Lymphangiectasia, Pancreatic exocrine insufficiency, Hepatic lipidosis Flashcards
What is lymphangiectasia
dilation and dysfunction of intestinal lymphatics
Primary LGE
limited to intestine +/- chylothorax
pretty uncommon
Secondary LGE
severe intestinal infilrative disease
e.g. IBD, lymphosarcoma, enteritis (severe inflammation)
intestinal lymph obstruction
Etiopathogenesis of LGE
GI disorders disturb protein balance along with mucosal barrier and lymph
drainage -> overdistended lacteals rupture and release (reflux) intestinal
lymph into gut lumen -> diarrhea and protein losses
Clinical picture of LGE
- weight loss and poor BCS
- pitting edema, ascites, pleural effusion from protein loss
- chronic diarrhea, steatorrhea, increased stool production
- panhypoproteinemia (loss of globulin), hypocholesterolemia, lymphopenia, hypocalcemia
Intestina biopsy of LGE
dilated, chyle-engorged lacteals and submucosal lymphatics, edema, lipogranulomas
Breed predilection for LGE
yorkies, maltese, dachshund
Goals of dietary management of LGE
- minimize lymph flow
- reduce lacteal and lymphatic distention
- limit fat intake (esp LCFA)
- minimize protein loss (occurs with decreasing lymph flow)
Key nutritional factors for LGE
- low fat diet (25% for dogs, >35% for cats), novel/hydrolized source (IBD), protein supplement (e.g. cooked egg whites); decrease lymphatic flow to allow for healing of lymph vessels
- fiber: low to high depending on BCS, avoid high fiber in low BCS patients; insoluble fiber -> decreased intraluminal fat digestion and micelle formation -> decreased LCFA absorption
- digestibility: 87% for protein, soluble CHO, fat; low residue foods -> reduced diarrhea from fat/CHO maldigestion -> reduced intestinal gas production
Vitamin and mineral nutritional factors for LGE
- vitamins: vitamin A, D, E product, 1 ml divided into 2 sites, IM q 3 m
- minerals: consider IV Ca; Mg, Zn, Cu may also become deplete if disease is severe/chronic
Pancreatic exocrine insufficiency (PEI or EPI), General Info
- maldigestion
- partial or complete deficiency of pancreatic enzymes -> poorly digested food
- chronic small bowel diarrhea
- frequent defecation of greasy, foul smelling, pale (gray/brown), voluminous stools
- weight loss/failure to thrive (low BCS, polyphagia [eat anything and everything], pica coprophagia)
- hemorrhages (vit K deficiency)
Breed predilection for PEI/EPI
German shepherds, rough coated collies, Siamese cats
Etiopathogeneis of Juvenile PEI
- atrophy of pancreatic acinar tissue
- clinical signs develop at 6-18 m of age
- animals are NOT dibetic
Etiopathogenesis of Acquired PEI
- inflammation and fibrosis associated with end-stage chronic pacreatitis
+/- diabetes mellitus
Mechanisms of PEI
- failure of intraluminal digestion and ineffective nutrient utilization
- impaired mucosal enzyme activity (lack of trophic pancreatic secretions, osmotic or secretory diarrhea)
Secondary concerns of PEI
- SIBOG (small intestinal bacterial overgrowth): lack of antibacterial factors from pancreatic secretions
- intestinal IgA deficiency (may be genetic component in German shepherds)
Key nutritional factors of PEI Digestibility Fat Fiber Fat soluble vitamins Water soluble vitamins
- high; >/= 87% protein, >/= 90% fat and soluble CHO
- moderate; dogs- 10-15% DMB, cats- 15-25% DMB; consider MCT as supplement or in diet (for extra cal)
- low fiber diet! (<5%)
- A, D, E (1 ml IM q 3 m); K1 (5-20mg q 12 hrs parenteral) if coaguopathies are detected
- cobalamin (B vit) [100-250 mg IM or SQ q 7 days for 2 wks]
Feeding management for PEI
- parenteral feeding may be your initial approach (but not always needed)
- reduce osmotic load by BID-TID feedings
- feed underweight patients at DER for optimal BW + 20% (this increases the likelihood of utilizing/gaining more cals)
- pancreatic enzymes (essential in successful mgt of PEI, dried powder extracts of bovine/porcine pancreas or fresh)
Pancreatic enzymes/RX for PEI
- though it is possible to feed fresh pancreas it is not recommended b/c of the associated health risks; powdered extracts are safer
- give powder with food or it won’t be useful
- antacids or H2 blockers are used to reduce gastric acid induced destruction of enzymes
- use abx like metronidazole when SIBOG
- use insulin with concurrent diabetes mellitus
What can be fed to PEI animals in addition to specially formulated Rx diets?
high quality adult maintenance diet
Mechanism of hepatic lipidosis
- excessive peripheral lipolysis
- increased TG synthesis in hepatocyte
- decreased fatty acid oxidation in hepatocyte
- decreased VLDL transport from hepatocyte
- protein deficiency
Clinical signs/diagnosis of hepatic lipidosis
- obese (but not always)
- anorexia, jaundice, weight loss, +/- hepatic encephalopathy,hematomegaly
- hyperbilirubinemia, elevated ALP (assoc with cholestasis)
- hypoalbuminemia, anemia, muscle wasting (b/c in catabolic state)
- fatty liver on histo
Dietary management of hepatic lipidosis
- nutritional support is essential or life threatening prognosis (prevent catabolism, inhibit peripheral lipolysis)
- avoid excess energy consumption- hepatic TG accumulation
- assisted feeding is necessary: NE tube (when can’t be anesthetized, E tube, PEG tube, parenteral, needed for 2-6 wks
- force feeding is inappropriate
Energy nutritional factors for hepatic lipidosis
- adequate daily energy intake
- increase daily fat at 25-40% DMB
- increase energy density >/= 4.4 kcal/g DMB
- feed at RER (IBW) in hospital- avoid refeeding syndrome
- increase to RER(IBW) x 1.1-1.2 at home
- hospitalized based on recovery progress
Protein and potassium nutritional factors of hepatic lipidosis
- increase protein to >30% DMB, but lower range if hepatic encephalopathy (b/c ammonia makes it worse)
- increase potassium; decreased via vomiting, pu/pd, anorexia, CRF; dietary goal of 0.8-1% DMB; hypokalemia: supplement 2-6 mEq potassium gluconate every day
L-carnitine for hepatic lipidosis
- can help drive beta-oxidation in mitochondria of liver
- synthesized in liver from lys and met
- some controversy as to value in hepatic lipidosis
- shown to protect obese cat from hepatic lipid accumulation
- during cal restriction: 250-500 mg/cat/day
Fat soluble vitamins, water soluble vitamins, SAMe, water for hepatic lipidosis
- vitmains K1 and E
- vitamin B complex
- SAMe: 20-40 mg/kg/d, given to protect liver cells from oxidative damage
- maintain hydration status, suspected lactate intolerance (so no LRS)