Gastrointestinal system & gastrointestinal emergencies Flashcards
What are the general causes of abdominal pain?
Distension of organ or organ capsule
Ischaemia
Traction
Inflammation due to underlying disease
Not treating issues relating to the abdomen can lead to?
Necrosis of tissue and loss of function of the abdominal organs and may result in SIRS, sepsis and MODS
What is a predisposed condition often found in young GSD that have pancreatic exocrine insufficiency?
mesenteric volvulus
A patient with both an increase in PCV and TP is likely to be what?
Dehydrated
A normal or increased PCV with a normal to low TP indicates?
Protein loss from the vasculature, acute abdomen, peritonitis, HGE.
A parallel decrease in PCV and TP indicates?
Haemorrhage (initially PCV may be normal or elevated and TP normal or reduced due to splenic contraction)
Which of PCV and TP is a more sensitive indicator of acute blood loss?
TP
Why may a patient have high glucose associated with an acute condition of the abdomen?
Diabetes, transient diabetes associated with pancreatitis, stress
Why may a patient have a low glucose associated with an acute condition of the abdomen
sepsis (not generally extremely low), hypoadrenocorticism
Loss of kidney detail, ‘streaky’ appearance or distension in the retroperitoneal area may indicate?
A space occupying lesion
Gas in the peritoneum on lateral or horizontal beam radiograph may indicate
GI perforation
Ruptured urinary bladder
Extension of a pneumomediastinum
Segmental gas or fluid distension in the small intestines is suggestive of
Gastrointestinal obstruction
Normal diameter of the small intestine
Dogs: 2-3X width a rib or no more than the width of an intercostal space
Cats: <2X the height of the central portion of L4 or 12mm
* all areas of the small intestine should be the same diameter
Modified transudate
Cells 300-5500/uL, protein 3-5g/dL, ND neutrophils, mesothelial cells, lymphocytes, RBC, macrophages
Congestion, RHSHF, liver disease, heartworm, neoplasia
Exudate
Cloudy or blood, protein >3g/dL, cells >5000-7000/uL, likely neutrophils +++, +- bacteria
Haemorrhage, septic peritonitis
Pathophysiology of pancreatitis
(diagram in notebook)
Common lab findings with pancreatitis
Increased liver enzymes + Tbil
Increased triglycerides, cholesterol etc
Neutrophilic leukocytes is or neutropaenia (often with left shift)
Increase/positive cPLI
Hypoalbuminaemia
+- anaemia and thrombocytopaenia
Low electrolytes
Elevated coags
Haemoconcentration
Ultrasound findings of patients with pancreatitis
Enlarged hypoechoic pancreas
Dilated pancreatic duct
Free fluid (often inflammatory)
Hepatobiliary dz
Thromboses/organ infarcts
+- masses
Biochemical marker for pancreatitis
CRP best we have so far
Treatment of pancreatitis
Early enteral feeding
Pain relief (opiates and lidocaine +- ketamine)
AM therapy if severe or concerns for bacteria
Eliminate underlying cause
Aggressive fluid resuscitation, consider colloids
Management of underlying illnesses
+- oxygen therapy
+- FFP (a-macroglobulins)
Frequent blood testing (pcv/ts, VBG, lytes, lactate, albumin, renal function, coags, glucose)
Intensive patient monitoring
Supplement electrolytes as needed (avoid Ca unless titanic otherwise promote ROS and free rads)
+- LD dopamine for haemodynamic support and may reduce microvascular permeability
Other supportive therapies
Why is early nutrition a must in pancreatitis
Those with SAP are in a catabolic state
Improves mucosal structure and function
Reduces chances of bacterial translocation
* if ileus or vomiting trickle feeds preferred
* supplement with glutamine
* watch for refereeing syndrome
Acute cholecystitis
Shetland sheepdogs and cocker spaniels are over represented
It is not always accompanied with inflammation
Bacterial (bacteria, parasites) or obstructive (mucocele, infarction) in nature
Signs of acute cholecystitis
Anorexia
Vomiting and diarrhoea
Abdominal pain
Increased ++ liver and biliary enzymes
Abnormal appearance of GB on imaging
Bacterial cholecystitis
Often caused by bacteria such as E. coli, clostridium, enterococcus, bacteroides and may be due to reflux of duodenal fluid or through portal system.
- Gas within the gall bladder indicates a gas forming bacteria present such as E. Coli or clostridium
Overall survival with either medical management or pref surgery = 61-82%
Obstructive cholecystitis
EHBO results in the dilation of the gall bladder and cystic duct within 24h but IH bile ducts within 5-7 days. Changes in liver and biliary enzymes will be apparent which may indicate hepatocyte necrosis, cholangitis and periportal fibrosis. +- choleliths
Choleliths
Most often an incidental finding and not always associated with cholecystitis
Occur due to mucin production and reduced GB motility producing either calcium carbonate or bilirubin pigment liths.
Surgery is generally required and carries a survival of about 78% in cats but only 41% in dogs
Gall bladder mucocele
Exclusive to dogs
Occurs when there is thick, mucin-laden bile within the gall bladder and ducts causing an obstruction to bile flow which leads to ischaemic necrosis of the GB wall and likely to rupture without intervention. Can attempt to medically manage however most of the time require surgery to avoid rupture and consequences of rupture
‘Kiwi fruit’ appearance
Medical management of GB mucocele
UDCA: immunomodulatory, increases GB motility, decreases mucin secretion
Levothyroxine
sAME: glutathione precursor and antioxidant
Amoxicillin
Omega FA
Hepatitis
Inflammatory cell infiltrate within hepatic parenchyma with cholangiohepatitis referring to the involvement of the intrahepatc bile ducts. There are many causes for hepatitis including: idiopathic (CCH, idiopathic feline hepatitis), viral (infectious CH, FIP), bacterial (leptospirosis, bartonellosis, septicaemia) or drugs/toxins
Mechanisms of hepatocellular injury
Hypoxia
Lipid perioxidation
Endogenous or intracellular toxins
Intracellular co-factor depletion
Cholestatic injury
Hepatocyte membrane injury
Hypoxic injury to hepatocytes
Cytokines & organelle injury > ATP depletion > free radical and oxidative injury
Toxin injury to hepatocytes
I.e. bile acid retention
Nuclei acid binding > impaired protein synthesis
Inflammation
TNF-a expression
Neutrophilic v. Lymphocytic idiopathic feline cholangitis complex
In both hepatic and biliary enzymes may or may not be increased
Mixed inflammatory infiltrates are seen in lymphocytic compared to neutrophilic
Treatment of neutrophilic involves antimicrobials whereas lymphocytic involved immunosuppressive therapy
IBD and pancreatitis may be associated with both
Hepatic tissue biopsies differentiate
Both are likely due to ascending bacterial infection from the GIT
Canine chronic hepatitis (CCH)
Idiopathic
Progressive, necroinflammatory disease likely with some immune-mediated process
Histopathologic assessment of liver tissue: lymphocytic, plasma cystic and may also be neutrophilic; apoptosis/necrosis, signs of regeneration with fibrosis
Treated with immunosuppressive therapy: UDCA, glucocorticoids, metronidazole, azathioprine, cyclosporine and +- copper chelation
Copper in CCH
These patients seem to have elevated levels of copper and unsure if primary copper storage disorder or if due to inability of diseased liver to excrete. In any situation chelation with d-penicillamine or trietine may be indicated
Leptospirosis and hepatitis
L. icterohaemmorhagiae or L. Pomona likely to induce hepatitis
May not test positive for first 2 weeks; infection may span 2-6 weeks
Usually induces ARF but hepatitis seen in 20-35% of cases
Treatment with doxycycline 5mg/kg q12
Bartonellosis and hepatitis
Likely henselae or clarridgeiae varieties and confirmed with PCR
Treatment with azithromycin (or: doxy, enro, rifampin)
Liver failure
Occurs when there is severe hepatocyte injury or dysfunction that leads to severe metabolic dysfunction, hepatic encephalopathy and coagulopathy.
Liver failure induces…
Coagulopathy
GI ulceration
Bacterial sepsis
Cardiopulmonary dysfunction
Ascites
CNS signs
How much of the liver can regenerate within a few weeks?
<75%
Acute v. Chronic liver failure
Acute liver failure likely to appear as hepatocellular necrosis as a primary lesion whereas chronic will have this as well as fibrosis, inflammation and hyperplasia of ductular structures.
Common clinical signs of hepatic failure
Hepatic encephalopathy (CNS abnormalities)
Hypotension
Lactic acidosis
Electrolyte abnormalities
Coagulopathy
Hypoglycaemia
Azotaemia
PU/PD (decreased ADH response, urea processing failure)
Icterus
GI signs
Consequences of hepatic failure
Higher risk of infection
Systemic hypotension
Portal hypertension
Pulmonary infiltrates
Renal dysfunction
Acid-base abnormalities
Haematology findings in patients with hepatic failure
Target cells
Acanthocytes
Anicytosis
Anaemia; nonregenrative indicates chronic where regenerative may be more acute process
Leukocytes is or leukopaenia
Biochemistry findings in hepatic failure
Increased liver enzymes
Increased TBil
Low cholesterol
Hypoalbuminaemia
Hypoglycaemia
Low BUN
ALT & AST
Found in cytosol of hepatocytes and leak when hepatocyte cell membrane disrupted (ALT shorter HL and therefore more specific for acute hepatic failure)
ALP
Found on the membranes of hepatocytes and biliary epithelial cells increasing in cholestatic disease
GGT
Specific for cholestatic disease
Albumin in liver failure
Altered albumin synthesis not detected until >66-80% of liver function lost and is a hallmark of chronic liver disease due to it having a long half life of 8 days. It is 25% of all proteins synthesised in the liver
How much cholesterol is synthesised in the liver
50%
When does hypoglycaemia occur in liver disease
When only 30% of liver function is present
UA findings in hepatic failure
Ammonium biurate crystals
Urate crystals
Bilirubinaemia
Treatment options for liver failure
Treat underlying disorder
Liver protectants
Routine supportive care
Treatment of HE
Treatment of coagulopathy
Seizure control (avoid benzodiazepines)
Vitamin E
Milk thistle
L-carnitine
Vitamin B complex
Gastroenteritis
Inflammation of the stomach and digestive tract
Stomach layers
Glandular; parietal cells (H secretion), chief cells (pepsinogen), mucosal (bicarbonate)
Mucosal; protects from effects of acids
Muscle: grinds, moves food
Small intestine areas and functions
- Duodenum
- Jejunum
- Ileum
Functions to breakdown/grind and absorb food/nutrients
Contains enterocytes, villi, microfilm etc
Infectious gastroenteritis pathogens
Clostridium
CPV-2
Campylobacter
Salmonella
Helicobacter
E. Coli
Cryptosporidia
Toxocaria
Trichuris (whip worm)
Hook worm
Urcinaria
Trichomonas
Histoplasmosis
HGE
Acute onset of haemorrhagic diarrhoea that is likely an immune response to bacteria, bacterial endotoxin or dietary ingredients. It is associated with a PCV >60%, vomiting, haemorrhagic diarrhoea, anorexia, depression.
Why do we quickly want to correct fluids in gastroenteritis
The GIT is a shock organ particularly in dogs and therefore poor perfusion to the gut worsens inflammation, promotes bacterial translocation and also promotes sepsis, and DIC.
Protein losing enteropathy (PLE)
Broad classification that indicates that there is massive plasma protein loss from the GIT. It causes disruption to the GI barrier and normal enterocyte function as well as deranged permeability of the tight junctions. This results in loss of albumin and antithrombin which leads to decreased oncotic pressure, pro inflammatory response and thromboembolism
Diagnostics and treatment of gastroenteritis
Faecal testing, systemic evaluation, determine underlying cause, imaging, albumin therapy, electrolyte and fluid therapy, radiographs, ultrasound, biopsies, nutritional support, try to avoid antibiotics, consider gastroprotectants.
Megaoesophagus
Congenital or acquired
Distension of vagus afferent system innervating the oesophagi is ineffective
Diagnosed either with plain radiographs or contrast radiographs
Treatment of megaoesophagus
Prokinetics
H-H2 blocker
PPI
Pyridostigmine
Prednisone
Mycophenylate
Azathioprine
Small, frequent meals from a height
Consider feeding tubes
Gastric empting disorders
Due to mechanical obstruction or defective propulsion and associated with chronic intermittent vomiting, gastric distension and weight loss. It is confirmed with a barium study and treated with small, frequent meals and prokinetics
Transit disorders
Include ileus, enteritis, nematode infestation, sclerosis, radiation eneteritis.
Can be a result of bacteria, bacterial endotoxin, surgery etc
Before beginning prokinetic therapy must rule out a mechanical obstruction
Functionality of the GIT
Can work independently of the CNS to control bowel function as no nerve fibres actually penetrate the intestinal endothelium so enterochromaffin cells act as neurotransmitters.
Serotonin in the GIT
95% of all serotonin in the GIT with ()% of that stored in enterochromaffin cells from stomach to colon
Main serotonin receptors in motility of the gut
Released from enterochromaffin cells into the Latin propria and overflow into intestinal luma and portal circulation.
5HT1P = peristalsis and secretions;
5HT4 = propulsive, peristalsis, neurotransmission, increases ACh
5HT3 = visceral hypersensitivity, vomiting and nausea
Cisapride
Acts on the 5HT4 and has broader prokinetic activity compared to metoclopramide. It improves kenesis of the entire GITso good for reflux, constipation and ileus. It is metabolised by the liver and CP450.
* out of favour due to side effects.
Metoclopramide
5HT4 agonist; 5HT3 and dopaminergic antagonist that increases entire GI motility but not so good in the colon. It crosses the BBB into the CRTZ so has been shown the have negative behaviour affects in some animals that can be balanced with diphenihydramine.
Ghrelin and motilin prokinetics
Stimulate GI motility and accelerate gastric emptying
Induce gastric hunger
Rikkunshito; cholinergic receptors and 5HT3
Erythromycin; motilin agonist, increases gastric emptying, accelerates colonic transit time
Acetylcholine inhibitors
I.e. ranitidine
Histamine H2 receptor antagonists that increase ACh able to bind in the proximal GIT to reduce gastrointestinal reflux without effects on transit time
Broad categories that cause GI haemorrhage
Ulceration
Disease causing coagulopathies
Vascular anomalies
Presentation of patients with suspected GI haemorrhage
Usually in a state of hypovolaemic chock due to blood loss, endotoxaemia and hypovolaemia. We need to establish what has happened and if the patient is on or exposed to things that are known to induce GI haemorrhage I.e. NSAIDs, rodenticides, hx of neoplasia, recent gastrointestinal surgery hepatic disease etc
Rectal exam findings that might indicate GI haemorrhage
Haematochezia = larger intestinal, colon or anal bleeding
Melena = likely reflects an upper GI bleed unless transit time reduced
Which of upper or lower GI haemorrhage seems to be more severe
Upper GI
Findings of blood tests that may suggest GI bleeding
Anaemia and if microcytic and hypochromasia may indicate a chronic bleed due to (Fe deficiency)
BUN:Crea >20 due to volume depletion and absorption of proteins from GIT * present in offer trauma so not diagnostic and likely not present if large bowel
Perioxidase bacteria in stool
PCV/TS may reflect changes similar to other haemorrhage patients
ACTH should be performed as addisons may induce
Thrombocytopaenia may be present
Liver and kidney enzymes likely to be elevated
Treatment of GI haemorrhage
Stabilise the patient
Identifying underlying cause and remove trigger
Consider blood products
Give gastroprotectants (PPI, H2, anti-emetics, sucralfate)
Ensure adequate DO2
Consider AB (Ceph and metro)
Do upper GI imaging if necessary
Mortality of GI haemmorhage
29-41%
Regurgitation v. Vomiting
Regurgitation is passive ejection of food where vomiting is active ejection of food
Ddx of regurgitation
Pharyngeal disease
Oesophageal disease
Oesophagitis
Mechanical obstruction
TRad findings in regurgitation
Aspiration pneumonia, megaoesophagus, lung/airway pathology
Treatment of regurgitation
Eliminate underlying cause
PPI, H2, anti-emetics, sucralfate
* prokinetics work on smooth muscle not striated muscle like found in oesophagus so won’t be beneficial
Treat aspiration pneumonia
High calorie diet, small and frequent meals form a height
Pathophysiology of vomiting
(Diagram in notebook)
Vomiting consequence
Dehydration
Hypokalaemia most common lyte disturbance in vomiting patients
Hypochlroaemic metabolic alkalosis common in GI foreign bodies
Oesophagitis
Treatment of vomiting
Treat underlying cause
IVFT
Anti-emetics
Treatment and prevention of electrolyte and acid-base disturbances
Withhold food if GI obstruction present
General types of diarrhoea
- Osmotic diarrhoea; excess luminal osmoses so fluid drawn into intestinal lumen
- Secretory diarrhoea; net increase into intestinal fluid likely due to poor absorption
- Altered permeability diarrhoea; damaged epithelial cells and tight junctions so vital subs lost > translocation
- Deranged motility diarrhoea; increased but more likely decreased contractions
Diarrhoea is more commonly _____ induced. What are common causes?
Iatrogenically
- chemotherapy; targets rapidly dividing cells including those of gastrointestinal mucosa
- antimicrobials; disrupt microflora
- NSAIDs
- lactulose etc
- acute, abrupt changes in diet
Primary GI causes of diarrhoea
Food reactions
Parasitism
Infection/bacterial overgrowth
Systemic viral infections
Fungus
Neoplasia
IBD
Lymphangiectasia
Extra GI causes of diarrhoea
Hepatobiliary disease
Pancreatic disease
Endocrine disease
* all causes generally affect absorptive ability of the gut or maldigestion
* cortisol is imperative to GI function so if low can result in malabsorption or maldigestion.
Diagnostics for diarrhoea
Faecal testing
Bacterial testing
ACTH/cortisol testing
Normal minimum database bloods
Folate and cobalam testing
Exploratory procedures
Treatment of diarrhoea
Identify and treat underlying processes
Remove iatrogenic cause if present
Alter diet: introduce low fat diet with hydrolysed protein
Bottom care
Kaolin
Probiotics
Immunomodulation in severe/refractory cases
+- antimicrobials
Peritonitis
Severe inflammation of the peritoneal cavity and is either due to a primary (less common) or secondary (more common) cause.
Primary: acute inflammation not associated with and intra-abdominal disorder I.e. FIP, salmonella etc that’s likely translocated
Secondary: acute inflammation associated with an intra-abdominal disorder I.e. trauma/surgery, neoplasia, foreign body etc
Exposure of peritoneum to sterile body fluids
This includes biles, urine, pancreatic and gastric enzymes. Pancreatic enzymes and gastric enzymes tend to produce a more severe inflammatory response
History and clinical signs of peritonitis
Recent trauma or surgery
Recent medications that may have caused GI ulceration
Parasite prevention history
Abdominal pain and distension
Lethargy/depression
Anorexia
Vomiting
Shock (cardiovascular/hypovolaemic)
Diagnostic testing for peritonitis
Imaging and abdominocentesis
Routine blood tests: neutrophils/neutropaenia, low or high K, increased coagulation times, increased liver and kidney enzymes, low protein
Dx peritoneal lavage; catheter into abdomen > 22ml/kg isotonic NaCl infused; collect sample
Stabilising peritonitis patients
- Resuscitative fluid therapy
- Confirm underlying cause and perform minimum database
- Consider blood components
- Treat electrolytes
- Pain relief
Goals of peritonitis surgery
Decontaminate
Reduced infection
Promote recovery
Drainage to further drain infectious fluids
Causes & risk factors for GDV
Genetic and environmental influences but deep chested, large to giant, adult dogs most at risk
- first-degree relatives that have had GDV
- increased thoracic depth-to-width
- lean body score
- advancing age
- eating quickly
- stress
- raised food bowls
- only dry food
- single large meals
- post prandial exercise
Brief pathophysiology of GDV
Unsure if dilation or volvolus occurs first > cardiovascular instability and decreased DO2 due to compression of low pressure abdominal veins > caudal vena cava flow rate reduced > reduced venous return leading to poor CO and reduced MAP > reduced DO2 to all organs, splanchnic pooling and portal hypertension leading to low IV volume and interstitial oedema > gastric distension and increased IA pressure result in poor diaphragmatic movement impairing ventilation, poor blood flow to gastrointestinal tract and organs > gastric necrosis and impaired gastric barrier (this is what causes high mortality) & may involve the spleen.
Whole body consequence of GDV
Lungs; hypercapnoea and hypoxaemia +- aspiration pneumonia
Spleen; torsion, avulsion, thrombosis, infarction
Liver; portal vein compression
Gut; bacterial translocation or necrosis due to impaired blood flow compromising integrity and function
Heart; cardiac arrhythmias due to ischaemia, reduced coronary blood flow, increased cardiostimulators and troponins
- mixed acid-base disturbances
- hypoxic brain injury
- repercussion injury
Diagnosis of GDV
Right lateral radiograph
Cranial displacement of the pylorus “popeye”, “double-bubble”
Treatment goals of GDV
Gastric decompression
Improve cardiovascular state
Reposition stomach and pexy
Correct lytes & AB
Stabilise arrhythmias
Management of aspiration
Management of conditions caused by the GDV I.e. reperfusion, organ damage etc
Nutrition in critically ill patients
Often critically I’ll patients are malnourished and poorer outcomes associated with patients only receiving <1/3 RER
Illnesses and stressors increase metabolic demands and increase inflammation leading to protein catabolism and delayed healing so appropriate nutrition must be implemented
Early nutrition
Crucial to positive patient outcomes
Consider: recent weight loss, recent food intake, current BMI and disease severity
Consider supportive feeding if anorexic 3-5 days and eating <75% RER
Hyporexia
Considered when a patient is eating <75% of their RER
Resting energy requirement
RER = 70(BW)^0.75
Lean body mass score
0 = marked wasting to 3 = good muscle tone
Assessing nutritional status of a patient
Body weight #1, weigh patients at least daily in hospital
Aim is to maintain body weight whilst hospitalised regardless if underweight or overweight
If <10% body weight lost they are considered malnourished
Don’t assume that overweight animals have reserves, they can be just as malnourished when critically ill
Some laboratory data with malnourished patients
Low albumin & LBM = lack of adequate protein and poor prognosis
Anaemia - lack of trace minerals I.e. Vit B
Hypokalaemia
+- low glucose
Omega 3 FA
Aim to reduce pro-inflammatory mediators and increase the anti-inflammatory response
Antioxidants
Aim to restore antioxidant stores lost during critical illness due to ROS and RNS
I.e. vitamin E, Ascorbic, selenium, glutathione
Immunomodulating nutrients
Arginine; cell growth, cell proliferation and wound healing (combats T cell suppression)
Glutamine; offers tissue protection, anti-inflammatory, immunomodulation, preserves metabolic function, antioxidant effects
Probiotics; reduce toxic bacterial metabolites, increase vitamin production, increased resistance to bacterial colonisation, reinforces the hosts natural defences (restore gut flora and barrier)
Nucleotides
- amino acids are building blocks for protein synthesis (preferred fuel for enterocytes)
Benefits of enteral nutrition
Most natural
Prevent villous atrophy
Maintains mucosal integrity
Preserves gut immunological function
What is the cause of metabolic alterations in sick patients
Catabolic state
Catecholamines, corticosteroids and inflammatory mediators
Malnutrition in critical illness results from
Catabolic state and inadequate intake
What must be stabilised before nutrition
Temperature and cardiovascular stability
Route of nutrition dictated by
GI function
Airway protective mechanisms
Length of hospital stay
Cost
Technical skill
Contraindications for enteral feeding
Uncontrolled vomiting
Oesophageal or upper airway dysfunction
GI obstruction
Ileus
Malabsorption
Maldigestion
Inability to control airway
Voluntary oral intake of food considerations
Quantify how much has been eaten
Avoid forceful feeding to prevent aversion
Consider appetite stimulants
- if eating <75% of RER consider feeding devices
NO/NG feeding tubes
Small fr silicone or polyurethane tubes passes via nose either into oesophagus or stomach
Short term use <14 days
Radiograph to confirm placement
Liquid foods only
O-tube
Requires anaesthetic procedure to place and technical skill
Tube placed through proximal to distal oesophagus
Longer use that NO/NG and more tolerated
Wider diet options
Must have normal oesophagus and GI function
Must be able to maintain airway
G-tube
Feeding tube directly into stomach usually via pexied cutaneous (PEG)
Nutrients feed directly into stomach (allows bolus feeding)
GI function must be normal but good for those with oesophageal dysfunction
Must be able to protect airway
Long term feeding but have to wait 24h before using
Must keep in for at least 10-14 days
Infection, dehiscence etc risk
J-tube
Feeding tube into the proximal jejunum
Nutrients provided distal to the pylorus and good for patients that can’t tolerate gastric feeding (gastro paresis, uncontrolled vomiting etc)
Must be kept in 5-7 days at least
Infection, leakage, migration and intestinal obstruction are risks
RER calculation and the considerations with regards to nutrition in critically ill patients
2-45kg = (BW X 30) + 70
<2 or >45 = (BW X 70)^0.75
* feed obese to ideal weight
* puppies may require above their RER
* goal is to maintain BW
* sepsis, burns, trauma etc may require above RER
General RER plan for enteral feeding
Day 1 25-50%
Day 2 <75%
Day 3 100%
Diets appropriate for enteral feeding
Highly digestible
Caloric dense (particularly if not tolerating large vol or reduced appetite)
Consider macro- and micro- nutrient requirements
Feed at least 35% protein cats and 25% protein dogs
* consider disorders I.e. low protein, low sodium etc
Monitoring enteral feeding
At least daily body weight
Review feeding orders at least daily
Monitor blood work
Manage feeding complications I.e. aspiration, refeeding syndrome, ileus, vomiting, diarrhoea etc
Parenteral nutrition
Given via the intravenous route in patients where enteral feeding isn’t possible or contraindicated but is not a replacement for enteral feeding. Three basic requirements:
1. Vascular access
2. 24hr nursing & POC biochemistry
3. Expertise to formulate a PN prescription and compound the admixture
- ability to tolerate the fluid
Catheters for parenteral nutrition
Preferably a dedicated central line or at least a designated port not being used by anything else
Can use peripheral catheters but must be for nutrition only and nothing hyperosmolar (I.e. 50% dextrose)
Must be placed and maintained aseptically, not to be disconnected unless discarding/discontinuing
Must be polyurethane or silicone based
Must have sterile dressing and inspected as least daily
TPN admixtures
Unlikely to provide complete nutrition but does provide the proteins, energy and water-soluble vitamins and potentially electrolytes.
Patients that are unlikely to respond well to TPN/PPN
Heart failure and Oliguria patients > fluid overload likely
Complications of parenteral feeding
Metabolic; hyperglycaemia, lipaemia, azotaemia, hyperammonaemia, refeeding syndrome
Catheter related; thromboses, infections, precipitation, malposition
Treatment of hyperglycaemia whilst receiving TPN
0.1U/kg insulin
TPN Plan for 5kg DSH; protein 35% (AA = 8.5%), lipids & dextrose 65% (70/30: 20% lipid and 50% dextrose), Vit B (0.2ml/100kcal), KPhos 8mmol/1000kcal (3 mmol/ml)
[note book]
TPN plan 40.2kg Rottweiler; protein 20% (AA 8.5%), 80% lipids and dextrose (70/30: lipids 20%, dextrose 50%), KPhos 8mmol/1000kcal (3mmol/ml), MgS 0.8mEq/100kcal (2.1mmol/ml); Vit B 0.3ml/100kcal
[note book]
Vacuum assisted drainage
Partially open wound covered with a reticulated polyurethane foam and pressure applied with a vacuum device at 75-125mmHg and left in place for 48-72 hours
Volume and albumin lost with peritoneal drainage
May require fluid and oncotic support
Closed suction drains
I.e. JP
Allows primary closure with drainage and has the benefit of removing infectious agents, inflammatory cells, and bacteria.
Able to obtain samples for cytology
Kept in place until drainage output is 5-10ml/kg/day
Resistant to mental and cellular debris obstruction
Inspect site at least every 24h
Paracentesis for peritoneal drainage
Used for decompression and sample collection of abdominal fluid
Increases patient comfort
Can use fenestrative Cathy’s to allow mor rapid fluid removal or decompression
Not to be left in
Patient may require sedatives to perform to prevent injury, complications etc
Should be done in L lateral to get the spleen out of the way
Indications for peritoneal draining
Septic peritonitis
Chemical peritonitis
Diagnostic sample collection
Dialysis
Increased IAP
Pancreatitis induced peritonitis
Patient comfort
RER 20kg dog
RER (30 X 20) + 70
670kcal/day
RER 1.8kg cat
RER = (1.8 X 70)^0.75
37.6kcal/day
Which of the following will affect gut motility and therefore affect nutritional treatment?
a. Body temperature
b. Perfusion
c. Blood pressure
d. All of the above
D
Nursing teams must wait how many hours prior to the first feeding through a gastrostomy tube?
a. 4–6 hours
b. 8–12 hours
c. 12–24 hours
d. 24–36 hours
C
Refeeding syndrome can occur with the reintroduction of nutrition and results in which of the following?
a. Rapid shift of electrolytes to the intracellular space
b. Rapid weight gain
c. Intractable vomiting
d. Increase in gastric acid production
A
Which of the following is not a macronutrient?
a. Carbohydrates
b. Fats
c. Vitamins
d. Proteins
C
Which of the following is not a fat-soluble vitamin?
a. Vitamin B12
b. Vitamin A
c. Vitamin K
d. Vitamin E
A
Which feeding tube could be maintained the longest, assuming no complications develop?
a. Nasogastric tube
b. Jejunostomy tube
c. Gastrostomy tube
d. Esophagostomy tube
C
A patient must consume at least what percentage of the calculated RER for voluntary oral intake to be effective?
a. 50%
b. 66%
c. 75%
d. 85%
D
What is the energy requirement for a 25^kg dog being treated for pancreatitis?
a. 750^kCal
b. 820^kCal
c. 960^kCal
d. 800^kCal + 0.75% illness factor
B
PVC feeding tubes should be used for what length of time?
a. 2–3 days
b. Less than 10 days
c. 14–30 days
d. As long as necessary and patent
B
Jejunostomy tubes are most appropriate for which type of patient?
a. Patients who need upper GI tract rest and minimized pancreatic stimulation
b. Any patient with anorexia lasting longer than three days
c. Patients with hypomotility that results in residual gastric contents
d. Patients that aren’t stable enough for general anesthesia but require additional nutrition
A
Endothelial injury, coagulopathy, and systemic vasodilation are major changes associated with:
a. GDV
b. sepsis
c. hemorrhagic diarrhea
d. gastrointestinal foreign body
B
In which of the following diseases should benzodiazepines not be used for sedation?
a. Hepatic lipidosis
b. Hepatic encephalopathy
c. GDV
d. Sepsis
B
Extrahepatic bile duct obstruction can be a complication of:
a. pancreatitis
b. parvovirus
c. acute hemorrhagic diarrhea
d. megaesophagus
A
The major reason to avoid NSAIDs in animals with gastric disease is:
a. sympathetic afferent pathways can be triggered, worsening GI disease
b. prostaglandin inhibition may worsen GI disease
c. steroidal anti-inflammatories are better tolerated
d. vagal pathways are stimulated, causing vomiting
B
Patients with parvovirus should receive nutritional support:
a. as soon as they will eat
b. 12 hours after the last incidence of vomiting
c. when diarrhea subsides
d. when vomiting is controlled
D
In dogs, which of the following is highly suggestive of septic peritonitis?
a. Blood glucose difference of greater than 20^mg/dL between paired peripheral blood and abdominal fluid
b. BUN difference of more than 2 times between paired peripheral blood and abdominal fluid
c. Lactate difference of greater than 1.4^mmol/L between paired peripheral blood and abdominal fluid
d. Potassium difference of less than 1.4 times between paired peripheral blood and abdominal fluid
A
The CRTZ contains all of the following receptors except:
a. 5-HT3
b. NK-1
c. alpha-2
d. beta-1
D
Maropitant is an inhibitor of which receptor?
a. 5-HT3
b. NK-1
c. H1
d. M1
B
- The endocrine portion of the pancreas is responsible for secreting which of the following?
a. Amylase
b. Lipase
c. Insulin
d. Trypsin
C
Active diaphragmatic and abdominal muscle contractions to force contents out of the stomach are called:
a. peristalsis
b. regurgitation
c. vomiting
d. diarrhea
C
