Lipomas and SI surgical colic Flashcards
What are the most common surgical lesion in the SI?
Strangulations are the most common surgical lesion
Discuss SI surgical colic?
- The majority of SI causes of colic require surgery
- palpable SI distension is an indication for surgery alone
- Remember SI should not be palpable in the normal horse
The small intestine is involved in the rapid transfer of ingesta towards the caecum anything that obstructs that ingesta will cause?
fluid to back up
Obstructions may be:
- physical: the most common cause
- neurological e.g. equine grass sickness
- vascular e.g. non strangulating infarction due to cyathostomes
What kinds of intestinal obstruction are there?
- Complete or partial
- Simple (wrapped around not occlude BS) or strangulating (occluding BS)
What is a simple obstruction?
Simple Obstruction
partial or complete obstruction of the lumen but, initially, no interference with the blood supply.
What is a strangulating obstruction?
Strangulating Obstruction
- blood supply to intestine is obstructed from the outset
- Won’t resolve even if you remove the obstruction
Define sequelae?
A sequela usually used in the plural, sequelae is a pathological condition resulting from a disease, injury, therapy, or other trauma. Typically, a sequela is a chroniccondition that is a complication which follows a more acute condition. It is different from, but is a consequence of, the first condition. Timewise, a sequela contrasts with a late effect, where there is a period, sometimes as long as several decades, between the resolution of the initial condition and the appearance of the late effect.
Discuss how pathological sequelae occur in simple obstruction of SI?
Simple obstruction of the small intestine
- Complete obstruction leads to sequestration of fluid oral to the obstruction in the intestine and eventually the stomach.
- >100 litres per day of fluid (saliva 10-15litres, gastric/intestinal/pancreatic secretions) pass through the small intestine
- If you obstruct anywhere along this it is no longer absorbed in hindgut. Moment you obstruct the SI you start a timer where horse starts loosing 4litres an hour of circulating volume
Depending on where obstruction occurs along SI depends how long it will take for stomach to fill up .
If we obstruct at ileum will take longer for stomach to fill as can fill SI space first
If we obstruct nearer stomach will fill much quicker
Depending where the lesion is is very important as more rostral lesion stomach will fill quicker and may rupture more acutely
Show this in a diagram?
What does a sequestration result in?
This sequestration results in
- reduction in circulating blood volume
- leading to increase in HR and PCV
- leading to hypovolaemic shock.
Progressive increase in intraluminal pressure causes
- hydrostatic loss of protein through the gut wall
- impaired blood supply leading to ischaemia
What are the causes of simple obstructions?
There are several causes of simple obstructions
- Adhesions (surgical, trauma, parasites)
- Neoplasia (leiomyomas)
- Abscesses
Discuss types of strangulation?
Depending upon the degree of compression of the intestinal blood supply, the strangulating obstruction is described as:
- Venous
- Arterial
Blood going in and not going out = Venous
Gut wall thickness does not change as no congestion but onset of clinical signs more rapid= Arterial
Discuss venous strangulation further?
- Arterial supply unaffected initially
- Venous occlusion leads to rapid mural congestion
- Intestine becomes dark red and oedematous
- Red blood cells present in all layers and quickly diapedese into the peritoneal cavity
- A sample of peritoneal fluid at this point would show RBCs a serosanguinous sample
Discuss venous strangulation further?
Increase in mural thickness and luminal distension increases pressure against the constricting structure
- e.g. the hernial ring, lipoma stalk, epiploic foramen
Eventually the pressure applied to the vessels exceeds the arterial pressure
Once the artery is occluded no further blood enters the strangulated segment
Discuss damage to the mucosa caused by venous strangulation?
The mucosa receives 80% of the intestinal blood supply
Therefore is most susceptible to damage after loss of BS
- begins to become necrotic within 1 hour
- necrosis commences at the apices of the villi
- extends to the crypts by approximately 4 hours
Discuss arterial strangulation?
- The pressure on the intestinal vessels from the outset obstructs both the veins and arteries
- Intestine wall does not increase in thickness
- Rapidly developing ischaemic changes result in the wall becoming paper-thin
- Very easy to rupture it therefore
- Shock develops very rapidly in this situation
Look at this arterial strangulation?
Discuss strangulation further?
Mucosal damage leads to bleeding into the lumen
- provides an ideal environment for bacterial multiplication
In the normal animal healthy mucosa is an effective barrier to endotoxins
- Once breached toxins pass through the damaged wall
- This results in systemic inflammatory response syndrome (SIRS) –Microbial toxins confounding the problem
The severity of the resulting SIRS (aka endotoxaemia) shock will depend upon?
- length and diameter of the intestine involved as larger bit involved the more bacteria can contribute to SIRS
- degree of vascular occlusion
- length of time the obstruction has been in existence. A vascular obstruction that has occurred for longer will create a more severe SIRs
- the most severe and rapidly fatal SIRS occurs following 360 degree complete torsion of the large colon
Strangulation obstructions cause?
- Severe pain
- Progressive increase in heart rate due to hypovolaemia
- Progressive deterioration in pulse quality
- Congested mucous membranes because of systemic changes causing vasodilation of peripheral BS causing more sequestration of blood in periphery
- Increase in capillary refill time
- Progressive increase in PCV and potentially total protein
- Increase in respiratory rate as not enough blood circulating to oxygenate our blood
- Marked changes in peritoneal fluid
Clinical diagnosis of SI surgical colic?
Hypovolaemia and SIRS
- (tachycardia, congested mucous membranes, delayed capillary refill time, increased PCV (>45%) and TP)
Distended loops of small intestine on rectal exam and ultrasonography
Nasogastric reflux
Serosanguinous peritoneal tap (>30 g/l)
Cause often only diagnosed at laparotomy
Discuss surgical management of SI colic?
- Advise owner (cost minimum £5000, recovery period, complications)
- Stabilise patient (nasogastric decompression, i/v fluids, NSAIDs for analgesia and reduce effects of SIRs, antibiotics)
- Prepare for surgery (prep surgical site)
Treatment of surgical colic?
Exploratory midline laparotomy
- If strangulation present this is corrected
- Ingesta removed through site of anastomosis or milked into caecum
- Intestinal viability evaluated, ischaemic or severely compromised regions resected
- Anastomosis of healthy sections performed
- in total approximately 50% of the SI can be removed once we get past 50% we are compromising the horses ability to absorb protein and water
- In a typical horse this is approximately 9m (or 30’)
