exam 2 notes

causes and clinical signs for oropharyngeal diseases

• causes

  • dental disease

  • trauma

  • foreign bodies

  • infection

  • ulcerative diseases

  • congenital anomalies

  • neoplasia

• signs

  • reluctance / refusal to eat

  • abnormal chewing movements

  • retention of feed “quidding”

  • protrusion and or swelling of the tongue

  • drooling and or excessive salivation (ptyalism)*

  • mandibular / maxillary swelling or drainage

  • halitosis

examination for oropharyngeal diseases

• observation: body condition, drooling, swelling of face or jaw, tongue protrusion, quid’s (feed balls) on ground

• give some feed and observe mastication

• oral examination

  • facilitated by sedation

  • irrigation of the mouth

  • manual / visual exam

  • thorough examination requires full mouth speculum and an effective light source, headlamp; mirror

• ancillary diagnostics

  • radiography, CT/MRI, oral endoscopy*

Trauma to oropharyngeal diseases

• lips, muzzle, cheek and tongue lacerations

  • superficial lacerations of lips, muzzle, and cheeks heal well by 2nd intention

  • primary closure for lacerations breaching oral mucosa

    • clean, local anesthetic, debride, 2-layer closure, no suture exposed at mucosa

    • these typically heal nicely due to ample blood supply

  • large tongue lacerations heal well when sutured; can amputate if needed

    • to level of frenulum if necessary with little problem

trauma fractures of the mandible and rostral maxilla

• kicks, collisions, cribbing, bite injuries, more

  • can result in fractures of teeth, incisor bone / premaxilla, mandible

  • fracture configurations range from bone fragments to complex bilateral fractures

• signs are drooling, lack of feed intake, mal-alignment and or instability, crepitus, soft tissue swelling, malodorous with time

• generally can be managed / repaired with good results

• some mandibular fractures are simple bone fragments

  • may present as sequestrum with draining tract

  • surgical removal and curettage

• minimally displaced unilateral fractures of mandibular bars

  • managed conservatively with soft feeds, oral rinses, time

• instability, malocclusion and bilateral fractures need stabilized

  • intraoral wiring for loose incisors, fractures of incisive bone / premaxilla and rostral mandible

  • wiring, bone screws and plates and external fixation for more complex and or caudal fractures

Oropharyngeal foreign bodies

• grass awns, splinters, and wires

• may locate in lingual, sublingual, intermandibular tissues, buccal recesses, hard palate, soft palate, pharynx

• results and signs can include

  • stomatitis, glossitis, cellulitis, abscess

  • salivation, halitosis, eating difficulties, feed refusal

• careful oral exam using speculum, light source, palpation; radiogrpahy and endoscopy

• removal followed by systemic antibiotics if indicated, NSAID, repeated oral lavage

other causes of stomatitis / glossitis

• dental points cause tongue / check lacerations; common

• parasite larvae: Habronema, Gasterophilus, Helicocephalobus,

  • Gastrophilus larvae cause stomatitis characterized by ptyalism; all may cause labial / oral granulomas

• oral ulcers: blister beetles, vesicular stomatitis virus, NSAID toxicity, caustic ingestion, uremia

• epulis: gingival hyperplasia associated with chronic irritation example erupting permanent teeth / caps

• lampus: benign swelling of hard palate caudal to incisors; eruption of permanent incisors or idiopathic

• manage inflammatory / ulcerative / infectious with oral rinses / lavage, NSAIDs, systemic antibiotics if indicated

salivary gland disease

• Sialoliths: may lead to duct rupture, fistula; sx removal

• trauma/lacerations of parotid gland and or duct

  • lacerated gland, duct/branches may result in salivary fistula

  • repair severed/lacerated parotid duct if possible

  • can be corrected with dissection and repair

  • gland can be destroyed chemically if needed

• obstruction of sublingual ducts mucoseal; marsupialize

• slaframine toxicity common in some areas

  • Red clover infected with Rhizoctonia legumencola

  • Herd outbreaks of ptyalism

  • remove from source

congenital oropharyngeal defects

• Cleft palate, tongue, mandible

• wry nose

  • dental anomalies (more later)

  • parrot mouth (overbite)

  • sow mouth (underbite)

  • shear mouth

  • oligodontia

  • supernumerary teeth

  • dentigerous cysts

developmental anomalies of teeth

• Oligodontia, supernumerary teeth, crowding of teeth

• parrot mouth: maxillary prognathism (or inferior brachygnathism); maxilla protrudes beyond mandible

  • severe overbite is a

    • major unsoundness

    • possibly heritable

    • corrective orthodontics sometimes performed

• sow mouth; mandibular prognathism (or superior brachygnathism)

  • lower jaw extends beyond maxilla; “underbite”

dentigerous cysts

• developmental anomaly; cystic structures in soft tissue over maxilla or mandible, often containing fragments of teeth

• often found at base of ear and are presented as draining tract

Oropharyngeal neoplasia

• melanoma at commissures

• squamous cell carcinoma

• less common

  • bone tumors: benign types are ossifying fibroma, osteoma; osteosarcoma is rare but majority occur in the head

    • ossifying fibroma in foals/yearlings; usually mandibular; resection via hemi-mandibulectomy; radiation also

  • primary dental tumors: odontoma, ameloblastoma

• tx and px depends on location and histological diagnosis

form and function of equine teeth

• Hypsodont teeth

  • long crown, short roots, enamel extends below gum line

  • incisors grasp, tear and pull the grass

  • cheek teeth are made for grinding the grass

• growth of crown continues until 6-9yr

• wear occurs at rate of 2-3mm / yr

  • reserve crown in alveolar bone erupts continually throughout adult life in response to wear, thus maintaining occlusion

  • length of reserve crown decreases gradually with this process; aged horse become “smooth mouthed”

adult dental chart and numbering systems

• anatomic: I1-3, C1, P1-4, M1-3

• Triadan: quadrants 1-4; upper right = 1, upper left = 2, lower left = 3 and lower right = 4; teeth numbered 1 to 11 in each quadrant.

• for example 1st upper right incisor is 101, last lower left molar is 311

• for deciduous teeth the quadrants are 5-8

deciduous teeth

• 24 in total

• the deciduous teeth are incisors and premolars; there are no deciduous molars

• at 6 months there are 3 deciduous incisors and 3 premolars in each arcade; 4×6 = 24 teeth total (excluding any wolf teeth)

• deciduous teeth are white with narrow neck

eruption times for permanent teeth

• permanent incisors (I1-3) erupt at 2.5, 3.5, 4.5 years

  • eruption times useful in aging young horses

• canine (C1) at 4 to 5 years (all males, some females)

• premolars: 2.5, 3 and 4 years for P2-4

  • (wolf teeth (P1) at 5-6 months when present)

• molars (M1-3) at 1,2 and 3.5 to 4 years

clinical signs of dental disease

• weight loss

• biting problems

• reluctance to eat

• retention of hay in the cheeks

• quidding

• tilting head when chewing

• halitosis (bad breath)

• bloody saliva

• facial/mandibular swellings

• drainage from maxilla or mandible

• malodorous, unilateral purulent nasal discharge

routine dental care

• exam at birth: occlusion, congenital defects

• exam 1-2x yearly as part of routine prevention

  • depending on age, diet, pre-existing problems

• “floating” to remove points and hooks on cheek teeth

• wolf teeth: usually removed at 1-2 yrs of age

• dental caps: deciduous teeth being shed as permanent erupts; remove if/when retained, especially premolars

• upper and lower P2s sometimes contoured for “bit seat”

• canine teeth: file down if sharp

points and hooks

• horses have prominent anisognathism; bottom jaw is narrow compared to upper

• mastication results in sloped arcades of cheek teeth

• sharp enamel “points” form on outside uppers and inside lowers; lacerations / ulcers on tongue and cheeks

• “hooks” form on upper P2 and lower M3

floating teeth: rasping / filling to remove points and hooks

• as needed in young horses with deciduous and erupting cheek teeth

• once annually for pastured horses

• 2x/yr for stabled horses

• as needed for horses with malocclusions, missing teeth

• hand floats or power instruments; careful with power float thermal injection

Incisor abnormalities

• retained deciduous incisors may lead to caudal displacement of permanent teeth

  • extraction of deciduous tooth indicated

• trauma to incisors

  • remove loosened deciduous incisors to protect permanent tooth bud

  • if permanent incisor, stabilization should be attempted

  • mandibular and maxillary fractures can displace or destroy tooth buds of permanent teeth

• fractures: many are non-problematic but

  • may involve associated boney structures, requiring fracture stabilization

  • pulp infection may occur can be managed with endodontics (vital pulpotomy / “root canal”); otherwise may require extraction

• extraction of incisors

  • involves chemical restraint local anesthesia, incision of gingiva directly over root, loosen periodontal ligament, complete extraction of root

  • need to keep opposing tooth reduced over time

• mal-alignment of incisor teeth

  • smile, frown, and tilt contours are associated with cheek teeth abnormalities

  • addressing malocclusion of cheek teeth is the key; rasping to change incisor contour is questionable

  • steps are overgrowth of individual incisors from absence or displacement of opposing tooth; regular rasping to keep level

canine teeth

• Blind (un-erupted) canine teeth

  • may cause mucosal irritation/ulceration and biting problems in 4-6yr old males/geldings, occasional female

  • incision over the un-erupted end encourages eruption

• elongated or sharp canine teeth

  • may cause bit problems

  • sharp canines enhance bite injuries

  • can be filed or cut

• very rarely a canine tooth requires extraction

  • due to fracture below the gum line and death of the tooth

  • canine extraction is difficult such that removal of a healthy canine should be avoided; bone flap approach

wolf teeth

• vestigial 1st premolar

• may cause bit problems if loose or sharp

• routinely extracted at 1-2yrs; loosen with periosteal elevator, extract with forceps

• “Blind” wolf teeth may cause subgingival enlargement and bit problems; remove surgically if needed

Premolar “caps”

• Deciduous premolars being shed as permanents erupt

• these are usually shed naturally; however

• permanent P3 and P4 erupt at 3 and 4 years and are prone to crowding with retention/delayed shedding of caps

  • erupt between permanent P2 and M1 which are already in place

retained premolar caps

• may cause a localized gingivitis

• often cause painless bony swelling around alveolus (“eruption pseudocyst”)

• these usually resolve with shedding / removal

• remove caps if they are truly retained

retained premolar caps and apical osteitis

• persistently retained caps at P3/P4 can lead to impaction and or displacement of permanent P3/P4

• with impaction there is expansion within the alveolus, lysis of supporting bone, and painful bony swelling around apex

• with progression the apex and surrounding alveolar bone can become infected (apical osteitis) and eventually the pulp

management of retained caps and apical osteitis

• remove retained cap(s)

• ± oral antibiotics based on presence / absence of painful bony swelling for example sulfas and metronidazole

• advanced infection leads to draining tract (mandible) or sinusitis (maxilla) and requires more aggressive intervention

• curettage of draining mandibular tracts

• sinus irrigation with maxillary sinusitis

• systemic antibiotics, often long term

• root end resections and apical seal are options

• extraction needed if fails to resolve

Dental decay / caries

• occurs most commonly at the occlusal surfaces of the caudal upper cheek teeth within the infundibula

• superficial decay at the surface of these teeth is common / typical generally non-problematic

• horses with unusually deep infundibula are prone to more extensive caries that can weaken tooth, promote infection of pulp cavity

• larger / persistent caries and infection

  • weakens the tooth, predisposes to splitting / cracking

  • infection may extend to root (apices)

  • endodontic techniques can be employed to seal caries

  • advanced dz requires extraction of tooth / fragments

Extraction of cheek teeth

• indications include infection, fracture, loose tooth, malposition, dental tumors

• extraction can be challenging depending on age of horse, and nature extent and location of disease

• intraoral extraction preferred; sinus trephination or sinus flap with repulsion, and lateral buccotomy, are more challenging and prone to complications

Malocclusions of the cheek teeth

• wave mouth:

  • older horses, usually at P4-M1; manage with regular floating

• step mouth:

  • “overgrowth” of cheek tooth because opposing tooth is absent; manage with cutting and or frequent rasping

• shear mouth:

  • excessive angle of the upper and lower occlusal surfaces; related to narrow mandible; causes “tilt” profile of incisors

  • creates razor sharp teeth causing lacerations of tongue and cheeks; frequent floating of cheek teeth

• smooth mouth

  • extreme wear of crown surfaces in older horses; pelleted feeds and removal of points

Periodontal disease

• generally the result of malocclusions

  • missing teeth, mispositioned teeth, wave mouth, shear mouth, step mouth, large hooks

  • result in diastema, spaces between teeth that trap feed

• progressive inflammation of the gingivae results in

  • resorption of alveolar bone, degeneration of periodontal membrane, pocket formation and loosening of the tooth

• chronically there is tooth decay and tooth loss; also can lead to osteomyelitis of supporting bone

• prevention: regular exams / dentistry to maintain normal occlusion

colic in horses

• colic = abdominal pain

• common but non-specific clinical signs in horses

  • multiple etiologies and severity

  • gastrointestinal: many conditions, stomach to rectum

  • non-GI: peritoneum, liver, urinary and repro tracts

  • “false colic” signs misinterpreted as abdominal pain, example rhabdomyolysis

• accurate diagnosis requires

  • knowledge of GI structure and function

  • understanding of pathophysiology of intestinal diseases

  • systematic approach to examination

anatomic and physiologic predispositions to GI disease

• the stomach is predisposed to gastric dilatation and rupture because the cardia is “one-way valve”

• the small intestine is prone to incarceration and strangulating obstructions

• large intestines:

  • important in water balance and nutrition, prone to acute inflammation leading to large fluid loses and PLE

  • prone to luminal obstruction, displacement, strangulation, and infarction

• small colon: prone to intraluminal obstruction, vascular injury

• motility patterns, natural openings and blood supply play roles in predispositions to obstruction and ischemic injuries

Mechanisms of intestinal pain

• Distension / stretching of intestinal wall

  • gas, fluid or ingesta; pain receptors in wall

• stretching / tension of the mesentery

• ischemia

  • incarceration, strangulation

  • vascular spasm / thromboembolism / infarction

• acute inflammation

  • intestinal mucosa / wall: enteritis (SI), typhylocolitis (LI)

  • serosa: peritonitis

mechanisms of intestinal injury: obstruction

• anatomical obstructions

  • simple obstruction

    • intra-luminal blockage and non-strangulating displacements

    • causes intestinal distention, tension on mesentery

  • strangulating obstruction

    • simultaneous occlusion of the intestine and blood supply

    • ischemia is usually acute, severe and rapidly progressive, with loss of bowel integrity and progression to devitalization, perforation

    • torsion, volvulus and incarceration / strangulating entrapment

mechanisms of intestinal injury; inflammation

• acute inflammation of the SI causes

  • Ileus (functional obstruction) fluid accumulation, SI distention, enterogastric reflux, gastric distension, abdominal pain, endotoxemia

• acute inflammation of the LI is common and causes

  • Ileus, fluid leakage and or secretion into lumen, diarrhea and fluid loss, PLE, abdominal pain, endotoxemia

• chronic inflammation of SI and or LI causes

  • malabsorption/ maldigestion, weight loss, sometimes hypoproteinemia

  • chronic, low volume diarrhea with LI

mechanisms of intestinal injury: non-strangulating ischemia and infarction

• classic cause is verminous arteritis associated with S. vulgaris larvae in cranial mesenteric artery and branches

• larval activity causes ischemia via arterial spasm, stenosis, and or thromboembolism

  • results in recurrent transient ischemia and pain or

  • infarction bowel injury, necrosis secondary peritonitis / perforation

pathophysiology of intestinal disease: cardiovascular compromise

• persistent and or progressive intestinal injury and abdominal pain result in circulatory shock due to:

  • Hypovolemia*

    • cessation of fluid intake

    • increase in insensible losses

    • fluid loss into intestinal lumen

    • strangulation obstruction

  • endotoxemia: cardiovascular effects of endotoxin*

    • depression of myocardial fx, loss of peripheral vascular tone/control (capillaries) => distributive shock

    • prominent with acute inflammatory or ischemic conditions

Primary (intestinal) endotoxemia

• endotoxin is the lipopolysaccharide (LPS) component of the outer cell membrane of gram-negative bacteria

• LPS is released into the intestinal milieu during normal reproduction and death of G-negative enteric bacteria

• in healthy animals, small amounts of endotoxin cross the GI mucosal barrier and enter the portal circulation

• scavenged and eliminated by Kupfer cells in the hepatic sinusoids

Endotoxemia

• Excess amounts of endotoxin in the systemic circulation (endotoxemia) occur via:

  • gram negative infection (G-neg sepsis)

  • primary / intestinal endotoxemia*

    • absorption of excess endotoxin and other bacterial products across damaged GI mucosal barrier, into portal circulation and or peritoneum

    • occurs especially when there is inflamed or injured bowel

• primary / intestinal endotoxemia is common in horses

  • GI dzs leading to inflammation and or injury are common

  • horses are highly sensitive to the pathophysiologic effects of endotoxin

• endotoxin interacts with mononuclear phagocytes and endothelial cells causing

  • widespread activation of the arachidonic acid cascade, massive release of pro-inflammatory cytokines, loss of vasomotor control and activation of the clotting cascade

• results in a systemic inflammatory response syndrome

  • characterized by hypotension, poor tissue perfusion, lactic acidosis and coagulopathy

• the terminal events are circulatory failure and DIC

primary (intestinal) endotoxemia

• simple GI stasis increases the amount of endotoxin absorbed across the GI mucosa

• GI distention, ischemia and or inflammation lead to

  • breakdown of the intestinal mucosa, resulting in

  • absorption of excess endotoxin across the bowel wall into the portal circulation

  • also enter peritoneal cavity when bowel wall is injured, taken up in circulation

Clinical manifestations of endotoxemia

• depression

• fever

• abdominal pain

• tachycardia

• increased CRT, weak pulses

• “toxic “ membranes

• hemoconcentration

• neutropenia

• left shift

• toxic change in neutrophils

• thrombocytopenia

• consumption of fibrinogen

• increased clotting times

clinical signs of abdominal pain

• restlessness

• curling the upper lip

• stretching

• looking at flank

• pawing the ground

• kicking at abdomen

• crouching

• dog sitting

• lying down

• rolling

• tachycardia and tachypnea

• sweating

• fasciculations

Diagnosis for colic you need to do

• thorough examination including

  • consideration of age, sex and breed

  • current and past medical history and preventive care

  • physical exam aimed at determining

    • the affected segment the intestinal tract

      • stomach, SI, LI, small colon or extra - intestinal

    • the nature and severity of the disease process

      • simple obstruction, strangulating obstruction, inflammation

    • cardiovascular status of the horse

Age, sex and breed predispositions with colic

• Newborn foals

  • meconium impaction

  • enterocolitis

  • uroperitoneum

• weanlings / yearlings

  • gastric ulcers

  • ascarid impaction

  • umbilical hernia

  • SI intussusception

  • foreign body

• adult horses in general

  • spasmodic

  • flatulent

  • gastric ulcers

  • impaction of large intestine

  • large colon displacement / volvulus

  • SI strangulations

  • typhlocolitis

  • verminous arteritis

• brood mares

  • parturition, uterine torsion, large colon displacement, large colon torsion / volvulus

• stallions

  • inguinal hernia (common), testicular torsion (rare)

• older horses, esp obese

  • strangulating pedunculated lipoma

• miniature horses especially youngsters

  • large and small colon impaction with sand, dirt, hair and foreign material (bedding)

history for colic

• history of current episode

  • duration, severity and progression of current signs

  • events surrounding the current episode

  • appetite, fecal production, water intake/access

  • response to treatment

• prior history and management

  • use, housing / environment, diet and water source

  • preventive health care: teeth, parasite control / deworming

  • changes in management / environment

  • previous colic or other medical problems

  • drug history-examples NSAIDs, antibiotics

examination for colic

• physical examination aimed at assessment of general condition, severity of pain, GI and cardiovascular status

• nasogastric intubation

  • gastric dilatation and reflux are generally indicative of primary gastritis or SI obstruction

• abdominal palpation per rectum can detect anatomical abnormalities

• abdominal ultrasound to visualize abdominal structures

• abdominal paracentesis can detect bowel compromise and or peritonitis (belly tap)

abdominal palpation per rectum

• may differentiate between medical and surgical conditions

• use a systematic approach

• landmarks / normally palpable structures are the aorta, cranial mesenteric artery, cecal base and ventral cecal band, pelvic flexure, spleen, and left kidney, urinary bladder, inguinal rings in stallions and geldings, ovaries and uterus in mares, peritoneal surfaces

abnormalities seen with colic

• dry or absent fecal balls in rectum / small colon

• fecal masses of LI, cecum, or small colon

• bowel distention; large versus small intestine

• tight mesenteric bands

• displacement of the spleen

• large colon displacements and strangulations

• abnormal peritoneal surfaces

• abdominal masses

abdominal ultrasound

• may differentiate between medical and surgical conditions

• trans-abdominal and trans-rectal

• detectable abnormalities include

  • small or large intestinal distention

  • changes in wall thickness

  • large colon displacements

  • sand accumulation in the large colon

  • small intestinal intussusceptions

  • inguinal hernia

  • enterocolitis

  • right dorsal ulcerative colitis

  • peritonitis, abdominal hemorrhage

clinical pathology with colic

• PCV and total solids help assess hydration / circulatory status; reflect protein losing enteropathy if present

• WBC will indicate stress, inflammation, infection and or endotoxemia, aiding diagnosis

• biochemical profile, electrolytes, blood gases, and lactate

  • provides assessment of circulatory status, guides fluid therapy

  • evaluation of organ function

• peritoneal fluid analysis* to assess intestinal integrity; also reflective of extra-intestinal disease

peritoneal fluid analysis for assessment of bowel integrity / intestinal compromise

• normal peritoneal fluid is light yellow and clear, WBC <5000/ul, protein <2.5g/dl

• generally remains WNL with simple LI obstructions

• vascular comprise (prolonged distention, incarceration, strangulation) leads to progressive changes

  • serosanguinous color (RBCs)

  • increases in WBC and protein (turbidity)

  • toxic changes in neutrophils as bowel wall becomes compromised (leakage of endotoxin)

  • dark fluid as bowel becomes necrotic, degenerate neutrophils

  • brown or green color, bacteria and plant material when bowel ruptures

principles of intervention with colic

• relief from pain

  • analgesics: xylazine / butorphanol, flunixin; detomidine

  • gastric decompression, cecal trocharization

• cardiovascular stabilization

  • volume expansion with IV fluids

• counteract effects of endotoxin

  • fluids, flunixin, plasma, polymyxin B

• ultimate goal: establish patent, functional intestine

  • fluids, laxatives and cathartics

  • surgical intervention (laparotomy)

Indications for surgical exploration with colics

• Clinical signs and progression are monitored over time

  • duration, severity and progression of pain, response to analgesics, rectal examination findings, naso-gastric intubation, peritoneal fluid analysis, and cardiovascular status

• surgical intervention is indicated with

  • progressive, severe and or unrelenting pain

  • obvious surgical lesion detected on rectal exam or US

  • progressive changes in abdominal fluid

  • progressive cardiovascular deterioration

  • unsatisfactory response to medical management

pre-surgical and anesthetic considerations

• stabilize CV status prior to induction

  • horse is compromised, anesthesia causes further hypotension

  • volume expansion / perfusion

• peri-operative antibiotics, anti-inflammatories

  • penicillin-gentamicin, flunixin

    • consider renal perfusion/function when giving these drugs

• NG tube in place

• Xylazine-ketamine-GG / diazepam induction, maintained on gas; goals are to maintain BP and limit time under anesthesia, myopathies are the primary risk

Exploratory laparotomy

• ventral midline incision, xyphoid to umbilicus

• initial inspection: apex of cecum should be on ventral midline, surrounded by ventral colon / sternal flexure

• look for discolored peritoneal fluid, fibrin on serosal surfaces, ingesta free in peritoneum

• decompress any distended intestine

• problem may be evident on initial inspection

• explore further by sweeping hand over viscera in all quadrants

• looking for distended loops of bowel, tight mesenteric bands, firm ingesta/fecal masses intra-abdominal masses

• detailed exploration

• feel root of mesentery and connections of cecum and colon for volvulus

• LI: check position by starting at cecum → ventral colon → pelvic flexure; nephrosplenic space

• run SI, palpate liver, right kidney, epiploic foramen

• exteriorize the colon and examine

• palpate / examine small and transverse colons

• decompression of distended SI and

• resection-anastomosis if needed

• pelvic flexure enterotomy to evacuate colon

• close abdominal wall with #2 absorbable (vicryl) methods vary; suture / staple skin; belly bandage

esophageal obstruction

• primary obstruction = intraluminal obstruction with feed or foreign body

• feed obstruction is the common form, referred to as “choke” or “simple choke”

• causes / associations/ predispositions for simple choke are

  • dental problems

  • course hay

  • grain, pellets or beet pulp eaten greedily

  • physical exhaustion (feeding immediately after a workout)

  • any cause of generalized weakness (example botulism)

  • pharyngeal dysfunction

  • previous choke

• additional causes of esophageal obstruction include

  • stricture

  • diverticulum

  • intramural masses example tumor (SCC), abscess/granuloma

  • extramural mass; cervical and mediastinal abscess, granuloma, or tumor

  • peri-esophageal scar tissue

  • functional obstruction: motility disorder and or mega-esophagus

primary obstruction with feed (simple choke)

• signs: are saliva and or feed from nose after being fed, anxious expression, extended neck, gagging, retching, coughing

• high cervical, thoracic inlet, heart base, cardia are common sites

• site of obstruction identified by passing NG tube or endoscope

  • also can palpate cervical obstruction

• endoscopy*, ultrasound, radiology to visualize

management of simple choke

• goals are to resolve the obstruction, manage complications, determine and eliminate the cause

• remove feed and water to avoid aspiration

• mild choke may resolve spontaneously

  • sedation can relieve anxiety and promote relaxation to encourage spontaneous resolutions; ex xylazine / acepromazine

  • however, prolonged obstruction (>4-6 hrs) increases the risk of esophageal damage, perforation and aspiration

• manual reduction via esophageal lavage is generally indicated (dont let the sun set on a choke)

• lavage via stomach tube and warm water

  • requires a-traumatic approach and patience

  • sedate to relax horse and drop head to avoid aspiration*

  • with tube placed proximal to obstruction repeatedly administer and drain small volumes of water to break up feed

  • can massage bolus if in cervical esophagus

  • special double lumen tubes are available

  • can place cuffed naso-trahceal tube to avoid aspiration

  • *do not forcibly push the obstruction aborad

• refractory / more severe impactions may require

  • irrigation under general anesthesia or

  • esophagostomy

• after relieving obstruction endoscopic exam to evaluate the degree of mucosal/esophageal injury is ideal

• for uncomplicated choke (minimal mucosal injury)

  • complete feed restriction for 24-48hours* (provide water

    • *esophageal motility is temporarily compromised subsequent to choke, predisposing to re-obstruction

  • re-feed with slurry initially for up to 7 days gradually return to normal diet depending on initial damage/progress

complications of simple choke

• acute complications include

  • mucosal injury / ulceration (esophagitis)

  • perforation (these dont do well depending on location)

  • aspiration pneumonia

  • dehydration and electrolyte depletion with prolonged chocke

  • manage with fluids, antibiotics, anti-inflammatory drugs, surgery as needed

• chronic complications are stricture, diverticulum, megaesophagus, recurrent obstruction

• prevention

  • proper dental care; alternative diets for aged / poor dentition

  • dont feed horses immediately after workout

  • avoid competition for feed

Esophagostomy

• employed rarely for cervical obstructions

  • refractory esophageal feed obstruction

  • foreign body retrieval

• performed standing or under general anesthesia

• place NG tube prior

• longitudinal esophagotomy over or below obstruction

• primary closure if esophageal tissue is healthy

• otherwise, delayed closer / second intention, feed esophagostmy (stomach tube in place

• antibiotic treatment indicated / necessary

• can be employed for healing of esophageal injury, or perforation from choke or foreign body

• also provides a means of enteral feeding in case of oropharyngeal disease that preclude oral intake

• esophagostomy placed below damaged site

• NG tube placed though esophagotomy site and sutured in place 2nd intention healing upon removal may fail to heal from fistula

esophageal perforation

• result of long-standing obstruction with feed, intra-luminal foreign body, NG tube, external penetration

• acute cervical perforation is potentially repairable if attended quickly and drainage established

  • diagnosis aided by endoscopy, US, radiographs, contrast

• primary closure if possible

  • otherwise, must heal by 2nd intention, guarded prognosis; place esophagostomy tube below for feeding

• intrathoracic perforation is fatal

  • severe, acute septic mediastinitis

Esophageal strictures

• usually the result of acute obstruction

  • also external trauma, reflux esophagitis, congenital

• signs are recurrent obstruction

  • diagnosis with endoscopy, contrast radiography

• bougienage techniques, endoscopic and other

• surgical techniques include

  • esophagomyotomy, partial or complete resection - anastomosis and patch grafting

• prevention is

  • diligent management of primary obstruction thorough post-obstruction evaluation and prolonged feeding of low-bulk diet when indicated

Esophageal diverticulum

• pulsion diverticulum

  • protrusion of mucosa and submucosa thru defect in the muscular wall, generally result of simple choke; has narrow neck / flask-like shape; fills with feed and leads to obstruction; diverticulectomy for correction

• traction diverticulum

  • consequences of scar tissue from perforation or other cervical injury, or esophagotomy / ostomy

    • contraction of scar tissue and traction on esophageal wall

    • leads to localized shallow diverticulum with wide neck

    • signs are intermittent, usually transient obstruction

    • generally causes minimal difficulty cna live with it

Esophageal motility disorders

• Megaesophagus is usually an acquired condition

  • prolonged obstruction (choke) may lead to permanent hypomotility and megaesophagus

  • can be a consequence of stricture or diverticulum

• Idiopathic megaesophagus in Freisian horses

• maybe as complication of neurological dz, example dysautonomia (grass sickness)

• dilated, hypomotile esophagus on endoscopy

• treatment options limited; elevate forequarters when feeding identify and treat any primary disease

Esophagitis

• Consequence of choke,

• reflux esophagitis

  • chemical injury from reflux or gastric acid/bile salts, affecting lower esophagus

  • complication of gastro-duodenal ulceration in foals (mostly) causing pyloric stenosis and gastric outflow obstruction

  • other causes of RE are SI obstruction causing entero-gastric reflux, gastritis and or gastric dilatation of any origin esophageal and gastric motility disorders incompetence of lower esophageal sphincter

• chemical injury from drugs (ex PBZ), toxicants, toxins (ex cantharidin)

other esophageal conditions

• Neoplasia

  • squamous cell carcinoma (SCC)

    • occurs in association with stratified squamous epithelium of the esophagus and stomach; esophageal SSC may present as choke

• congenital abnormalities

  • rare

  • idiopathic megaesophagus in Friesians

  • persistent right aortic arch vascular ring anomaly (stricture)

  • 4th bronchial arch defect

Disorders of the stomach

• gastric ulceration

• gastric dilation

• grain overload

• gastric impaction

• gastric rupture

• neoplasia

Equine gastric ulcer syndrome

• common condition and cause of poor performance and or ill-thrift across domestic equine populations

  • occurs in all ages, sexes, breeds and classes

  • performance horses are at highest risk

  • prevalence varies (11% go 90%)

• etiopathogenesis is incompletely understood

  • multifactorial including confinement, feeding practices, NSAIDs and a variety of physiological and social stressors

  • clearly intensive management practices associated with training and performance are major contributors

clinical signs in adult horses for gastric ulcers

• in adult horses, signs are vague and non-specific, and most cases go unrecognized; common complaints are

  • reluctance / refusal to work*

  • anxious demeanor “grouchy”

  • aversion to cinch, touching flank

  • diminished appetite

  • sometimes loss of condition

• some (minority) show abdominal pain, typically as recurrent bouts of mild-moderate, intermittent colic

  • EGUS may be the most common cause of recurrent colic in adult horses

equine gastric ulcers syndrome in foals

• very common and believed associated with illness, physiologic and or psychic stress in early life

  • common in neonates and suckling foals with diarrhea

  • lack of maternal interaction in neonatal period/ early life due to illness or death of dam, or illness of foal

  • stress of weaning psychosocial stress and disease

  • NSAIDs foals appear more sensitive to toxic effects

• glandular and pyloric disease may be more common in foals vs adults

• as with adults, most cases are subclinical

• in clinically evident cases, signs and complications tend to be more pronounced / severe compared to adults

• poor appetite / suckling behavior

• abdominal pain*

  • colic after suckling

  • recumbence rolling up on back

  • abdominal pain can be marked and or persistent

• Bruxism and ptyalism suggest advanced disease and many indicate ulcerative duodenitis

Diagnosis for equine gastric ulcers

• clinical diagnosis response to treatment

  • condition is common, especially in athletes, stressed adn or sick horses, and horses on NSAIDs

• endoscopic examination of the stomach is definitive (and ideal)

  • requires 2.5-3m scope

  • graded based on severity

endoscopic appearance of gastric erosion and ulceration

• top: mild hyperkeratosis of squamous mucosa adjacent to margo plicatus, indicating mild erosive disease (gastrophilus larvae are observed on the adjacent glandular mucosa)

• below: extensive erosion of squamous mucosa with sloughing of epithelium

• top: severe diffuse squamous ulceration involving lesser curvature

• below: thickened, hyperkeratotic appearance of deep, focal squamous ulcers in the chronic phase

general principles of management of gastric ulcers

• management changes****

  • take athlete out of work when possible

  • reduce confinement / increase turnout

  • change diet: free choice hay/pasture, stop grain

  • for non-athletes ID and eliminate stressors, illness

• stop any NSAID use

• pharmacologic suppression of gastric acidity

anti-ulcer drugs (acid suppressive therapy)

• horses with clinical squamous ulceration uncomplicated by glandular disease

  • proton pump inhibitor omeprazole (Gastroguard, Boehringer-ingelheium)

    • 4mg/kg q 24hrs for 28 days

    • recheck gastroscopy at 28 days

  • H2 receptor antagonists (ranitidine preferred, currently unavailable*)

    • off label use in US common

    • oral tablets

    • recheck gastroscopy at 4-6 weeks

    • H2 agonists work well and are inexpensive

  • off label pantoprazole and famotidine protocols also exist

  • injectable formulations very useful in managing EGUS in foals

• horses with glandular disease

  • Omeprazole (gastroguard)

  • sucralfate 12mg/kg orally q12h

  • treat for 4 weeks, recheck gastroscopy

  • frequently need continued treatment and treatment failures are common after 8 wks consider alterantives

  • alternatives are injectable omeprazole and misoprostol these are off label usages

  • in refractory cases, management changes are critical including various means of enrichment to address psychosocial aspects

management of foals with EGUS, gastroduodenitis

• foals with clinical signs (colic) often have extensive disease, including glandular ulceration adn or duodenitis; gastroscopy

• treat any primary dz, identify adn eliminate physiologic and social stressors, eliminate any NSAID use

• treat aggressively with anti-ulcer drugs, including injectable IV pantoprazole and oral sucralfate

• with suspected duodenitis / gastric outflow obstruction, motility modifiers ex bethanicol, metaclopramide

  • some require pyloric bypass surgery to relieve outflow obstruction; gastroenterostomy; guarded prognosis

• note: incidence and clincal consequences of ulcerative duodenitis in adults is not well documented

preventive use of ulcer drugs

• intermittent use in performance horses

• stressful events such as weaning, shipping

• sick, hospitalized horses

• maybe horses on NSAIDs

Gastric dilatation

• primary gastric dilation: risk/ complication of carbohydrate overload “grain overload)

  • ingestion of excess amounts of highly fermentable feed

  • grain, extruded feeds, rich alfalfa, lush pasture

  • results in excessive gas production, gastritis and fluid production

• Secondary gastric dilation: result of small intestinal obstruction

  • leads to enterogastric reflux

  • likely the most common cause of gastric dilation

• in either case the risk is gastric rupture (fatal)

  • horses have small stomach relative to body size (8-10L) perhaps 20 liters when maximally distended

  • no mechanism for regurgitation / vomiting (lower esophageal sphincter is normally one way valve)

gastric dilatation clinical signs and diagnosis

• signs are abdominal pain, NG reflux, caudally displaced spleen, gastric dilatation, distended SI with secondary

• Dx/evaluation: nasogastric intubation, rectal exam, ultrasound

• primary gastric dilatation / CHO overload may present with history of exposure, acute and progressive abdominal pain, gastric rupture or enterocolitis

• horses with secondary gastric dilatation have distended small intestine and other signs of SI dz depending on cause/type

management of gastric dilation

• gastric decompression via nasogastric tube

• dilation secondary to SI obstruction recurs until SI problem is resolved

  • leave tube in place and work up case

grain overload (carbohydrate overload)

• horses gains access to the grain bin

  • corn, barley, oats, sweet feed, commercial pellets

  • also rich alfalfa and lush pasture

• may present as acute gastritis and gastric dilation

  • characterized by acute progressive abdominal pain and gastric reflux; gastric rupture is a major risk and fatal

• severe cases evolve into a syndrome of enterocolitis, often severe with lactic acidosis, endotoxemia and laminitis

management of known or suspected grain overload

• assess the situation critically / carefully in order to determine the level of exposure

• pass NG tube to assess stomach contents / gastric pressure; attempt gastric lavage

• with no clinical signs (colic/GD), treat as follows:

  • mineral oil under gravity flow

  • NPO for 24 hours; monitor closely for 72 hrs

• if colic, reflux and or toxemia are present, decompress adn plan for intensive care

Gastric impaction

• uncommon, poorly defined, fair to poor prognosis

• defined as dehydrated mass of ingesta retained beyond 16 hours of abstinence

• possible predispositions

  • poor dentition

  • course roughage (oat hay, straw), beet pulp, bran

  • possible sequelae to gastritis / grain overload

  • persimmon seed phytobezoars are a known specific cause

  • gastric squamous cell carcinoma (SCC)

  • Fresians appear predisposed via inherent motility issue

• usually vague signs of poor appetite, maybe mild, intermittent colic; rarely acute abdominal crisis

gastric impaction: diagnosis and management

• abdominal ultrasound: large radius of stomach curvature and splenic displacement; gastroscopy

• medical tx for impacted feed is oral hydration with crystalloid solutions

• oral infusion of carbonated beverage for persimmons

• may be dx-ed at exploratory laparotomy; transmural hydration and massage of mass followed by medical tx

• prognosis for idiopathic impaction with gastric enlargement is guarded risk of recurrence rupture

gastric rupture

• terminal event of acute gastric dilation or gastric impaction

  • other possible causes and predispositions not clearly defined; perhaps mural disease ex stomach worms, gastric SCC

• rupture results in acute septic peritonitis, rapid development of endotoxic shock and death

• typically presented in severe endotoxic shock with history of abdominal pain or found dead

• diagnosis on ultrasound, abdominocentesis, necropsy

• euthanasia

Gastric neoplasia

• squamous cell carcinoma is the most common form of gastric and esophageal neoplasia in horses

• generally teen-aged and older

• arises from the squamous epithelium of stomach / esophagus

  • may become transmural and invade adjacent organs

• weight loss and or chronic colic; choke with esophageal

• Dx: gastroscopy/biopsy, maybe peritoneal fluid analysis

• poor prognosis

small intestinal obstruction

• in general SI obstruction causes gas and or fluid distention of the SI, enterogastric reflux, gastric distension, and abdominal pain.

• causes: adynamic ileus, intraluminal obstructions, incarcerations, intussusceptions, adhesions, and various strangulation obstructions

• strangulating obstruction leads rapidly to bowel compromise, peritonitis, and CV compromise; prompt sx intervention is needed

• further most simple SI obstructions eventually lead to bowl injury and usually require surgical intervention

signs of obstruction:

• abdominal pain

• nasogastric reflux

• SI obstruction

adynamic ileus

• inhibition of propulsive bowel activity results in functional obstruction

• causes are:

  • post-operative complication of laparotomy, especially for SI dz

  • enteritis

  • peritonitis

  • neonatal weakness / hypoxemia syndromes

• managed with treatment of any primary disease, decompression via NG tube, ± motility drugs

• *without a specific diagnosis / functional cause, signs of SI obstruction should prompt exploratory laparotomy

simple intraluminal obstructions of the small intestine

• ascarid impaction

  • jejunal obstruction in weanling aged foals

  • often precipitated by deworming foal with heavy burden

  • medical tx early is possible; guarded px for surgical dz

• ileal impaction

  • coastal (Bermuda) hay and tapeworms are risk factors

  • gradual progression (hours) of SI distention and colic

  • generally a surgical condition, although medical management is possible with early diagnosis/intervention

• foreign bodies

  • baling twine, plastic bags, more; surgical in most cases

SI incarcerations

• epiploic foramen entrapment; cribbing is a risk factor

• mesenteric rents: SI becomes incarcerated via teras in mesentery or gastrosplenic ligament becomes fluid filled and engorged prone to volvulus

• inguinal entrapment in stallions (inguinal hernia): post breeding or heavy exercise; some breed predispositions

• umbilical and inguinal hernias in foals, body wall defects, diaphragmatic hernia

• these are surgical conditions presenting as gradually progressive (hours) SI distention and abdominal pain

SI intussusceptions and adhesions

• Intussusceptions

  • jejunum, jeunual-ileal, ileo-ileal, ileo-cecal

  • perhaps more common in young

  • perhaps associated with hypermotility/enteritis

  • tapeworms may be associated with ileocecal intussusception

  • surgical and may require resection-anastomosis

• intestinal adhesions

  • complication of laparotomy, esp SI obstruction / resection

  • any cause of peritonitis

  • localized or focal bowel injury ex infarction / parasites

  • post-surgical adhesions present later with colic / distended SI

  • surgical intervention; px depends on location and extent

Strangulating small intestinal obstructions

• strangulating pedunculated mesenteric lipoma

  • mature horses, especially older overweight mares

• small intestinal volvulus; all ages, unknown etiology

• strangulation / torsion / volvulus associated with Meckels diverticulum

• these present as acute, persistent and progressive abdominal pain and require prompt surgical intervention

obstructive conditions of the large intestine

• large colon and cecal impactions

• sand accumulation

• ureterolithiasis

• LC displacement

• large colon volvulus

• intussusception

• obstructive disease of the large intestine cause abdominal pain and include simple (intraluminal) obstruction, nonstrangulating displacements and strangulating obstructions (torsion, volvulus, intussusception). most intraluminal obstructions with course or dry ingesta (impactions) are treated medically. severe or persistent impactions, large accumulations of sand, enterolithiasis, most non-strangulating displacements and torsion/ volvulus require surgical correction

impactions of the large intestine

• accumulation of firm desiccated ingesta in the lumen of the LC or cecum, resulting in physical obstruction

• water restriction*, stall confinement, poor dentition, course roughage, sand, NSAIDs, and stress are predispositions

• can occur as a complication of any disease that causes reduced fluid intake or fluid loss

• LC impactions are most common, and initially arise at sites in where luminal diameter narrows, ie pelvic flexure and or transverse colon

• impacted ingesta and gas accumulate orad to these sties, leading to gas distention of large intestine and thus pain

• cecal impactions are less common; some may involve motility disorder

Large colon impaction

• usually there is intermittent, mild to moderate abdominal pain and abdominal distention

• mass of firm ingesta palpable when left colon involved

• generally these horses remain physiologically stable and are managed medically

• advanced cases may become complicated showing persistent / progressive pain and cardiovascular deterioration and may require surgical intervention

• most can be managed medically

• restrict feed and provide water

• control pain

• oral and IV fluids

• laxatives and cathartics

  • mineral oil, DSS, psyllium, MgSO4 / NaSO4

• surgery indicated with progressive pain and or failure of medical treatment (not typical)

  • evacuation of colon through pelvic flexure enterotomy

• good prognosis in general; sx cases more complicated

cecal impaction

• firm ingesta filling cecum

• risk factors / predispositions as with LC impaction but

• some are associated with orthopedic sx, prolonged hospitalization and NSAID use and

• some may involve a primary motility disorder

• diagnosis by abdominal palpation per rectum

• medical tx if early; aggressive fluids and laxatives

• surgery sooner rather than later; spontaneous perforation with minimal premonitory signs can occur

  • typhylotomy and evacuation

• true motility disorder is considered a progressive condition that will culminate in cecal rupture without surgery; cecal bypass via ileocolostomy

sand accumulation

• sandy environments, bare pastures, feeding hay on the ground are predispositions to sand accumulation in LI

• sand irritates the colonic mucosa

  • sometimes resulting in intermittent diarrhea (sand colopathy)

• tends to accumulate in the RDC, resulting in

  • abdominal pain from tension on mesentery, large colon impaction and or obstruction of transverse colon

  • also predisposes to displacement, torsion / volvulus

• diagnosis by

  • history of exposure, characteristic sounds on auscultation, detection of excessive sand in feces, abdominal ultrasound / radiography, and inadvertent enterocoentesis

• medical tx: psyllium hydromucilloid

  • 400g/500kg in feed or via NG

  • protocol depends on amount of sand, clinical signs (colic or not)

  • IV fluids and analgesics as necessary

• may require celiotomy; large sand accumulations, obstruction at transverse colon, failure of medical management; evacuation of sand via PF enterotomy

• prevention: husbandry-avoid feeding on the ground; intermittent feeding of psyllium

Enterolithiasis

• Mg-ammonium phosphate stones in large colon

• regional; CA, AZ, IN and FL

• associated with alfalfa hay, high mineral and pH in colon

• can be single or multiple and quite large

• chronic colic and or acute abdominal crisis by wedging in transverse colon / small colon

• dx with abdominal x-ray, maybe US, or exploratory sx

• surgical removal required

Large colon displacements, torsion, and volvulus

• because most of the large colon is not directly attached to the body wall the left colon can move freely within the abdominal cavity (the floating colon)

• predisposes the colon to several forms of entrapment, displacement, torsion and volvulus

• primary affects adult horses; post-parturient mares particularly prone

left dorsal displacement of the large colon

• “nephrosplenic entrapment

• non-strangulating displacement in which the left colon becomes incarcerated within the nephrosplenic space

• lodged between the base of the spleen, left kidney, and neophrosplenic ligament

• intermittent mild-moderate pain, depending on stage

• dx by rectal exam, US

• some resolve spontaneously

• med txs: 1) controlled vigorous exercise 2) IV phenylpehirne or 3) anesthetize and roll

• surgical correction via laparotomy often best option

Right dorsal displacement of the large colon

• the figure shows a complete right dorsal displacement of the LC

• the large colon is displaced between the cecum and right body wall and wrapped around the back of the cecum, running transversally across the caudal aspect from right to left with the pelvic flexure directed forward

• partial or incomplete displacements are often found at laparotomy

• may possibly progress to torsion and or volvulus

• a non-strangulating displacement resulting in progressive signs of pain and abdominal distention

  • pain varies depending on the position of the colon and degree of gas distention

  • over time, distention progresses, the levels of pain and cardiovascular compromise increase, and the colon is vulnerable to volvulus

• dx: pain, distention, lack of fecal production, abnormal rectal exam; often the colon can be clearly felt passing across the caudal-dorsal aspect of cecum; ultrasound

• surgical correction is required; generally good prognosis