Colic Flashcards
non strangulating colic
muscle spasm, intestinal damage, tense mesenterium
lead to
vasoconstriction
splenic contraction
sweaitng
pain, exhaustrion
stragnulating disorders
local circulatory disorder and fluid sequestration
lead to
hypovolaemia
enteritis
wall permeabiliity and dysbacteriosis
lead to endotoxaemia
consequences of endotoxaemia
inflammatory mediators
DIC
organ dysfunction
vessel dilation
SIRS
consequence of peripheral circulatory failure
tissue perfusion
haemoconcetration
azotaemia
metabolic acidosis
aim of examination of colic horse
decide between medical and surgical therpay
what 2 systems should you focus on for the examination
cardiovascular and gi
normal heart rate
28-40bpm
potential rupture heartbeat
> 100bpm
physical exam of colic horse
behaviour
posture
body surface
skin tent test
skin temp
rectal temp
signs of colic in CV system
tachycarida, abnormal premature atrial depolarisation, tachypnoea, labored breathing
abdomen exam - visual
degree of distension
location of distension
scrotum exam - visual
enlarged
hot/cot
pain/no pain
ausculatation of abdomen location
left and right paralumbar fossa
left and right lower abdomen behind the costal arch
types of sounds
weak = mixing of ingesta
louder = propulsion of ingesta
longer, toilet flushing sound = right paralumbar fossa, ileo caecal, caeco caecal activity
sounds heard behind the xiphoid cartilage
colon
increased borborygmi
early stages of enteritis and colitis
reduced or absent sounds
impaction
obstruction
hypoperfusion
ileus
dislocation
torsion
aim of rectal palpation
diagnosis
distension
displacement
normally palpable in horse
14
rectal mucosa
bony pelvis
internal inguinal rings
small colon
bladder
cervix, uterus, ovaries
abdominal aorta
left kidney
spleen
pelvic flexure
left vetnral and dorsal colon
nephrosplienic ligament
base of caecum
peritoneum
FLASH
fast localised abdominal sonography of horse
7 regions for US
ventral abdomen
left middle 1/3 of abdomen
right middle 1/3 of abdomen
gastric window
duodenal window
renosplenic ligament
cranial vetral thorax
what is an indicator of right dorsal displacment of large colon
visualisation of colonic mesenteri vasculature
normal liquid from NG tubing
<0.5L
pH of normal NG tubing
<=5
needle technique of abdominalcentesis
18-19G needle at 90o angle
into ventral part of abdominal wall
teat cannula technique of abdocentesis
23-25g needle with 1-2ml of LA
short stab incision
edta tube for
nucleated cell count
cytology
plain tube for
TP
lactate
glucose
normal abdocentesis findings
small amount of fluid
pale/straw yellow
clear (newpaper test)
<25g/l TP
< 5.0 x10’9/L NCC
no RBC
lactate levels in colic
increased lactate levels due to low O2 delivery and inadequate oxygen utilisation
cause of spasmodic colic
individual susceptibilty
nutritional failure
cold water
meteorological factors
migratroy parasites
pathogenesis of spasmodic colic
smooth muscle spasm
hypermotility
vagotonia
clinical signs of spasmodic colic
sudden, mild, moderate colic
short bursts
normal vitals
increase borbogymi
spasm
gas production
loose faeces
differential diagnosis of spasmodic colic
tympany
ileus
impaction
acute gastric dilation
acute enteric
pregnancy colic
urinary colic
treatment of spasmodic colic
spasmolytics - buscopan
nsaids
hand walking
activated charcoal or other absorbents via NG tubing
IV fluids
prognosis of spasmodic colic
good if treated early
proximal enteritis is due to
unknown
fusarium spp
clostridium, salmonella isolated from reflux
diet change - increasae in concentrates
pathogenesis of proximal enteritis
increased secretion
decreased absoprtion
fluid and electrolyte loss
hyperperistalsis
macroscopic changes
haemoconcetnration
hypovolemia
decreased tissue perfusion
oliguria
microscopic changes
hepatic changes
peritoneal fluid
changes of peritoneal fluid in case of proximal enteritis
higher TP than in ileus
disproportionate TP to NCC
pathogenesis of increased secreation due to proximal enteritis
Na and Cl transported from intersitial to epithelium and to gut lumen
water follows ions
what contribute to secretion
bacterial toxins
inflammatory mediators
2 mechanisms for secretion
cAMP, cGMP system
Ca system
macroscopic changes of proximal enteritis
dark red haemorrhages
yellowish bands
microscopic changes of proximal enteritis
degeneration, necrosis, sloughing
neutrophil infiltration
haemorrhage on serosa
heptatic changes of proximal enteritis
ascending infection
endotoxins in portal system
biliary stasis
biliary hyperplasia
inflammation
clinical signs of proximal enteritis
lethargy
reflux
raised bcv
decreased peristalsis sounds
distended small intestinal loops
Lab analysis of proximal enteritis
increased PCV, TP, lactate
Hypo - Na, Cl, K
increased AST, AP, GGT
prerenal azotaemia
metabolic acidosis
abdo centesis of proximal enteritis
dark yellow, turbid
increased cell count
TP > 35g/l
differential diagnosis of proximal enteritis
mechanical ileus
pancreatitis
ileal impaction
alimentary lymphoma
prognosis of proximal enteritis
surgical is better than earlier
complications of proximal enteritis
laminitis
decreased body weight
thrombonphlebitis
treatment of proximal enteritis
NG tube
fluids
AB
nsaid
analgesia
prokinetic drugs
parenteral feeding
fluids for aggressive rehydration in proximal enteritis
7% NaCl crystalloids
AB for proximal enteritis
gentamicin
enrofloxacin
penicillin
metronidazole
nsaid for proximal enteritis
flunixin
analgesia for proximal enteritis
butophanol
prokinetic drugs for proximal enteritis
lidocaine
metoclopramide
parenteral feeding of proximal enteritis
dextrose
amino acids
lipids
isotonic solution
first 12hrs - 35%
second 12hrs - 60-65%
after 24hrs - 100%
prevention of laminitis
palaption of hooves and digital arteries
cie poots
cast
ACP and low molecular weight heparin
direct causes of diarrhoea
increase faecal water and electrolyte content
hypersecretion and malabsorption
indirect causes of diarrhoea
acute colonic inflammation
enterotoxins bind to secretory receptors
VFA and Na malabsorption
abnormal microflora produces dissolved metabolites
abnormal intestinal motility
sequalae of diarrhoea
significant and fast loss of Na, K, Cl, HCO3
loss of plasma to intestinal lumen
dehydration, metabolic acidosis, shock, renal insufficiency, death
bacterial causes of acute colitis
salmenellosis
clostridiosis
neorickettsiosis
parasitic causes of acute colitis
strongylosis
cyathostominosis
anoplocephalosis
toxic causes of acute colitis
AB associated diarrhoea
right dorsal colitis
cantharidin toxicsosis
misc causes of acute colitis
intestinal anaphlaxia
carb overload
sand enteropathy
4 clinical forms of salmenellosis
carrier state
lethargy, anorexia, fever, neutropenia
peractue, acute entercolitis
speticaemia +/- diarrhoea
clinical signs of salmenellosis
depression
anorexia
fever, tachycardia, tachypnoea
colic signs
profuse, watery diarrhoea
severe dehydration
prolonged CRT
acute laminitis
reflux
mm are dry, dark red, dirty red, purple
rectal palpation of salmenellosis
large amounts of gas and fluid in caecum and large colon
lab analysis of salmenellosis
PCV > 80%
low TP
leukopenia, neutropenia, thrombocytopaenia
hypo - Na, Cl, K
metabolic acidosis
prerenal azotaemia
diagnosis of salmenellosis
5 faecal samples
rectal biopsy
PCR
characterisitcs of salmenellosis
zoonotic
enterotoxin -> pge synthesis –> increased secretion –> diarrhoea
salmonella enters enterocytes
fibrinonecrotic typholocolitis
interstitial oedema
intramural thrombosis or infarct
ulcer in large intestine
cause of clostridiosis
c. perfringens A,B,C
c. difficile
clinical signs of clostridiosis
death without diarrhoea
typholocolitis
acute laminitis
typhlocolitis signs in clostridiosis
depression
anorexia
fever, tachycardia, tachypnoea
colic signs
profuse haemorrhagic diarrhoea
dehydration
brick or dirty red mm
diagnosis of clostridiosis
anaerobic culture
ELISA
PCR
cyathostominosis 3rd larval stage
may stay in hypobiotic state in caecal and large colon wall
cyathostominosis 4th larval stage
migrate though large intestinal mucosa
clinical signs of cyathostominosis
seasonal - early spring following deworming
typhocolitis
typhocolitis in cyathostominosis
colic signs
severe diarrhoea
decreased body weihgt
dehydration
sc oedema on limbs and ventral abdomen
death
diagnosis of cyathostominosis
isolation of larva from faeces
rectal biopsy
large colon biopsy
antiobiotic associated diarrhoea
disruption of normal flora
similar to salmonellosis
diarrhoea developes 2-6days of AB therapy
AB associated with antiobiotic associated diarrhoea
clindamycin
lincomycin
TTC
trimethoprim
erythromycin
rifamicin
metronidazole
diagnosis of antiobiotic associated diarrhoea
rule everything else out
right dorsal colitis
after phenylbutazone admin
gastric ulcers
thickened wall of right dorsal colon
diagnosis of right dorsal colitis
lapratomy
necroscopy
cantharidin toxicosis
toxin of blister beetles
difficult to diagnose
clinical signs of cantharidin toxicosis
anorexia
lethargy
fever
tachycardia
colic signs
diarrhoea
mixed shock
oral, lingual vessicles and ulcers
pollakuria, haematuria, diluted urine
colitis x AKA
intestinal anaphlyaxia
clinical signs of colitis x
hypovolaemia and endotoxic shock
abdo pain
profuse diarrhoea
weakness
collapse
death without diarrhoea
colitis x and IgE
IgE mediated type 1 hypersensitivity localised to large intestine
IgE independant anaphylactoid rxn
which part of the large intenstines is hanging freely
left part (pelvic flexure)
aetology of colic
horses cant vomit due to sharp angulation of pylorus
free pelvic flexure
change in diet
poor quality concentrate
low fibre
decreased water parasites
EGUS affects
any region affected by gastric acid
EGUS effects
hyperkeratosis to perforation
2 types of EGUS
equine squamous gastric disease
quine glandular gastric disease
ESGD primary
associated with intensive managemnet in animals with normal gi tract
ESGD secondary
occurs secodary to delayed gastric emptying resulting from other disease states
EGGD types
autonomically - cardia, fundus, antrum, pylorus
descriptively - focal/multifocal/ diffuse. mild/ mod/ severe
prevalence of EGUS
TB > sport > foals> regular adults
cause of ulcers
imbalance of
- inciting factors - hcl, pepsini, bile
- protective facotrs - mucus bicarbonate, pge, circulate
acid exposure
extrinsic factors
- NSAIDS, cox1, stress, conc low feeds, low fibre, decreased salive, delayed gastric emptying,
exercise - pressure increases
treatment of ulcers
continuous feeding
ppi
h2 antagonists - ranitidine
misoprostol
sucralfate
acute gastric dilation and impaction
pathogenesis
o Fermentation: gas, volatile fatty acids, lactate
o Fluid influx in to lumen of stomach - > gastric dialation and colic, sometimes gastric rupture
o Gastric dialation, colic
o Pressure on diaphragm, compromised respiration
o Decreased venous return
o Hypovolaemic shock
o Gastric rupture
acute gastric dilation and pimpaction
clinical signs
o Sudden onset, fast progression
o Severe, continuous colic, sweating
o Tachycardia
o Decreased GI motility
o Negative rectal findings
o Diagnostic nasogastric tubing
o Haemoconcentration, Hyperlactataemia
o Enlarged stomach on ultrasound visible on left side
acute gastric dilation and pimpaction
diagnosis
NG tube
US
acute gastric dilation and pimpaction
treatment
o Spasmolytics, analgesics
o Stomach tubing and lavage o IV fluid therapy
primary gastric content
acute gastric dilation
secondary gastric content
reflux
caused by ileus
methods to open abdomen
ventral midline
paramedial approach
inguinal approach
median approach (seperate prepuce)
parainguinal
suprapubic paramedia
lesions of intestinal wall
distension
ischaemic mucosa
vascular closure
distension
in case of stranguation
can cause permanent damage after 4hrs
ischaemic muscosa
tips of villi will die
endotoxins enter blood
mainly in small intestine
reperfusion injury
infiltration by neutrophils
adhesions (postop ileus)
right side of taenia
antimesenteric side
when to operate in case of colic
violent colic
worsening clinical signs and lab values
tympany
swollen intestinal wall
how to assess intestinal viability
fluorescin dye
surface oximetry
doppler
histopath
small intestine stragulation obstructions
- Volvulus
- Epiploic foramen
- Pedunculated lipoma
- Mesenterial tears
- Intussusception
- Inguinal hernia
-Umbilical hernia - Diaphragmatic hernia
small intestines non stragulation obstructions
- Ileum impation
- Muscular hyperthrophy
- Ascarid impactions
- Duodenitis, proximal jejunitis
- Neoplasia
- Gastroduodenal obstruction
- Miscellaneous simple obstruction
symptoms of duodenitis - prox jejunitis
fever
leucocytosis
reflux
elevated temp
DONT DO SURGERY
caecum disorders
- Caecum impaction
- Caecocaecal invagination
- Caecocolonal invagination
- Caecum volvulus, torsion
- Caecum infarction
type I caecum impaction
hard –> mechanical
type II caecum impaction
fluid –> paralytic
(worse)
need to do a jejunumcolostomy
diseases of ascending colon
- Large colon tympany
- Impaction
- Displacement
- “Sand colic”
- Enterolithiasis
- Large colon displacement
- large colon torsion
RDD
dight dorsal displacement
apex of caecum located in pelvis
LDD
tympanic ventral colon btw spleen and left abdomen
heart rate < 40
lower pcv
no blood flow to spleen
most violent colic
volvulus / torsion
full torsion
no artery or venous blood supply
half torsion
150o rotation
veins are obturated but artery can still bleed - DEATH
diseases of descending colon
impaction
lipoma pendulans
enterolith
non intestinal colic diseases
- Cardiovascular
o A. iliaca thrombus, pericarditis - Thorax
o Pleutitis, pleuropneumonia - Abdomen
o Neoplasia
o Abscess
o Peritonitis
o Haematoma - Liver
o Cholelithiasis
o Cholangiohepatitis - Spleen
o Abscess
o Splenomegaly - Urinary tract
o Nephrolith
o Pyelonephritis
o Cystitis
o Bladder rupture - Mare genital tract
o Ovulation
o Theca granuloma tumor
o Uterine torsion
o Contraction - Stallion genital tract
o Testicle torsion
o Orchitis - Muscle bone
o Laminitis
o Rhabdomyolysis
o Ligamentum prepubicum rupture - Nervous system
o Tetanus
o Botulism
o Lyssa
o END
4 types of abdominal hernias
- umbilical hernia
- Traumatic hernia
- Postoperative hernia
- Prepubic tendon rupture
