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Surgery > Abdomen > Flashcards

Abdomen Flashcards

1
Q

What is localised peritonitis

A

Localised inflammation and irritation of parietal peritoneum occurs with all inflammatory GIT conditions e.g., cholecystitis/appendicitis manifesting as pain and tenderness

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2
Q

Why does generalised peritonitis occur

A

Serious condition due to
- Irritation of peritoneum from infection e.g., perforated appendix: manifests over time: underlying condition Sx progress to severe acute abdominal pain
- Chemical irritation of peritoneum from leaking intestinal contents e.g., perforated ulcer: often superimposed infection occurs (e. coli, bacteroides)

Manifests suddenly with acute severe abdominal pain, generalised collapse and shock

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3
Q

Sequelae of generalised peritonitis

A

Manifests suddenly with acute severe abdominal pain, generalised collapse and shock

Leads to generalised inflammation throughout peritoneal cavity and spread of inflammatory exudate through peritoneum –> intestinal dilation and paralytic ileus

Complications include septicaemia and toxaemia and death

Continuing pain/swinging fever/elevated WCC after Tx suggests subphrenic/paracolic/pelvic abscess –> Ix and guide drainage with USS or CT

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4
Q

What is the cause of spontaneous bacterial peritonitis

A

MCC = haematogenous spread of infection to peritoneum in liver cirrhosis patient with ascites

Organisms: E. coli, klebsiella, enterococci

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5
Q

How does spontaneous bacterial peritonitis present

A

Consider in all patients with ascites who deteriorate (pain and pyrexia may not be present)

Fever, renal dysfunction, septic shock, encephalopathy, without obvious cause

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6
Q

Investigation of secondary peritonitis

A

FBC, UEC, CRP, lipase +/- blood cultures +/ LFTs (e.g., cholecystitis) +/- B-HCG

Erect CXR to assess for free air under diaphragm

USS or CT

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7
Q

Investigation of SBP

A

Ascitic tap/aspiration for MC&S and cell counts (neutrophils v. v. important  elevated = start Tx)

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8
Q

Mx of secondary peritonitis

A
  1. Resuscitation
    a. NGT for bowel decompression
    b. Venous access
    i. IV fluid administration
    ii. IV broad spectrum antibiotics = gentamicin + metronidazole 500mg BD + amoxicillin/ampicillin 2g QID
    * Can change gentamicin to tazocin after 72 hours if cultyre not back
    * PO step down = amoxicillin + clavulanic acid (875mg + 125mg) BD
  2. Surgical Tx
    a. Peritoneal lavage of abdominal cavity
    b. Treatment of underlying condition
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9
Q

Mx of SBP

A

IV broad-spectrum antibiotics = IV 2g ceftriaxone daily
IV infusion of 20% albumin

Prophylaxis given high recurrence rate
- Criteria = ascites, low protein concentration in ascitic fluid, cirrhosis and either liver failure or impaired renal Fx
- Trimethoprim + sulfamethoxazole 160mg + 800mg daily PO

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10
Q

What is acute appendicitis

A

Acute inflammation of vermiform appendix

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11
Q

What is the aetiology of acute appendicitis

A
  • Obstruction of appendiceal lumen by faecolith, normal faecal matter, lymphoid hyperplasia, tumour (esp. carcinoid), infective organism e.g., parasite
  • Generalised appendiceal wall inflammation (idiopathic)
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12
Q

What is the pathophysiology of acute appendicitis

A
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13
Q

What is the epidemiology of acute appendicitis

A

MC in children and adolescents
- Peak 10 – 30

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14
Q

What are the clinical features of appendicitis

A
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15
Q

DDx for appendicitis

A
  • Mesenteric adenitis (children, after URTI, generalised lymphadenopathy, lymphocytosis)
  • Gastroenteritis (pain often before V&D)
  • Terminal ileitis secondary to CD or yersinia infection
  • Meckel’s diverticulitis
  • Leaking PU down R. paracolic gutter (CXR and AXR for free air)
  • Gynaecological: Ruptured cyst, ovarian torsion, ectopic pregnancy, PID
  • Nephrolithiasis
  • UTI
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16
Q

Complications of appendicitis

A
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17
Q

Ix of appendicitis

A
  • FBC (leucocytosis with predominant neutrophilia)
  • UECs
  • CRP (elevated)
  • UA
  • B-HCG in women of childbearing age
  • +/- G&H in preparation for surgery
  • USS in children/pregnant women
  • USS or CT if Dx not clear clinically  thickened, enhanced appendiceal wall, obstruction/appendicolith etc., surrounding inflammatory changes e.g., fat stranding
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18
Q

Mx of appendicitis

A
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19
Q

What kinds of gastric resections are there

A

Total or subtotal gastrectomy
Billroth I and II = gastroduodenostomy
Roux-en-Y = oesophago- or gastrojejunostomy

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20
Q

Complications of gastric surgery

A
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21
Q

What kinds of bariatric surgery are there

A

Gastric Banding
Gastric Sleeve
Roux-en-Y Gastric Bypass
Biliopancreatic Diversion +/- Duodenal Switch

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22
Q

Describe the gastric banding procedure including outcomes and complications

A

Adjustable band around upper portion of stomach leaving small pouch below cardia  reduces intake

Outcome: 45-50% of excess weight loss with high quality intensive follow up and continual band adjustments

Complications: band can erode into stomach, band failure due to band slippage, stomach prolapse through band, or consumption of high calorie liquids

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23
Q

Describe the gastric sleeve procedure including outcomes and complications

A

Large part of greater curvature removed leaving a narrow tube-shaped remainder  reduces intake and removes most of Grehlin-secreting area of stomach to reduce appetite

Outcome: 60% excess weight loss and no malabsorption

Complications: long staple line can leak despite reinforcement with glue, sleeve can expand over time

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24
Q

Describe the Roux-en-Y Gastric Bypass including outcomes and complications

A
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25
Q

Describe the Biliopancreatic Diversion +/- Duodenal Switch including outcomes and complications

A

Outcome: 75-85% weight loss and rapid T2DM cure independent of weight loss

Complications:
- severe malabsorption and deficiency syndromes
- internal herniation risk
- leakage at staple line

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26
Q

General risks of bariatric surgery

A
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27
Q

Causes of RIF mass

A
  1. Appendiceal abscess
  2. Cecal tumour
  3. CD
  4. Ovarian tumour/cyst
  5. Pelvic kidney/transplanted pelvic kidney
  6. Carcinoid tumour
  7. Iliac lymphadenopathy
  8. Amoebiasis
  9. Ileocecal TB
  10. Psoas abscess
28
Q

Causes of LIF mass

A
  1. Faeces (can be indented)  loaded sigmoid
  2. Sigmoid or descending colon cancer
  3. Diverticular disease
  4. CD
  5. Transplanted pelvic kidney
  6. Psoas abscess
  7. Iliac lymphadenopathy
  8. Ovarian tumour/cyst
29
Q

Ix of iliac fossa mass

A
  • FBC, UEC, CRP, B-HCG, blood cultures (+/- AFBs), ANCA/ASCA, plasma 5HIAA, chromogranin A, serotonin etc.
  • 5HIAA in 24 hour urine, bHCG
  • Faecal MC&S +/- microscopy for cysts/trophozoites, faecal calprotectin
  • Abdo or pelvic USS/CT/PET or scintigraphy
  • Colonoscopy + biopsy
30
Q

What causes gastric outlet obstruction

A

In adults GOO is MCC from malignancy: mostly pancreatic cancer that invades into duodenum and causes a blockage
(previously MC was ulceration)

Children MCC is pyloric stenosis due to hypertrophy of pyloric muscle

31
Q

How does GOO present

A

Over course of day become fuller and fuller –> evening or next day vomit undigested food –> feel instantly better

Ex: classically have succussion splash (shake pt from side to side to produce sloshing noise in epigastrium)

32
Q

How does PUD cause RIF pain

A

Sometimes when an ulcer perforates the fluid that is released is acid rich and it tracks immediately down the right paracolic gutter –> relatively sudden onset of pain that tracks down to the RIF (Valentino syndrome)

33
Q

What is a hiatal hernia

A

Protrusion of intra-abdominal contents through lax/widened oesophageal hiatus of diaphragm into thoracic cavity.

34
Q

What are the types of hiatal hernia

A

Type I/Sliding: distal oesophagus and GEJ slide upwards through oesophageal hiatus into posterior mediastinum (present in 30% > 50yo)

Type II/Rolling/Para-Oesophageal: gastric fundus prolapses through oesophageal hiatus into thoracic cavity alongside oesophagus while GEJ remains in anatomical position below diaphragm

Type III/Mixed: both GEJ and gastric fundus prolapse through oesophageal hiatus into thorax

Type IV/Complex: any type of hiatus hernia along with herniation of intraabdominal contents other than the stomach e.g., spleen, colon, small intestine, omentum

35
Q

Risk factors for hiatal hernia

A
  • Increasing age: weakening of phreno-oesophageal ligament
  • Obesity: increased intra-abdominal pressure pushes stomach against hiatus + deposition of fat in and around crura and hiatal widening
  • Smoking: loss of elastin fibres in diaphragmatic crura
  • Collagen metabolism disorder
  • M > F
  • Previous gastro-oesophageal procedure or structural abnormalities of oesophageal hiatus/phreno-oesophageal ligaments
36
Q

Clinical features of type I hiatal hernia

A

Loss of anti-reflux mechanism and impaired clearance into stomach –> increased GOR –> retrosternal discomfort (worse when supine/bending/stooping), chronic cough, hoarseness, regurgitation, dysphagia, wheeze/aspiration etc.

37
Q

Clinical features of type II hiatal hernia

A
  • Substernal chest pain: can be mistaken for angina pectoris
  • Early satiety
  • Retching
  • Ulcer Sx and haematemesis
  • UGI haemorrhage and haematemesis
  • Obstruction –> pain and non-bilious vomiting
  • Ischemia –> necrosis –> mediastinitis and death (retrosternal chest pain radiating to back, tachycardia, fever, subcutaneous emphysema, SVC syndrome)
    ** Bowel sounds in thoracic cavity!
38
Q

DDx of hiatal hernia

A
  • GORD
  • Angina pectoris
  • Pheumonia
  • Gastric outlet obstruction
  • Gastric atonia
  • Oesophageal motility disorder
39
Q

Ix for hiatal hernia

A
  1. CXR –> retrocardiac air fluid level
  2. Gastroscopy = main diagnostic test +/- Ix of GORD complications
  3. +/- UGI contrast study/barium swallow
  4. +/- manometry/pH monitoring
40
Q

Mx of hiatal hernia

A
41
Q

Complications of hiatal hernia

A
  • UGI
  • Obstruction
  • Ischaemia and necrosis
  • Mediastinitis
  • Dysphagia
  • Reflux oesophagitis
  • Stricture formation
  • Barrett’s oesophagus
  • Oesophageal cancer
42
Q

Complications of hiatal hernia surgery

A
  • Post-op haemorrhage
  • Mesh infection
  • Biologic mesh –> recurrence
  • Permanent mesh –> erosions
  • Fundal necrosis (ligation of short gastric vessels and L. gastric artery)
  • Transient dysphagia
  • Diarrhoea (vagal damage)
  • Transient bloating
43
Q

What is a hernia

A

Protrusion of a structure through an abnormal opening/weak point in the wall of it’s containing cavity

Viscera herniate through abdominal wall into hernial sac lined by peritoneum

44
Q

What is the pathophysiology of hernia formation

A
45
Q

What are the types of abdominal wall hernias

A

Ventral Hernia: epigastric, umbilical, Spigelian, parastomal, ventral incisional
Groin Hernia: inguinal, femoral
Pelvic Hernia: sciatic, obturator, perineal
Flank Hernia: superior and inferior lumbar triangle

Richter hernia: incarceration of only part (anti-mesenteric portion) of bowel wall in abdominal wall defect –> ischaemia without obstruction (MC in femoral hernias)

46
Q

What kind of inguinal hernia is most common

A

Indirect

47
Q

Describe an indirect inguinal hernia

A

Patent processus vaginalis (hernial sac) allows herniation of viscera through deep inguinal ring through inguinal canal (with spermatic cord/round ligament) and superficial inguinal ring (lateral to inferior epigastric vessels).

Manifest early or in adulthood with progressive dilatation of deep ring and distension of hernial sac with intra-abdominal contents

48
Q

Describe a direct inguinal hernia

A

Arise medial to deep inguinal ring  advancing age and increased abdominal pressure contribute to attenuation of abdominal wall and herniation through defect in Hesselbach triangle medial to inferior epigastric vessels.

49
Q

What is a pantaloon hernia

A

indirect and direct inguinal hernia concomitantly (often with lipoma of spermatic cord)

50
Q

What is a femoral hernia

A

Arise from femoral ring bounded by:
- Anterior = inguinal ligament
- Posterior = pectineus muscle
- Medial = lacunar ligament
- Lateral = femoral vein

51
Q

What is a reducible hernia

A

Hernial contents can be returned to cavity via opening through which herniation occurred either with gentle pressure or with relaxation (e.g., when supine)

52
Q

What is an incarcerated hernia and it’s sequelae

A

Hernial contents becomes entrapped by neck of hernial sac and cannot be reduced –> restricted venous outflow –> oedema and obstruction of arterial inflow –> Strangulated hernia = hernia with compromised blood supply (–> obstruction, necrosis, perforation, peritonitis)

53
Q

What are the risk factors for hernias

A
  • Chronically raised intraabdominal pressure (constipation, obesity, abdominal mass, pregnancy)
  • CT disease/collagen vascular disease
  • COPD/smoking/chronic cough
  • Heavy lifting
  • FHx
  • Low BMI
  • Male
  • 1st year of life
54
Q

How do hernias present

A
55
Q

How are hernias Mx

A
56
Q

What are considerations and CIs in hernia Mx

A
  • Previous hernia repair may influence surgeon’s approach
  • Lower abdominal surgery e.g., open appendicectomy may be a relative contra-indication for laparoscopic repair (adhesions)
  • Strangulation is absolute contraindication for laparoscopic repair
57
Q

What are complications of hernia Mx

A
  • Wound seroma or haematoma
  • Wound infection
  • Testicular ischaemia/atrophy (.7%)
  • Rare: vascular or visceral injury
  • Hypoaesthesia or painful neuroma (cutaneous nerves injured/divided) –> chronic pain affects 2-4%
  • Main late complication = recurrence (15%)
  • Emergency + elderly + comorbidities = greater overall complications: bowel resection from strangulation
58
Q

Causes of intestinal obstruction

A
59
Q

Pathophysiology of bowel obstruction

A

Bowel obstruction →stasis of luminal contents and gasproximal to obstruction → ↑ intraluminal pressure, which leads to the following:

  • Gaseous abdominal distention → sequestration of fluids within distended bowel loops (third spacing) →dehydration and hypovolaemia
  • Vomiting→ loss of fluid and Na+, K+, H+, and Cl-→ hypokalaemia, metabolic alkalosis, hypovolaemia
  • Compression of intestinal veins and lymphatics → bowel wall oedema → compression of intestinal arterioles and capillaries → bowel ischaemia →
    • ↑ bowel wall permeability → translocation of intestinal microbes to peritoneal cavity → sepsis
    • Necrosis and perforation of bowel wall →peritonitis
    • Anaerobic metabolism and lysis of ischaemiccells → accumulation of lactic acid and release of intracellular K+→ metabolic acidosis and hyperkalaemia
  • Proximal lumen distension → gas and fluid level and muscular hypertrophy
  • Proximal gut obstruction → vomiting
  • Distal gut obstruction → constipation
  • Distal lumen collapse
  • Systemic effects → dehydration, infection
60
Q

Bowel obstruction Ix

A

FBC, UEC, CRP, lipase, amylase, glucose
Consider coags and group and hold
ABG and arterial lactate

XR supine and erect
+ with water soluble contrast study (gastrogaffin enema or oral preparation) –> helps to predict need for surgery and may help to demonstrate site of obstruction

CT abdomen and pelvis can localise the lesion accurately

61
Q

Clinical features of intestinal obstruction

A

Abdominal colic
Vomiting (profuse in upper gut, maybe be absent in lower gut obstruction)
Obstipation (constipation and no passage of flatus

Distension
Increased high pitched bowel sounds
Marked tenderness suggests strangulation –> urgent surgery

Check hernial orifices and rectum

62
Q

What is seen on XR with intestinal obstruction

A

SBO:
- Distended loops of bowel proximal to obstruction
- Fluid levels on erect film

LBO:
- caecum and ascending colon are distended

63
Q

Mx of intestinal obstruction

A

Resuscitation with IV fluids (.9% normal saline with potassium)

NG decompression

Increasing temp, HR, pain, WCC –> urgent CT and possible laparotomy
- removal of obstruction
- gangrenous: resection
- decompression with metal stents in malignancy
- defunctioning colostomy in critically ill pts
- unkinking and deflation of sigmoid volvulus with flexible sigmoidoscopy (recurrent = sigmoid resection)

64
Q

Groin lump DDx

A
65
Q
A

Surgery (17 decks)

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