Small Animal Surgery Flashcards
What are the Halstead’s Principles?
- Haemostasis
- Approximation of tissues
- Adequate blood supply
- Strict asepsis
- Tension free close
- Tissue handled atraumatic
- Dead space reduced
What is the Anatomy of the Abdomen?
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.
What are Hernias?
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
What is the Sequelae to Hernias?
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
What are the Aims and approach to hernia repair?
- Return contents
- Close ring to prevent recurrence
- Remove redundant tissue
- 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
Describe Ventral Abdominal Hernias (Do not breed)
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
Causes of Caudal Abdominal Hernias?
- 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
- Traumatic
Tx: Require sutures at inguinal lig., ext. rectus fascia & int. oblique abdominal
What is Femoral Hernias?
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
What is a Traumatic Hernia (False Hernia)
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
What is an Incisional Hernia?
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
What is a Perineal Hernia?
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
Describe the Pelvic Diaphragm
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
Explain the aetiology and consequences of of Perineal Hernia
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)
Diagnosis and Treatment of Perineal Hernia?
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:
- Wound infection
- Faecal incontinence
- UT malfunctions
- Tenesmus
- Sciatic n. paralysis
- Recurrence
What are Diaphragmatic Hernias?
- 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)
How to diagnose and treat Diaphragmatic Hernias?
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
What is the composition of the Peritoneum?
- 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
Explain lymphatic drainage
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
Explain the formation and promotion of adhesions?
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
Describe the components and uses of the Omentum?
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
Describe Pathophysiology of Peritonitis
- 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
What are the results of peritonitis?
IRH MISS HIM
(I really have miss him)
- ↑ IAP
- ↑ Hypovolaemia - Impairs ventilation - Respiratory acidosis & hypoxaemia
- Via reflex diaphragmatic rigidity & ↑ IAP preventing ventilation - Hypoproteinaemia
- Protein fluid moves from IV to cavity - Metabolic acidosis
- Impaired oxygenation via respiratory acidosis - Intrahepatic cholestasis
- Alteration of bile flow → icterus - Severe catabolic state
- Via 25% increase in metabolic rate & massive protein loss into cavity - Septic shock
- Adrenergic stimulation → ↑ venous p. → injury to gut mucosa & translocation of flora - Hypovolaemia
- Protein fluid from IV to cavity - Fluid sequestration in bowel lumen via reflex ileus
- ↑ IAP → ↓ CO & return - Hypotension & ↓perfusion → metabolic acidosis/hypoxia - Impaired renal function
- Renal insufficiency → ↓ clearance of toxins → ARF - Myocardial depression
- Via hypoxic pancreas
What are the classifications of Peritonitis?
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
- 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
Diagnosis of Peritonitis?
- 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
Treatment for Peritonitis?
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
- Analgesia – Lignocaine CRI (Cf. opioid was sig.)
- Debridement
- ↓ Intra-ab Bacteria, FB, Adjuvants & peritoneal fibrin - Lavage
- 200-300ml/kg Warm saline or until fluid returns clear
- ↓ Bacteria, blood clots, debris, inflam cells BUT evidence conflicting/not sig. - Serosal Patching
- Reduces suture line disruption to prevent collagen & ECM degradation → dehiscence
- Provides fibrin seal, mechanical support, resistance to leakage, provides blood supply - Omentalisation
- No evidence but is recommend to wrap organ in omentum - Drainage
- Closed or open, vacuum assisted is easier to manage - 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
Explain Sepsis and SIRIS
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
What causes Multiple Organ Dysfunction (MODS)
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%
What causes Ileus?
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
What is Reflex Rigidity?
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
Describe the anatomy and function of the spleen
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
- Cranial Mesenteric:
- Jejunal
- Ileocolic → Middle colic, Right colic, Mesenteric ilial branch - Caudal Pancreaticoduodenal
- 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)
How to Diagnose and Treat Splenomegaly?
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
Causes of Inflammation or Splenitis?
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
Causes of Cellular Hyperplasia?
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)
Causes of Congestion in Spleen?
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
Causes of Cellular Infiltration?
Cellular infiltration
Causes:
- Myeloproliferative lymphosarcoma/lymphoma & mastocytosis +- Mx neoplasia
- Histiocytic sarcoma (Bernese, Rottweilers, Golden)
- Amyloidosis
Causes of Nodular Hyperplasia?
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
Other pathologies in Spleen: Segmental Infarction, Plaques, Neoplasia, Haemangiosarcoma?
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
Explain diagnosis and treatment for Splenic Torsion?
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
Explain Diagnosis and treatment for Splenic Trauma?
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
Explain causes and types of splenic neoplasia?
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
Explain the Anatomy of the Oral Cavity
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)
Important surgical factors and prep of the Oral Cavity?
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
Explain Neoplasia as a Disorder of the Tongue?
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
Describe Palate diseases and Defects?
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
Describe Acquired Oronasal Fistula?
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
Explain Disorders of the Tonsils
Mx: 70%
MST: 2m
Incidence: 50% normal
LN’s have metastatic dz
Sx:
- Palliation
- Biopsy & Suture tonsillar crypt
- Ligature
- Tonsillectomy: No BOAS evidence
What are the Tumours of the Oral Cavity?
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
Diagnosis and Treatment for tumours of the oral cavity?
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
What is Salivary Gland Disease?
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
What is Salivary Mucocele?
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
Explain the anatomy of the Oesophagus?
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
Explain the complications with the Oesophagus in Surgical?
- 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
Explain the Surgical Approach with the Oesophagus?
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
What causes Oesophageal Foreign Bodies?
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
Explain Vascular Ring Anomaly (Oesophageal Obstruction)
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
