Dogs and Cats 12 Flashcards
1
Q
Regurgitation what results from, anatomy of canine and feline and what signs indicate that it is regurgitation
A
- Oesophageal disease
○ Caning: 2 layers skeletal muscle for most length
○ Feline: greater smooth muscle component LOS is a ‘physiological’ sphincter only
○ Oesophageal disease dogs >cats
Signs of regurgitation - Passive process (cats less passive)
○ No nausea or retching (but pain sometimes due to FB)
○ No repeated swallowing attempts - Involves oesophagus
○ No bile or digested food
○ Distension of cervical oesophagus may occur - Variable signs
○ Timing relating to feeding, presence of food, amount of vomitus blood
2
Q
What are 3 important questions to ask owners to determine whether vomiting or regurgitation
A
- Was there lick lipping or swallowing before/after vomiting
- Stomach heaving -> active forceful process
- Is there a yellow green tinge to the vomit, what does it look like?
3
Q
What are the 5 afferent pathways of vomiting
A
- Receptors and afferent pathways
a. Peripheral receptors in viscera (mechanoreceptors, chemoreceptors, 5-HT receptors (serotonin)
§ Stretch, torsion, inflammation, ulceration
b. Chemoreceptor trigger zone (CTZ) has no BBB and is stimulated by drugs and metabolites
§ Circulating endogenous or exogenous toxins/metabolites
c. Vestibular apparatus (H1, M1 receptors)
§ Motion, inner ear, CNS disease
d. Higher centres - central nervous system
§ Fear, anxiety and stress
e. Synapse at vomiting centre (close pox to other centres) may also have direct stimulation
§ Input for other areas, CNS disease
§ Receptors -> chemoreceptors, D receptor, 5-HT receptor
§ THIS IS THE ONE WE ARE TARGETTING WITH ANTI-NAUSEA DRUGS
4
Q
What are the 2 main efferent pathways of vomiting
A
- Efferent pathways
○ Autonomic nervous system inhibits motility gastric body, oesophagus and sphincters
○ Somatic nervous system driving force
5
Q
What are the 4 main causes of vomiting
A
1. Abdominal or gastric inflammation ○ Stimulate mesenteric receptors 2. Obstruction/delayed gastric emptying a. Distention and irritation of mucosa b. Toxins to CTZ 3. Systemic disease a. Toxins to CTZ, peripheral and central receptors, decreased GI motility, secondary gastritis 4. Central nervous system disease
6
Q
Differential diagnosis for ACUTE vomiting what are the GI ones
A
Non-fatal and self-limiting - MAINLY
○ Dietraty indiscretion/sensitivity
○ Overeating
- Potentially life-threating - need to confirm or rule these out
○ Gastroenteritis - dehydration and electrolytes are severe enough
○ Septic or other peritonitis
○ Pancreatitis
○ Acute haemorrhagic diarrhoea syndrome (leads to SI disease)
○ Intestinal obstruction
§ FB, intussusception, volvulus, mass
7
Q
What are the non-GI differential diagnosis for vomiting
A
- Systemic infections ○ FeLV, FIV, leptospirosis, canine distemper - CNS/vestibular disease - Toxins ○ Drugs, chemotherapy, heavy metals - Metabolic disorders ○ Kidney - uraemia, hypercalcemia ○ Adrenal - hypoadrenocorticism ○ Liver ○ diabetes mellitus ○ Peritonitis ○ DKA ○ Pyometra
8
Q
When a vomiting animal comes in what are the 4 main questions to ask
A
- Does any fluid/electrolyte/acid-base imbalance or pain need to be corrected
- Does the animal have potentially infectious condition
- Does the animal have metabolic condition and required specific treatment? - blood tests
- Does the animal have a condition that required urgent, surgical intervention
9
Q
What are some important questions to ask during history of a vomiting animal
A
- Is it a critical animal
○ If yes stabilise and ask questions whilst doing this
○ If no, take your time - Is it vomiting or regurgitating
- Does it seem to be primary GI disease
○ Age, onset, diarrhoea and vomiting (if so more likely)
○ Where there other signs -> PU/PD, progressive loss of appetite - Do I have a suspicion of what I am dealing with
- List of important information
○ Duration and progression
○ Pre-existing clinical signs
○ Vaccination status
○ Dietary history - including treats, potential to roam, toxins, scavenge
○ In-contact animals
○ Concurrent clinical signs
10
Q
What are some important things to do especially for physical exam of vomiting animal
A
- Evaluate ALL body systems
- Assess for dehydration or signs of systemic illness and pain
○ If dogs have low blood pressure may not respond to pain as well - need to correct - Check mouth
○ For linear FB cats, ulceration - Abdominal palpation
○ Organomegaly, FB - Rectal examination
○ Provides stool sample (important for infectious disease), detects melena and rectal disease
11
Q
In terms of history and physical examination what indicates when to treat vomiting dog non-specifically
A
- History suggestive of possible self-limiting cause
○ Only vomiting that resolves with fasting present - No evidence of metabolic compromise
- Majority of these cases will resolve with non-specific treatment
12
Q
In terms of history and physical examination what indicates when to investigate further for a vomiting dog
A
- Historical evidence of systemic or severe disease
○ Jaundice, anaemic, vomiting of faecal like material (severe disease) - Animal systemically unwell
- Abnormal physical findings
○ Palpable mass, melena, significant pain - No response to non-specific treatment
13
Q
What are the 3 main steps in a vomiting investigation (after history and physical exam) and how to achieve
A
STEP ONE: rule out metabolic disease
- Haematology, biochemistry (including electrolytes) and urinalysis (prior or at same time as IV fluids if possible)
○ Assess hydration/electrolyte status
○ Assess renal/hepatic function
○ Assess for presence of anaemia/hypoproteinaemia
- Lipemic serum - no eating/vomiting - pancreatitis?
STEP TWO: rule out infectious disease
- Faecal parvovirus in at-risk dogs
STEP THREE: rule out surgical emergency
- Abdominal radiographs first and most important imaging modality
- Need 3 views, although 2 is sometimes enough
- Can do quick abdominal ultrasound
14
Q
What signs suggest surgical emergency and clinical signs of GI obstruction
A
- No prior signs of illness
- Known scavenger
- Younger (usually)
- Dogs > cats
- Severe signs
Clinical signs of GI obstruction - Abdominal pain
- Vomiting (Metabolic alkalosis - vomiting up gastric acid)
- Failure to pass faeces
- Dehydration
- Absent gut sounds
Rarely abdominal distention
15
Q
After basic investigation of a vomiting case in clinic what should you have ruled out
A
- Non-fatal and self-limiting ○ Overeating or garbage ingestion ○ Dietary indiscretion/sensitivity - Potentially life-threatening ○ Peritonitis (see fluid) ○ Gastroenteritis (not ruled out yet) ○ Pancreatitis ○ Acute haemorrhagic diarrhoea syndrome ○ Intestinal obstruction (partial may still be present) § GB, intussusception, volvulus ○ Remove most metabolism - except hypoadrenocorticism - Systemic infections - CNS or vestibular disease - Toxins - Metabolic disorders ○ Uraemia, liver disease, hypoadrenocorticism, hypercalcaemia
16
Q
After basic investigation of vomiting and still haven’t found an answer what are some further investigations
A
- Ultrasound - referring vet
○ For linear FB/s or partial obstruction detection
○ Assess all abdominal organs including pancreas - Fluid analysis if present
- Contrast studies - not really done due to good ultrasound
○ Difficult to do in vomiting animals - BIOPSY - exploratory lapartomy, endoscopy
17
Q
linear foreign bodies what species most common in, what results in and diagnosis
A
- Common in cats (>dogs)
- One end fixed (tongue, pylorus) and length of FB causes ‘brunching’ up of intestines
○ Elastic waistband - Vomiting, depression, anorexia (only in cats)
- Examine base of tongue and may palpate
- Rarely visible on plain radiography
18
Q
Intussusception what results in, most common sites and predisposing causes
A
- Telescoping of one intestinal loop into an adjacent segment
- Most common sites
○ Ieocolic junction
○ Jejunojejunal - Predisposing causes
○ Active enteritis in young puppies/kittens
○ Acute renal failure, neoplasia (older animals), previous intestinal surgery)
19
Q
Intussusception clinical signs and diagnosis and treatment
A
Clinical signs - Acute ○ As for other intestinal obstruction ○ Be vigilant if animal not recovering from enteritis as expected ○ May reduce in and out - Chronic ○ Hypoproteinaemia ○ Weight loss Diagnosis and treatment - May palpate - Ultrasound best for diagnosis - Always look for underlying cause - Surgical correction
20
Q
SNAP cPL what test is it for, sensitivity and specificity and what else could an increase indicate
A
SNAP cPL test for canine pancreatitis
- Lipase produced exclusively by the pancreas
- Not altered by prednisolone
○ Sensitivity (very few false negatives) is high in acute forms
○ Sensitivity lower in more chronic forms
○ Not specific in regards to cause of pancreatic inflammation
§ MAY BE HIGH IF SEPTIC PERITONITIS (need to rule this out with surgical interventions above)
- SNAP test
21
Q
If you have a dog that is sick for 3 days, vomiting, lethargy, anorexia with normal imaging and ultrasound but no stress leukogram on bloods what would you do next
A
○ Recurrent disease, associated with anorexia, NO STRESS LEUKOGRAM - hypoadrenocorticism
§ Run cortisol testes - found to have Addison’s disease
22
Q
Aortic arch vascular ring anomaly what is it, what animal occurs within
A
kitten with regurgitation when moving from liquid to solid food
- Aortic arch vascular ring anomaly - congenital anomalies of aorta arch may encircle and constrict the oesophagus and prevent oesophagus from opening up
○ Persistent right aortic arch with the ligamentum arteriosum passing dorsally over the oesophagus - constriction of the oesophagus dorsal to the heart base
○ Liquid food moves through but solid get stuck
23
Q
What are the 2 main causes of regurgitation and causes within
A
1) obstructive
a. luminal obstructions
b. extraluminal obstructions
2) non-obstructive
a. congenital - 30%
b. acquired - 70%
24
Q
What are the main causes of obstructive regurgitation
A
a. Luminal obstructions
§ FB, neoplasia, hiatal hernia (pyloric sphincter weakness), oesophageal structure, infectious (spirocercosis - Europe)
§ Doxycycline - if tablets stay in oesophagus highly irritative (give with water)
b. Extraluminal obstructions
§ Vascular ring anomaly -> in the kitten case ABOVE
§ Neoplasia
25
what are the main causes of Non-obstructive regurgitation
a. Congenital - 30%
§ Missing receptors for Acetylcholine to work
§ Siamese, jack Russel, Newfoundlander (congenital or acquired)
b. Acquired -> 70% -> megaoesophagus
26
What are some causes of megaoesophagus
- idiopathic
- neuro-muscular - myasthenia gravis (25% of all acquired cases), polymositis
- generalised inflammatory myopathies - immune-mediated, infectious
- distemper
- endocrine - hypoadrenocorticism, hypothyroidism
- GIT - oesophagitis
- paraneoplastic - thymoma
- toxic - lead, prganophosphates, snake venom
- incidental (not pathogenic) - excitment/general anaesthesia, vomiting
27
Myasthenia gravis what results in, what occurs, 3 types and main signalment
Megaoesphagus
□ Myasthenia gravis (25% of all acquired causes)
® Antibodies destroy the AcH receptors
® Two types
◊ Focal (oesophagus, pharynx, larynx, face)
◊ Generalised -> generally go downhill faster
® Two hits 2-3 years or >9 years
® GSD, Goldern, Abyssinian, Somali, Siamese
28
Regurgitation work up what involved and additional diagnostics
1. Thoracic radiograph
2. Fluoroscopy (movement) -> when don't get answer from radiograph
3. Endoscopy
- Risk of aspiration pneumonia - NOT WHEN UNDER GA
Other diagnostics
- CBC - inflammation/infection, lead toxicity (basophilic staining)
29
CBC - inflammation/infection, lead toxicity (basophilic staining) what are the 4 main diseases looking for with regurgitation and what need to confirm with
1. Hypoadrenocorticism -> electrolytes (ensure ACTH is low first then)/ACTH stimulation test
2. Myasthenia gravis -> Anti-acetylcholine receptor antibody
§ Confirm immune-mediated process
§ Does not differentiate primary vs secondary
§ Congenital -> NOTHING TO DO WITH ANTIBODIES -> wouldn't see a difference on this test
□ The receptors will not be present
3. Neuromuscular disease -> creatinine kinase
4. Hypothyroidism -> T4 and TSH (BOTH
30
What are the 2 main complications of regurgitation
- Nasal discharge -> bilateral mucopurulent
| - Aspiration pneumonia -> productive cough, dyspnoea
31
List the 3 main things within non-specific treatment for regurgitation
1. Feeding
§ What type of food and how much
□ Frequent, small meals, high calories, consistency (Depends on patient)
§ Bailey chair
□ Up right dog, let the gravity do its job
□ For 20-30mins
§ Feeding tube into the stomach - takes dedication
2. Antacid
3. Fluid therapy
32
What are the 3 main options for specific treatment of regurgitation and describe within the specific causes that you treat this way
```
1. Treat underlying disease
§ Remove foreign body
□ Endoscopically
□ Surgically
□ Risk of stenosis
□ Additional treatment
® Soft food, antacids, steroids □ Prognosis -> guarded to good
§ Stricture
□ Bougienage
□ Balloon dilation - can relapse so can be expensive
□ Prognosis: good (but can be expensive)
§ Vascular ring anomaly
□ Surgery
□ Prognosis: guarded
§ Hiatal hernia
□ Surgery
□ Prognosis: good
○ Antibiotic treatment for aspiration pneumonia
§ Spirocercosis
§ Treatment - ivermectin, doramectin
§ Prognosis good unless becomes sarcoma
○ Medicament options (pyridostigmine)
§ Idiopathic - GO OVER
□ Treatment: supportive
□ Prognosis poor to guarded
§ Hypoadrenocorticism's
□ Treatment
§ Myasthenia gravis
□ Treatment: pyridostigmine, corticosteroid, supportive
□ Prognosis - poor to guarded
```
33
Defintiion and detection of acute abdomen
- A sudden onset of abdominal clinical signs, pain or discomfort from abdominal pathology
Detection
- As part of your major body system assessment you illicit abdominal pain.
○ This may be as simple as pain on abdominal palpation
○ OR
○ You detect other clinical signs related to the abdomen such as a palpable fluid wave.
- Stoic animals may not reveal pain on examination but show it in their gait or stance (stiff limbed, reluctant to walk, prayer dog stance)
- 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
34
What is the main aim of treating the acute abdomen
- The basic aim of treating the acute abdomen is to determine if the problem requires surgical or medical care to treat the problem or to reach a diagnosis
35
What are the 6 main mechanisms of abdominal pain
1. Distension
2. Traction
3. Ischemia
4. Forceful GIT contractions
5. Acute invasion or denuding of the bowel
6. Secondary inflammation ( abdominal nerve endings stimulated by proteinases and vasoactive substances)
36
Acute abdomen GIT which differentials require surgical treatment
- Gastric Dilatation/Volvulus
- Mesenteric Torsion
- GIT obstruction from foreign body/neoplasia/adhesions
- GIT linear foreign body -
- GIT necrosis/ulceration/perforation
- Duodenocolic ligament entrapment
- Mesenteric thrombosis/embolism
- Portal venous thrombosis??
- Perineal hernia (herniation)
37
Acute abdomen GIT requiring medical treatment
- Severe Gastro-enteritis (viral/bacterial/parasites/toxin/HGE)
- Pancreatitis
- Obstipation
- Colitis
38
What are some urogenital causes of acute abdomen
- Urethral obstruction s/m
- Prostatitis/prostatic abscess s/m
- Dystocia s/m
- Uroabdomen s/m
- Pyometra/uterine rupture s/m
- Cystitis/cystic calculi s/m
- Ureteral obstruction s
- Pyelonephritis s/m
- Renal abscess s/m
Vaginal rupture
39
what are some Hepatobiliary system causes of acute abdomen
* Bile peritonitis s
* Acute hepatitis/cholangiohepatitis m
* Biliary obstruction s
* Necrotizing cholecystitis s
* Liver lobe torsion s
* Hepatic abscess s/m
40
What are some other causes of acute abdomen
* Haemoabdomen (usually parenchymatous organ rupture) s/m
* Neoplasia s/m
* Penetrating wounds/evisceration s
* Splenic torsion and splenitis s
* Splenic abscess s/m
* Surgical contamination s
* Strangulated hernia s
* Pansteatitis s/m
* Sclerosing encapsulating peritonitis s
41
What are the 6 most common causes of acute abdomen
1. haemabdomen,
2. uroabdomen,
3. septic peritonitis,
4. bile peritonitis,
5. intestinal obstruction,
6. GDV, perforated stomach or proximal duodenum, pyometra, abdominal wall perforation
42
Acute abdomen what do you perform first and the 5 steps within
STABILISATION
1. IV fluids
2. anaglesics
3. oxygen
4. antibiotics
5. other symptomatic treatment
43
Anaglesia for acute abdomen what are the main drugs to use when and what if doesn't control, also what not to use
- Opioids are the cornerstone of treatment - acute pain
○ Begin with a pure agonist eg methadone/morphine unless suspect biliary stasis
○ When controlled reduce to partial agonist such as buprenorphine
○ Butorphanol does not have a long enough action to be used for prolonged analgesia
○ If severe consider a CRI of an opioid (fentanyl) as this evens out peaks and troughs
- If opioids are not rapidly reducing/controlling the pain then add in other agents as CRIs
○ Ketamine
○ Lignocaine - local blocks
○ Medetomidine
○ Or intra-abdominal/intrathoracic /local blocks of
○ Lignocaine (stings for a short time)/bupivicaine (stings for a longer time)
§ Switch from lignocaine to bupivicaine
DO NOT USE NSAIDS IN PATIENTS THAT ARE HAEMODYNAMICALLY UNSTABLE OR HAVE GIT/RENAL INVOLVEMENT
44
After stabilisation during acute abdomen what is the next step and 5 things within
- At this point if the patient is requiring immediate treatment collect blood (and if possible urine)
- Immediately run
1. PCV/TS (always assess together)
2. Glucose
3. BUN via an azostix
4. Electrolytes/blood gas/lactate
5. Blood Smear
○ Hold blood for haematology, biochemistry, coags(ACT—needs to be run immediately/APTT/PT).
45
In terms of acute abdomen and measuring PCV,TS what does decrease TS, increased PCV, Increased PCV and TS, decreased PCV and TS, PCV does not drop as rapidly as TS
1. Decreased TS - protein loss from the vasculature – rule out peritonitis
2. Increased PCV (60-90) and normal to low TS – HGE is major differential with appropriate signalment and clinical signs
3. Increased PCV and TS – dehydration
4. Decreased PCV and TS – haemorrhage is probable (remembering that splenic contraction can mean that
5. PCV does not drop as rapidly as TS and that the changes take at least 6-8 hours to significantly change) –splenic rupture; GIT ulceration; liver rupture, coagulopathy
46
Blood glucose measurement in acute abdomen what means with increase, decrease and what else should you look at
- Increased
○ Dogs– stress, diabetes, severe pancreatitis
○ Cats – stress or diabetes
- Decreased
○ Sepsis
○ Hypoadrenocorticism
- Look at serum colour -> always recorded
47
BIN measurement in acute abdomen when increased and what to check and what to rule out
```
- Increased
○ Pre-renal
○ Renal
○ Post-renal
○ False positive
- If high check creatinine to see if renal system is involved
- If high alone rule out GIT haemorrhage
```
48
Blood smear in acute abdomen what is the main thing you are looking for, normal range and what are the 4 other things you are looking for
- Examine every cell line
- Look for platelets to check for platelet clumps and count per HPF
- Normal 8-15
- Spontaneous bleeding from thrombocytopenia alone usually less than 2
○ More than 4-5 then bleeding not from low platelets alone unless have dysfunction
- Low platelets common in DIC
• Look for signs of
1. Regeneration - Anisocytosis, macrocytosis, polychromasia
2. DIC – schistocytes, rbc fragments
3. Leucocytosis with or without a left shift
4. Leukopenia
49
After stabilisation and running bloods what is the next step in acute abdomen
1) signalment
2) history
3) physical exam - abdomen
4) imaging
50
In terms of signalment what is important for acute abdomen
- Use signalment to streamline your diagnostic plan
○ Eg young animals – infectious/foreign body more likely than immune mediated/neoplasia
- Older entire animals need close assessment of their reproductive systems
- Obese animals may have pancreatitis
- Recent surgery needs to be factored into the differential diagnosis list
51
History what is important for acute abdomen
```
- Information required
○ Onset of signs - gradual or rapid
○ When last normal
○ Last food/water intake
○ Increasing/decreasing food/water requirements
○ Any ‘not the usual’ food in last three to four days -> pancreatitis
○ Change of routine lately
○ Is the patient an indiscriminate eater
○ Exposure to potential toxins
○ Are there other animals affected
○ History of trauma
○ Vaccination history
○ Worming history
○ When does pain occur (constant vs fluctuating: more marked after eating)
```
52
In terms of physical examination what is important
- Further careful palpation and percussion of the abdomen should then be undertaken in an attempt to identify abnormalities of size, irregular shapes/surfaces
- Attempt to further localise the focus of pain
i. e. : right upper quadrant, cranial abdomen, caudal abdomen
- Perform a rectal
- Perform imaging if indicated
53
Imaging for acute abdomen what are the 3 main questions to ask and the 3 main choices for imaging
○ Do we need to go to surgery?
○ Do we need to sample?
○ What management is required?
Choices
1. Radiographs
- For example large tympanic abdomen (GD vs GDV), known ingestion of a FB ( to look for signs of obstruction)
2. Ultrasound
- AFAST to look for fluid or alternatively a full diagnostic scan
- You may decide you need both modalities to increase your clinical information
3. CT/MRI are increasingly available and may be considered
54
What are the 9 steps in reading the abdominal radiograph
1. Serosal detail - good, increased or decrease
2. Gastrointestinal tract
○ Position
○ Contents
○ Degree of distention
3. Liver
4. Spleen
5. Kidneys
6. Urinary Bladder
7. Prostate/uterus
8. Thorax
9. Skeletal structures
55
Intraabdominal serosal detail on radiograph what causes increased, good and poor
○ Increased: - highlight margins of organs
§ Free peritoneal or retroperitoneal gas
○ Good- can see the margins of the organs
○ Poor- ddx:
§ Young animals - brown fat higher water content (fat similar opacity to organs) - important to use signalment
§ Thin animals - fat provides the contrast (without loss of margins) - doesn't need a lot of fluid to decrease the serosal detail
§ Abdominal effusion
§ Peritonitis
§ Carcinomatosis
56
Evaluation for abdominal fluid what is the test to do and scoring system and what is important to do afterwards
- Scoring -> Does it have fluid -> or not fluid (if don't see fluid look at both longitudinal and transverse views)
- Abdominal fluid score -> score out of 4 (get 1 every image that has fluid)
○ DOES NOT QUANTIFY THE FLUID
-> to quantify the fluid get sample -> ultrasound guided
57
Fluid analysis what does it help rule out, what are the 3 ways to collect and what is important to do before abdominocentesis
- Helps rule out/in septic peritonitis, uroabdomen, bile peritonitis, haemorrhage, neoplasia, chronic vs acute inflammation
- Collect via
1. Ultrasound guided abdominocentesis
2. Blind abdominocentesis
3. Diagnostic peritoneal lavage
- Consider performing radiographs before performing abdominocentesis especially if using methods 2 or 3
○ Going to add air when stick the needle in
58
Blind abdominocentesis what need to do, how achieve and steps within
- Clip, surgically prep the area
- Use the four quadrant approach
- Closed or open technique
- Two needles simultaneously may help
Fluid collection
- Collect the fluid aseptically in edta and plain (non-gel) tubes
- Make smears for cytological assessment
- Reserve some for aerobic and anaerobic culture
- If low cellularity spin the sample as you would urine
- If the sample clots then you have hit a blood vessel or organ or it is a very very recent bleed
59
Diagnostic peritoneal lavage when would use, what need to be done in preparation and steps within
fluid anaylsis if not getting fluid from other
- Empty bladder
- Prepare skin aseptically
- Infuse 20ml/kg warm isotonic fluid into abdomen— 0.9% NaCl
- Watch for discomfort or increased respiratory rate/effort (putting pressure on diaphragm)
- Roll patient side to side
- Allow gravity to fill bag– may need gentle abdo pressure to aid this
○ Place bag lower than the patient
- Collect fluid as for other methods for analysis remembering it is diluted!
60
What are the 3 steps in fluid analysis
1) gross examination
2) classification
3) tests to run on teh fluid
61
Gros examination of the fluid what does different colours or textures indicate
○ Clear – no injury or generalised peritoneal disease
○ Opaque and bloody – intra-abdominal haemorrhage
○ Darker on repeat sample –continuing i-a haem.
○ Turbid or cloudy peritonitis
○ Bluish to greenish tinge – bile leakage or upper GIT leakage
62
Test to run on the fluid what are the 6 main ones and what indicates what
a. Run paired fluid and serum
§ Bacteria -> Bacterial peritonitis
§ Toxic neutrophils -> Suppurative peritonitis
§ Plant fibres -> GIT leakage
§ Neoplastic cells
§ Intra-abdominal neoplasia
b. Glucose/Lactate (sepsis)
§ Glucose
□ 1.1mmol/l lower than paired serum glucose highly correlates with septic peritonitis
§ Lactate
□ >2.5mmol/l dogs 100% sensitive 91% specific other causes - pyogranulomatous pancreatitis
® Anaerobic metabolism
□ Cats 67% specific: intestinal neoplasia, pancreatitis
§ A gradient of -1.5mmol/l (effusion to venous) lactate was also 90% accurate in diagnosing dogs with septic peritonitis (cats 78%)
c. Triglycerides (if chylous)
d. Creatinine/Potassium (uroabdomen)
e. Bilirubin
f. Amylase/ lipase (pancreatitis)
63
Diagnostic Peritoneal Lavage fluid analysis -> if use this mechanism what PCV, RBC and WBC count are significant
○ PCV 2% mild i-a haem.
○ PCV 3-10% moderate i-a haem.
○ PCV >10 % significant i-a haem.
○ RBC count > 0.2 x 10¹² significant i-a haem.
○ WBC count >1 x 10¹² mild to moderate peritoneal irritation
○ WBC count > 2x 10¹² marked peritoneal irritation, significant peritonitis
64
Diagnostic Peritoneal Lavage fluid analysis -> if use this mechanism what does amylase>serum, alkaline phosphateas>serum, bilirubin positive, creatinine>serum mean
○ Amylase > serum -> Pancreatitis
§ Trauma to pancreas or small bowel leakage
○ Alkaline Phosphatase > serum
§ Significant intestinal trauma, ischemia 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
65
Gastric dilation and volvulus what normally see on radiograph and what do you see with GDV, what is the key differentiating feature
○ Different stages of rotation will result in different radiographic appearance
○ Normal -> fundus dorsally , pylorus ventrally
○ GDV CLASSIC -> Fundus ventral and caudal, pylorus dorsal and cranial
○ Commonly see megaoesophagus
- KEY DIFFERENTIATING FEATURE IS THE POSITION OF THE PYLORUS
○ Also compartmentalisation -> see two gas filled areas separated by soft tissue
66
Spleen abnormalities can see on radiograph which is rare and which is common
1) splenic torsion - rare -> C-shaped spleen
| 2) splenic mass - common - some are benign (haematoma) most are malignant, look at liver for metastasis
67
Uterus how to image via radiographs, what is the main finding
- To image uterus -> Image bladder and slide probe cranially
- Pyometra - fluid can be anechoic or echogenic
○ Often coupled with cystic endometrial hyperplasia
68
Antibiotic use in acute abdomens when use broad vs narrow spectrum, administration route and the 3 types of therapies
- Broad versus narrow spectrum
- Use broad spectrum when concerned about gut content leakage/contamination
- Use narrow spectrum if you have found only one type of bacteria on your tests
○ eg gram negative rods in a urine sample
- The preferred route of administration is intravenous
- Choice is also dictated by the organ that is being targeted
1. Empiric therapy
2. Broad-spectrum therapy
3. Combination -> if unsure on whether gram positive or negative
69
Antibiotic use in acute abdomens what to do in terms of susceptibility testing and what 6 questions need to ask yourself before administration
```
Susceptibility testing
- Don't delay initial resuscitation or put patient at risk!!
- To guide de-escalation
- Be familiar with your lab’s panels
Ask yourself:
1. What organism is likely?
2. What tissue?
3. Recent antibiotic exposure?
4. Hospital or community acquired?
5. Is it life-threatening?
6. How long?
```
70
What 3 combinations are good broad spectrum choices for acute abdomen and what additional one can you add
1) ampicillin + enrofloxacin, gentamicin
2) cefazolin + gentamicin
3) clindamycin + enrofloxacin, gentamicin
consider adding metronidazole for added anaerobic cover
71
How to classify pancreatitis and what does acute pancreatitis mean
1. Acute, chronic, recurrent
2. Mild, moderate, severe
Acute pancreatitis
- Acute = inflammation or necrosis centred on the pancreas or peri-pancreatic fat
- No exocrine atrophy
- No fibrosis
72
Acute pancreatitis what is normal pathophysiology and then what happens/causes acute pancreaitis
- Normal
○ Zymogen (precursor for digestive enzymes) and lysosomal granules kept separately in the cell
○ Zymogen aren't activated until they are in the small intestine (by enterokinase - cleaves and activates)
○ PSTI mops up accidentally activated trypsin
- Causes of Disease -> fusion between lysozyme and zymogen granules -> ACTIVATION OF ZYMOGEN WITHIN CELL
○ Increased acinar acidosis
○ Decrease amount or function of PSTI
○ High fat/low protein diets - MOST COMMON -> urolithiasis diets
§ Cats not normally associated
○ Hyperlipidaemia
○ Drugs (azathioprine, KBr)
○ Trauma
○ Hypoxia
73
Acute pancreatitis what are the 4 things in the development
- Activation enzymes stimulates neutrophil migration and activation of cytokine cascades
- Can stop at mild, clinically insignificant or
- Cause pancreatitis (local) inflammation or variable severity or
- Can cause systemic inflammation and severe multi-organ disease
74
What are the main clinical signs for acute pancreatitis in cats and why
```
- Vomiting (not high percentage that vomited) -> MOSTLY LETHARGIC AND STOP EATING
○ Dehydration, hypovolaemic shock
- Diarrhoea
- Abdominal pain
○ Acute fluid collection, peritonitis
- Jaundice
○ Associated with hepatic lipidosis (period of not eating) -> hepatic encephalopathy
- Cardiac arrhythmias
- Acute renal failure
- Hepatopathy
- Respiratory distress
- CNS signs
Anatomy
- Disease in pancreases, disease in gall bladder
```
75
What are the main clinical signs in dogs and why
- Anorexia
- Vomiting - - due to inflammation and stimulation of mesenteric receptors, blood borne emetic agents
- Abdominal pain
○ 3 most common above
- Jaundice (generally occurs as they are getting better, bile duct obstruction or inflammation)
- Co-current diabetes ketoacidosis
Anatomy
- Pancreases associated with duodenum, colon, spleen, stomach
○ Septic peritonitis - pancreases inflamed as sitting in puss
○ NOT ALWAYS THE PRIMARY PROBLEM
76
What are the 7 mains ways to diagnose acute pancreatitis and the gold standard
1. Clinical signs and suspicion -> lipemic serum
2. Non-specific moderate increase in liver enzymes, signs of dehydration and inflammation
3. Pancreatic enzymes considered poor markers - NOT USEFUL
4. Logically most dogs with AP have a degree of peri-pancreatic fat necrosis (bright and white) - diagnosis by ultrasound
5. Spec-canine pancreatic lipase - DOGS
6. Pancreatic lipase immunoreactivity - CATS
7. Cytology - fine needle aspirate of pancreases
Gold standard -> clinical signs, history, imaging (radiograph and ultrasound -> can confirm and can also rule out other things like septic peritonitis)
- bloods but mainly to rule out other metabolic causes
77
Pancreatic enzymes how good are they at diagnosing acute pancreatitis
- NOT USEFUL
○ Lipase greater than 3x upper reference interval
§ Sensitivity 73%
§ Specificity 55%
○ Amylase greater than 5 x upper reference interval
§ Sensitivity 62%
§ Specificity 55%
78
Spec-canine pancreatic lipase what species used in, for what, how good is it and interpretation of results
DOGS - pancreatitis
○ Studies shown localised to pancreas only
§ Studies have shown this to be low or no detectable in dogs with EPI (exocrine pancreatic insufficiency)
○ Lots of abstracts then SNAP test developed
§ Sensitivity from 21-73% - greater in severe cases
§ Specificity 80-85%
○ Interpretation of results
§ <200ug/L - healthy dogs
§ 200-400ug/L - equivocal
§ >400ug/L - consistent with pancreatitis
○ Not able to be correlated to outcome/clinical severity from current studies
ALSO -> doesn't say if primary or secondary issue
79
Pancreatic lipase immunoreactivity what species used in, for what, how good is it
CATS - pancreatitis
○ Species specific
○ Reference interval: 1.2-3.8 ug/L
○ Less affected by other disease
○ May be difference in diagnostic utility for chronic vs acute forms of the disease
○ Specificity 91% -> BUT ONLY TESTED ON SMALL SAMPLE SIZE OF SEVERE CASES
○ Probably not useful in less severe cases
80
Cytology in the diagnosis of pancreatitis why used in cats and dogs
○ Very useful in cats -> could be lymphoma
○ DOGS - not useful - inflammation, necrotic but no diagnosis
○ Safe
○ Strong overlap between inflammation/dysplasia and neoplasia
81
Treatment for pancreatitis list the things needed
```
P - perfusion
A - analgesia
N - nutrition
C - control vomiting
R - reduce gastric acidity
E - evaluate for complications
A - aspirate fluid collection
S - steroids
```
82
Perfusion why is it important for treatment of pancreatitis, recommendations for fluids and how fast
- Pancreatic microcirculation is susceptible to hypertension -> why see pancreatitis post-operatory
○ Change in circulation -> blockage of capillaries -> oedema -> influx neutrophils
- Recommendations
○ Early fluid resuscitation essential
○ Lactated ringers solution superior to normal saline
§ Potentially due to reducing acinar acidosis and down-regulating NF-kappaB
- RAPID restoration if in NON-CARDIGENIC shock
- Consider colloids if unable to restore volume without pulmonary oedema
- Be careful with fluid rates in cats
- plasma -> probably no benefit unless treating platelet issues
83
analgesia for pancreatitis - EXAM what do you need to do
1. ASSUME pain is present, recognise and quantify level of pain
○ Re-assess frequently
2. Start with maximum analgesia thought necessary then STEP DOWN
Anticipated levels of pain associated with acute pancreatitis
84
Mild pancreatitis pain what anaglesia do you use
- Buprenorphine - start at 30-40ug/kg for 4-6 hours
- Can add gabapentin (approx 10mg/kg q 12-24h) if needed
- When pain is controlled, reduce dosage of buprenorphine not frequency
85
Moderate pancreatitis pain what anaglesia do you use
- Baseline = buprenorphine 30-40ug/kg q 4-6 hours
○ + ketamine CRI start at approx 20ug/kg/minute
○ + lidocaine CRI start at approx 40 ug/kg/minute
○ + gabapentin if needed
- Once pain improving
○ Reduce ketamine incrementally (stop when reach 5 ug/kg/minute)
○ Reduce lidocaine incrementally (stop when reach 10 ug/kg/minute)
○ Reduce buprenorphine dosage then frequency
86
Severe pancreatitis pain what anaglesia do you use
- Baseline = buprenorphine 30-40 ug/kg q 4-6 hours
○ + ketamine CRI start at approx 20 ug/kg/minute
○ + lidocaine CRI start at approx 40 ug/kg/minute
○ + gabapentin if needed
- Consider fentanyl - last resort
- Consider morphine epidural
- Refer to an ICU
- Once pain improving, treat and withdraw drugs as per moderate
87
Pancreatitis anaglesia what drugs to avoid
- Fentanyl -> slams GI -> want to get them to eat, one thing that will help resolution
○ However pain trumps this
- Morphine -> only as epidural as makes the dog vomit,
- Medetomidine -> reduces pancreatic perfusion
- Tramadol -> can cause anorexia and other side effects
88
Controlling vomiting what are the 8 main anti-emetics for pancreatitis and the 3 main ones
a. Phenothiazine - MAIN
b. NK-1 receptor antagonist - MAIN
c. Dopaminergic antagonists - MAIN
d. 5-HT3 antagonists
e. Narcotics
f. Anticholinergics
g. Butorphanol
h. Anti-histamines
89
Controlling of vomiting in pancreatitis what want to block, the goal and the main thing used
Act to block -> peripheral and central receptors that lead to stimulation of vomiting centre
Goal
- Unlikely to resolve ALL episodes vomiting
- Concurrently control nausea
- Allow feeding
- Minimise continued fluid losses
What use?
- Maropitant - NK-1 receptor blockage -> substance P decrease THEREFORE reduce pain as well
- If poor emetic control, signs of nausea -> add in ondansetron (0.5mg/kg slow IV then PO q 12-24 hours OR 0.5 mg/kg/h for 6 h)
90
Gastric acid suppression drugs in pancreatitis when use
○ Melena
○ Haematemesis
○ Regurgitation consistent with reflux oesophagitis
91
Complications for pancreatitis
- Associated with feeding
○ Aspiration pneumonia
○ Poor intestinal motility
- Extra-hepatic bile duct obstruction -> ignore
- Associated with disease
○ As before: treat primary condition as needed
92
Aspirating fluid in treatment of pancreatitis what results from, when do and complications
- Acute fluid collection develop within the first 2-3 weeks -> may be area of necrosis
- True pseudocysts develop approximately 6-8 weeks later
- Virtually never infected in dogs
- Biggest risk for mortality is surgery
- THEREFORE -> if not causing pain then ignore, if causing pain - percutaneous drainage
93
Corticosteroid in treating pancreatitis what are the theoretical benefits, bad, when use
- Theoretical benefits
○ Inhibit release of pro-inflammatory mediators
○ Decreased sequestration of neutrophils
○ Reduce adhesion of primed neutrophils to endodelial surface
○ Reduces release of eleastase and free radicals from neutrophils
○ Reduces pulmonary vascular permeability
○ Enhances acinar cell apoptosis
○ Increases production of pancreatitis-associated protein (PAP)
- BUT -> possibly hydrocortisone, low rate infusion
- Need to get everything else sorted before recommending routinely (perfusion, analgesia, nutrition etc)
- If all else is failing and animal is dying -> USE
94
discharging pancreatic cases what discharge with and monitoring
- Remove/avoid triggers if known
- Discharge with low-fat diet; moderate to high soluble fibre
○ 1 week if not lipaemic, transitioning back to normal diet over about 4-6 weeks
- Discharge with 3 weeks pancreatic enzyme supplements and analgesia (gabapentin over tramadol)
- Check fasting serum triglycerides and cholesterol 1-2 weeks later
95
What are some signs that suggest gastric disease is more serious
- Abdominal pain - often post-prandial
- Weight loss (dependent on underlying and concurrent disease)
- Excessive distention
- Decreased appetite
- Melena - in order to detect has to have large amount of blood - SEVERE AT THIS POINT
- Vomiting (and haematemesis)
96
Chronic vomiting what are the 4 main steps
1) hstory - is it chronic
2) physical exam
3) assessment
4) treatment
- non-specific, specific
97
in terms of chronic vomiting history what specially asking for
- Ensure vomiting and not regurgitation
- Ask about possible precipitating factors
- Determine if evidence of delayed gastric emptying or other signs of diffuse GI disease
- Do signs persist despite fasting?
- Are there signs of systemic illness such as weight loss?
- Progression?
- Obtain full dietary, prophylaxis and travel history
98
in terms of chronic vomiting what are important aspects in physica exam
```
- Complete physical examination
○ Thyroid palpation (any cat >6yo)
○ Abdominal palpation
○ Rectal examination (dogs) - always
- Assess hydration status
- Determine if animal is systemically well
```
99
in terms of assessment of chronic vomiting case what are the 3 situations and what do
1. Obvious cause -> TREAT
2. No obvious cause -> animal systemically well -> non-specific treatment
3. Evidence of systemic disease or serious consequences resulting from V
○ Initial stabilisation, minimum database
100
non-specific treatment of chronic vomiting what don't you use, most important and other treatments
```
- Anti-emetic don't have a place in chronic disease
Most important treatment -> Dietary therapy
Gastric acid suppression
1. antacids - NOT INDICATED
2. diffusion barriers (sucralfate)
3) histamine H2 receptor anatagonists
4) proton pump (H+K+ATPase) inhibitor
5) prostaglandin E1 analogues
```
101
antacids what are they, what do they do, indications and contraindications
- Aluminium or magnesium hydroxide
- React with HCL to form conjugate chloride salt and water
- Indications: uraemic patients to bind PO4 -> ONLY INDICATION
- Contraindications:
○ Need very frequent admin to prevent rebound hypersecretion
○ May cause constipation, renal calculi if contain calcium
○ Will interfere with absorption many drugs
