Dogs and Cats 12 Flashcards
Regurgitation what results from, anatomy of canine and feline and what signs indicate that it is regurgitation
- 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
What are 3 important questions to ask owners to determine whether vomiting or regurgitation
- 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?
What are the 5 afferent pathways of vomiting
- 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
What are the 2 main efferent pathways of vomiting
- Efferent pathways
○ Autonomic nervous system inhibits motility gastric body, oesophagus and sphincters
○ Somatic nervous system driving force
What are the 4 main causes of vomiting
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
Differential diagnosis for ACUTE vomiting what are the GI ones
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
What are the non-GI differential diagnosis for vomiting
- 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
When a vomiting animal comes in what are the 4 main questions to ask
- 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
What are some important questions to ask during history of a vomiting animal
- 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
What are some important things to do especially for physical exam of vomiting animal
- 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
In terms of history and physical examination what indicates when to treat vomiting dog non-specifically
- 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
In terms of history and physical examination what indicates when to investigate further for a vomiting dog
- 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
What are the 3 main steps in a vomiting investigation (after history and physical exam) and how to achieve
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
What signs suggest surgical emergency and clinical signs of GI obstruction
- 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
After basic investigation of a vomiting case in clinic what should you have ruled out
- 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
After basic investigation of vomiting and still haven’t found an answer what are some further investigations
- 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
linear foreign bodies what species most common in, what results in and diagnosis
- 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
Intussusception what results in, most common sites and predisposing causes
- 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)
Intussusception clinical signs and diagnosis and treatment
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
SNAP cPL what test is it for, sensitivity and specificity and what else could an increase indicate
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
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
○ Recurrent disease, associated with anorexia, NO STRESS LEUKOGRAM - hypoadrenocorticism
§ Run cortisol testes - found to have Addison’s disease
Aortic arch vascular ring anomaly what is it, what animal occurs within
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
What are the 2 main causes of regurgitation and causes within
1) obstructive
a. luminal obstructions
b. extraluminal obstructions
2) non-obstructive
a. congenital - 30%
b. acquired - 70%
What are the main causes of obstructive regurgitation
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
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
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
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
Regurgitation work up what involved and additional diagnostics
- Thoracic radiograph
- Fluoroscopy (movement) -> when don’t get answer from radiograph
- Endoscopy
- Risk of aspiration pneumonia - NOT WHEN UNDER GA
Other diagnostics
- CBC - inflammation/infection, lead toxicity (basophilic staining)
CBC - inflammation/infection, lead toxicity (basophilic staining) what are the 4 main diseases looking for with regurgitation and what need to confirm with
- Hypoadrenocorticism -> electrolytes (ensure ACTH is low first then)/ACTH stimulation test
- 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 - Neuromuscular disease -> creatinine kinase
- Hypothyroidism -> T4 and TSH (BOTH
What are the 2 main complications of regurgitation
- Nasal discharge -> bilateral mucopurulent
- Aspiration pneumonia -> productive cough, dyspnoea
List the 3 main things within non-specific treatment for regurgitation
- 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 - Antacid
- Fluid therapy
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
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
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
What are the 6 main mechanisms of abdominal pain
- Distension
- Traction
- Ischemia
- Forceful GIT contractions
- Acute invasion or denuding of the bowel
- Secondary inflammation ( abdominal nerve endings stimulated by proteinases and vasoactive substances)
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)
Acute abdomen GIT requiring medical treatment
- Severe Gastro-enteritis (viral/bacterial/parasites/toxin/HGE)
- Pancreatitis
- Obstipation
- Colitis
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
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
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
