Exam 1 Flashcards

(103 cards)

1
Q

Lec 1

A

General Evaluation of the GI System

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2
Q
  1. Basic Evaluation
A
  1. History

Signalment
-Sex
-Age
-Breed

Feeding & Housing
-Appetite
-Manure
-Changes

Metabolic Status

Cardiovascular Status

  1. Colic Symptoms (not a diagnosis but a C/S)
    -Looking or biting at sides
    -Stretching out
    -Kicking at belly
    -Excessive rolling
    -Pawing
    -Lip curl
    -Not eating
    -Excessive lying down
  2. Physical Examination

-Pain
-General: Hydration, septicemia, endotoxemia (purple, darker reddish MMs, prolonged CRT)
-Focused: Gastro-intestinal: Gut sounds, feces
-Extra-intestinal: reassess after removing obstruction

The Colic workup

-Detailed history
-Signs of colic
-PE
-Rectal exam
-Nasogastric intubation
-Hematology
-Serum chemistry
-Abdominal ultrasound
-Abdominocentesis
-Ancillary diagnostics

Laboratory

-CBC, inflammatory markers
-Biochemistry: lactate (normal <2mmol/L), Poor prognosis >6mmol/L and or peritoneal lactate 2x serum
-Glucose: (normal 80-100 mg/dl) poor if >300mmol/dl
-Electrolytes (acidosis):

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3
Q

Dehydration Status

A

> 8%
HR: 81-100 or >100 bpm
CRT: 4 sec or >4 sec
PCV: 50 or >50
TP: 8 or >8
Cr: 3-4 or >4
Eyes: +, ++ (sunken)
MM: dry, red or cyanotic

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4
Q
  1. Naso-gastric tube
A

Techniques
-Pass & check
-See it on the left side, jugular groove
-Negative pressure should be present

Analysis
-Obstruction (see choke)
-Reflux: Obstruction, ileus
-Reflux: volume, color, odor, consistency, feed material

Indications
-Routine medication administration
-Relieve choke
-Nasogastric decompression

Complications
-Epistaxis
-Aspiration
-Perforation

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5
Q
  1. Rectal exam
A

Preparation
-Yourself
-The client
-Your patient
Restraint
-Sedation
-Additional measures
-Prior preparation prevents poor performance

Normal findings
-Bladder
-Female reproductive tract in the mare
-Inguinal canals and Urethra of the stallion
-Caudal border of the spleen
-Nephrosplenic ligament
-Caudal pole of the left kidney
-Mesenteric root
-Ventral cecal tenia (no tension should be palpable)
-Cecal base ( should be empty in the normal horse)
-Small colon containing fecal balls
Pelvic flexure

Abnormal findings
-Crepitus (usually means rupture, anaerobic bacteria)
-Irregular or rough surfaces
-Masses
-Firm tubular small bowel
-Tight bands
-Painful areas
-Gas filled LI
-Impacted LI

Complications
-Rectal tear

Paracentesis: Abdominocentesis

Indications
Surgery
-Diagnosis
-Prognosis
-Cost

Techniques
-Patient preparation
-Neddle vs. teat cannula
-Use of ultrasound
-Complications

Analysis
-Gross aspects: color, smell, turbidity
-Lab analysis
-Prognosis bad if: abnormal values

Normal
-Volume: slow drip; not profuse or streaming
-Color: yellow and clear
-Leukocyte count: <5000 cells/uL
-Differential count: <50% neutrophils
-TP: <2.5 g/dL (usually <1.5 g/dL)
-Lactate: <2mmol/L

Complications
-Cellulitis
-Abscess
-Bleeding
-Splenic puncture
-Bleeding
-Omental herniation

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6
Q
  1. Endoscopy
A
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7
Q
  1. Ultrasound
A

Technique
-Probe 2-5 MHz curvilinear transducer
-Clip, clean, coupling gel
-Sedation if needed

Approach
1. Consistent systematic approach
2. Position of transducer and maker
3. Depth of the field of view

FLASH
-Fast Localized Abdominal Sonography - 15 min
1. Ventral
2. Gastric
3. Spleno-renal
4. Left middle third
5. Duodenal
6. Right middle third
7. Thoracic

Details

-Location
-Peristalsis
-Wall aspect
-Diameter
-Content
-Abnormal structures

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8
Q

FAST - Left Abdomen (gastric)

& Left Abdomen (nephrosplenic)

A

-Dorsal edge of Spleen
-Stomach wall
-Gastrosplenic vein

-Spleen

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9
Q

Left Abdomen

A

Left Abdomen

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10
Q

Right abdomen (liver, duodenum, colon)

A

Right Abdomen Kidney

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11
Q

Right
Abdomen

A

Ventral Abdomen and Chest

-Large colon
-Fluid
-Pleural effusion

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12
Q
  1. Radiographs
A
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13
Q
  1. Fecal exam
A
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14
Q
  1. Absorption tests
A
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15
Q

Colic 101

A

-History
-PE
-Rectal exam
-Nasogastric tube: most common
-Assess & control pain
-Flunixine meglumine: Benamine
-Sedation
+/- Butorphanol
-Surgery referral
>90% of cases are medical
-Intensive care & monitoring may be needed

Medical

-Pain management: NSAIDs, alpha-2 agonist, opioid
-Anti-spasmodic: N-butylcopolammonium (Buscopan)
-Phenylephrine (for nephron-splenic)

No reflux
-Water
-Electrolytes
-Laxatives

Instructions for owners
-Monitor
-Call ifs..
-What to do

Refer if
-Severe pain (uncontrolled or recurring)
-HR>60 BPM
-Abnormal rectal exam (not impaction)
-Reflux on nano-gastric tube
-Dehydration/Toxemia
-Abnormal abdominal fluid

How to refer
-Have owner organize trailer
-Call clinic
-Manage pain: <30 min: Xylazine IV, 1-2hr: Detomidine IV, indwelling NG tube, IV fluids ?
-Fluids

What if you can’t refer?

-More medical management in the field
-Go back out and treat again
-IV fluids?
-Analgesics
-Time
-Trocarisation
Euthenasia if nothing works

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16
Q

Colic Surgery

A

-May be a diagnostic and treatment
Pain based decision, not progression in case

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17
Q

Lecture 2

A

Fluid Therapy

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18
Q
  1. Bable to estimate dehydration in an equine patient based on physical exam and laboratory finding
A

<5%
-NSF: no significant findings

5%
-Dry, tacky MMs, +/- mild depression

7%
-Moderate skin tent
-Tachycardia
-Slow jugular refill

10%
-Moderate to marked skin tent
-Decreased pulse pressure
-Cold extremities
-Depressed

12%
-Marked skin test
-Signs of shock
-Obtunded

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19
Q
  1. Be able to formulate a fluid therapy plan based on physical exam and laboratory findings
A

Goals of Fluid Therapy
1. Restore intravascular volume
2. Improve perfusion to tissues
3. Overcome regional circulatory deficiency

Phases of Fluid therapy

Emergency
-Shock dose
-60-90 ml/kg
-1/4-1/3 dose and reassess, then 20-30 ml/kg
-10-20 L bolus
-Foals: 1L bolus

Replacement
-Deficit + maintenance + continuing loss
-Deficit volume = % dehydration * BW (kg)

Maintenance
-2-4 ml/kg/hr
-~ 1L/hr
-Foal: 3-5 ml/kg/hr, includes oral fluids

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20
Q
  1. Describe different fluid types and when they should be indicated
A

Types

  1. Crystalloid

Examples
-Isotonic
-Hypertonic saline: rapid, transient increase in blood volume. Max dose: 4ml/kg. Short duration 45 min. Decreases ischemic/reperfussion injury. Administer 10L isotonic fluid per L of hypertonic to correct intracellular fluid deficit
-Hypotonic

  1. Colloid
    Indications
    -TP<4mg/dL
    -Albumin <2mg/dL
    -COP <12mmHg
    Actions
    -Expand plasma vol
    -Oncotic pressure support
    -Restore effective circulating vol
    -Albumin = 75% oncotic pressure of plasma

Synthetic Colloids
-Hetastrach
-Pentastarch
6% solution in Isotonic saline: COP = 30-37 mmHg
-Dose 10-20 ml/gj
-Platelet disfunction, renal injury

  1. Plasma

Indications
-COP = 20mmHg
-Source of albumin and clotting factors
-Need 10L to increase TP by 1.0 g/dL
-0.05BW(kg) *(TP desired - TP patient)/ TP donor

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21
Q

Electrolytes

A
  1. Electrolytes

Indications
-When severe deficit
-Hypocalcemia: ex cantharidin toxicosis, “Thumps”
-Hypoglycemia: ex foals septicemia, NMS

Calcium
-Skeletal muscle contraction, neuronal function, GI smooth muscle function
-Ionized vs. total measurements
-Hypocalcemia: endotoxemia, functional SI disturbance, endurance horses, postpartum dairy cattle

Tx
-Hypocalcemic: 500 ml 23% Calcium Gluconate per 5-20L fluids
-Normocalcemic: 50-100 ml 23% calcium gluconate per 5-20 L of fluids

Potassium

-Hypokalemia: reduced intestinal motility, muscle weakness, lethargy

Tx
-0.5 men/kg/hr
-10-20 meg/kg/hr = 50-100 men/5L bag

Sodium

-Cerebral edema, osmotic demyelination
-<0.5 meg/L/hr or 8-12 mew/day
-Hypernatremia: prolonged water deprivation or fluids administration.
Tx
-0.45% NaCl, 5% Dextrose
-Hyponatremia: profound colitis, sepsis
Tx
-Polyionic with added NaCl, 3% NaCl

Chloride

-Hypochloremia: GI loss or sequestration, often with metabolic alkalosis, hyperkalemia, and hyponatremia
Tx
-Underlying cause
-0.9 %NaCl IV

Dextrose

Indications
-Early lactation ketosis
-Nutritional support in foals
-Uroperitoneum foals
-Urolithiasis in farm animals

Tx
-2.5-10% Dextrose solution CRI
-100 ml 50% dextrose per 1L = 5% solution

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22
Q

Enteral Therapy

A

Indications

-GI tract functional
-Maintenance requirement needed
Impaction colic

Advantages

-Fluid directly into GI tract
-Stimulates colonic motility
-Decreases expense
-Decreases need for precise adjustment

Tx NG-tube
-Nasogastric tube
-2-6L dose
-Funnel
-Leaving the tube in place?
+/- Electrolyte powder

Tx Indwelling feeding tube

-2-5L/hr
-Coil set
-Carboy
-Isotonic electrolyte solution
-135 meq/L Na, 95 meq/L Cl, 5 meq/L K & 45 meq/ HCO3

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23
Q
  1. Describe routes of administration and when they would be indicated
A

IV Catheter Locations

-Jugular
-Lateral thoracic
-Cephalic

IV catheter types

-Over the needle: short, Abbocath (24-48 hours), Mila (long term up to 14 days)
-Over the wire: Silastic, flexible, used in foals, camelids, 1-2 lumens

Administration Set
-Stat set
-Coil

Transfer set
-Connect fluid bags
-Allows 4 bags to be hung: 5L (2-4 bags), 10-20L “hung”
-Attached to section of braided mane
-Attached to catheter

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24
Q

Monitoring Clinical Signs & Lab work

A

-HR normalization
-Increased pulse quality
-Improved mentation
-Decreased CRT
-Increased urine production
-Warming extremities

Lab Work
-PVC/TS
-USG: neonates common
-Blood serum lactate: normal <2mmol/L
-Electrolytes: if supplementing or in fluids >24hrs

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25
Lecture 3 Esophagus & Stomach
26
Esophageal Obstruction (Choke)
1. Examination 2. Definition -Choke: most frequent esophageal problem 3. Etiology -Ravenous eaters -Geriatric horses -Sedated or exhausted horses -Grain, hay, beet pulp, carrots, chewing issues, size of feed -Remove all the food after a horse has been sedated due to increased risk for choke 4. Epidemiology 5. C/S -Horse anxious -Extended neck -Nasal discharge -Coughing -Ptyalsims -Dysphagia -Distended esophagus 6. Pathophysiology 7. Dx -Clinical signs -Naso gastric tube (stops at obstruction site) -Endoscopy: not always necessary. Examine Trachea (aspiration signs) and esophagus for lesions, withdrawing scope and inflating esophagus. -Ultraound -Radiographs 8. Tx a. Remove all feed and water b. Make patient comfortable & let esophagus relax -Sedate: low head carriage to avoid aspiration c. Pass tube: up to obstruction, lavage gently (head down), track water and outflow. Gentle push Tx - variations -Wait give drugs and check back in 2-4 hrs -Sedation (alpha agonist + butorphanol) -Oxytocin -N-butylscopolammonium bromide -Tubes sizes vary -Correct dehydration -General anesthesia Aftercare -Restriction of food 48hrs -Progressive re-feed -Endoscopy of trachea and esophagus -NSAIDs and antimicrobials -Monitor for fever and other signs 9. Prognosis/complications -Excellent if no complications -Ulceration -Aspiration pneumonia -Metabolic alkalosis -Stricture -Perforation -Stomach rupture **Follow up exam**
27
Esophagitis
1. Examination 2. Definition 3. Etiology 4. Epidemiology 5. C/S 6. Pathophysiology 7. Dx 8. Tx 9. Prognosis
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Other Esophagus diseases
29
Equine Gastric Ulcer Syndrome
1. Examination -40-90% exercise induced stress overexercised -Endoscopic view -Ultrasound -Nasogastric tube 2. Definition 3. Etiology ESGUS: squamous -Acidic conditions -Exercise intensity -Training, fasting, transport, stabling, time at work -NSAIDs -Dietary: grain vs. pasture Prevention -High % heals with Omeprazole -4 weeks -Add H2 receptor antagonist -Change management practices -Supplements EGGUS: Glandular -Acidic conditions -NSAIDs -Helicobacter? -Gender, trainer, no grass turn out, no roughage -Unprocessed grain, exercise **No impact of time in work** Prevention -Low % heals with Omeprazole -6 weeks tx -Doxycycline, Sulcralfate, Pectin-lecithin, Misoprostol -Supplements -Gastric hyperplasia-biopsy 4. Epidemiology 5. C/S -Colic -Poor appetite -Weight loss -Pain on tightening of girth -May or may not show clinical signs 6. Pathophysiology 7. Dx **Endoscopy** -Withhold food for 16 hours -Withhold water for 1 hour -Fecal occult blood? -Sucrose marker? 8. Tx -Proton pump inhibitors: Omeprazole for 28days -Histamine receptor antagonists: Cimetidine, Ranitidine, Famotidine Mucosal Protection -Sucralfate -Misoprostol Antiacids -Magnesium hydroxide -Aluminum hydroxide -Lidocaine if severe colic Prokinetics -Bethanecol -Metoclopramide -Erythrmycin -Cisapride **Omeprazole as prophylaxis** Gastrogard: Treats ulcers, prescription tube Ulcergard: Prevent ulcers, OTC tube 9. Prognosis
30
31
32
Acute Grains Overload
1. Examination 2. Definition 3. Etiology 4. Epidemiology 5. C/S -Depend on severity -Red-purple MMs -Tachycardia -Tachypnea -Colic -Abdominal distention -Severe lameness -Trembling -Sweating -Diarrhea -No intestinal sounds **Endotoxemia, Colic:gas, motility, Lameness, laminitis, flounder** 6. Pathophysiology 7. Dx -Hx -C/S -Polycythemia -Neutropenia with left shift and toxic changes -Gastric reflux -Tight bands on rectal exam 8. Tx Asymptomatic -Prevent absorption -Lavage stomach -If no reflux: 1 lb Epsom salts or 1 lb activated charcoal -Mineral oil, biosponge -Prevent endotoxemia and sequelae -1mg/kg Flunixin meglumine then 0.3 mg/kg q8hrs -Antihistamine: Diphenhydramine, Doxylamine -Remove all feed for 24hrs -Cryoprophylaxis for laminitis 9. Prognosis -Excellent if tx before C/S Symptomatic grain overload -IV fluid: hypertonic saline -Follow by polyionic -Plasma fluid -1mg/kg flunixin meglumine then 0.3mg/kg q8hr -Lidocaine (motility, analgesia, neutrophil margination) -Leave NG tube in place: receives gas, if no reflux 1/2 lb Mg sulfate, 1/2 charcoal, 1/2 gallon warm water **Polymyxin to bind endotoxin (if normal renal function)** -Pentoxyfylline -Laminitis prevention Prognosis: depends on complication present
33
Gastric Dilation and Rupture
1. Examination 2. Definition 3. Etiology -Primary: impaction, grain overload, water intake, air -Secondary: ileus obstruction 4. Epidemiology 5. C/S -Acute colic -Reflux -Hemoconcentration -Hypokalemia -Hypochloremia -Rupture: septic shock, pain that suddenly stops -Tachypnea, tachycardia, wearing, muscle fasciculations 6. Pathophysiology 7. Dx -NG tube -Ultrasound -Abdominocentesis -Rectal palpation 8. Tx -NG-rube -Pain medication -Euthanasia 9. Prognosis -Poor
34
Gastric Impaction
1. Examination 2. Definition 3. Etiology -Unknown -Poor dental care -Grain overload -Ingestion of persimmons -Severe hepatic disease -SCC 4. Epidemiology 5. C/S -Inappetence -Acute and recurrent colic -Improves when food withheld -Worsens if refed 6. Pathophysiology 7. Dx -Gastroscopy -Ultrasound 8. Tx Type 1 -Accumulation of food, normal size stomach -Enteral fluids 1L/100kg isotonic electrolytes q2h Type 2 -Accumulation of food, increased stomach size -Add IV fluids -Prokinetics: Bethanecol, Erythromyin Type 3 -Phytobezoar (persimmon seeds) -Diet coke (>< laminitis, caffein toxicosis) -1L/hr for 1-3 days -700 ml/12 hrs Surgery 9. Prognosis
35
Others- Stomach
36
Lecture 4 - SI
1. Duodenitis proximal jejunitis 2. Equine proliferative enteropathy 3. Inflammatory bowel disease -Simple obstruction
37
Small Intestine
1. Medical -DPJ -EPE -IBD Thickening -EPE -IBD Obstruction -Ascarid -Ileal 2. Mixed issues -Ileal impactions -Ascarids 3. Surgical -Volvulus strangulation -Herniation Entrapment -Intussusception
38
Duodenitis Proximal Jejunitis - DPJ
Etiology -Unknown -Possible Clostridium difficile, Perfringes, Salmonella -Feeding practices Pathophysiology -Inflammation -Edema -Hemorrhage C/S -Serositis (petechia & ecchymosis) -Increased secretion -Decreased motility -Pancreas, liver involvement -Possible infection -Fever not always present -Dehydration eventually -Acute colic, depression -Tachycardia -Tachypnea **Pain wanes after NG decompression** -Depression remains Dx -Lots of reflux -NG-tube orange-brown, fetid reflux -Dehydration -Electrolyte, acid base, liver enzymes tests -Rectal palpation: multiple loops distended SI -Ultrasound: distended SI, decreased motility -Abdominocentesis: yellow - turbid (to serosanguinous) -Increased TP -Normal WBC -Acidosis -Elevated liver enzymes Tx -Reflux: NG-tube q 12hr -Fluid: correct imbalances -Combat endotoxemia + inflammation and sequelae -Benamine -Polymyxin -DMSO -Laminitis prevention -Penicillin, Metronidazole per rectum -Add gentamicin if low WBC -Prokinetic agents: Lidocaine, Metoclopramide, erythromycin lactobionate, Cisapride Response -Improves Nutrition -Avoid oral food for several days -Consider parenteral nutrition Surgery -If they are painful, costly Prognosis/Complications -Resolves if aggressive Tx -Peritonitis -Infarction -Aspiration pneumonia -Adhesions -Laminitis
39
Equine Proliferative Enteropathy - EPE
-Weanlings -Foals -N. America: August-February Etiology -Lawsonia intracellularis Epidemiology -Disease of pigs (subclinical) -Rodent reservoir -Often no obvious exposure to pigs -Transmission: oro-fecal -Risk factor: stress Pathophysiology -Distal jejunum and Ileum -Invasion of proliferating crypts in Ileum -Excessive mitosis, hyperplasia -Thick corrugated mucosa -Decreased absorption capacity C/S -Lethargy -Anorexia -Colic, diarrhea -Concurrent disease -Peripheral edema -Protein loss Dx -Hx -PE -Hypoproteinemia <5g/dL -Hypoalbuminemia <2g/dL -Ultrasound: thickened SI, excessive abdominal fluid **PCR and Serology combine to be definitive** -PCR fecal sample or rectal swab definitive diagnosis -Serology: IFAT, ELISA, IPMA (immune peroxidase monolayer assay) -Silver stain of biopsy -Test herd mates Tx -Antimicrobials 2-3 weeks -Young: Macrolides (Azithromycin, Clarithromycin) -Older: OTC IV, then oral Doxycycline -Others: Rifampin, Chloramphenicol, Mino -Supportive colloids -Parenteral nutrition -Antiulcer -Continue until issues resolve Prognosis -Good with early therapy Prevention -Separate foals -Regular PE, TP, serological status -Pest control -Extra-label vaccine (pig vax intra-rectally)
40
Inflammatory Bowel Disease
**Adult horses** a. Granulomatous enteritis (GE) b. Multisystemic eosinophilic epitheliotropic enterocolitis (MEED) c. Eosinophilic/lymphocytic-plasmocytic/basophylic enterocolitis d. Idiopathic focal eosinophilic enteritis (IFEE) Pathophysiology -Intestinal thickening -Protein losing enteropathy C/S -Progressive weight loss -Intermittent abdominal discomfort -Edema Dx -Anemia -Hypoproteinemia -Umtrasound -Absorption test -Biopsy Tx -Steroids -Surgical (IFEE)
41
Simple Obstructions of SI
1. Ascarids: young horses Etiology/Risk factors -Heavy infestation Parascaris equorum -Weanling foals -Poor deworming history C/S -Untrhiftyness -Poor hair coat -Colic 1-5 days Dx -NG-reflux: may contain dead worms -Ultrasound and rectal exam: Distended SI Tx -Medical: intestinal lubricants, IV fluids, pain control. Slow onset antihelmintics (Fenbendazole - Panacur) -Surgery may be needed 2. Ileal: adults Etiology/Risk factors -Adult horses -South Eastern USA -Coastal bermuda grass hay -Tapeworms (Anoplocephala perfoliata) -Ileal hypertrophy -IBD C/S -Colic -Progressive abdominal distension -Decreased gut sounds -Rectal exam & Ultrasound Distended SI -NG reflux -Abdominocentesis normal Tx -Medical: reflux, pain control, IV fluids -Surgical: pain, changed abdominal fluid Prognosis -Good
42
Lecture 5 - Small Intestine 2
Surgical Structures Not exteriorized -Stomach -Duodenum -Transverse colon -Rectum
43
Sometimes Need surgery
-Ileal impaction (thicker, gateway to cecum, bermuda grass hay contributor) -Ascarid impaction -Duodenitis-proximal jejunitis -Foal inguinal herniation (congenital) -Intestinal hypertrophy
44
Always Need Surgery
45
Strangulating Lipoma
-More common in older horses >20 years old 3x more likely -Strangulating lipoma: Arabians, QH, Saddlebreds, ponies C/S -Painful -Depressed -Dead gut = doesn't hurt -Decreased GI sounds -Trauma to face due to severe pain, rolling -Dehydration -Endotoxic, MMs injected -Evidence of trauma Dx -C/S -Rectal exam: tubes 8-10 cm , distended SI, shrink wrapped colon -NG tube: reflux!! but may not show right away bc intestine is long and takes a while to get full. Blood work -Dehydration -Increased PCV/TP -Leukopenia if early endotoxemia -Increased lactate >2mmol/L -Ultrasound: >4cm diameter >4mm thick wall Abdominocentesis -Serosanguinous -Lactate >2mmol/L -TP>2g/dL Prognosis -Mid-jejunum best -Proximal ileum not best -Towards duodenum or end of helium = worst -Endotoxemia = bad -Longer affected area = worse Tx -Surgery: resection and anastomosis
46
Epiploic Foramen entrapment
-Space between caudate lobe of the liver, portal vein and gastropancreatic fold -Risks: cribbing -Often involves ileum = bad -Careful not to rip the portal vein, bleed out on the table
47
Diaphragmatic Hernia
Congenital or acquired (trauma) -Large Intestine: interfere with respiration. Entire large colon can herniate -Small intestine: more likely to herniate -Challenging diagnosis and treatment -Radiographs -Ultrasound -Exploratory surgery: ventral tears: suture or mesh -Later laparoscopic repair if dorsal
48
Entrapment in the Gastrosplenic ligament
-No breed or age predisposition -No need to repair rent -Enlarge it at surgery so nothing else can get trapped there
49
Umbilical Hernia
-Medium size (two fingers) -Strangulating intestine: painful, swollen, heat, non-reducible -Ultrasonography
50
Small intestine volvulus
-Foals, Racehorses, endurance horses C/S -Twisting of intestine and mesentery Tx -Resection
51
Small intestinal entrapment in other structures (Gastrosplenic ligament, diaphragmatic hernia, umbilical and inguinal hernia, intussusception)
Intessusception -Ileo-cecal or jejuno-jejunal -Abnormal motility: TAPEWORMS -Surgery: resection
52
Inguinal/Scrotal Hernia
-Stallion -Tennessee walkers, Saddlebreds, Standard breeds -Unilateral -Indirect: through vaginal ring -Rectal and external palpation -ultrasonography -Surgery: resection, hemi-castration, external inguinal ring closure
53
Small Intestinal Surgery
-Enterotomy -Resection and anastomosis: jejunojejunostomy, jejunoileuostomy, jejunocecostomy. -Hand sewn end to end: Single or double layer. Member vs. Cushing Common complications -Ileus: everything backs up till the stomach, NG-tube helps relieve. Reflux -Adhesions: when excessive inflammation -Endotoxemia: laminitis **Motility affected by surgery** -SI detention: shortening of villi = increased inflammation -Loss of mesothelial cells -Neutrophil infiltration -Edema -Decreased perfusion -Ischemia and reperfusion injury: free oxygen radical formation, inflammation, motility affected -Devitalized intestine: bacterial translocation
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Post Operative Ileus treatment
-Prevalence 10-55% -Mortality 13-86% Risk factors -Increased PVC at admission -Surgery/anesthesia length -Length of resection Tx -Supportive care -Reflux regular every 2-4 hours -IV fluids, replace + maintenance -NSAIDs -Time -Prokinetics The Lidocaine Debate -Dose must be precise -CRI -Anti-inflammatory -Prokinetic? mixed reviews
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Adhesions
-25% of cases -Foals at higher risk -Fibrin over damaged areas -Inadequate fibrinolysis Causes -Post-op ileus -Ischemia -Foreign material -Serosal abrasion NO DRY GAUZE -Excessive tissue handling -Large suture Tx -Re-laparotamy -Mild-manage intermitent colic -Prevention: Carboxymethycellulose, good tissue handling
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Endotoxemia
-Lipopolysaccharide in the blood -Equidae: sensitive compare to other species -Toxic dose 2 ug/kg C/S -Mild colic -Decreased borborygmi -Restlessness -Sweating -Anorexia -yawing -Depression -Pale MMs, later brick red, purple +/- toxic line with prolonged CRT -Increased HR, RR, Temp, later decreased temp, venous filing, and pulse strength +/- Lose manure -Scleral reddening -Profound depression Systemic Inflammatory Response Syndrome -Endotoxemia is one of the triggers for SIRS -Profound neutropenia with a left shift -Hyperglycemia -Hypovolemia -Azotemia -Increased cardiac troponin -Lactic acidosis Tx -Remove the source -Prevent LPS and host infection **Polymyxin B binds and neutralizes endotoxin** -Endoserum/hyperimmunized J5 plasma - Antitoxin antibodies -Decrease inflammatory response: NSAIDs, DMSO?? -Supportive fluid therapy to prevent shock & laminitis
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Laminitis and Endotoxemia
-Not completely understood why -LPS administration does not cause laminitis -Endothelial damage and direct platelet activation -Coagulopathy
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SI prognosis
Non-strangulating -80-90% good Intra-op -Mid jejunum 75% -Ileum <5% -Duodenum <10%
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Lecture 7
Large Intestine Medical
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Large Intestine
Impactions Diarrhea Inflammation -SI obstruction leads to reflux -LI obstruction lead to bloat, usually -High HR, dehydration, and shock = refer -Always pass a stomach tube. Reflux suggests a SI lesion. Refer -Serosanguinous abdominal fluid often indicates dead bowel. Refer -Rectals can be dangerous to both horse and veterinarian. Only do if safe and necessary. Palpate changes may include distention (gas or impaction) or displacement (spleen, guts) Review anatomy -Cecum can be auscultated in the upper right abdominal quadrant. It sound like a drain is opened or a flushing
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Large colon impaction
1. Sand -Ventral diaphragmatic/sternal flexure 2. Pelvic flexure -Straw/hay/boredom -Lack of water 3. Cecum -Hospitalization -Typical risk factors -Tapeworms **Note: Small intestine: Ileum = Coastal bermuda hay, Ascarid: poor deworming**
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Pelvic Flexure Impaction
Predisposing factors -Poor ability to chew -Coarse roughage -Decrease water intake -Decrease motility -Excessive fluid loss Clinical signs -Pain: slow onset, mild, intermittent, severe -Anorexia, abdominal distension, decreased fecal output -Heart rate varies with level of pain Typical case -Horse moved from pasture to stall -Eats excessive straw/hay -Water supply broken in winter Dx -Hx, C/S -NG-tube: no reflux -Rectal exam impaction -Abdominocentesis: normal Tx -Do not feed -Allow water if no reflux -Pain management -Fluid/laxatives: oral, water, mineral (controversial), magnesium sulfate, DSS -IV if impaction is severe 4-5 L/hr Prognosis -Good
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Sand Impaction
Predisposing factors -Access to sandy soil -Feeding hay or grain on sandy ground -Lack or roughage -Mineral content C/S -Pain: acute, intermittent, severe or chronic -Anorexia, abdominal distension -Decreased fecal output -HR varies with level of pain -Diarrhea if chronic Dx -Auscultation sound of waves -May not find sand in feces, glove test -Rectal palpation -Ultrasound -Radiographs -Bowel necrosis possible under the weight of the sand Tx -Pain management -Fluids and laxatives -Psyllium hydrophilic mucilloid (Metamucil) 400g/500kg q6hr until resolves, then SID x7d -Water, other laxatives -Psyllium and probiotics -Limit feed -Surgical Prevention -Prevent overgrazing -Do not feed off the ground -Prophylactic psyllium (7 days q 4-12 mts) Prognosis -Good for mild to moderate -Unless intestinal wall debilatized
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Acute Diarrhea
Diagnostic Approach -Hx and PE -Fecal exam -Blood and serum -Other tests -Response to treatment Infectious -Bacteria -Parasites -Viruses Non-infectious -Toxicity -IBD -Sand impaction Complications -Sepsis -Endotoxemia -Immune compromise -Superinfection -Infarction -Thrombosis -Laminitis -Coagulopathy -Inflammation -Sepsis -Impared CV function -Colitis, typhlocolitis, isolation
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Equine Coronavirus - ECov
-Enveloped, ++RNA virus -Beta coronavirus 1 linked to enteric fever and diarrhea -Infection starts in SI (necrosis, sloughing villi) -Anorexia, lethargy, fever >> diarrhea, colic -Leukopenia -Hyperammonemic encephalopathy
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Salmonellosis
2500 serotypes -S. enterica serovar typhimurium = most frequent -Risk factors: stress, carriers, surgery, broodmares, antibiotics -Zoonosis -Virulence -Spread C/S -Acute colitis -Profuse diarrhea, occasional pain or colic -Fever, tachycardia, depression, dehydration -Sepsis, shock, endotoxemia, CV shock -Vascular leak syndrome -Coagulopathy -Culture: 3-5 fecal samples 12-24 hrs apart -5-10g of feces -Mucosal biopsy -PCR screening, quatitative Tx -Fluid therapy, plasma or colloids -Flunixine meglumine -Total/partial parenteral nutritional support -Antimicrobials -Anticoagulants? Prognosis -If >10d diarrhea and sepsis = poor prognosis Prevention -Biosecurity measure -Cleaning, disinfection, isolation
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Potomac Horse Fever
a.k.a Equine Monocytic Ehrlichiosis -Neorickettsia risticii (obligate intracellular bacterium) -Infected trematodes -Mayflies and caddisflies -Horse ingest infected fluke larvae -Oral or water transmission -Snail 1st, Insect 2nd -June-november -Area close to river -Pasture or stable -80% of horses will nor develop clinical signs -20% will develop C/S C/S **Biphasic fever** -Diarrhea, colic, fever, anorexia, depression -Leukopenia, toxemia, hypoproteinemia -Laminitis: 30% of affected horses: may be the only clinical sign -Abortions Dx -Neorickettsia risticii PCR on fecal or blood -PCR on buffy coat of blood -Serology Tx -Antimicrobials -Oxytetracycline IV, followed by oral -Several days treatment -Fluid, plasma, colloids -Vaccination available but many different strains. Early spring and early summer
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Clostridial Diarrhea
C. difficile -Colitis in adults -Toxin A (enterotoxin) -Toxin B (cytotoxin) -Risk: antimicrobial administration, hospitalization C. perfringes -Occasional cause of colitis -Hemorrhagic diarrhea -Sepsis -5 types (A-E) based on exotoxin -Age, environmental persistence C/S Foals -Hemorrhagic diarrhea -Sepsis -Gas and fluid filled SI Adults -Diarrhea -Abdominal discomfort -Fever -Colitis -Severe Toxic colitis -Moderate illness Dx -Culture isolation -ELISA antigen test -Extra testing required to determine if isolates are toxigenic -PCR -Toxin A/B II ELISA **Culture + PCR, Toxin-ELISA** Tx -Supportive care -Antimicrobials: Penicillin, Metronidazole, Vancomycine if resistance -Saccharomyces boulardii (yeast), probiatics -Gastro-intestinal protectants: Di-tri octahedral smectite powder (Biosponge) -Transfaunation
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Other Diarrhea Causes
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NSAIDs Toxicity - Right dorsal colitis
-Phenylbutazone, Flunixine meglumine C/S -Hypopotreinemia -Hypoalbuminemia -Right dorsal colitis, diarrhea, colic Dx -Ultrasound: edema RDC -Succeed fecal blood test -Rule out
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Diarrhea - General Therapy, Fluids, endotoxemia, etc.
Oral fluids -Water -Electrolytes: 30 ml of 50% dextrose, 12 g Baking soda, 10 g KCl Intravenous -Hypertonic saline: 2-4 ml/kg bolus -Follow with crystalloids (10L for each L of hypertonic) -Crystalloids: plasma-lyte, Normosol, Lactated Ringe. KCl 20-40 mEq added per L (0.5 mEq/kg/hr) -Colloids: plasma, hydroxyethyl starch (hetastarch, Penastarch) Endotoxemia -Plasma 2L -Flunixin meglumine -Polymyxin for laminitis -Pentoxifylline -Prevent founder -Prevent thrombophlebitis -Slow IV B-vitamins -Intestinal protectants -Nutrition
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Lecture 8 LI surgery
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Cecal Impaction
Type 1: mechanical obstruction, fecal material Type 2: dysfunctional motility Etiology -Poor dentition -Poor quality hay -Lack of access to water -Post anesthesia/hospitalization -Tapeworms -NSAIDs -Lack of exercise C/S -Reduced fecal output -Mild pain -Reduced borborygmi -Decreased cecal emptying Dx -Rectal palpation -Cecum is attached to the dorsal body wall, can not pass your hand over the cecum, helps differentiate from Left colon Tx -Some respond to medical, others need surgery **Monitor carefully for 24-36 hours if not improving with medical management, then recommend surgery** Medical Tx -Laxatives: Magnesium sulfate, mineral oil, NG-tube -IV fluids -Analgesics: NSAIDs **Be careful with Alpha2 agonists = decreased motility, may delay surgery -Prokinetic? **Neostigmine can cause too much contraction and lead to rupture** Surgical Tx -Typhlotomy "dump the cecum" -Jejunocolostomy or ileocolostomy -Can't remove the cecum, complete cecal bypass
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Nephrosplenic entrapment
a.k.a "Left dorsal displacement" -Space between the left kidney and spleen Risk -TBs, WBs, anything round barreled -Yearlings **Not seen in foals, ponies, nor minis** Dx -Mild to severe colic -Ultrasound: spleen pushed ventral, can't see left kidney -Rectal exam: feel something coursing up to the left -Can be hard with short arms Tx 1. IV phenylephrine (in saline IV slowly) and exercise 2. Fluid therapy 3. +/- Rolling (under GA) 4. Surgery: correct displacement Surgical Tx -Ventral midline laparotomy initial correction -Hand assisted laparoscopic nephrosplenic ablation -Recurrence 8%
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Right dorsal displacement
Etiology -Generally associated with impaction -Risk: none specific -Recurrence more common than with other types of displacement C/S -Mild to moderate pain -Severe pain if >/= 180 degree torsion -PE paramenters WNL -Blood work: dehydration, elevated GGT (stasis in liver) Dx -Rectal palpation -Taenia palpable in the wrong direction +- impaction -Ultrasound +/- Reflux Tx -Pain management: NSAIDs, alpha-2, butophanol -Fluid therapy, enteral, IV or combination -Trocharization if surgery not an option -Aseptic prep, 14g catheter, antibiotics Sx -Pain -Deterioration of condition -Colic >24hrs -Replace colon into proper anatomic position +/- pelvic flexure enterotomy "dump" the colon empty -Lots of lavage during sx, change gloves. Two layers closure: simple continuous + Cushing
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Large colon torsion - Impaction
-Sometimes need surgery -Sand impaction, feed material, Enteroliths (always need surgery) -Pelvic flexure enterotomy Colon Torsion -The most painful colic -Rapid referral -Common in post parturient mares -Typically at the base of the cecum Dx -Hx, C/S -Elevated HR, dehydration, very painful, abdominal distension -Rectal: severe gas distension -Bloodwork: dehydration, elevated lactate -May show signs of endotoxemia Tx -Surgical -Untwist colon +/- enterotomy, +/- colon resection -Difficult anesthesia management: arterial blood pressure low, endotoxemia when un-flip colon Post-Op -Look terrible for the first 24 hrs -NSAIDs -Antimicrobial - Broad spectrum -Colloids: hetastarch, plasma -Anti-endotoxic medications, Polymyxin B, Hyperimmunized plasma, Endoserum -Lidocaine -Ice boots for laminitis Prognosis -Impactions/displacements: Good >95% -Torsions: 50/50 Post op management -Antibiotics: penicillin K (IV), or procaine (IM). -Gentamicin +/- Metronidazole -IV fluids 2x maintenance -If refluxing, need to replace that loss too -Supplementation: Calcium gluconate (23%), KCl -Colloids if TP<4 g/dL, Albumin <2g/dL -Equine plasma, Hetastarch (10ml/kg increases oncotic pressure) Monitoring -Fecal output -Pain -Feed/water intake -Watch for laminitis, diarrhea, colic signs -Reflux q2hrs -PCV/TP, CBC, Chemistry, Electrolytes -Feeding: LI = water first, grass or hay 12-18hrs later. Slow SI= water 24 hrs, feed 48 hrs, small particles, alfalfa leaves, grass best. -Exercise: Day 60-90 turn out with no forced exercise, after 90 days training if no other problems Complications -Incision dehiscence: rare. Heavy horses, older >1 yo. -Hernia: 8-10% of cases -Edema: common, drainage -Infection: 8-30% cases -Diarrhea -Peritonitis -Post operative elius (POI) -Adhesions 8-26% -Laminitis: 2-9% -Phlebitis: 3-18%
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Lecture 9 Disorders of small colon and abdomen
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Enterolithiasis
-Take a long time to form -Risks: alfalfa, Arabias, region -Right dorsal colon, small colon (transverse colon) C/S -Variable -Gas distension -Mild-moderate pain Dx -Often surprise at surgery -Radiographs -Continue to be painful despite medical colic treatment = referral Fecalith -Very similar to enteroliths -Can break them apart **Common in minis & ponies with colic** -May resolve medically: IV, enteral fluids, pain management -surgery: enterotomy or manual break up
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Small colon impaction
Risk -Altered motility -Coarse feed -Poor dentition -Fall/winter not drinking **Salmonellosis** C/S -Usually diarrhea -Mild pain, then worse -Decreased manure production: 10x more likely to have diarrhea than LC impaction Dx -Tubular small colon -"wall" of manure -Blood on the sleeve, mucosal irritation -Leukopenia with left shift Tx -Medical: fluid therapy IV and oral. Laxatives, flunixin meglumine. Antibiotics if severe leukopenia, septicemia -Surgery: enterotomy or enema passing a garden hose Prognosis -Tend to develop endotoxemia, reduces prognosis
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Abdominal abscess
Intra-abdominal Abscesses -Relatively rare Etiology -Bastard strangles =Streptococcus equi -Pigeon fever = Corynebacterium pseudobtuberculosis -GI perforation -Wound -Foaling complication -Unknown causes C/S -Low grade persistent fever -Low grade chronic colic -Weight loss and decreased appetite Tx -Long term antimicrobial therapy -Drainage?? not first choice
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Equine Small colon Lesions
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Peritonitis
Primary -Actinobacillus equuli, Strep zooepidemicus -Only one type of bacteria present Internal abscess -Strep equi subsp equi, R. equi, C. pseudotuberculosis GI perforation -Foreign body -Impaction -Multiple types of bacteria present Wound Castration -Aseptic peritonitis - inflammation Post-Op colic surgery -Increased risk with resection and anastomosis or enterotomy Neoplasia Hemoabdomen Dx -Hx of chronic low-grade colic, inappetence, depression, weight loss chronic -PE: fever, decreased motility, dehydration -CBC: chronic inflammatory leukogram -Serum chemistry: Increased SAA, chronic hyperglobulinemia -Rectal exam: may be unremarkable -Abdominal ultrasound: increased fluid, flocculent: mixed echogenicity **Fibrin "tags"** Abdominocentesis -Culture and sensitivity -Red top tube: does not have anything = culture and sensitivity -Purple top: EDTA = Cytology -Total nucleated cell count Normal <5000/uL Acute septic peritonitis: 100,000/uL After colic surgery: 150,000-200,000/uL -pH: Decrease with septic peritonitis -Glucose: decrease (consumed by bacteria) **Definitibe diagnosis and cause = surgery** Tx -Surgery? -Antibiotics -Abdominal drainage -Abdominal lavage: LRS, normal saline. Instill 10L - walk horse 20-30 minutes - open drain Prognosis -Depends on the cause -Actinobacillus equuli - favorable -Higher mortality if post op complication 56% fatal
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Peritonitis
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Gastric rupture
GI perforation -Sick but can sometimes survive -Endotoxemia -Depends on how big of a leak (bacteria) and for how long Tx -May be able to resect leaky bowel GI rupture Stomach > Cecum > LC -Rapid onset of septic shock -Elevated HR >70, dark red/brown/purple MMs -Prolonged CRT -Hypothermic -Sweating -Shivering -Severe depression: not colicky -Rectal: free gas -Ab tap: Plant material **Euthanize ASAP**
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Hemoabdomen
Etiology -Trauma horse kick -Post-op colic: resection and anastomosis - slipped ligature -Chemical peritonitis -Increased risk of adhesion formation: mild colic, decreased PCV = pale MMs Dx and Tx as for other types of peritonitis +/- treat blood loss
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Rectal tears
Etiology -Palpation per rectum -Foaling trauma/dystocia -Idiopathic, tend to be transversely oriented -Risk factors: Arabians, Minis: max size 7 glove palpation. -Risk >9 yo more often Legalities -Malpractice, bad luck -Protect yourself: sedation, restraint, Buscopan or lidocaine Grades and Tx Grade 1 & 2 **Mucosa or muscular tear** -Do not rectal for 2-4 weeks -Systemic antibiotics? Trimethoprim-sulfadiazine, Ceftiofur -Laxative diet, fresh grass, pellets, bran mashes, mineral oil Grade 3 **Mucosa, submucosa, and muscularis** -Refer -Prior to referral: epidural and pack rectum -May develop endotoxemia -NSAIDs -Broad spectrum antibiotics: Penicillin, Gentamicin, Metronidazole -Suture? -Repeatedly evacuate rectum? -Surgery and pelvic flexure enterotomy -Low bulk feed and laxative diet Grade 4 -Laparotomy -Loop or end colostomy: by-pass procedures -Rectal liner: suture in a sleeve via laparotomy Prognosis -Grade 1 & 2 = excellent 93% -Grade 3 = poor -Grade 4 = Grave
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Rectal Prolapse
Relatively rare Type 1 -Mucosa and submucosa: diarrhea, parasitism, rectal tumor Type 2 -Full thickness to rectal ampulla Type 3 -Rectum with small colon intussception Type 4 -Entire rectum and small colon: Foaling
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Equine Euthanasia
Methods -Overdose of pentobarbital: most common -Dose 1ml/10 lbs Others -KCl: only if horse is anesthetized -Gun shot -Captive bolt -Intrathecal lidocaine (only is anesthetized) Pentobarbital 1. Premed Xylazine + Ketamine induction 2. 1ml/10lbs 3. Jugular vein catheter preferable 4. Horse falls down before entire amount is given, don't stop give the rest 5. Check for heart beat and corneal reflex. -It can take a while, be patient and let owners know
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Disorder of Equine Liver
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Diagnosis of Liver Disease
History and C/S -Not evident until >60-80% parenchyma non-functional -Often Acute onset Acute -Hepatic encephalopathy -Abnormal behavior -Depressed, aggressive, bizarre -Icterus -Jaundice -Unsafe to handle horse Chronic -Weight loss -Intermittent fever -Intermittent colic -Diarrhea -Ascites -Pruritus -Photosensitization
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Hepatoencephalopathy
-Hepatic dysfunction or porto-systemic shunt -Does not differentiate acute vs. chronic failure -Behavioral changes: yawning, stridor, aimless wondering, incoordination, depression, sudden neurological behavior , blindness Pathophysiology -Neurotoxins (ammonia) -False neurotransmitters (serotonin) -Imbalance nero-transmission (GABA, glutamate)
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Laboratory Tests, Ultrasound, Liver Biopsy
Cholestatis induction Problem: biliary hyperplasia & cholestasis. High in young animals (colostrum), RACEHORSES, right colonic displacement, proximal enteritis -GGT: liver -ALP: Kidney & pancreas Cytosol leakage Problem: Acute insult, short life, not stable. Inflammation, infection, metabolic disease, toxins, neoplasia -IDH (SDH) -AST -LDH **Bilirubin direct & indirect. Bile acids, triglycerides, clotting factors, ammonia** Ultrasound -Size, location, vessel diameter, texture -Abscess, cholelithiasis, neoplasia, fibrosis -Right last rib to 10th intercostal space Liver Biopsy **Check clotting time first ** -Diagnosis and etiology (use for culture and prognosis) -Right 14th ICS (tuber coax - point of shoulder) -Ultrasound guided when possible
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Equine Liver Viruses
Equine parvovirus hepatitis (EqPV-H) -Acute disease -Strong association with Theiler's disease Nonprimate equine Hepacivirus (EqHV) -Not associated with Theiler's disease -Acute and chronic **USDA requires donor horses to be tested for viral hepatic diseases before products can be use/donated**
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Acute liver Disease
1. Theiler's disease -Common acute failure -Adult horses -Post-vaccinal Hepatitis -Idiopathic acute hepatic disease -Most likely EqPV-H -Transmission is unclear: product recipient -No known contact Risks: biologic product administration (TAT, other). Brood mares, recently castrated males. Season spring/summer C/S -Acute hepatic failure 2-3 months after biologic product -Anorexia -Hepatoencephalopathy -Icterus -Pica (persistent eating) -Yawning, fever, dermatitis -Weight loss, edema, icterus, ARDS -50-60% acute mortality Dx -Increased AST >1000 IU/L, LDH, SDH -Increased GGT >100IU/L, ALP -Increased total and unconjugated bilirubin, bile acids -Decreased BUN -Hyperammonemia -Increased PT, APTT -Decreased Albumin -PCR -Biopsy: hepatocyte necrosis Tx -Focus on controlling Hepaticenphalopathy -Supportive care -Dextrose, balanced electrolytes -Decrease diet protein, increase carbohydrates, sorghum, milo, beet pulp -Antioxidant and anti-inflammatory -Systemic antimicrobials -Neomycin, luctalose, mineral oil (decreases risk of HE) -Sedation -Corticosteroids -Prognosis: guarded 2. Tyzzer's disease **Foals** Etiology -Clostridium piliforme: spore forming intracellular anaerobe. Multiple strains in environment -Transmission: fecal-oral. Colonization GI tract, liver -Risks: time of the year, Spain mare on lush pasture. Resident status -Foal ingests mare's feces -Bacteria absorbed by portal circulation - liver C/S **Acute 7-42 days old foals** -Liver, intestine, heart -Septic shock and liver failure -Seizures, coma, sudden death -Leukopenia, hemoconcentration, hyperfibrinemia -Hypoglycemia -Severe acidosis -Increased IDH, AST, LDH, GGT, ALP Dx -Post mortem -Acute multifocal hepatitis, lytic hepatic necrosis, enteritis -Culture: difficult -PCR **Intrahepatocellular filamentous bacteria in silver stain Tx -Supportive care -High dose Penicillin, Gen, Metronidazole. -Septic shock parenteral nutrition Prognosis -Highly fatal
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Chronic liver disease
1. Choalongiohepatitis -Bacteremia -Ascending infection -Jaundice -Fever -Occasional colic -Anorexia Cholelithiasis -Recurrent episodes with colic and weight loss -Biliary obstructions -Liver disease **Middle aged horses** -Stasis Labwork -Increased highly GGT, ALP -Increased bilirubin, and bile acids -Inflammatory profile Ultrasound -Hepatomegaly -Bile duct dilation -Increased echogenicity -Choleliths crania-ventral part of the liver 6-8th ICS Biopsy: culture, histopath Endoscopy Tx -Long-term antibiotics -Penicillin gen 3 -Cephalosporin, TMS -Enrofloxacin + Metronidazole -DMSO 3-5 days to dissolve stones -Fluids dextrose included -NSAIDs -Bile salts -Choleithotomy, choleitoripsy -Prognosis: fibrosis, clinical signs, location 2. Pyrrolizidine toxicosis -Chronic progressive, often delayed intoxication -USA: Senecio, Crotalaria -Only eaten if sparse food or in hay, pellets -Cumulative dose -Delayed signs Pathophysiology -Pyrrolizidine alkaloid activated to Pyrrols in liver -Absorption into portal circulation then liver -Pyrrols cross-link DNA in dose dependent manner **Antimitotic, megalocytic effect** -Damage specific to prevent division of hepatocytes -Liver failure -Veno-occlusive disease -Portal hypertension C/S -Photosensitization -Liver failure -Weight loss -Icterus -Abnormal behavior -Diarrhea -Stridor Dx -Increased GGT, ALP, bile acids, bilirubin -Ultrasound: increased echogenicity -Biopsy: chronic hepatitis **fibrosis, bile duct proliferation, megalocytosis** -Run a clotting profile before doing biopsy Tx -May improve and relapse possible -supportive therapy -Pentoxifylline, SAMe Prognosis -Poor
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Hyperlipemia
-Hepatic lipidosis -Life threatening -Fatty liver and serum cloudy with lipids -High caloric need but low intake Risk -Well-conditioned, middle aged -Ponies, donkeys -Early lactation, late pregnancy Pathophysiology -Negative energy balance -Fat mobilization -Triglycerides synthesis -Secretion Very low density lipids -Fat accumulation and deposition C/S -Anorexia -Depression -Weakness -Incoordination -Diarrhea -Colitis Dx -Opaque plasma -Increased bilirubin -TG>500 mg/dL -Azotemia -Fatty liver infiltration Tx -Emergency -Treat primary disease -IV fluids -Nutritional support: enteral nutrition critical care meals MD's choice -Heparin? -Insulin - hyperglycemia
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Therapy for liver Disease
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Other