibly low rate infusion
* need to get everything else sorted before recommending routinely
Follow up for pancreatitis?
Peritoneal Defence Mechanisms
Pathophysiology of peritonitis
•
Fluid loss & Vasodilation
- > reduced cardiac return
- > reduced
cardiac output ->
reduced systemic perfusion
•
Reduced perfusion
– anaerobic metabolism, production of MCD
•
Acidosis
Secondary to:
•
Poor perfusion of organs
•
Poor renal perfusion inhibits renal buffering mechanisms
•
Reflex rigidity inhibits ventilation
•
Catecholamine and cortisol responses result in
hyperdynamic
state
^ O2 demand
•
Poor perfusion and disruption to mucosal barriers promotes
bacterial translocation.
•
Endothelial damage and circulatory stasis promotes
hypercoagulable
state
worsened by loss of clotting factors
Peritonitis–> SIRS
Adjuvants for Peritoneal Inflammation
Causes of Peritonitis
Surgical management of septic peritonitis
Most common cause of peritonitis? Others? Risk factors post surgery?
Causes of leakage from the GIT
Pre-operative considerations for peritonitis
Approach, suture materials, and suture patterns for peritonitis?
Debridement and important surgical steps when treating peritonitis?
Purpose of lavage for peritonitis sx? How much?
Omentalisation in peritonitis surgery
Serosal patching in peritonitis surgery
Closure options peritonitis sx
When should you use primary closure without drainage for peritonitis surgery?
when should you use open peritoneal drainage in peritonitis surgery?
•
Cranial 1/3
-2/3 of the linea
alba left partially
open with a loose simple continuous
monofilament suture pattern (1-
6 cm gap)
•
Falciform
ligament excision
•
Tack omentum to areas of leakage to
prevent occlusion of opening
•
Sterile technique for bandage changes
– in
surgical suite under GA
– allows serial re
-
inspection
•
Bandages weighed to assess fluid loss
•
Mean open drainage duration 4 days in
retrospective clinical studies (Greenfield
1987,
Woolfson
1986)
•
Criteria for closure unclear but recommendations:
(Woolfson
1986)
•
Improvement in colour and clarity of drainage fluid
•
Reduction in volume drainage fluid
•
Absence bacteria on cytology
•
Repeat culture at closure
– 40% patients had different
MC&S results (Greenfield 1987) and positive results
increased mortality (
Woolfson
1986)
•
Nosocomial infection recognised complication
•
Superiority of open drainage not established in any
trials in clinical reports in either humans or animals
Primary closure vs. open drainage peritonitis?
Closed suction drainage potential problems and benefits (peritonitis sx)?
Closed suction drainage
VAC Laparostomy peritonitis sx
•
Technique similar to open but:
•
Visceral protective layer (?)
•
Open cell foam
•
Suction catheter
•
Circumferential Occlusive film seal
•
Continuous
Neg
pressure
-75-
125mmHg via
Suction unit
•
Changed q 48
hrs
•
Time to closure:
•
2 days
Post operative support peritonitis
Prognosis for peritonitis sx
What does fasting lead to?
Role of nutrition in healing after GI disease
What is interventional nutrition?
Partial parenteral nutrition
Slide
36
Partial parenteral nutrition
•
Formulation complex
•
Add glucose, amino acids then lipids
Can add water soluble vitamins
•
Sterile conditions
•
Room temperature maximum 24 hours
•
Dedicated sterile IV catheter
•
Can be started at 100% Day 1 (but at 0.7 RER)
Total parenteral nutrition
Complications parenteral nutrition
Enteral feeding post op
Enteral nutrition post intestinal surgery?
When to commence enteral feeding?
What is NPO mean?
What is assisted nutrition?
Oesophagostomy tubes
O tubes: 12-14 F cats; 16-18 F larger dogs
Method of insertion of O-tube
cont.
•
Enlarge incision so forceps can push through hole
•
Grab end of tube
•
Pull back towards mouth
- expand opening if wish
•
Turn the tube around in mouth and push down the
oesophagus
•
Do a little wiggle/flip and ensure kink is gone and no tube in mouth
•
Pull out to
predesignated
spot, quick skin prep
•
Secure with
pursestring
then a
chinese
finger trap suture with non-
absorbable suture material
Gastrotomy tubes (G tubes)–general? Biggest risk?
Gastrotomy tube feeding advantages and disadvantages?
How much do you feed dogs with enteral feeding?
How much to feed cats (enteral feeding)?
What are the goals with how much to feed with enteral feeding?
Random tips with enteral feeding
What to feed with enteral feeding?
Immunomodulators with enteral feeding
Glutamine
•
Amino acid used by enterocytes as energy source
•
Reduces villus blunting and bacterial translocation
•
Variable outcomes in human studies, but safe except in
renal or hepatic disease
•
Difficult to supplement in enteral formulations
When to use immunomodulators with enteral feeding?
Role of HCl? Pepsinogen? Somatostatin? Gastrin? Mucous?
Signs of gastric disease
What do you need to consider with chronic vomiting?
When to go with symptomatic treatment with chronic vomiting?
Important questions to ask with history with chronic vomiting
Physical exam of animal with chronic vomiting
Assessment of animal with chronic vomiting?
How to treat symptomatically with chronic vomiting
* anti-emetics do not have a place with chronic vomiting
* Dietary therapy
* Decide what is most important: hypoallergenic, soluble fibre and highly digestible, Omega 3
** there are more possible tx (antacids, diffusion barriers, H2 receptor antagonists, proton pump inhibitors, etc.)
Antacids in the treatment of chronic vomiting
Diffusion barriers (Sucralfate) tx of chronic vomiting
* Indications: treatment of gastric ulceration and reflux oesophagitis
* Administration- apart from food and other drugs (30 minutes except digoxin, tetracyclines, fluoroquinolones it’s 2 hours)
H2 receptor antagonists in the treatment of chronic vomiting
•
Cimetidine
(Tagamet) q 6
-8 h
•
Ranitidine (Zantac) q 12h
•
Famotidine (Pepcid) q 24h
•
Nizatidine
(Tazac)
•
REDUCE DOSE BY 50% IF IMPAIRED RENAL
FUNCTION
PPI tx in chronic vomiting
•
Omeprazole
(Losec
)
•
Effective dose is higher than in many guides:
–
- 5
- 1.5 mg/kg PO q 12 hours in ICU
–
Then 0.5 mg/kg q 24 hours
•
Oral
omeprazole
more effective than IV
pantoprazole
•
Used
for:
gastrinomas, gastric carcinomas,
reflux oesophagitis, mast cell tumours
•
Need to taper down
PE1 analogues tx chronic vomiting
DDX of chronic vomiting
*IBD
* dietary intolerance
* intestinal lymphoma (cats>>dogs)
* chronic pancreatitis
* Secondary diseases:
- hyperthyroidism (cats)
- renal failure
- liver disease
- heart disease
- hypercalcaemia
- hypoadrenocorticism etc…
Haematemesis
Ulcerative disease
Gastric ulceration causes
Consequences of GI ulceration
Initial tests to run in chronic vomiting
Approach to gastric ulceration
* blood work unremarkable
* gastric distension on abdominal radiographs
* Couldn’t see much on ultrasound
Pyloric antral hypertrophy
Chronic vomiting in cats?
•
ALL chronic inflammation in gut will lead to
lymphocytic-
plasmacytic
inflammation
- difficult to
differentiate inflammation from small cell lymphoma
•
Often chronic history
•
Diarrhoea not always observed
•
Pruritis
may be manifested as vomiting of hair balls
•
Only SEVERE disease will cause weight loss
Dietary sensitivity as a cause of chronic vomiting in cats
•
Cats have a short digestive tract (
c.t
. dogs) and are
obligate carnivores
•
Therefore, require highly digestible diets
•
Diets picked for cats with suspected dietary sensitivity
should have highly digestible or
hydrolyzed
protein
sources
•
No correlation to ELISA or RAST testing
Different foods relationship to microflora
IBD
Post-FeLV most common site for lymphoma in cats??
Intestine
* Classification of lymphoma: small cell lymphocytic, large cell (lymphoblastic)- large granular cell
Small cell lymphoma?
* Diagnostic difficulties
- not always changes on U/S
- where to biopsy
- how to biopsy
- how to interpret biopsy: PARR testing (antigen rearrangement) useful, and may be diagnostic on duodenal sample even if lymphoma is in ileum
* Potential causes: genetic predisposition, any chronic inflammation: IBD, Helicobacter?, cigarette smoke exposure, FIV (no effect on prognosis)
Large cell lymphoma
Clinical signs of chronic pancreatitis in cats
Diagnosis of chronic pancreatitis
Clinical priorities when presented with a chronic vomiting (but well) cat….
* Diet–> antibiotics–> immune suppressives
* Should see response in 1-2 weeks
* If do, continue diet for 6 months if completely balanced, and then can try other previous diets. Approx 50% won’t relapse
* If partial response: can try alternative hydrolyzed or hypoallergenic diet– may be variable individual response
If chronic vomiting cat does not respond to diet….
Antibiotic trial–> amoxicillin 20 mg/kg bid for up to 6 weeks
* Metronidazole 10 mg/kg bid for maximum 3 weeks
* Again, should respond within 1-2 weeks and after 3-4 week course may only need dietary management
** If still no response to diet… need to “support the cat”
* need to be happy with diagnostics
Last stop in chronic vomiting cat no response to diet firstly or after antibiosis….
U/S: may be normal or show loss of layering with IBD, small cell lymphoma
- may show masses, lymphadenopathy, focal intestinal thickening or effusion and can get samples
Diagnosis of IBD
If you diagnose IBD:
- Prednisolone: 1-3 mg/kg daily (once or in divided doses), start to taper every 3-4 weeks until reach minimum effective dose, continue diet and continue antibiotics for first 2 weeks of prednisolone, side effects: PU/PD and alopecia (minimal) and development of diabetes is a risk
- Other corticosteroids: Dexamethasone: only if can’t give oral medication, and not eating well enough to place in food, 1/6 to 1/8 of the oral pred dosage q 36-48 , profound immune supprssion OR Budesonide: not evaluated in cats
- Other immunosuppressives: only if histological diagnosis! Chlorambucil: current choice as add on, generally well tolerated, Ciclosporin: be careful with latent toxoplasmosis, not evaluated in feline IBD
- Other therapies: Omega 3 fatty acids- may interfere with palatability of diets and cause diarrhoea, extrapolated dosage is 17-25 mg/kg/day EPA; 8-18 mg/kg/day DHA…. Probiotics: lack of translational benefit in people, well tolerated in cats, recent abstract suggest not effective feline IBD
If you diagnose small cell lymphoma
Tx: still support (cobalamin), still give antibiotics and diet
- initial therapy:
- prednisolone 3 mg/kg once daily, reducing to 1-2 mg/kg once daily when have clinical remission
- Chlorambucil
* Treat concurrent disease
- What are potential concurrent diseases?
Cholangiohepatitis: antibiotics +/- immune suppressive, vit K if severe
Pancreatitis (usually chronic): nutritional support, analgesia
Hepatic lipidosis: nutritional support
Treatment?
80% of our adult patients are affected
Painful and unhealthy
Oral defence mechanisms
Important points of PD
What is periodontitis?
process of periodontal disease?
Arrow= action site of periodontal disease
What is pellicle?
Plaque (biofilm) needs the pellicle to develop
Plaque v. calculus (on crown and root, tartar more human term)
What is gingivitis and periodontitis?
Stages of pellicle and plaque deposition?
Steps of plaque formation and role of pockets?
What is the central component of periodontal disease?
What are the local secondary factors adding to plaque?
Periodontal disease progression
Key to tell owners about PD?
What is attachment loss?
Local and systemic effects of PD?
Consequence of scalings and extraction– healthy vs. diseased animal?
PD Systemic effects
What is the treatment of Feline Chronic Gingiostomatitis?
Why is dental anaesthetics different?
Advanced age = diminished organ function, possible concurrent disease
Dental anaesthetic plan
When do we use analgesia during a dental?
- Pre-operatively
- Peri-operatively- local nerve blocks
- Post-operatively
Prior to a dental procedure?
Common medications that may be used days prior to
procedure include:
-
NSAIDS
-
Tramadol
-
Gabapentin
-
Amantidine
-
Fentanyl patches ?
Common pain medications that may be used in
premedication
include:
-
Opiods
–
eg
methadone,
hydromorphone
, buprenorphine,
butorphanol
-
NDMA antagonists-
eg
Ketamine
-
Alpha-2 agonists-
eg
medetomadine
Nerve blocks, why bother?
Local nerve block drugs?
Complications of dental procedures
Volumes for nerve blocks
How to perform a nerve block?
Commonly used local nerve blocks and less commonly used?
Post op dental analgesia
Consider:
Ta b l e t s
: NSAIDS
eg
carprofen
, meloxicam and
robenacoxib
,
opiods
eg
tramadol. Some tablets are smaller than others.
Robenacoxib
and
tramadol can be taken on an empty stomach.
Liquid oral medications
: NSAIDS
eg
meloxicam (need to be given with
food)
Opiods
eg
tramadol (it is very bitter), buprenorphine
bucchally
(0.04mg/kg cats, can be expensive long term)
Transdermal
:
Opiods
- compounded codeine, fentanyl patches
(requires longer planning)
Indications for dental radiographs
* fractured tooth to assess crown and root
* investigate soft or hard tissue enlargement, asymmetry or instability
* investigate supernummery or missing teeth
* Determine presence or abscence of deciduous or permanent teeth
How much are we missing without x-ray?
Good exam question!
How to take dental radiographs
Two common dental RG techniques
Parallel technique
Shadow is a true representation of the height of the building
Shadow is a lengthened representation of the height of the building
Shadow is a foreshortened representation of the height of the building
angle for maxillary PM and M?
What angle for incisors and canines in a dog?
What angle for cat incisors and canines?
Generalised megaoesophagus
Likely aspiration pneumonia
Other than RG, testing for oesophageal problem?
What do you assess imagery wise with the stomach?
* Assess size: no greater than 3 intercostal spaces wide; fundus typically 2 x wide as pylorus
* Contents
* position: cranial to 12th rib
* Is this a surgical abdomen?
Stomach filled with food
Right lateral radiograph, fluid filled pylorus
* take the left lateral radiograph to ensure it is just the pylorus and not a mass
Gas filled stomach cat
Delayed emptying, chronic pyloric obstruction
Who do you take to surgery?
A- a lot of poo in the stomach– treat medically
B- GDV compartmentalization– SURGERY (patchy irregular mineralization of the ribs is normal)
Assessing the SI in a dog?
Normal SI
Normal to have gas in the colon
Intestines have a lot of gas– go back to the patient: is it vomiting? etc.??
Determining whether there is a SI obstruction rules
Contrast agents
Normal barium contrast study in the GIT
Lymphoid follicles
lymphoid follicles in tonsils, Peyer’s patches, spleen, adenoids, skin, etc. that are associated with the mucosa-associated lymphoid tissue (MALT).
A lymph follicle is a dense collection of lymphocytes, the number, size and configuration of which change in accordance with the functional state of the lymph node. For example, the follicles expand significantly when encountering a foreign antigen. The selection of B cells, or B lymphocytes, occurs in the germinal center of the lymph nodes.
Contrast within the stomach and duodenum showing a linear foreign body
contrast study showing intussusception
Complete dental treatment
Attachment loss
Aim of dental treatment
Probing and charting
Perio-probing
True pocket depth = probing depth + attachment loss
Severity of periodontitis is based on??
Third degree furcation
What is a dental chart?
What is gingival surgery and open root planning?
Antimicrobial treatments for the mouth
What are the 12 steps of dental treatment?
Home-care advice for dental treatment
Control of plaque
Two imp. points to note:
- Penetration of AM drugs into this biofilm is difficult. Abs have very limited success in treating PD.
- Once disease is established, thorough dental treatment under GA needs to be performed, not given homecare. Home care is used for prevention of disease. You cannot prevent a disease that is already established.
When is homecare for restoring grade 0 an option?
Homecare dental mechanical examples
Home care brushing
Homecare chemical examples
What is this called?
Exodontia
So how do you know when to extract?
For other cases (
eg
grade 3/4 PD), you need to take into account:
-
Will the owner be
able
or
willing
to perform homecare (
eg
owner might
have arthritis in their hands, fractious cat, time poor client, unmotivated
client)?
-
What level of home care are they happy to do (daily care? Passive care
only?)
- Is this the only dental likely to be performed for a long time (
eg
cost issues,
risky anaesthetic)?
-
Is the tooth an important strategic tooth (
eg
canines or
carnassials
)?
-
Is the tooth likely to be useful (maxillary molars in cats are not of great
use, are there any teeth opposing it?)
-
Are there any other treatment options (
eg
referral for root canal,
orthodontics, guided tissue regeneration, restoration)?
Exodontia instruments
What can happen with multi-rooted teeth even when they appear mobile?
RG taken to check for tooth 106 (canine). Also has a persistent 504 (extra root).
Extraction complications
Steps for extraction of a tooth- simple
Surgical extraction multi rooted tooth
Example of a multi rooted tooth with one sound root and one diseased root
Lacerated roots where they are stuck together– different root shape– may use different tools– good to take RG to know
Releasing incisions
Incise along the sulcus (pocket)
Used to elvate the attached gingiva and then the mucosa
Sectioning different types of teeth
Extractions hints and tips
Deciduous teeth
Must be extracted otherwise PD will develop rapidly
Two teeth of the same type should never be present at the
same time- so if the deciduous isn’t gone when the adult
erupts- it is retained!
Deciduous teeth are often removed due to being retained,
fractured, and malocclusions (they occur in puppies- so
check!)
Remove deciduous teeth
Exam question!
Feline Tooth Resporption
TR is commonly like an iceberg. Difficult to see and mostly below the surface.
* Lesions are seen most commonly in the mesial premolar teeth, secondly in the other distal teeth (frequently in upper and lower carnassials) but any tooth can be involved
Feline TR
Lesions affecting the canine teeth may manifest as what
appears to be
gingival recession
with enhanced
exposure of the root.
These are likely to be
‘
super-eruption
’
as a result of
osteoblastic
activity in the
periapical
alveolar bone
resulting in obvious exposure of the root.
Clinical signs of Feline TR
Prevalence of Feline TR
Feline TR aetiology
Pathophysiology of feline TR
Diagnosis of feline TR
Radiography:
Missing teeth
are most often the result of advanced TR
which leads to crown loss… A gingival
‘
bump
’
where a
tooth should be is an indication of total
resorption
.
•
If tooth remnants protrude, there will be a marked gingival
reaction & radiographs will demonstrate retained roots.
Furcation exposure– not TR!
Stages of TR
Two phases of odontoclasts in TR
Type 1 TR. Radiolucency in the tooth with normal PD structures.
Type 2 TR (replacement resorption) significant resorption evident and loss of PD ligament space.
Mixed findings, such as where one root may be type 1 and the other type 2
Treatment of feline TR?
At this time,
extraction
is the recommended treatment.
•
It is advisable that dental prophylaxis and effective home
care (
including plaque control
) be considered as a
‘
preventative
’
measure.
•
Dental checks every 6 months, and annual dental
examinations (including full mouth
radigraphy
) is
recommended.
•
Note that at the time of treatment of gross TR lesions,
there may be subclinical (
as yet microscopic
) lesions in
other teeth! These will become evident given time
What is crown amputation as a treatment of feline TR? When should you not use this technique?
Oral masses- B or M?
SCC
Assessment of oral masses
Orthodontic basics
In dogs and cats we performing orthodontic
correction to enhance function and prevent disease.
We accept that animals
need a functional and pain free
bite, not necessarily a perfect bite.
•
Malocclusions may be
acquired
or
hereditary
.
•
“Dental” (Class I) malocclusions may not always be
hereditary.
•
“Bony” (Class II, III and IV) malocclusions are generally
considered to be hereditary.
Normal occlusion in a dog
Class 1 Malocclusions
Class II malocclusions
Class III Malocclusion
What to look for with occlusion
Orthodontic adjustments
What it tipping?
Problem with crowded mouth
Base narrow mandibular canine
teeth
Base narrow mandibular canine
teeth
Treatment options in orthodontics
What is endodontics?
Pulp anatomy
Endodontic principles
Tertiary dentine
Aetiology of pulp and periapical disease
Aims of endodontic treatment
Accomplishment of endodontic aims of treatment
Rabbit dental anatomy
Signs of dental disease in a rabbit
Causes of dental disease congenital and acquired
Dental disease more common in rabbits:
- housed in traditional hutch/lack exercise
- fed large percentage commercial mix or pellets
- little hay/grass/veggies in diet
Recommendations for dental health in rabbits
Dental examination in rabbits
Acquired dental disease: progressive signs in rabbits
Grade 1 dental in a rabbit
Grade 2 dental rabbit
Sites of bone penetration by cheek teeth in a rabbit
Grade 4 dental in a rabbit
Grade 5 dental disease in a rabbit
Treatment of dental disease in rabbits
Dental abscess treatment rabbit
Marsupialisation
Dental abscess treatment
Corticosteroids and rabbits?
NO!!!!! Use NSAIDs
GP dental anatomy
Ferret dental anatomy
Rats and mice dental anatomy
General GIT rabbit
Rabbit caecum
Abnormal production of caecotrophs (ISS)
Abnormal caecotrophs cause, treatment/prevention?
Causes of uneaten caecotrophs that may adhere to fur around anus
Treatment for GI stasis/ ileus
Most common cause of GI stasis is an inappropriate diet
Mgt of GI Stasis in a rabbit
* GI stimulants: Metoclopramide, cisapride, sucralfate, ranitidine (prokinetic effect equal to cisapride and antacid actions
* Exercise
* Massage
* Feeding e.g. critical care
* Prevention: Diet!!
GI stasis rabbits
Bloat in a rabbit
Stomach tube can be difficult to get anything out because of what rabbits eat, even if you use a wide bore
Surgical approach to bloat
Ileus v. Bloat & Obstruction
General Guinea Pig GIT
GP Gastrointestinal stasis & Dysbiosis/ Antibiotic induced Diarrhoea
Faecal impaction
Coccidiosis rabbits and GPs
Ferret GIT
GI FB in a ferret
Helicobacter mustelae in Ferrets
Eosinophilic Gastroenteritis in a ferret
Rat and mouse GIT
What is diarrhoea?
Faecal scoring system
When is diarrhoea acute?
Can still have severe SI disease without overt diarrhoea
The presence of detectable diarrhoea usually indicates?
PATHOGENESIS OF DIARRHOEA
WHAT IS osmotic diarrhoea?
What is secretory diarrhoea?
How does increased intestinal permeability cause diarrhoea?
Right heart failure, may notice diarrhoea before ascites
How does deranged intestinal motility cause diarrhoea?
What is a common mechanism of diarrhoea?
Systemic disease that causes diarrhoea
*adrenal- hypoadrenocorticism unknown why diarrhoea
Questions to ask about diarrhoea
DOes the animal need interventional treatment in hospital or at home?
Is the disease likely to resolve without much investigation?
How are we going to investigate?
DDX for diarrhoea
* Primary lymphangiectesia
* Dietary indiscretion
* Dietary sensitivity
* Lymphoma or other diffuse neoplasia
* Neoplastic partial obstruction
* IBD
* Viral, protozoal, bacterial, fungal, parasitic infection
* Partial FB obstruction
First look with patient with diarrhoea
* Boxer– IBD or colitis
* History– first ask about the diarrhoea
- How long?
_ has it changed or progressed?
- Continuous or intermittent?
- SI or LI in origin helps us decide if we are really worried or a little worried
Differences between SI and LI diarrhoea
Melena worried SI
No pigment or color– worry about bile duct obstruction because no bilirubin being delivered
Fresh blood and mucoid?
Second and third part of diarrhoea history
Third get more background
- Vaccination
- Env and in contact animals
- any medications
- prophylaxis (worms)
- diet: full history if chronic, abridged if acute but association if present
Physical exam of animal with diarrhoea
After initial evaluation of animal with diarrhoea what can you determine?
Worry don’t have sufficient exocrine pancreas function
Animals are often bright and happy
What is serious with animal with diarrhoea?
Is it distressing to the owner?
When might you treat without investigating?
Basics of non-specific treatment with diarrhoea
*haematology
* biochem (including electrolytes)
* urine analysis
* T4 (cats)
* TLI
What can that tell you??
* Low protein or anaemia–> protein losing enteropathy
* evidence of metabolic disease
OR NOTHING
With an animal with diarrhoea, what do you do if nothing found with screening?
Serum trypsin like immunoreactivity
* this is not a test for a sick dog or cat
* Animals with EPI are well but skinny with diarrhoea
So don’t delay other diagnostics in a sick animal while waiting for TLI (2-3 days)
Sensitivity and Specificity of TLI?
Serum folate and cobalamin with animals with diarrhoea?
Normal absorption of folate and cobalamin (B12)
What happens in cats and dogs with chronic GI disease with serum folate and cobalamin? Why?
Pancreatic lipase and diarrhoea
Faecal analysis with diarrhoea
Faecal PCR with diarrhoea?
Miscellaneous laboratory testing with diarrhoea
Imaging and diarrhoea
Can aspirate LNs too– but not always helpful
U/S can be normal even with really severe disease, U/S can’t give a histological diagnosis and very operator dependent
Gold standard for diagnosis? But when don’t you use?
Don’t use in acute disease
Endoscopy with chronic diarrhoea
8-16 biopsies from each area
Exploratory laparotomy with chronic diarrhoea
What is acute diarrhoea? What do we want to know?
Less than 14 days in duration
** Know how to assess accurately animals that present with acute diarrhoea to determine the optimal diagnostic testing
** Does the animal need in clinic treatment?
* Is it likely to be self limiting?
* Is it infectious?
When might you suspect infectious?
Take precautions to not spread!!!
Diagnosis with acute diarrhoea suspect infectious
Infectious diarrhoea acute DDX
Suspect hookworm? Acute diarrhoea
Suspect roundworm?? unlikely with acute diarrhoea
Common suspects for bacterial diarrhoea
Commensal– each can be isolated from 25% of dogs and cats
Campylobacter causing diarrhoea??
Clostridium as a cause of diarrhoea??
E. coli as a cause of diarrhoea?
PCR or culture and get E. coli– no surprise– only worry with chronic disease
FISH testing– can see E. coli invading into mucosa
Salmonella as a cause of diarrhoea?
Protozoa as a cause of diarrhoea?
4 mechanisms of diarrhoea
Consequences of diarrhoea
What is a hernia?
* Classifications
- true or false
- congenital or acquired
- acute or chronic
- incarcerated
- strangulated
- auto-penetrating
Why do we fix hernias?
Loss of domain
* treatment of choice: open the abdomen and leave it open
* Can use pressure sensors to test for
Or can stretch
How do we fix hernias?
Exam question
Reconstructing large hernial defects
*Mesh - polypropylene, Polyglactin 910, (teflon)- more commonly in humans, PSIS: porcine SI submucosa
If you have a hernia and the animal is vomiting…?
Likely strangulating
Muscle flaps to reconstruct large defects
VAC- applying negative pressure to an area
compartment separation- separating different abdominal muscles to allow the abdominal wall to stretch out
wall partitioning- allows it to expand (Z expands into straight line)
Scrotal hernias
Inguinal and scrotal hernias
Femoral hernias
Traumatic and incisional hernias
* usuall blunt force trauma- dogs: hit by car, cats: high-rise syndrome
* At regions of abdominal wall attachment
- paracostal (cats)
- dorsolateral
- prepubic
* Loss of domain
Incisional hernias
3 possibilities exam question
Anatomy of the perineal hernia
Aetiology/ pathophysiology of perineal hernias
Causes of perineal hernia
Non-surgial options of perineal hernias
Surgical options of perineal hernias
Adjunctive surgery to perineal hernia
Complications of perineal hernias
Cryptosporidium as a cause of small intestinal diarrhoea
Unlikley (same as Giardia) unless immunocompromised
** No mucus, blood in diarrhoea
* Can sometimes see on faecal
* PCR sensitive
* Tx: diet +/- anti-protozoals
* Not cure
Giardia as a cause of small intestinal diarrhoea
* PCR test
* Snap ELISA test
* tx: Fiber +/- Febendazole first
( Don’t worry about Isospora)
Tritrichomonas as a cause of diarrhoea
Viral causes of diarrhoea
* Enteric coronavirus
* Distemper
* Parvovirus
Coronavirus
Distemper
Parvovirus: CPV 2
* Usually puppies
* Often low socio-economic areas
* Not guaranteed treatment success
* Breed susceptibility: Rottweiler, Dobermans, Labradors, American Staffies, German Shepherd
* Signs: Anorexia, Vomiting then diarrhoea, dehydration
* Falst positive- not with vaccination?
* False negatives- not enough sample or too late
Parvovirus Treatment
New treatment trial parvo
Parvo Prevention
* If recovered- immune > 20 months
* Treat for Giardia etc.
* Vaccinate other puppies in household
- probably too late
- virus can survive in environment for months (just in time for next litter)
AM spectrum of disinfectants
Feline Diarrhoea RealPCR Panel
Canine Diarrhoea RealPCR Panel
When is diarrhoea not infectious?
Non-infectious diarrhoea in kittens/puppies
* Osmotic
- milk
- change in diet
- over-eating
* Dietary indiscretion: common, not pyrexic, older, good vaccination history, known to be scavenger, usually supportive treatment only
Canine Haemorrhagic Gastroenteritis (HGE)
* All ages, toy, miniature breeds
* Vomiting precedes diarrhoea by few hours
* Depression and shock quickly develops
* Marked elevation PCV (60-70) with normal skin turgor
* WCC, biochemistry and imaging usually normal
Canine HGE treatment
General treatment acute diarrhoea
Outpatient and inpatient diet diarrhoea
So if chicken and rice– brown rice– with pumpkin and/or carrots (add fiber)– metamusil perhaps
Antibiotics with diarrhoea
* metronidazole
* ampicillin or amoxycillin-clavulonate
(no indication if treating as outpatient except parvo CSU protocol)
Prebiotic??
Prebiotic– fiber
What about drugs to stop the diarrhoea?
* Remember any treatment that slows gut transit time may result in firmer stool but may actually exacerbate the problem by allowing for translocation of bacteria or continued absorption of toxins
* Most causes of diarrhoea in small animals already have decreased motility secondary to primary process
* Treatment
- ideally IV fluid therapy as dehydrated
- if owners have cost concerns, and are able to spend a lot of time then may be possible for frequent administration of oral fluids (electrolyte solution not 100% necessary as not vomiting, but won’t hurt)
- no indication for other treatment
- feed little and often either homemade highly digestible food (steamed chicken with no skin, grated carrot and brown rice or chicken, white rice and metamucil) or a prescription diet designed for this like Hills ID
Treatment
- this dog needs IV fluid therapy as dehydrated and showing some signs of systemic inflammation. At home treatment should not be recommended
- Antibiotics are unlikely to be needed if dog is eating (below), and should ideally wait for culture results– if deteriorates before results received, then can administer metronidazole 10 mg/kg PO bid to protect against bacterial translocation
- no need for gastric protectants (the blood is coming from the intestine, and so they won’t help) unless the dog starts to vomit
- assume potentially zoonotic/contagious and practice barrier nursing in clinic
- feed little and often either homemade highly digestible food (steamed chicken with no skin, grated carrot and brown rice or chicken, white rice and added metamucil) or a prescription diet designed for this like Hills ID
Treatment
- IV fluids +/- glucose
- give B multivitamin
- early nurtition- interventional if needed
- anti-emetics as needed: cerenia not licensed for puppies <12 weeks old, so consider using ondansetron however should be OK
- possible needs antibiotics (metronidazole OK)
- fenbendazole when will tolerate it
Treatment
- Fenbendazole
- Feed a highly digestible diet, then gradually introduce to a kitten diet
- little and often feeding
- avoid milk
Chronic diarrhoea
* Greater than 14 days duration
* We’re talkinga bout SI here
Chronic diarrhoea DDX
Most of the DDx caused by metabolic disease result in a sick dog with a poor appetite, whereas the primary GI diseases (in bold) cause an increased appetite. However, IBD and Neoplasia can cause either an increase or a decrease in appetite, depending on severity and location.
Small + large intestinal signs DDX
Initial options with chronic diarrhoea
* Treatment trial- When should we do this? The dog or cat is WELL, maybe there are concurrent signs of pruritis, in which case dietary trial + fenbendazole is indicated.
– well, good appetite, no abnormalities on exam, association with food or concurrent pruritis–> dietary trial (see IBD), Fenbendazole
* Investigate a little
- no response to treatment trial, weight loss, concurrent vomiting or other clinical signs, owner concerned
* Get a good history– full dietary
* Perform a good physical exam- include a digital rectal exam
How to investigate chronic diarrhoea
Signs of concern with chronic diarrhoea
Aetiology of Exocrine Pancreatic Insufficiency (EPI) in dogs
Exocrine pancreatic functions
What is EPI?
EPI clinical signs
EPI Diagnosis
EPI treatment
EPI prognosis
Approach to poor responders EPI
When to investigate a lot with chronic diarrhoea
What if albumin is low?
So remember that globulin is very large, and so can’t escape through the glomeruli. When there is increased intestinal permeability, globulins can escape!
Protein losing enteropathy
Not a diagnosis
A description of a problem
** Clinical signs effusion when serum albumin < 15 g/L
** Often GI signs are not very obvious
Diagnosis: GI Lymphoma in Dogs
GI lymphoma in cats
GI lymphoma in cats: treatment
Diagnosis of GI neoplasia– in dogs?
Intestinal lymphangiectasia
dilated lacteals and pitting oedema in the picture
* Often secondary to other diseases as for IBD
* Yorkies pre-disposed
* lose protein, lymphocytes and chylomicrons into gut lumen
* Usually resolves if treat underlying condition
* If idiopathic then:
- prednisolone
- low fat diet
IBD
Aetiology of IBD
Histological classification of IBD
Clinical classification of IBD:
- dietary responsive enteropathy
- antibiotic responsive enteropathy
- true inflammatory bowel disease (IBD) that requires immune suppression
What does that mean?
No difference in clinical signs– except in severe cases– no difference in histology
Dietary responsive diarrhoea
Antibiotic responsive diarrhoea
Immunosuppressant responsive diarrhoea (true IBD)
Breed predispositions for IBD
Any breed- no cat breed predisposition, older than 1 year, exacerbated by stress, if pure bred concurrent pruritis or young more likely to be food responsive
Clinical signs IBD
* Same for diet-responsive enteropathy
Remember usually not true food allergy, but can be usually with pruritis as well
* Same for antibiotic responsive enteropathy
Initial options treatment IBD
- Treat potential parasitic disease: Fenbendazole (50 mg/kg sid 3 days), treats whipworm, potentially treats Giardia as well
Well dog tx chronic diarrhoea
- Treat dietary sensitivity (1. Treat potential parasitic disease)
Novel protein
* Hydrolysed soy diet beneficial in recent study
Why? The decreased allergenic stimulation OR
* Fibre promotes colonic transit time via stimulation segmental contractions
* Fibre alter bacterial population
* Fibre increases porduction of SCFA
* Fibre absorbs large amounts of faecal water
Not usually true hypersensitivity
- need to withdraw (get response)
- rechallenge (get recurrence)
- over 75% food responsive GI disease do not recur with re-challenge
- Treat dysbiosis
Treatment trial end
Faecal microbial transplantation
* well evaluated in people
* unknown in IBD
* increasing use
Biopsy
Sick dog or albumin < 20 g/L–> biopsy
* Biopsy to start, and then give all three options: immune suppression–>antibiotics–>diet
Glucocorticoids
Reduce by 10-25% per day- dosage first then frequency. Aim for < 0.5 mg/kg every second day.
Additional immune suppressive
I start azathioprine at 1-2 mg/kg every second day, others start at 1-2 mg/kg once daily for 2 weeks then reduce to every second day.
Regardless, check WBC at 2 weeks, 4 weeks, 8-12 weeks, then every 3-6 months.
Do not use in cats.
* Azathioprine
- In severe cases start at time of prednisolone
- alternatively prednisolone sparing when tapering the dose
- takes 1-2 weeks to reach therapeutic effects
- side effects include pancreatitis and leucopenia
- monitor white cell count regularly
* Chlorambucil
- recent abstract suggests better than azathioprine in treating protein-losing enteropathy
IBD in cats: remember the differences
So what do you do with a well cat with diarrhoea?
What to do if sick cat with diarrhoea or if ruled out metabolic disease and diet?
Develop a DDX for animals with large intestinal diarrhoea based on history and physical examination– exam hint
Role of the LI
Signs of LI disease
What is colitis?
DDX for colitis
Clinical approach to LI diarrhoea
So, in other words… investigate if:
- a Boxer or French Bulldog
- Weight loss
- Diffuse diarrhoea
- Systemically unwell
Treatment trial with LI diarrhoea?
90% of animals with LI diarrhoea, this will work
What if the treatment trial for LI diarrhoea doesn’t work… what next?
How to biopsy the colon?
Preparation for colonoscopy
Colonoscopy v. Proctoscopy
Occult trichuriasis in which whipworms may be grossly evident in the cecum but not in the descending colon
Cats with LI diarrhoea
L-P colitis
Lymphocytic Plasmocytic Colitis– similar to IBD
Sulfasalazine– aspirin enema but orally??
Clostridial colitis
Granulomatous colitis
Granulomatous colitis in Boxers (histiocytic ulcerative colitis- HUC)
Diagnosis of HUC
* Histologically a mucosal infiltrate of plasma cells, lymphocytes and PAS- positive macrophages
* Severe mucosal ulceration
* Patchy distribution
Prognosis pre-2004 v. now of Granulomatous colitis in Boxers
Prognosis pre-2004
* Traditionally thought to be a disease with a poor prognosis and treated with immunosuppressives
* Some reports of spontaneous resolution or regression of severity in older animals
The condition was then classified as histiocytic ulcerative colitis to emphasize the presence of periodic-acid Schiff (PAS) positive macrophages throughout the colon (Sander & Langham). Typical histologic appearance of granulomatous colitis differs from other forms of canine inflammatory colitis in that there is severe mucosal ulceration and infiltration of the sub-mucosa and lamina propria with PAS positive macrophages (Hall et al). The distribution of inflammation throughout the colon may be patchy and multi-focal (ref).
Tritrichomonas foetus
Clinical signs of Tritrichomonas foetus
Diagnosis of Tritrichomonas foetus
Prognosis of Tritrichomonas foetus
* Most cats will recover spontaneously
* However, many will have very severe clinical signs
Treatment of Tritrichomonas foetus
Irritable bowel syndrome
* Characterised by diarrhoea (usually LI), vomiting and abdominal cramping
* Diagnosis of exclusion
- main DDX IBD with associated pain
* Empirical treatment with anti-cholinergics and fibre supplementation
- NB careful with altering motility without histology
* Reduce stresses
What if LI diarrhoea w/o mucus?
Same diseases that cause colitis
Haematochezia predominantly
Rectal Masses– neoplasia
Rectal masses- non-neoplastic
DDX dyschezia/ tenesmus
Anal sacculitis
Anal sac adenocarcinoma
Constipation and obstipation
Diagnostic/therapeutic approach to Constipation and obstipation
Performing enemas
Idiopathic megacolon
Idiopathic megacolon: treatment
* Severe megacolon (obstipation):
- If dilation only: Colectomy
- If hypertrophy:
- < 6 months duration: pelvic osteotomy or colectomy
- > 6 months duration: Colectomy
