Small Animal Surgery Flashcards

1
Q

What are the Halstead’s Principles?

A
  • Haemostasis
  • Approximation of tissues
  • Adequate blood supply
  • Strict asepsis
  • Tension free close
  • Tissue handled atraumatic
  • Dead space reduced
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2
Q

What is the Anatomy of the Abdomen?

A

Linea Alba
Widest at the cranial abdomen

Composed of: External & internal abdominal obliques and transverse abdominal muscles

Attaches: To pubis via prepubic tendon (Cr Pubic ligament)

Prepubic Tendon
Dog: Attaches to pectineus, rectus abdominis & Aponeurosis of abdominal obliques

Cats: Doesn’t exist – is instead separate attachments of the pectineus & abdominal m.

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3
Q

What are Hernias?

A

Any full thickness defect or weakness in the abdominal wall that allows protrusion of abdominal contents

Composed of:
a) Ring – Anatomic limits of wall defect
–> True Defect: May be within a true aperture in body wall – covered by mesothelial membrane
–> False Defect: Made by blunt trauma – no sac & has risk of adhesions
–> Acquired Defect: Iatrogenic, e.g., surgery – no sac & has risk of adhesions

b) Sack – Mesothelial membrane (e.g., peritoneum)
c) Protruding contents

Locations:
- Cranio-Ventral Mid: Umbilical, substernal
- Lateral: Parasternal, dorsal lateral
- Caudal: Congenital scrotal, inguinal
- Traumatic: Prepubic, femoral

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4
Q

What is the Sequelae to Hernias?

A

a) Space occupying effects:
Abdominal wall becomes tightened as it adapts to the organ displacement
Issues: Abdominal compartment syndrome, tension on repair, acute pulmonary issues

b) Incarceration:
Luminal obstruction of hollow organs, usually by small inelastic rings (Femoral, scrotal)
Bladder: Usually entrapped within perineal, ventral, inguinal & traumatic – decompress*
Intestine: High mortality if hernia is ~ same size
Uterus: Only issues if pyometra or gravid

c) Strangulation:
Herniated contents are incarcerated and undergo devitalisation – may be delayed in traumatic hernias due to adhesions
Reversible: Early venous obstruction Irreversible: Arterial strangulation causing necrosis

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5
Q

What are the Aims and approach to hernia repair?

A
  1. Return contents
  2. Close ring to prevent recurrence
  3. Remove redundant tissue
  4. Use patients own tissue if suitable

Dx:
- Reduction of contents & palpation
- Radiograph (Abdominal strip)
- CT
- US to rule out DDx

Surgical Approach:
Hernial sac is ligated/amputated as close to canal or ring as possible
a) Over Hernial Ring: If uncomplicated & no evidence of obstruction or strangulation
b) Midline Celiotomy: If due to trauma or risk of strangulation/obstruction

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6
Q

Describe Ventral Abdominal Hernias (Do not breed)

A

Cause:
- Failure of embryogenic folds (Cephalic, caudal, lateral)
- Polygenic inherited character

Associated with:
- Fucosidosis
- Cryptorchidism
- Ectodermal dysplasia
- Incomplete caudal sternal fusion
- Concomitant diaphragmatic hernia

Omphaloceles
Large midline defects cause abdominal organs to protrude from the body in a transparent sac. Hard to repair and are usually PTS (put to sleep)
Umbilical:
Most common type. May be acquired via excess traction at birth but is RARE
Dx: Palpation in dorsal recumbency at umbilical scar
Tx:
- <2-3mm: Treat conservatively
- Larger: Surgical repair usually at ovariohysterectomy, tension free using Linea alba

  • Spontaneous closure can occur ~6m
  • Resect all irreversibly damaged organs
  • Recurrence is uncommon
  • Neuter all patients

Prognosis: Good. Guarded if strangulated, open at birth or multiple hernias

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7
Q

Causes of Caudal Abdominal Hernias?

A
  1. Congenital defect of Inguinal ring

Scrotal hernia - Indirect *Emergency
Viscera enters the vaginal process
Host: Young male dogs, increased with cryptorchidism
Consequence: Narrow inguinal canal causing high incidence of strangulation (GIT!)
CS: Dark swelling of caudal scrotum, pain, inflammation, hydrocoele, cord-like swelling
DDX: Orchitis, abscess – can rule out hernia if spermatic cord is normal size
Tx:
- Castration recommended
- +- Scrotal ablation
- +- Laparotomy if strangulated
- No post op Ab unless hollow lumen

  • Suture both int. & ext. rings (Simple interrupted to allow spermatic cord, pudendal & n.)

Inguinal Hernia - Direct:
Less common, organs pass through inguinal rings
Host: Mature females – wider/shorter inguinal canal which ↑ by obesity & hormones
Consequence: Large w/ low incidence of strangulation
DDx: Lipoma, mammary tumour, fat, LN’s - DO NOT FNA unless US first
CS: Soft painless swelling in inguinal region, uni or bilateral
Tx:
- Bilateral: Midline approach
- Suture inguinal opening partially
- +- enlargement of cr. ring to reduce

  1. Traumatic
    Tx: Require sutures at inguinal lig., ext. rectus fascia & int. oblique abdominal
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8
Q

What is Femoral Hernias?

A

Location: Protrusion through the femoral canal, lateral to the inguinal canal, usually caudomedial to the femoral vessels. Femoral ring is located at the inguinal ligament
Composed of:
a) Muscular lacuna: Femoral n. within iliopsoas m.
b) Vascular lacuna: Craniomedial to muscular lacuna – contains Saphenous n., femoral a. & v.,

Causes:
- Iatrogenic transection of pectineus m.
- Blunt trauma = avulsed cr. Pubic & inguinal lig

Dx: Palpate caudal to the inguinal ligament
Tx: Approach parallel to inguinal lig., or midline. Sutures placed btwn. Inguinal lig. & pectineal fascia

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9
Q

What is a Traumatic Hernia (False Hernia)

A

Associated w/: Diaphragmatic hernia or pelvic fracture due to increased abdominal pressure

CS: May be masked by signs of trauma, migration of contents may change site of swelling

  • Acute: Painful, Chronic: non-painful
  • Bulging mass & asymmetry
  • Swelling ↑ with ab contraction

Dx: Assess abdominal strip for break & chest rads +-US if fluid
Tx: Acute: Midline approach Chronic: Over hernia to avoid adhesions +- enlarge ring
Aftercare: Encourage standing +- hobbles

Complications: Seroma, haematoma, infection,
skin dehiscence – recurrence is uncommon

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10
Q

What is an Incisional Hernia?

A

When abdominal suture is disrupted. May be acute (<7d) or chronic (wks → years)

Pathogenesis:

  • ↑ intra-ab pressure (Pain, preg, obesity)
  • Entrapped fat btwn hernia
  • Inappropriate suture material
  • Chronic steroid treatment
  • Poor post-op care

CS: Wound oedema/inflam, serosanguinous drainage, +- evisceration by patient

Tx:
Acute:
- Early aggressive supportive therapy
- Sterile bandages +- E-collar
- Superficial: Close ab wall defect
- Deep wounds: Open peritoneal drainage
- Use monofilament abs or non-abs
- DON’T debride edges

Chronic:
- Debridement
- Reconstructive surgery

Prognosis:
- Good if no complications & limit exercise (2wks)
- Shock/contamination ~<40% mort
- ↑ hospitalisation: Small body, high lactate, evisceration

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11
Q

What is a Perineal Hernia?

A

Failure of pelvic diaphragm due to weakness or separation causing dilation of rectum and protrusion of prostate, bladder, intestine, rectal flexure, retroperitoneal fat/omentum, periprostatic cysts into perineum

Hosts: Males (89-93%) cf. females, middle-age to old dogs

CS: Constipation, obstipation, tenesmus, perineal swelling, +- UT signs ass. w/ bladder retroflexion

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12
Q

Describe the Pelvic Diaphragm

A

Functions: Maintain ab contents in abdomen & provide structure for rectum & other structures that transverse the pelvic canal

Muscles:
- Coccygeus m.
- Levator ani *Most common fault
- Ext. anal sphincter m.
- (Int. obturator m.)

Location:
- Most common: Between levator ani, ext. anal sphincter & internal obturator (Caudal Perineal)
- Least common : Between Bulbospongiosus, ischiourethral, ischiocavernous m.
- MAINLY right > left side

Important Structures: Sacrotuberus lig (Sciatic n. runs close, do NOT ligate)., Int. pudendal a/v/n., Caudal rectal n., Caudal gluteal a., Sciatic n., AND semitendinosus m., sup. Gluteal m., pelvic diaphragm

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13
Q

Explain the aetiology and consequences of of Perineal Hernia

A

Aetiology:
1. Congenital Predisposition
2. Rectal Abnormalities *RRRGRANP
- Rectal deviation (100%)
- Rectal dilatation (40%)
- Rectal diverticulum (Rare)
- Gender related differences
- Neurogenic atrophy
- Prostatic disease
3. Hormonal Imbalance: Androgens (2.7x risk if entire), relaxin
4. Prostatic Enlargement
Results in straining to defecate against a potentially weakened diaphragm
5. Structural Weakness of Pelvic Diaphragm
Short tail breeds w/ under developed levator ani & coccygeus
Surgical Importance: Poor suture holding power & absence of suture points
6. Chronic Straining

Consequences:
- Dilation/deviation of terminal rectum
- Faeces impaction
- Diverticulum
- Retroflexed Bladder: (20-30%), +- azotaemia, Hyperk – Emergency (Catheter, cystocentesis, cystopexy)

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14
Q

Diagnosis and Treatment of Perineal Hernia?

A

Dx:
- Rectal Exam: Lack of support (Finger lateral inside anus), check prostate/straining causes

  • Radiography
  • Cystography
  • Barium meal
  • US

Tx:

*Requires combination of techniques

  • Pre-op
    Bloods, urinalysis, Ab’s, remove faeces, empty anal sacs, pack rectum w/ gauze, purse string suture butthole
    +- urinary catherer. CONTRAINDICATED: Enemas
  • Standard Technique
    Reappose m. of pelvic diaphragm – preplace all sutures before tying
    Sternal recumbency – PRESERVE the pudendal n. overlying int. obturator
    Problems: Suturing degenerate tissue, tension on repair
  • Transposition of Internal Obturator
    Provides good support ventrally, used in combination w/ other techniques
  • Prosthetic Mesh Repair
    Used when severe atrophy is present – polypropylene
  • Transplantation of Semitendinosus
    Used for ventral midline defects, particularly after bilateral repair
  • Transplantation of Superfial Gluteal
    Used to reinforce standard repair dorsally – in combo with int. obturator flap
    BUT increased incision & trauma
  • Cystopexy/Vas Defernsopexy
    Used when bladder is retroflexed, usually pexy colon at same time → PH 1wk later
    Vas deferns connects to prostate, pull it forward and pexy
  • Castration
    Important in prostomegaly (4-6wk healing) but also lower recurrence rate
  • Alternatives
    Porcine SIS, Porcine dermal collagen, Fascia lata autograft/allograft, tunica vaginalis fascia post castration

Post-Op:

  • Remove purse string
  • Digital rectal support check
  • Medication to ↓ strain
  • Low residue diet
  • +- Antimicrobial

Complications:

  1. Wound infection
  2. Faecal incontinence
  3. UT malfunctions
  4. Tenesmus
  5. Sciatic n. paralysis
  6. Recurrence
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15
Q

What are Diaphragmatic Hernias?

A
  • Musculotendinous partition
  • Strong central tendon (21%)
  • Muscles: Par sternalis (D & V), Pars costalis (L), Paired lumbar crura (R > L– L, I, M)
    –> Right is larger than left
    Divided into lateral intermediate and medial
  • Nerves: Splanchic N. & Sympathetic trunk – btwn lateral crus & 13th rib bilaterally

Openings:
1. Aortic Hiatus (Dorsal): Aorta, azygos, hemiazygos, lumbar cistern thoracic duct
2. Oesophageal Hiatus: Oesophagus & blood supply, dorsal & ventral vagal trunks
3. Caval Foramen (Ventral): Vena cava

Cause: Trauma - Direct or indirect (Sudden ↑ IAP w/ glottis open)
IAP: Intra Ab Pressure

Location: Costal > Central tendon; Cats: Circumcostal (59%),
Dogs: Radial (40%), Circumcostal (40%)
- Most commonly herniated organ: Liver (88%)

CS: *Depends on system affected
- Obstruction, cardiorespiratory, incarcerated
- Dyspnoea!
Causes: Compression/atelectasis, hypoventilation, V/Q, dysrhythmia, pleural/peritoneal pressure equalises, pain/mechanical
- Pleural effusion: Mostly liver, thin cranial vena cava & hepatic V. walls, lymphatic distension
- Strangulation: Via adhesion bands; Ischaemia, perforation, abscessation, cranial vena cava (CVC) pressure (rare)

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16
Q

How to diagnose and treat Diaphragmatic Hernias?

A

Dx:
- Thoracic palpation of apex beat to define side of hernia (80% accuracy)
- Radiographs: Partial loss of diaphragm line (66-97% - NOT DIAGNOSTIC)

  • US (93% A)
  • CT & MRI
  • Contrast studies: Not indicated, false negatives (obstruction)

Sx Approaches:
- Midline Coeoliotomy:
Indications: Most traumatic & all congenital perito-pericardial hernias (UNLESS adhesions)
Adv: Don’t need to know position of tear
Dis: Adhesions difficult, hard to suture concave

  • Median Sternotomy:
    Allows extension of midline coeliotomy
    Adv: Adhesions can be visualised
  • Lateral thoracotomy:
    Performed on side of hernia CI: Bilateral hernia, perito-pericardial hernias

Tx:
Timing: Earliest opportunity in a stable patient

  • Coeliotomy and examine for hernias
  • Avoid kinking VC when repositioning liver
  • +- Freshen chronic edges
  • +- Chest drain
  • Circumcostal: Sutures anchored on costal arch & ab wall
  • Materials: Pig SIS, Silicone, Polypropylene, Fascia lata, Muscle flaps (Rectus & transverse ab)
  • Pulmonary Reinflation: Lateral thoracostomy tube w/ gradual reinflation, esp. chronic or reperfusion issues – Pressure of 10mmH20

Issues:
a) Prolonged expansion: Valsalva effect = ↓ return of blood to heart
b) Over inflation: Ruptured parenchyma = haemorrhage, pneumothorax, pulmonary oedema

Post-Op:

  • Expel residual air pre-close
  • Radiographs
  • IVFT
  • +- Analgesia
  • +- Ab if herniated liver/perforated viscous
  • Monitor CV & RR: Pa02, MAP, CVP
  • Inadequate RR: 02 sup, thoracostomy tube aspiration, auscultate thorax, blood gas analysis
  • Intermittent/cont. suction of fluid/air
  • Remove tube when <2-3ml aka ~6hr

Complications: (~50%)
- Death:
a) <24hrs: Haemo/pneumothorax, oedema, shock, pleural effusion, dysrhythmia
b) >24hrs: Rupture, obstruction, strangulation of GIT or unrelated disease

  • Ascites
  • Gastric ulceration
  • Oesophagitis
  • Megaoesophagus (Transient)
  • Hiatal Hernia (↑IAP = ↑ Laxity)
  • Recurrence

Px:
- Post-op 80-90% success
- 15% Mortality prior to presentation
- ↑ Mortality: Anaesthesia time, soft tissue injury, orthopaedic injury

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17
Q

What is the composition of the Peritoneum?

A
  • Fluid:
    Cell type: Acellular – Primarily macrophages (50%) and Lymphocytes (40%)

Composition: Small albumin, H20, low wt. molecules, SG <1.016 lacks fibrinogen

Role: Non-clotting surfactant, dilutes chem mediators, smooths mesothelial surfaces, removes particles, limits adhesions

Flow: From all surfaces to the diaphragm (lymphatic plexus for fluid collection)

  • Micro layer:
    a) Serous Layer: Has squamous cells with microvilli
    b) Extensive lymphatics
  • Macro Layer:
    a) Membrane: Clear, thin, translucent
    b) Layers: Parietal & visceral
    c) Peritoneal Cavity: Small volume of clear fluid
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18
Q

Explain lymphatic drainage

A

Movement: Through the mediastinal LN via passive diaphragm stretch & -ve intrathoracic pressure

Importance:

  • Peritonitis is likely to form into bacteraemia <6mins
  • ↑ Sternal LN suggest peri/retroperitoneum inflam/neoplasia as ONLY omentum can absorb particles & bacteria in the peritoneal cavity

Factors affecting matter clearance:

  • Gravity
  • Resp. movement
  • GIT activity
  • Diaphragm movement
  • Intra-peritoneal pressure
  • Particle size (<10um only)

Healing of Peritoneum
Timing: All defects close in 5-7d regardless of size
Mesothelial Cells Involved: Edges & depths of defects, adjacent mesothelial surfaces

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19
Q

Explain the formation and promotion of adhesions?

A

Formation
- Initiated by: Peritoneal injury → inflammation
- Inflammatory cells & fibrin release → fibrinolysis in 3-4d assuming good perfusion

– Either:
A) Inflammation subsides: Adhesions may breakdown

B) Ischaemic tissues/persistent inflammation: Fibrin is infiltrated w/ fibroblasts producing collagen & permanent fibrinous adhesions persisting >4-5d

Promotion:

  • Suturing peritoneum
  • Endotoxemia
  • Intestinal manipulation
  • Bowel distension
  • Desiccation of serosa
  • Foreign body contamination

Prevention:

  • Preventing desiccation
  • Gentle tissue handling
  • Haemostasis
  • Precise sutures
  • Lavage of clots & FB’s

Dissolution:

  • Adequate mesothelial O2 & nutrition
  • Lack persistent inflam
  • Plasminogen activating substances

Advantages
- Increases blood supply in compromised tissue
- +- Limit leakage from viscus

Disadvantages
- Clinical disease via restrictive adhesions which compromise lumen and +- strangulate

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20
Q

Describe the components and uses of the Omentum?

A

Location: Inside of the peritoneal cavity

Components:
a) Lesser omentum: Attached to greater curvature of stomach & liver
b) Greater omentum: Attached to lesser curvature of stomach & pancreas (Has omental bursa)

Function:
- Isolates & seals source of infection/inflammation via adhesion
- Absorbs bacteria & other matter
- Rich blood supply
- Immune function (PMN, lymphocytes, macrophages, lymphatic drainage)

Use of Omentum

  • Aid sealing of adhesions
  • Highly movable, create flaps anywhere
  • Through diaphragm for oesophageal healing
  • Blood supply for non-healing wounds outside abdominal wall

Disadvantages:
- Causes adhesions on viscera → local abscesses/focal peritonitis (Can be good cf. general)
- Complicates ab tube drainage
- Obstruction of GI via adhesions

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21
Q

Describe Pathophysiology of Peritonitis

A
  • Primary innate defence:
    Complement system (C3a & C5a release) stimulates neutrophil chemotaxis & mast cell/basophil degranulation
  • Other innate defence:
    Bacteria absorption via diaphragm lymph, phagocytosis, abscess formation & NK cell activity
  • Secondary specific defence:
    Mediated by lymphocytes, provides a 2nd amplification system response to sepsis
  • Immunoglobulin production:
    Produced by peritoneum assosciated. Lymphoid tissue & omental lymphoid tissue

Inflammatory response:

  • ↑ protein rich fluid
  • Neutrophils & macrophages
  • Activation of complement
  • Opsonisation
  • Mast cell ↑ of perm
  • Fibrinolytic inactivation
  • Fibrin blocks stomata
  • Peritoneal rel. lymphoid resp

Adjuvants:
- Gastric mucin: Anticomplement effects → Inhibits phagocytosis
- Haemoglobin: Interferes w/ chemotaxis, phagocytosis & intracellular killing (Provides iron)
- Bile salts: Lower surface tension & alter cell adhesion → RBC lysis & Hb release
- Barium
- Peritoneal fluid: ↑ bacteria, ↓ bacterial clearance, ↑ mortality rates

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22
Q

What are the results of peritonitis?

A

IRH MISS HIM
(I really have miss him)

  1. ↑ IAP
    - ↑ Hypovolaemia - Impairs ventilation
  2. Respiratory acidosis & hypoxaemia
    - Via reflex diaphragmatic rigidity & ↑ IAP preventing ventilation
  3. Hypoproteinaemia
    - Protein fluid moves from IV to cavity
  4. Metabolic acidosis
    - Impaired oxygenation via respiratory acidosis
  5. Intrahepatic cholestasis
    - Alteration of bile flow → icterus
  6. Severe catabolic state
    - Via 25% increase in metabolic rate & massive protein loss into cavity
  7. Septic shock
    - Adrenergic stimulation → ↑ venous p. → injury to gut mucosa & translocation of flora
  8. Hypovolaemia
    - Protein fluid from IV to cavity - Fluid sequestration in bowel lumen via reflex ileus
    - ↑ IAP → ↓ CO & return - Hypotension & ↓perfusion → metabolic acidosis/hypoxia
  9. Impaired renal function
    - Renal insufficiency → ↓ clearance of toxins → ARF
  10. Myocardial depression
    - Via hypoxic pancreas
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23
Q

What are the classifications of Peritonitis?

A

Primary Peritonitis
Primary inflammation in absence of an evident intra-abdominal source of infection or penetration
E.g., Spontaneous Bacterial Peritonitis
Characteristics: Mainly monoclonal & Gram + bacteria

Px: No difference, 50% survival
Tx: Oral route for cats

Secondary Peritonitis
1. Aseptic Peritonitis

Types:

  • Mechanical e.g., Iatrogenic, Gossypiboma
  • Starch, e.g., Gloves → Granulomatous
  • Chemical, e.g., GI fluid, bile, urine, IP Ab
  • Sclerosing encapsulating (Chronic)
  • Parasitic, e.g., T. Gondii
  • Protozoal, e.g., Neospora
  1. Septic Peritonitis
    Mortality: 50% - Increased when albumin <2, left shift, ↓TP, hypotension & dehiscence (85%)

CS: Ab enlargement/pain (Praying position), tachypnoea, malaise (V+, D), temperature variation (Cats = hypo), lack of bowel sounds, +- Peritoneal effusion → SIRS

Causes:
- GI:
Most common
Cause: Surgical wound dehiscence
↑ Risk: Pre-op peritonitis, low albumin, FB
Consequence: 5% dehiscence (W/ Bacteria & FB removal if no peritonitis)
Px: >50-68% mort w/ peritonitis – level of dehiscence affects px

  • Pancreatic:
    Cause: Ruptured abscess? Occurrence: Pancreatitis present in 50% peritonitis cases
  • Genitourinary:
    Occurrence: Rare
    Location: Bladder, pyometra, prostate
  • Hepatobiliary:
    Cause: Cholelithiasis, GB rupture, Necrotising chelcysititis
    Px: 14% Mortality, GB rupture – 50% survival (Septic) or 100% (Non-septic)
  • Penetrating wounds
  • Sx complications
  • Peritoneal dialysis

Pathophysiology:
- Severity: Depends on site (20-80% Mort), ↑ distal = ↓ Px, e.g., Pyloric leak 2nd NSAID 63%m
- Virulence: Adjuvants are synergistic, e.g., bile, barium, Hb, Mucin
- Poly-Microbial: Gram negative, e.g., E.coli, Bacteroides Fragilis

24
Q

Diagnosis of Peritonitis?

A
  • Abdominocentesis: *Most important
    Technique: Awake/sedated → EDTA, plan & culture → Insert 1-3cm caudal to umbilicus

cf –> clinical findings?

Lavage Method:
Insert dialysis/14G catheter, IP 20-22ml/kg saline ONLY infused if no fluid on catheter insertion

Evaluation:
Leukocyte & Bacteria: Morphology is more important than total no.

Warranted Sx Exploration: Toxic/Degenerative neutrophils, bacteria, plant material

Uroabdomen: Creatine or K+ increased cf. serum

Free Intraperitoneal Bile: Bilirubin 2x serum

GI Ischaemia, pancreatic injury/inflam: ↑ Amylase or lipase cf. serum

Septic Effusion: >2.5mmol Lactate – not reliable in cats (Use cytology & NCC instead)

Septic Peritonitis: <2.75 glucose! More than 1-2mmol difference is 100% Dx

Ddx: No absolute cell count can determine between normal post Sx response & infection

DO NOT USE peritoneal drain to monitor fluids → Degen neutrophils, incorrect lactate/glucose

  • Ab Radiographs: Loss of serosal detail, ‘ground glass’, free air
  • Thoracic Radiographs: Double effusion – 3.3x more likely mort.
  • Ultrasonography: Free fluid
  • CT: Useful in trauma
  • Bloods:
    Non-specific: ↑ MPV, PCT, PDW, thrombocytosis/penia, neutrophil toxicity, TWCC & band %
    Non-survivors: ↑ GGT, ALT, Blood lactate >2.5mmol/L & Lactate clearance <42%/12hrs
25
Q

Treatment for Peritonitis?

A

Tx:

  • Fluid & E- Therapy: Aggressive, Colloids & crystalloids
  • Surgical drainage!!
  • Antimicrobials:
    Mainly broad bactericidal (Ampicillin-Gentamicin-Metronidazole), NO Fluoroquinolones
    C&S rec. (BUT 71% no change in outcome, 20% inappropriate change in outcome)
  • NSAIDS: Controversial, only AFTER fluids, e.g., Flunixin – ↑ Px, ↓ adhesions/abscesses (Dog)

Sx:
Goals:
- Eliminate source of contamination, reduce FB/bacterial load/Inflam cells, prevent PI

  • Supply nutrition
  • SI Monofilament suture for bowel/omentum/serosa
  1. Analgesia – Lignocaine CRI (Cf. opioid was sig.)
  2. Debridement
    - ↓ Intra-ab Bacteria, FB, Adjuvants & peritoneal fibrin
  3. Lavage
    - 200-300ml/kg Warm saline or until fluid returns clear
    - ↓ Bacteria, blood clots, debris, inflam cells BUT evidence conflicting/not sig.
  4. Serosal Patching
    - Reduces suture line disruption to prevent collagen & ECM degradation → dehiscence
    - Provides fibrin seal, mechanical support, resistance to leakage, provides blood supply
  5. Omentalisation
    - No evidence but is recommend to wrap organ in omentum
  6. Drainage
    - Closed or open, vacuum assisted is easier to manage
  7. Primary Closure – ONLY IF
  • No ICU/plasma available
  • Monobacterial infection
  • Non-GI Infx source
  • Localised inflam is removed
  • Little/no foreign material left

Post-Op:
- Nutritional Support:
Prevent: Immunosuppression, ↓ energy store, weakness, delayed healing, organ failure

Enterocyte Nutri Benefits: ↓ Permeability, maintain structure/function, preserve biliary IgA

Methods:
NGT! (Allows drainage), Gastrotomy, Jejunostomy, Parental (Glutamine), Transfusion (+- Rejection), Analgesia (Return of GI function)

Px:

  • Closed Drainage: 70-85%s
  • Open Drainage: 52-89%s
  • Primary closure: 54-67%s
  • Location: Higher in GIT, ↑ Px
26
Q

Explain Sepsis and SIRIS

A

Mortality: 25% w/o mods (multiple organ dysfunction syndrome)

Cause: Must result specifically from infection

Pathophysiology:

  • ↑ O2 consumption
  • Endotoxin release → activation of complement & macrophages
  • Fever → ↑ Survival & defences, ↓ bacterial proliferation
  • Vasodilation & increased vascular permeability → Heat, pain, swelling, redness

Systemic Inflammatory Response Syndrome (SIRS)
Identical to sepsis but results from a non-infectious insult

Diagnosis Criteria: *≥2 are required

Clinical Manifestations:
1. Hyperdynamic phase: Bounding pulse, Red MM, fever, tachycardia/pnoea
2. Advanced Disease/Decompensated shock: Hypotension/thermia, pale MM, Weak pulses\
Septic Shock
Causes acute circulatory failure & persistent arterial hypotension

27
Q

What causes Multiple Organ Dysfunction (MODS)

A

Altered organ function in acutely ill patient req., intervention to maintain homeostasis of ≥2 systems

Cause: Severe sepsis leads to an uncontrolled inflam response
Mortality: 70%

28
Q

What causes Ileus?

A

Cause: Early peritoneal inflammation (peritonitis)→ sympatho-adrenergic reflex inhibition

Result: Block myenteric cholinergic neurons

Prevention: Spinal anaesthesia & adrenergic blockade

Benefits: Impedes intraperitoneal circulation to stop spread of contaminants

Disadvantages: Can cause bacterial translocation against gut wall in sterile peritonitis → sepsis

Adynamic Ileus
Functional – ileus w/ no mechanical obstruction

Causes:
- Ischaemia
- Chronic bowel distension
- Endotoxemia
- E- imbalance
- Effects of Anaesthesia

29
Q

What is Reflex Rigidity?

A

Reflex Rigidity
Cause: Peritoneal irritation causes rigidity of abdominal (34-64% cats) & diaphragmatic muscles

Localisation:
- Peritoneum: Can be localised as innervated by somatic n.
- Visceral Organs: Innervated by visceral n. that respond to stretch – difficult to localise

Consequences:

  • Interfere w/ resp movements
  • ↓ Intraperitoneal circulation
30
Q

Describe the anatomy and function of the spleen

A

Anatomy

Location:
Dorsally tethered to greater curvature of stomach via gastrosplenic lig., tail is along the ventral midline

Vasculature
1. Celiac:
- Hepatic a. → Right gastric, Gastroduodenal
- Splenic a.: Gives rise to left pancreatic a., enters spleen & continues as left gastroepiploic a.
- Left gastric a.: Anastomose w/ short gastric a.
- Splenic v.: Drains into gastrosplenic v. → portal vein

  1. Cranial Mesenteric:
    - Jejunal
    - Ileocolic → Middle colic, Right colic, Mesenteric ilial branch
  2. Caudal Pancreaticoduodenal
  3. Caudal Mesenteric:
    - Cranial Rectal
    - Left colic

Function
Immunosurveillance:
- Filtration: Removal of IgG covered RBC’s & platelets (IMHA, IMT)
- Synthesis: IgM (Early immune defence), B cells, T cells
- Phagocytosis: Ag at margin → white pulp → B-cell production → lymphocyte trapping
- Foetal immune development

Haematopoiesis:
- Platelet Storage: 30% mass
- RBC Storage: 10-20% dog mass
Separated into pools: Rapid: 90%, released <30s, Intermediate: 9%, 8m, Slow: 1%, 1hr
- Extramedullary (Foetal) Haemopoiesis
- Removal of abnormal RBC’s (Acanthocytes/spherocytes)

31
Q

How to Diagnose and Treat Splenomegaly?

A

Generalized Splenomegaly
Inflammation
Cellular hyperplasia
Cellular infiltration
Congestive enlargement

Diagnose:
- Radiography: More on right lateral view then left lateral

  • US: Hyperechoic changes –> nodular hyperplasia, primary or metastatic focal neoplasms and fibrosis from healed infarction or haematoma
  • MRI & CT
  • Baseline HCT & Coagulation panel –> FNA & Tru-Cut
  • Needle Track Seedling

Sx:
- Considerations: Coagulopathy, Hypotension, Ventricular arrythmia (Lignocaine CRI), PCV <20% (Blood transfusion pre-op but only auto-transfuse if trauma to avoid neoplastic dissemination)

  • Splenorraphy:
    Indication: Small lacerations/punctures

Warning: Incomplete haemostasis
Closure: Interrupted mattress (4-0, 5-0 abs, monofilament), gel foam (Mimics abscess on CT), Enclosure w/ absorbable mesh bag for external tamponade

  • Partial Splenectomy:
    Indication: Splenic focal abscess or injury NEVER in neoplasia

Closure: Staples, CO2 laser, ultrasonic cutting, bipolar sealing device (<7mm, 3x a., 2x v.)

  • Complete Splenectomy:
    Indication: Neoplasia, splenic torsion, severe trauma, generalised infiltrative dz, Immune-mediated dz

DO NOT de-rotate splenic torsion as releases bacterial products

Closure: Double ligate splenic a./v., 1x left gastroepiploic & short gastric a.,
Use stapling device, haemostatic clips (<3mm), ligatures (4 total)

  • Post Op: Inspect portal/splenic V. for thrombus, & inspect haemorrhage post removal
  • +- Prophylactic Gastropexy:
    Removing mass creates abnormal movement of stomach → stretch of gastrosplenic, hepatoduodenal & hepatogastric → Twists on long-axis
    5.3% increased risk – some found non
32
Q

Causes of Inflammation or Splenitis?

A

Causes: Bacterial, protozoal, viral, or fungal
- Dog – Bacteraemia, low-grade septicaemia, chronic infectious disease (Necrotic debris)

Types:
- Infectious: Neutrophilia
- Pyogranulomatous: Cats – FIP

  • Lymphoplasmacytic: Chronic, subacute or mycotic/mycobacterial
  • Eosinophilic:
    Cats – Hyper-eosinophilic syndrome, Dogs – eosinophilic gastroenteritis
33
Q

Causes of Cellular Hyperplasia?

A

Causes:
a) Red & White pulp:
- IMHA: Extramed. haematopoiesis & reticuloendothelial via IgG-erythrocytes

  • IMT
    b) Macrophage hyperplasia: Histoplasmosis, Leishmaniasis
    c) Lymphoid hyperplasia: Chronic stimulation
    d) Splenic myeloid metaplasia: Histocytosis – Px poor (70%m)
34
Q

Causes of Congestion in Spleen?

A

Congestion
Hosts: Cats cf. dogs are unlikely to have physiological splenic enlargement – most likely pathologic

Causes:
1. CHF: Rs-CHF → venous congestion in liver → portal hypertension → splenic venous stasis
2. Portal hypertension: Viral, toxic, neoplastic, inflammation
3. Vascular Outflow Obstruction: Splenic torsion, CVC/PV obstruction, Ab mass, GDV
4. Relaxation of Splenic Capsule: Barbiturates, ACP

35
Q

Causes of Cellular Infiltration?

A

Cellular infiltration
Causes:
- Myeloproliferative lymphosarcoma/lymphoma & mastocytosis +- Mx neoplasia
- Histiocytic sarcoma (Bernese, Rottweilers, Golden)

  • Amyloidosis
36
Q

Causes of Nodular Hyperplasia?

A

Hosts: Older dogs – usually benign

Path:
- Lymphoid, erythroid, myeloid & megakaryocyte nodules
- Distinct from haematomas
- Fibro-histiocytic nodules are distinct & intermediate stage to a malignant histiocytoma

37
Q

Other pathologies in Spleen: Segmental Infarction, Plaques, Neoplasia, Haemangiosarcoma?

A

Segmental Infarction
Hosts: Uncommon in dogs

Location: Subcapsular areas (Poor perfusion & venous return)

Cause: Hypercoagulable states, splenomegaly, cardiac dz, neoplasia, liver/renal dz, excess CCsteroids

Dx: CT w/ contrast, MRI w/ gadolinium – sensitive +- US

Plaques
Siderotic: Benign gold brown/black via stored iron from erythrophagocytosis & Hb breakdown

Siderocalcific (G-Gandy Bodies): White-yellow dry crusts on margins +- brown (Fe), Blue (Ca), Yellow (Bilirubin) via senile changes or old areas of haemorrhage

Neoplasia
Types: Lymphoid, Mast-cell, histiocytic, plasma cell, myeloproliferative, HAS etc..

Locations: 9% of cardiac mass, 29% cardiac HSA also splenic, Cardiac HSA Mx rate 42%

Haemangiosarcoma
Path: Solitary mass of well-differentiated endothelial cells → well-formed vascular space

Ddx: Haemangiosarcoma → Poorly differentiated/arrangement

Other
- Hamartoma: Benign lesion, rare and identical on U/S to other forms

  • Abscess: Uncommon in dogs, rare in cats
  • Cyst
38
Q

Explain diagnosis and treatment for Splenic Torsion?

A

Hosts: Uncommon, more often in deep-chested large dogs, NOT in cats

Cause: Unknown – potentially spontaneous resolving GDV

CS >3d:

  • ↓ Gastric motility, tympany,
  • Venous → arterial occlusion
  • Blue/black c-shaped spleen
  • Vague signs, e.g., V+, D+

Dx:
- Haematology: Leucocytosis, anaemia, thrombocytopenia
- Biochemical: Non-specific +- ↑ Hepatic & pancreatic enzymes
- Radiographs: Lack of splenic outline, ab detail ↓ in effusion +- C-shaped spleen/gas
- CT: Cork-screw mass w/ no contrast enhancement
- US: General hypoechoic splenomegaly, lacy parenchyma, infarction (Gas shadows, thrombi, adhesions, no colour-doppler flow)

Treatment:

  • Supportive treatment
  • Prophylactic gastropexy
  • Splenectomy: *EMERGENCY
    Do not de-rotate → Intravascular release of sequestered blood, thrombi, TNF, FR, VA

Staples & haemoclips are inadequate due to thickening of perivascular tissue

Examine pancreas for damage & Ischaemia

Px: Guarded to good – chronic has better success

39
Q

Explain Diagnosis and treatment for Splenic Trauma?

A

Consequence: Massive haemorrhage

Dx: Lavage, FNA/Biopsy, gastrocentesis, gastronomy tube, abdominocentesis (PCV fluid)

Tx: Stabilise, IV analgesia, abdominal compression, Blood?, Splenorrhaphy, splenectomy (P/C)

Px: Good-Excellent if survive peri-operative

40
Q

Explain causes and types of splenic neoplasia?

A

Types:
- Cats: Lymphosarcoma, MCT, 37-73% neoplastic
- GSD, Retrievers: HSA, splenic haematoma, 33-66%

Px: 50:50 benign vs malignant, if haemorrhage 20:80 benign vs malignant → most malignant are HSA

Haemangiosarcoma
Origin: Vascular endothelium
Spread: Mx to RA, Tracheobronchial & Pulmonary LN’s – Rapid grow
Hosts: ~9-11yrs
Consequences: Non-traumatic Haemoabdomen (88%)

Grading:

  • Stage 1: Splenic Mass
  • Stage 2: Ruptured splenic mass
  • Stage 3: Metastasis (Liver)

Px:

  • Peri-operative mort 7.6%
  • Every ↓ 10K platelets ↑ death 6%
  • PCV <30 2x more likely to die
  • Intra-operative arrythmia x2
  • Surgery: 3wk-3m
  • Surgery & chemo: 5m
  • Surgery, chemo, L-MTP-PE: 9m
  • > 1yr survival – 7%
  • Non-neoplastic 1yr – 64%

Adjunct therapy: Chemo/immune/radiation therapy – used for microscopic disease Mx <11/hpf

  • Cyclophosphamide, etoposide, piroxicam, MST ↑ 6m, easy

Post-op Complications:

  • Vascular compromise (Pancreatic, portal V.)
  • GDV?
  • Infection?
  • ↓ Oxygen transport
  • DIC – 12.2% solid tumour
  • Arrythmia (V-Tach, VPC)
    Cause:
    a) myocardial ischaemia/hypoxia due to ↓ return/hypovolaemic shock via mass rupture
    b) Impaired venous flow via Compression of CVC
    RF: Anaemia, hypotension, leucocytosis, mass rupture
    Tx: Lignocaine CRI (Unstable, ECG complexes, Rapid VT/R/T) OR Sotalol PO home

Risk Factors: Platelet count, anaemia, arrythmia, spleen size (Inverse), visible lesions, cardiac mass

41
Q

Explain the Anatomy of the Oral Cavity

A

Lips & Cheeks
- Innervation: CN 7 & 5

Tongue
- Extrinsic Muscles: Styloglossus, hyoglossus, genioglossus
- Innervation: Hypoglossal n.
- Blood Supply: Lingual a., branch of the external carotid

Soft Palate
- Control: Tensor Veli Palatini (Taut), Levator Veli Palatini (Elevation)

Tonsil
- Blood Supply: Tonsillar a. branch of the lingual a.
- Connection: Mandibular and medial retropharyngeal LN.

Lymphatics
- Important LN’s: Medial retropharyngeal, mandibular, parotid
- Drainage: Superficial cervical
- Access: Single ventral incision exposes all 3 LN’s
- Exploration: CT! LN mapping, Dyes/radioactive (Tumours), Palpation (Insensitive)

42
Q

Important surgical factors and prep of the Oral Cavity?

A

Important Surgical Factors
- Good blood supply speeds up healing but may also be ass. W/ significant haemorrhage
- Bacteria present in mouth but is balanced by antibacterial saliva
- Tension on suture causes high breakdown
- Bypassing feed is important for protecting suture

CS of Oral Cavity Dz

  • Change in face/head shape
  • Drooling, dysphagia, poor breath
  • Haemorrhage from mouth
  • Oral pain, anorexia
  • Nasal discharge
  • Mass on palpation

Prep of Oral Cavity
Hard to achieve asepsis but decrease bacterial load via:

  • Anti-microbials (+ anaerobes)
  • Tx Periodontal dz 2-3d prior
  • Regular antiseptic flushing
  • ET tube is cuffed
  • +- Pharyngeal packing

Oesophagostomy Tube
Indication: Feeding whilst mouth is unavailable – Must have normal oesophageal function!
Location: Distal tip must be in distal oesophagus not stomach & can remove at any time

43
Q

Explain Neoplasia as a Disorder of the Tongue?

A

Types: Malignant melanoma, squamous cell carcinoma, fibrosarcoma, osteosarcoma

Malignancy: 64-93%
Mx: Local LN & lungs
Px: Depends on size

Tx: Glossectomy – Dogs > Cat toleration & adaption of oral structure, excellent survival rates

44
Q

Describe Palate diseases and Defects?

A

Congenital Defects
- Primary Palate AKA Hare Lip: Includes Lip & premaxilla
- Secondary Palate: Includes soft palate +- Hard palate

Surgical Principles:
- Aim for multiple layer closure
- Tension relieving incisions
- Preserve supply of major palatine a.
- Overlap flaps in large bony defects

Methods:
- Hard palate defects: Nasal mucosa & oral mucosa
- Soft palate defects: Nasal mucosa, oral mucosa & palate muscle
- Sliding Flap Technique – Hard palate:
Cut down the sides of the hard palate, Rx in middle & suture together

Risk: Major palatine a. is near incision site

  • Hinged Pouch Flap Technique – Hard Palate:
    Create a flap in the hard palate using an incision & periosteal elevator
    Rx on both sides and suture the oral & nasal mucosa together
  • Hinged Pouch Flap Technique – Soft Palate
    Indication: Cleft palate
45
Q

Describe Acquired Oronasal Fistula?

A

Cause: FB, Trauma, dental associated (Canines!)

Principles:

  • Remove barriers to healing
  • Protect repair via oesophagostomy tube!
  • Multiple layer closure
  • Tension free closure
  • Buccal mucosal flaps if required
46
Q

Explain Disorders of the Tonsils

A

Mx: 70%
MST: 2m
Incidence: 50% normal
LN’s have metastatic dz

Sx:

  • Palliation
  • Biopsy & Suture tonsillar crypt
  • Ligature
  • Tonsillectomy: No BOAS evidence
47
Q

What are the Tumours of the Oral Cavity?

A

Types (In order): MM (30-40%), SCC (20-20%), FSA, AA, OSA

Melanoma, Squamous Cell Carcinoma, Fibrosarcoma,
AA: Acanthomatous ameloblastoma , Osteosarcoma,

Analgesia: Maxillary NB. For rostral analgesia

Clinical Appearance:
- MM: Involves gingiva, small old dogs, dark pigment or amelanotic
- SCC: Involves gingiva, Older large dogs, usually flat & ulcerative
- FSA: Involves gingiva, middle-older dogs, around maxillary carnassial tooth & hard palate
- OSA: Medium-larger dogs, in maxillary or mandible
- AA: Medium-larger dogs, often rostral, looks like a SCC and often displaces teeth

48
Q

Diagnosis and Treatment for tumours of the oral cavity?

A

Dx:

  • CT & MRI: Superior
  • Thoracic Rads: Underestimates bone loss
  • LN’s: Palpation is inaccurate - 40% normal = Mx & 50% enlarged have no Mx → cytology!
  • Genetic Marker: Chromosome 30 – Poor Px
  • Ki67: Correlates w/ Mx & clinical stages
  • COX2, KIT, EGFR, SOZ, Metalloproteinases: Aggressive histological behaviour MM
  • Histological type changes Px not Sx approach

Tx:
- Surgery: 2-3cm of bone, 1cm of soft tissue, 72% success
- Viral vectors: Immunotherapy kills cancer cells
- Electrochemotherapy: Bleomycin, electroporation intralesional remission for stage 1/2
- Radiation therapy: Adjunct hypofractioned 3-6, Remission ~70%, Survival ~5-7m

49
Q

What is Salivary Gland Disease?

A

Hosts: Dogs ONLY!
Main Glands: Parotid, zygomatic, mandibular, sublingual (Molar in cats)

Minor Glands: Lingual, labial, buccal, tonsillar, palatine, molar

Functions of Saliva:

  • Lube ingesta
  • Thermoregulation
  • Oral cavity cleaning
  • Buffer weak acids
  • ↓ Oral bacteria growth
  • Protect surface epi
50
Q

What is Salivary Mucocele?

A

Cause: Leakage of saliva into surrounding tissue due to rupture of glands/ducts – ? trauma
Location: Mandibular and/or sublingual,

CS:

  • Painless swelling
  • CS ONLY if obstructs normal function
  • Gradually enlarges +- regresses
  • Tissue irritation → lined with GT
  • Aspirate saliva w/ large bore needle

Anatomical Location:
- Cervical:
CS: Soft painless swelling under ventral chin
- Sublingual AKA Ranula
CS: Soft painless fluid swelling under tongue, usually unilateral
- Pharyngeal:
CS: Only Dx once obstructing pharynx/larynx, ONLY one that causes important CS
Dx: Laryngoscope pharyngeal swelling, Aspirate saliva

Tx:
- Surgical Removal:
Removes: Both mandibular/sublingual chains on the affected side – sig. reserve
Approach: Lateral, ventral to digastricus m. or orally
Important Structures: Internal & external maxillary v., facial v., external jugular

  • Recurrence of Mucocoele: Remove contralateral glands
  • Ranula AKA Sublingual: Marsupialisation
  • Pharyngeal: Drained and mandibular + sublingual removal
  • Cervical: Opening is optional; done if large or caliculi present
51
Q

Explain the anatomy of the Oesophagus?

A

Layers: Mucosa, submucosa, muscularis, adventitia – lacks serosa

Stretch: Lateral/transverse stretch > Longitudinal

Blood Supply:
- Cervical: Cranial & Caudal thyroid arteries

  • Cranial 2/3rds: Bronchoesophageal
  • Caudal: Oesophageal branches of aorta, intercostal arteries, left gastric artery

Innervation: Close association with vagus n.

Species Difference:
- Dog: Has striated muscle throughout with distinct longitudinal mucosal folds

  • Cats: Change from striated to smooth m. & longitudinal to transverse folds at heart base

Location: Small amount in ab (Sphincter function!), moves through diaphragm, terminates at stomach cardia

52
Q

Explain the complications with the Oesophagus in Surgical?

A
  • Lack serosa: No fibrin seal or pluripotent stem cells
  • Segmental blood supply: Intramural! & collateral supply must be preserved, ligation of cervical & thoracic blood supply causes necrosis
  • Lack omentum: Cannot patch wounds
  • Constant movement (Swallow, resp): Can place G/J-tube, withhold
    food/water 24hrs-7d
  • Tension at surgical site
53
Q

Explain the Surgical Approach with the Oesophagus?

A

Surgical Approach
- Cervical Oesophagus: Ventral (On LHS)
- Thoracic Oesophagus:
a) Cranial Thorax: L/R ICS (intercostal); sternal
b) Caudal thorax: L ICS 7, 8, 9

Surgical Principles:
- Gentle tissue handling
- Min contamination
- Accurate apposition
- Careful electrocautery
- Appropriate suture materials

Suturing:
- Suture: Strength layer is the submucosa, 1-2 layer close (If 2 layers, can tie mucosal layer knots in the lumen), appositional pattern (SI)!

  • Bio-fragmentable anastomotic ring
  • Oesophageal Substitution
  • Oesophageal Patching: Omentum, muscle, pericardial graft
54
Q

What causes Oesophageal Foreign Bodies?

A

Cause: Sharp bones, dental chews (small dogs)

Hosts: Terriers <3yrs, old dogs

Locations: Thoracic inlet, heart base, caudal oesophagus

CS:

  • Regurgitation, salivation, inappetence
  • +- ulceration, oesophagitis
  • +- Pneumomediastinum, mediastinal abscess
  • +- Stricture weeks later

Tx:

  • Endoscope & specialised Grasper to remove Per os (Best option)
  • If in distal oesophagus, Push it down into stomach
  • +- Fluoroscopy
  • Thoracotomy: If above fails, worse Px

Post-Op: Inspect for perforation/ulceration & treat with
- Sucralfate, Proton pump inhibitor, H2 receptor blocker
- Analgesia
- Gastrostomy tube if severe

Complications: Oesophagitis, ischaemic necrosis, dehiscence, leakage, fistula, diverticula, strictures

Px: Worse in older dogs (longer duration & perforation), mortality ~5%, strictures ~2%, Sx good

55
Q

Explain Vascular Ring Anomaly (Oesophageal Obstruction)

A

Type:

Persistent Right Aortic Arch – Between the AA (Right), lig. arteriosum (Dorsal), PA trunk (L), heart base (Ventral)

Cause: Hereditary – recommended to neuter

Host: German Shepherds, Irish Setters, Labs, Greyhounds, Siamese, Persians

CS: Develop soon after weaning, regurgitation of food/fluid

Dx: Barium swallow

Consequence: Oesophagus filled/dilated w/ food cranial to obstruction at heart base

Tx: 4-5th ICS thoracotomy to transect ligamentum arteriosus

Px: Good if Tx early, lifelong risk of aspiration pneumonia, persistent regurgitation common, 18% die in first 2m, 1/5 fail to respond

56
Q
A