exam 3

debridement throudh grass tetany

primary wound closure

for a fresh, clean, sharply incised wound w minimal trauma and contamination. Closure is done in the 6-8 hr golden period

first intention healing

appositional healing. when edges of a clean wound are brought together and closed

delayed primary wound closure

closure 1-3d after injury, before granulation tissue appears. mildly contaminated, minimally traumatized. some debridement is performed

second intention healing

would allowed to heal w/o surgical closure, closes due to contraction and epithelization. used w dirty, traumatized, contaminated wounds where cleansing and debridement is necessary. would closure may be difficult bc size or location of wound

secondary closure

sutured at least 3-5 days after injury, granulation tissue is present. Used when wound is severely contaminated, traumatized, second intention healing is not desirable

primary contact layer

direct contact w wound. adherent or nonadherent. occlusive or semi occlusive.

secondary contact layer

absorbent and padded. conforming layer that covers primary later and supports the wound

tertiary contact layer

holding and protective layer. nonocclusive is preferred for air and moisture transfer.

casts

stabilize fractures distal to elbow/stifle. immobilize limbs to protect ligament or tendon repairs. can also stabilize wound. cast material is tertiary later.

bandage aftercare

assess toes for warmth, color, swelling. foul odor can indicate tissue damage. restrain animals from chewing bandage and restrict exercise.

colic workup

general physical, nasogastric intubation for reflux, rectal exam by DVM only, full lab work, may need abdominocentesis

ileal impaction

mechanical obstruction of the lumen of the ileum. pain level varies

at risk for ileal impaction

most common in SE US and associated w coastal BGH or tapeworms

ileal impaction treatment

medical or surgical

strangulating lipoma

stalk of the lipoma wraps around the intestine causing ischemia. usually severely painful

at risk for strangulating lipoma

older horse population

strangulating lipoma treatment

surgical correction

ischemia

restriction of blood floe causing a lack of oxygen

lipoma

benign fatty tumor

proximal enteritis-jejunitis

unknown etiology, horses are usually depressed and febrile. moderate to severe gastric reflux is present

proximal enteritis-jejunitis treatment

typically medically but surgery is occasionally performed

left dorsal displacement

pelvic flexure gets caught in the nephrosplenic ligament. varying degrees of pain

left dorsal displacement

occasionally can be resolved medically but usually requires surgery

right dorsal displacement

pelvic flexure courses cranially and either resides in the diaphragm or moves to the right side of the abomasum between the cecum and the body wall - mild to moderate pain

right dorsal displacement treatment

medical versus surgical management is determined based on the degree of pain

large intestine impaction primary locations

in pelvic flexure or in junction of right dorsal and transverse colon. acute change sin diameter and physical obstruction. mild or intermittent pain

large intestine impaction cecum

occasionally occurs. motility issue is cause, secondary to hospitalization. impaction in cecum can rupture.

large intestine impaction treatment

most can be treated medically but surgery is occasionally indicated

volvulus

longitudinal twist of the colon, usually clockwise. causes ischemia with severe and unrelenting pain. thought secondary to gas accumulation in colons

at risk of volvulus

broodmares

volvulus treatment

surgery is necessary for correction but prognosis is generally poor

strangles causative agent

streptococcus equi, a gram + bacteria. does not survive long in env unless in moist conditions like nasal discharge. high morbidity, low mortality.

at risk of strangles

primarily in horses 1-5 years old

strangles shedding

continues weeks after recovery

strangles transmission

inhalation or ingestion after direct contact w mucoid discharges. bacteria adheres to nasal/buccal mucosa and set up house lymph nodes associated w upper respiratory tract

most common lymph nodes affected by strangles

submandibular lnn and retropharyngeal lnn

guttural pouch

diverticulum of the eustachian tube, many important structures lie within pouches like carotid artery and cranial nerves.

strangles clinical presentation

fever, serous to mucoid nasal discharge, swollen lymph nodes.

strangles swollen lymph nodes

initially firm, soft after 7-10 days and rupture. severe swelling can cause dysphagia and dyspnea

strangles disease course

23 days

strangles diagnosis

clinical signs, PCR, culture and sensitivity of drainage from lymph nodes and nasal or pharyngeal swabs

strangles treatment

isolation, supportive care like NSAIDs and fluids, antibiotics if necessary

sequelae of strangles

guttural pouch empyema and purpura hemorrhagica. internal abscessation, septicemia, endocarditis, retropharyngeal abscesses

purpura hemorrhagica

immune mediated disease that causes vasculitis. inflammation of blood vessels causes leaks - horse experiences generalized edema

strangles prevention

IM and IN vax available. IN stimulated local immunity, a MLV vax and complications have been reported

laminitis causes

diseases leading to sepsis, endocrine disruption, support limb laminitis, black walnut shavings in bedding (less common)

laminitis etiology

due to loss of laminar attachments between the laminar epithelium between the dermal and epidermal layers - causes inflammation, insulin resistance, and decreased laminar blood flow. bone displacement

symmetrical displacement

sinking of P3

palmar/plantar displacement

most common - loss of dorsal laminar attachments and cant counteract the pull of the DDFT. tip of P3 falls and sinks

acute presentation of laminitis

initial presentation. no displacement of P3

subacute presentation of laminitis

>3 days of signs. no displacement of P3

chronic presentation of laminitis

displacement of P3 has occurred, regardless of duration

laminitis clinical signs

extremely painful, reluctance to walk, camped out appearance, hooves are warm, bounding digital pulses

laminitis diagnosis

radiographs and physical exam findings (posture, gait, pain, hoof testers, bounding digital pulses)

acute laminitis treatment

stop pain and inflammation, support the foot (use deep stall bedding and remove shoes to shift to sole support)

chronic laminitis treatment

several weeks after inflammation has resolved shoeing can be attempted. there are many approaches to achieve proper hoof/coffin bone alignment

displaced abomasum

condition where the abomasum moves to an abnormal location, can displace on the R or L side.

affected by displaced abomasum

can affect any ruminant at any time but most common in lactating dairy cows

displaced abomasum risk factors

elevated BCS, reduced DMI, negative energy balance, post-parturition, low calcium

displaced abomasum historical findings

usually <30 DIM, decreased DM intake, decreased milk production, may be ketotic, signs of colic w RDA, elevated NEFAs and BHBA

displaced abomasum physical exam findings

pings, colic and shock w RDA/volvulus, depression, urine/blood ketones, elevated HR, dehydration, decreased stool

displaced abomasum treatment

correct fluid and electrolyte, provide energy/glucose precursors, pain management. each case evaluated independently

displaced abomasum fix

mild cases medical management; moderate/severe surgical management (L flank abomasopexy and R flank omentopexy)

rolling displaced abomasum

roll from right to left lateral

displaced abomasum prevention

maintain proper BCS, ensure proper nutrition in dry period, TMR opposed to grain, appropriate fiber content, monitor milk production

displaced abomasum prevention post-partum

monitor temp, uterine size, and presence of ketones

traumatic reticuloperitonitis

hardware disease

hardware disease effects

primarily in dairy cattle but can occur in any ruminant

hardware disease etiology

cattle are indiscriminate eaters, metal gets picked up in hay or by grazing. once swallowed the object can enter rumen or reticulum.

hardware disease in rumen

if object enters the rumen, ruminal contractions move the object over the ruminoreticular fold

hardware disease in reticulum

objects are trapped in the reticulum due to the honeycomb mucosa and its ventral location. object can penetrate the reticular wall during reticular contractions, increased pressure applied to the GI contents from a late gravid uterus, or straining during parturition

hardware disease pierces reticulum only

seeds bacteria; localized peritonitis or generalized peritonitis

hardware disease pierces diaphragm

seeds bacteria; pleuritis, pericarditis, and pulmonary abscesses

hardware disease clinical signs

acute drop in milk production, increased body temp heart rate and respiratory rate, arched back, careful gait, uneasy movement, grunt when rising, positive grunt test, resist withers pinch, chronic cases an develop vagal indigestion

pleuritis or pericarditis results in

higher body temp, tachycardia, shallow respirations, muffled heart sounds, signs of congestive heart failure

signs of congestive heart failure

jugular vein distention, brisket edema, submandibular edema

hardware disease diagnosis

clinical signs and history, labwork, peritoneal fluid analysis (sometimes challenging bc infection can be walled off), ultrasounds

hardware disease labwork

elevated WBC count on a CBC; elevated fibrinogen and total protein

hardware disease diagnosis

abdominal - in area of reticulum; localized peritonitis can be IDed

thoracic - ID pericarditis and pleuritis

abdominal radiographs - referral institutions necessary

hardware disease surgical treatment

rumenotomy to remove object, post op broad spectrum antibiotics, supportive care as needed

hardware disease medical treatment

broad spectrum antibiotics, magnet admin, supportive care as needed

hardware disease prevention

magnet admin around 1year; avoid using bailing wire, avoid grazing cattle around construction, complete removal of old fences and buildings in grazing areas

ketosis

metabolic disorder with subclinical and clinical presentations

ketosis effects

primarily dairy but also small ruminants and camelids. holsteins and older cows are more at risk. most common in parturition to 6 wks postpartum

ketosis risk factors

excess bcs at calving, other postpartum diseases, high milk production, poor cow comfort, stress, nutritional imbalances, severe negative energy balance

ketosis clinical findings

drop in DMI, abnormal stool, depression, decreased BCS, ketotic breath, neurologic signs

ketosis pathophysiology

negative energy balance means high glucose demand without enough input and so adipose mobilization occurs (gluconeogenesis). NEFAs are mobilized to acetyl coa in the liver. complete oxidation of acetyl coa occurs via citric acid cycle, which is dependent on presence of oxaloacetate intermediate. in this situation, oxaloacetate has been depleted to feed gluconeogenesis, so excess acetyl coa is put into ketogenesis to produce ketones.

ketones produced

acetone, acetoacetate, beta-hydroxybutyrate (BHB; most common ketone)

ketosis diagnosis

clinical signs and production stage, ketones in urine/milk/blood (blood test necessary to detect BHB

ketosis treatment

provide glucose precursors, corticosteroids, vitamin b12 for krebs cycle

ketosis prevention

proper nutritional management in transition period, prevention of over conditioned cows in late lactation

hypomagnesemia

grass tetany - metabolic disorder due to low Mg resulting in low Mg in CSF

effected by grass tetany

lactating adult animals (esp on lush pasture or silage) and fast growing claves w high Mg demands, milk only diets, or secondary to scours

grass tetany etiology

occurs when Mg intake does not meet demands required for maintenance and lactation and no readily available Mg stores in body.

Mg requirements

maintenance: 3mg/kg body weight

lactation: 120 mg/kg milk

grass tetany risks

lush pastures low in Mg; periods of decreased food intake; soil or grass high in K or fertilized with N; lactation

grass tetany Mg absorption

Mg absorbed in rumen from forages. high K/low N and low Na/P intake decrease Mg absorption in rumen

Mg needed for

most cellular pathways, ATP formation, ATPase

grass tetany developing signs

clinical signs develop when plasma calcium is also low. lush pastures are also low in Ca and can result in metabolic alkalosis

metabolic alkalosis

urine pH >8.5 , decreases mobilization of Ca stores