Pallor, Jaundice and Fluid Therapy Flashcards
Erythrocyte physiology
Fate of old and damaged erythrocytes?
Hemolytic (pre-hepatic):
* Rapid destruction of RBCs causes release of bilirubin into blood
* Increase in unconjugated bilirubin expected
* Animal expected to be anaemic
- Anorexia in horses
* Horses that have been anorectic for more than 1-2 days are mildly icteric
* Unconjugated bilirubin concentration increased
Definition of anaemia
Factors to consider when interpreting hematocrit (PCV):
* Species
* Age (changes in neonates)
* Hydration status
* Excitement or pain (horse)
* Breed (hot v. cold blooded horses)
** Anaemia is functionally defined as a decrease in the blood’s O2 carrying capacity
Partial pressure determined by O2 solubility
Approximately 98% of O2 carried in the blood is bound to haemoglobin
Clinical signs of anaemia
Anaemic patients Haemoglobin Saturation curve
Clinical signs of anaemia
* exercise intolerance, lethargy, depression (dementia)
* Tachycardia (increase in HR)
- increase tissue DO2
- systolic murmur
* Tachypnoeic (increased RR)
- ensure complete arterial oxygenation
* Cool extremities and weak peripheral pulses
- redistribution of blood to vital organs
* Signs of shock (blood loss > 30-40% of blood volume)
Severity of clinical signs depends on
Chronic v. acute blood loss and anaemia
How can clinical signs of anaemia give a clue to aetiology?
Diagnostic approach to anaemia
* Classification by bone marrow response:
* Regenerative anaemia: appropriate bone marrow response
- blood loss
- hemolysis (increased RBC destruction)
* Non-regenerative anaemia: bone marrow fails to increase erythropoeisis
- indicates abnormal bone marrow
- other cell lines often affected
Regenerative v. Non-regenerative
Peripheral signs of a regenerative response by the bone marrow
Peripheral signs of a regenerative response can be absent in:
Because the presence of a regenerative response is unreliable, a “mechanistic” approach to diagnosing anaemia is often used…
Haemorrhagic Anaemia
* Anaemia accompanied by hypoproteinaemia
- PCV and protein normal acutely
- splenic contraction may obscure anaemia acutely in horses
- protein may be normal with haemorrhage into a body cavity
Haemorrhagic anaemia internal v. external haemorrhage
Haemolytic anaemia via haemolysis
* Anaemia with a normal or slightly increased (protein)
* Erythrocyte morphology can suggest aetiology
- Heinz bodies
* Signs of an inflammatory reaction
- neutrophilia
* Hyperbilirubinaemia (unconjugated)
* Anti- RBC antibodies
- Coombs test or flow cytometry
Intravascular v. extravascular hemolysis
Anaemia via inadequate production
What is shock?
Severe haemodynamic and metabolic derangements that lead to an imbalance of oxygen delivery and oxygen consumption, leading to decreased cellular energy production
Circulatory shock
Hypoperfusion due to pumps not working
* Hypovolaemia
* Cardiogenic
Non-circulatory shock
* Hypoxic
* Metabolic
What is hypovolemic shock?
Causes of hypovolaemic shock
How might the body respond to hypoperfusion?
Shock pathophysiology
Angiotensinogen–> angiotensin I–>ANG II
- Vasoconstriction
- Facilities release of norepinephrine
- increased vascular sensitivy to norepinephrine
- increase Na and H2O resorption in proximal tubule
Oxygen delivery must meet oxygen consumption or else…
What happens when there is cellular oxygen and energy debt?
Clinical parameters in hypovolaemia
Definition of distributive shock? Causes?
Clinical signs of Distributive shock?
What is obstructive shock?
Causes of obstructive shock
Obstructive shock clinical signs
Cardiogenic shock definition
Causes of cardiogenic shock
Clinical signs of cardiogenic shock
Definition of metabolic shock
Causes of metabolic shock
Clinical signs of metabolic shock
Hypoxic shock
Causes of hypoxic shock
Clinical signs of hypoxic shock
Functional types of shock
Approach to treating shock
* First principles…what sorts of questions would you ask yourself when approaching a patient that looks like “flat?”
Is it shock?
Other “objective” information”:
- Haemodynamic
– heart rate
– MAP < 80 mmHg
– decreased urine output (UOP)
* Other objective information
- tissue perfusion parameters
- lactate > 2.5 mmol/L
- arterio-venous CO2 gradient
- Venous O2 saturation
* Non-specific changes on blood work
- circulatory
– ALT, AST, BUN, Creatinine
* Others, depending on type of shock
Tissue perfusion parameters
If so, what type of shock is it?
Is it a type that requires fluid therapy?
If it requires fluid, is there any reason to be cautious?
Is fluid therapy contraindicated?
What other therapies will you administer?
Conclusions of shock…
How much of body weight is water? Other compartments?
60%
10 kg dog, how much body water? How many L intravascular? Interstitial? Intracellular?
Water movement in the body
3 types of fluid therapy
Classifications of altered tissue perfusion
Identification of need: tissue perfusion
Identification of need: evidence of poor/abnormal tissue perfusion
What tests can assess tissue perfusion.. OBJECTIVE assessment
Is there a single parameter that reliably identifies abnormal tissue perfusion?
Flow chart of findings when poor/altered tissue perfusion–> auscult heart–> what might you find?? Lungs??
Vascular access for fluid resuscitation
Most common route of fluid resus?
Central venous catheter
Intraosseus catheter for acute resuscitation
What to use with acute resuscitation fluids? What NOT to use?
What not to use:
hypertonic crystalloid fluids, 5% dextrose in water
Increases ICF > ECF
Rates and volumes depends on?
Figuring out rates and volumes– species?
Severity of hypoperfusion/shock– in determining rates and volumes?
Rates and volumes
Risk factors for adverse effects
Types of fluids
Isotonic crystalloids
Hypertonic Saline
Hypertonic saline effects
Synthetic colloids
* if low COP, low total protein
* small volume resuscitation
* Combination with HTS
* Adverse effects:
- coagulation impairment
- renal failure in people
- in dogs?
Packed Red Blood Cells (whole blood)
Final volume depends on??
Resusucitation endpoints?
Objective:
ECG: HR decrease
Arterial BP: MAP > 65-70 mm Hg
Urine output > 2 ml/kg/min
Lactate < 1.5 mmol/L
PCV: more than 20%
Safety endpoints of fluid resuscitation?
Time in fluid resuscitation?
Resuscitation strategy
Hypoperfusion Hypovolemia/ Sepsis–> Fluid bolus–> reassessment???
Key points of acute resuscitation?
Determine presence and severity of anaemia… how?
Regenerative or non-regenerative?
Regenerative anaemia
Other changes that support regeneration
* Polychromasia
* Increased MCV +/- decreased MCHC
* Macrocytic and hypochromic/ macrocytic normochromic
* Increased RDW
* Nucleated RBC
Regenerative: haemolytic or haemorrhagic?
Presenting problems and clinical signs of anaemia?
Common histories of anaemic patients
Problem lists that point to anaemia’s aetiology
Haemolytic anaemia
IMHA
Extravascular haemolysis?
intravascular haemolysis
Why does IMHA occur?
Typical signalment of IMHA
Typical presentation of IMHA
Typical findings on physical exam of IMHA
* enlarged liver +/- spleen
* Jaundice, orange coloured urine
* Abdominal pain, lymph node enlargement, fever
* Red coloured urine
Physical exam findings in IMHA if concurrent immune mediated destruction of platelets
Initial management:
* Rest, oxygen (fly by or oxygen pen), get IV access, ensure have resuscitationg code, collect blood samples: EDTA (purple), blood smear, plain/lithium heparin (yellow/green), +/- citrate (blue)
- PCV/ TP and blood smear
- Minimum data base (haemogram, biochemistry)
* Collect urine
** look for underlying cause- why? when?
- Prior drug history (including vaccines, over the counter and preventive health care)
- Travel history- ticks, heartworm, other infectious causes
- Prior diseases
- Prior transfusions, pregnancies
- Search by RG, U/S, cross match blood type, tests of clotting function, infectious disease panels (geographically dependent), blood gas analysis, check bone marrow sample…
- No underlying cause found… Ruby has primary IMHA
Diagnosis IMHA
Then what would be abnormal?
When would you perform the Coomb’s Test? What is it?
Treatment of IMHA
Immunosuppresive doses of prednisolone
* Mainstay of initial treatment, rapid
* Or IV dexamethazone day 1 then prednisolone day 2 onward
* Until normal PCV and no spherocytes or auto agglutination, then slowly taper every 2-4 weeks while monitoring red cell count
* Side effects common: increased thirst, increased urination, increased appetite, increased panting, muscle wasting, weakness, poor wound healing, GI ulceration, increased liver enzymes and liver size, thin skin, hair loss, clots, increased risk of infection, diabetes, Cushing’s disease
** First immunosuppressive medications tapered
What is another option aside from Prednisolone for treatment of IMHA
Or Cyclosporine
- give one hour before or two hours after food
- give once or twice a day by mouth
- for refractory cases
- can monitor blood levels prior to next dose after 2-4 weeks
- rapid in action
- does not suppress bone marrow
- high cost, compounding
- side effects: vomiting, diarrhoea, anorexia, overgrowth of gums, papilloma like skin lesions, hair loss, increased risk of infection, cancer?
- manage GI side effects with twice a day dosing/ giving with small amounts of food
* Lots of other immunosuppressives tried, good evidence is lacking
- Leflunomide- GI side effects common
- Mycophenolate mofetil- GI side effects common– similar side effects to Azathioprine, less bone marrow suppression and pancreatitis, relatively expensive
- Liposomal- encapsulated clodronate
* Human immunoglobulin (rapid onset, IV in emergency setting)
Treatment of IMHA other than Immunosuppressives
Monitoring/ nursing of IMHA
Prognosis of IMHA
Negative prognostic factors in IMHA
Complications of IMHA
DIC- 20-45% of cases
- low platelet counts, prolonged clotting times, low fibrinogen, increased fibrinogen degradation products
* Relapse
16% of cases, restart treatment and taper more slowly, may require lifelong treatment
Outcome of Ruby with IMHA
Immune mediated thrombocytopenia
Mycoplasma haemofelis
Clinical signs
* Vary with species, strain, stage of infection, concurrent disease (FIV/ FeLV)
* Acute: pale, lethargy, anorexia, weight loss, dehydration, pyrexia, splenomegaly (jaundice)
* Transmission: fleas, fighting, contaminated transfusions, ?transplacental
Diagnosis of Mycoplasma haemofelis
Treatment of Mycoplasma haemofelis
Babesiosis
* 2 days for transmission to occur
* RBC fragility + anti- RBC Ab–> intravascular/ extravascular haemolysis
* Sludging of RBC–> organ failure + hypoxia
* Acute infections
* Chronic infections
* Subclinical infections
* B. canis- 10-21 day incubation period
* B. gibsoni- 14-28 day incubation period
Secondary complications and diagnosis of Babesiosis?
Toxin/ drug induced acute anaemia
Pathophysiology of toxin/ drug induced acute anaemia
Microangiopathic haemolytic anaemia
Electrolyte abnormalities + acute anaemia?
Congenital RBC defects and acute anaemia
* Pyruvate kinase deficiency
- Autosomal recessive
- Chronic moderate to severe haemolytic strongly regenerative anaemia
– impaired RBC glucose metabolism, decreased RBC lifespan
– BM exhaustion (myelofibrosis, osteosclerosis): MST 1-5 years
– cats: mild to moderate signs, may live to old age
** only supportive treatment
** Phosphofructokinase deficiency (PFK)
- energy depleted RBC –> low grade anaemia, marked regeneration
- Marked RBC alkaline fragility
– IV haemolysis with exercise, hyperthermia, severe barking
** May have normal life span
What is anaemia?
Clinical presentation of anaemia
Signs of anaemia on physical exam
Hypoperfusion v. anaemia?
White gums… then….
Look at PCV- if normal but white gums– circulation problem
Low PCV– anaemia
3 to 5 days
How to tell if Chronic– can test later again and see if same
Causes of non-regenerative anaemia
Cause and severity of anaemia in dogs
Questions for the owners with anaemia
Assessing severity, chronicity of anaemia– how does your patient look?
- is anaemic
- doesn’t have anaemia
- Main difference from 1 HR and RR normal
- Anaemic, collapsed, really trying to compensate
Symptomatic treatment with anaemia
Anaemic patient work-up
How to collect bone marrow
How is cytology and histopathlogy complementary in anaemia?
* Chronic non-generative anaemia (8 months)
*PU/PD
* Tiredness (agility dog)
* Not much on the exam except overweight
Biochem
Cholesterol- going down
Albumin- low
Creatinine- high
K- normal
Na- slightly low
Biochem
Cholesterol- going down
Albumin- low
Creatinine- high
K- normal
Na- slightly low
- Inflamm
- Endocrine *** mild anaemia, expect stress leukogram– lymphocytes are high– unusual… specific gravity– dog is not concentrating… Na is decreasing. Wondering about the liver with cholesterol. ADDISON’S??
- Bone marrow
- CKD– specific gravity– dog is not concentrating
- Iron deficiency anaemia
** U/S very small adrenal gland
What is it? Tx?
Confirms addison’s
A month after starting Addison’s treatment
Work up
FeLV/FIV snap test, negative Mycoplasma
Physical exam– Unremarkable
* Imagine- unremarkable
Work up
FeLV/FIV snap test, negative Mycoplasma
Physical exam– Unremarkable
* Imagine- unremarkable
What’s next?
Treatment?
Sammy, Cocker ME, 12 yo
Alopecia
Large testicle
Enlarged nipples
Bone marrow aspirates- lack of cells
Hyperoestrogenism treatment
Other causes of bone marrow aplasia
Chronic anaemia non-regenerative, microcytic, hypochromic and thrombocytosis
IRON DEF
Iron deficiency anaemia picture? Causes?
Iron deficiency treatment
Chronic anaemia conclusion
Chronic anaemia work-up
Components of the haemostatic system
The clotting cascade
Haemostatic defects– categories
Primary haemostatic defects
Secondary Haemostatic Defects
Haemostatic defects
Tests of haemostasis
* Platelet count
* Prothrombin time (PT)
* Activated partial thromboplastin time (aPTT)
* SCA 2000/Coag Dx
Blood smear
Buccal mucosal bleeding time
Activated Clotting Time
* Use pre-warmed tubes and heating block
* Begin timing when blood first enters tube
* End point is first visual evidence of clot
* Reference ranges vary
Prothrombin time
Activated Partial Thromboplastin Time
* History
* Full physical exam
* Diagnostic tests
- PCV/TS/CBC (Chronicity/ severity)
- Blood smear (platelet count/ RBC morphology)
- ACT or PT/aPTT
- ?BMBT
- Chem screen for organ assessment
- Imaging to look for haemorrhage, masses and other disease
History in regards to a bleeding patient
Clinical signs of haemorrhage you might find on PE
* Short, narrow pulse profile
* HR 225 quiet sounds
Reassessment after fluids (3L crystalloids in 1 hr)
* High, narrow pulse profile
* HR 140
Owners report ate rat poison
What would you expect the PT and PTT to be in this dog and why?
What would you recommend and why?
Classifications of Haemoabdomen
Aetiology of traumatic haemoabdomen
Aetiology of Non-traumatic Haemoabdomen
Most common causes of haemoabdomen
Initial stabilisation of haemoabdomen
Diagnosis of haemoabdomen
Surgery or no surgery? Haemoabdomen
Indications for laparotomy
Exploratory laparotomy
Exploratory laparotomy with haemoabdomen
Surgical haemostasis
* Pressure/ tamponade (temp 5-10 mintutes)
* Ligation with suture ligatures or vessel sealing device
* Abdominal packing
* Topical haemostatic agents- gelfoam, surgicel
Metastatic rate of splenic mass
Splenic mass– most common? Diagnosis?
Study of acute non-traumatic haemoabdomen– causes? Prognsis?
Splenic masses- Haemangiosarcoma
Vascular anatomy of the spleen
Where do you ligate splenic vessels? What do you have to be careful not to ligatein order to avoid risk of pancreatic ischaemia?
Indications for splenectomy
Performing a splenectomy
* Biopsy other organs as indicated (especially liver, LNs, omentum, peritoneum)
* Lavage abdomen thoroughly
* ensure all bleeding controlled
* Histopathology
- submit entire spleen
- bread loaf, fix in formalin
Splenectomy complications
* Criteria for treating
- HR > 150 bpm
- Multiform ventricular beats
- R on T phenomenon: superimposition of an ectopic beat on the T wave of preceding beat. Likely to initiate sustained ventricular tachyarrhythmias.
- Hypotension during ventricular arrhythmias
* Treatment:
- Lidocaine bolus (2 mg/kg IV bolus) then CRI (30-80 microg/kg/min)
- supplemental O2
- treat hypovolaemia
- procainamide 20-40 ug/kg/min IV
** Other complications
- Continued bleeding
- Vascular compromise to pancreas: damage to pancreatic artery arising from splenic artery, release of MDF 2o to pancreatic ischaemia
- Acute portal vein thrombosis- hypercoaguable state
- DIC
HSA Prognosis with surgery alone
Splenic HSA prognosis with surgery + doxorubicin? Surgery + Metronomic chemo
Splenic torsion- signalment? Diagnosis? Tx?
* Do not derotate spleen– inflammatory mediators, thrombi
* Manually ligate vessels instead of staples
* Careful inspection of pancreas for compromise
* Prophylactic gastropexy
Non splenic causes of haemoabdomen
Summary haemoabdomen
Functions of the liver
Potential manifestations of liver disease
Bilirubin metabolism
Physical examination– what are you looking for?
Acoholic faeces
* Assess the size and contour of the liver
If the liver is small and smooth what is a possible DDX?
Congenital vascular diseases e.g. portosystemic shunts– NOT JAUNDICED!!!
If the liver is small and bumpy??
End-stage liver disease: Cirrhosis & Fibrosis
If the liver is large and smooth?
* Infiltrative disease: Lymphoma, amyloidosis,
* Lipidosis
* Acute hepatitis
* Vacuolar hepatopathy
* Hard working!
Large and bumpy liver??
* Neoplasia: adenoma (primary), metastatic
* nodular hyperplasia
* Abcesses/ cysts
What must you rule out before treating primary liver disease?
How to diagnose liver disease?
Serum bile acids
- responsible for fat absorption
- reflects enterohepatic circulation and hepatocellular function
- only do if indicated clinically and not if high bilirubin
- bile acid stimulation test also affected by:
– steroid hepatopathy and extra-hepatic disease
– failure of GB to contract
– Intestinal integrity and transit time
–?breed
Liver changes don’t always mean primary liver disease
Haemotology with liver disease
Diagnostic imaging liver disease
Swiss cheese!
FNA cytology in the diagnosis of liver disease
Blind FNA sites for liver FNA
Biopsy: needle v. wedge?
Acute hepatopathies aetiology? Hepatocellular injury?
* Any inflammatory, toxic, neoplastic or infectious insult to the body has the ability to cause acute liver disease
In many casees the underlying aetiology cannot be identified, especially until the animal is stabilised so immediate treatment when clinical signs are directly attributable to liver disease is appropriate
Signs and diagnosis of acute liver disease
Prognosis of acute liver insult
General treatment of acute hepatopathies
What do you do if concerned about hepatic encephalopathy?
General treatment of acute HE
Avoid potentiating factors when treating acute HE (or any liver disease really!)
Acetaminophen toxicity
Anti-oxidants in the treatment of liver disease?
Ursodeoxycholic acid
Biliary system disease
(e.g. well dog, jaundiced, high ALP)
Approach to figuring out if hepatic or post-hepatic jaundice
Gall bladder mucocoele
When is Extrahepatic Bile Duct Obstruction (EHBDO) a surgical emergency?
Idiopathic nodular hyperplasia
* often appears nasty on U/S
* Needle biopsies may not distinguish from adenomas
* Need large wedge biopsy for definitive diagnosis
* Do not use this disease an excuse for a sick dog
Neoplasia and the liver?
Vacuolar hepatopathy
* Causes: hyperA, diabetes mellitus, pancreatitis, lipid metabolism disorders, chronic stress, severe hypothyroidism, glucocorticoid administration
Chronic hepatitis
Causes of chronic hepatitis
Breed specific hepatopathies diagnosis– clinical signs?
Breed specific hepatopathies diagnosis?
What hepatopathy might this Bedlington terrier have?
Copper toxicosis
Hepatopathy?
Hepatopathy?
Chronic active hepatitis
Hepatic fibrosis
Idiopathic hepatic fibrosis
Treatment of these chronic conditions of the liver– what we need to know
General tx for chronic canine liver disease
Anti-copper medications
Anti-fibrotic agents
Inflammatory liver disease of cats
Acute v. chronic Cholangiohepatitis (CCH)
Other types of inflammatory liver disease in cats
Clinical signs of CCH
Difference in clinical signs in acute CCH, chronic CCH and LPH of cats
Clinical pathology of liver disease in cats
Diagnostic imaging of liver disease in cats
Diagnosis of feline liver disease– cytology and biopsy
Treatment CCH/LC (cats)
Treatment of LPH
Prognosis of CCH? LPH?
Hepatic lipidosis in cats
* Usually period of anorexia/ illness precedes HL
* Other factors may be involved
- Carnitine deficiency
- weight loss
- insulin deficiency
- hepatic factors
* Older to middle aged cats
Clinical signs of hepatic lipidosis in cats
Diagnosis of hepatic lipidosis in cats
* Imaging
- hepatomegaly on Xray
- hyperechoic on U/S
- evaluate rest of abdomen for other disease
* Cytology
- can be blind FNA
- See cytoplasmic vacuolation within hepatocytes
- usually FNA is diagnostic
- check clotting times before biopsy
Treatment of hepatic lipidosis
* Nutrition ASAP
- Oesophageal or gastrostomy
- titrate up to 100% day 4
- balanced commercial diet
- monitor re-feeding syndrome
- can discharge with tube in place
- no need for appetite stimulants
Prognosis of hepatic lipidosis
Other liver disease of cats
Hepatic lymphoma
Shiva, 3yo, FS German Shepherd
Chief complaint- lethargy, not eating, reluctance to rise
LN (last normal)- 4 days ago
Progression- hiding 4 days ago, self-limiting, eating normally up until today
Shock secondary to hypoperfusion
Any reason to be extra cautious with Shiva?
** You should be especially because because if we suspect Shiva is bleeding then we could cause her to bleed more
RR 40, RE normal
Resp auscultation clear all fields
Resp effort and pattern normal
Pale MM
Distended abdominal palpation, fluid wave present, difficult to palpate deeply
Hypovolaemic but could be distributive (vasodilation)
Clinical assessment of hypoperfusion
Mild to severe hypovolaemia?
* Supplemental oxygen– increasing dissolved oxygen (only 3%)– can help in severe cases… generally speaking not a huge difference… so if this dog was resistant, okay
*SpO2
* Venous blood gas, PCV/TP– lactate!!! pH would be useful to know. (doesn’t include unless you have a machine that has it on it).. PCV/ TP could be normal if the bleed was acute
* AFAST- run this before PT/aPTT
* ECG
* Blood pressure- guides your treatment– if it is normal, you don’t have to rush into giving fluids straight away. Sub-normal you have to give fluids to bring it back up.
** Peripheral vasoconstriction– toxicities, compensating for hypovolaemia… if BP comes up normal… they are compensating and doing the job right now.
VPC’s and Free
Abdominal Fluid
Defibrinated from the peritoneum
Free blood– when it is has been sitting the abdomen for a while becomes defibrinated…. really recent– might still clot
3.
When would you give a transfusion?
< 20% PCV = transfusion as can’t go to surgery
If you don’t have the blood, belly rap!! Slow bleeding considerably– increasing intrabominal pressure > the pressure of the bleed
Chest radiographs– in case of mets….
Would give some fluids– perhaps half maintenance.. trying to keep blood pressure
YES!!
In the veterinary profession, we are lucky enough to have the option of euthanasia to avoid unnecessary pain and suffering. You haven’t failed as a vet, the owner hasn’t failed as an owner
2.
What are you specific concerns?
Won’t be suffering… there is a chance they won’t make it, there is a chance they will pull through and have a good quality of life
Hypotension, dysrhythmias, hypothermia, cardiopulmonary arrest
No, would not treat
Yes
Asystole
What anaesthetic drugs should you be careful of with Shiva?
Avoid
Acepromazine- hypotension and potential interference with clotting
Alpha 2 agonists– decreased CO
Cautious of propofol/ Alflaxan- potential for apnea and CV depression
Ketamine– causes CV depression if relative adrenal insufficiency
Anaesthesia monitoring
e.g. small dog, haemoabdomen, big fluid bolus, reasonably stable for surgery, transfusion and methadone 0.1 mg/kg IV
No ventricular arrythmias… nervous about propofol/ alfaxan
High dose fentanyl, medium dose medazolam, and lignocaine
** dull mentation and CV depression this would be enough
* Mainted it on sevoflurane (less soluble than iso so can change depth better)
* Kept it on fentanyl and lignocaine CRI interoperatively to reduce the amount of sevo you need….
Dog was still hypotensive but did well
