Gastrointestinal Emergencies Flashcards

1
Q

What is peritonitis and how can it occur?

A

Inflammation of serosal membrane (makes up the visceral and parietal peritoneum) that lines the abdominal cavity

can occur spontaneously - primary

or breakdown of the peritoneal membranes -> foreign substances entering cavity - secondary

Subsequent inflammation uniform pattern

Infectious or sterile

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2
Q

Describe the structure of the serous membrane

A

Lined the abdominal cavity

Visceral peritoneum any part of the serous membrane not lining the abdominal wall

Parietal pleura any part that lines the wall

Cavity contains only small amount of fluid

Cavity divided into greater and lesser sac connected by the foramen of Winslow

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3
Q

What is primary peritonitis? Cause, symptoms, diagnosis

A

Spontaneous bacterial peritonitis - infection of ascitic fluid that can’t be attributed to any intra-abdominal ongoing inflammatory or surgically correctable condition

Ascites- pathological collection of fluid within the peritoneal cavity
can be caused by cirrhosis (portal hypertension + decreased liver function less albumin -> fluid move SI to cavity)

❌abdominal pain, fever, vomiting usually mild

Aspirate ascitic fluid - neutrophil count >250cells/ mm3

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4
Q

What is secondary peritonitis? Causes

A

Surgical peritonitis - result of an inflammatory process in peritoneal cavity secondary to inflammation, perforation or gangrene of infra-abdo or retroperitoneal structure

Common causes: peptic ulcer disease, appendicitis, diverticulitis (can all lead to perforation), post surgery

Non-bacterial causes: tubal pregnancy that bleeds (cavity not enclosed in females), ovarian cyst - bloody highly irritant

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5
Q

Clinical presentation and treatment of peritonitis

A

Presentation: abdominal pain most common -gradual or acute (diffuse suggests perforated viscera)

Lie v still, knees flexed, shallow breathing

✅ control infectious source surgery, eliminate bacteria and toxins antibiotics, maintain organ system function intensive care

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6
Q

What is bowel obstruction?

A

Mechanical or functional problem that inhibit is normal movement of gut contents - can affect large or small intestine, all ages

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7
Q

Common causes of bowel obstruction in children, symptoms, treatment

A

(Intestinal atresia and)

Intussusception - one part of the gut telescopes into adjacent section (cause not well known, lead point is mass that preciouses the telescoping action, e.g. meckel’s diverticulum (leftover umbilical cord) or enlarged LN

Can extend far may prolapse out of rectum

If lymphatic drainage impaired -> oedema -> can impede arteries -> infarction

Abdo pain, vomiting and haematochezia

✅air enema, surgery

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8
Q

Common causes of bowel obstruction adults

A

Adhesions

Incarcerated hernias

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9
Q

Causes of small bowel obstruction, symptoms, diagnosis

A

Intra- abdo adhesions (fibrous bands) occur post >50% abdo surgeries , greater omentum involved 80% and bowel 50% (-> ❌abdominal pain, secondary infertility)

Damage to mesothelium (direct trauma, post operative infection) -> capillary bleeding -> exudation of fibrinogen

Hernias can narrow lumen enough (incarcerated groin hernias most common)

Inflammatory bowel disease crohn’s, repeated episodes inflammation and healing

❌nausea and vomiting (bilious) most common early, absolute constipation late, abdominal distension

History- abdo pain cramps, intermittent. Examination - abdo distension, increased/ absent bowel sounds, hernia. imaging

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10
Q

Causes of large bowel obstruction, symptoms

A

Typically older generation

Colon cancer (60% of mechanical obstruction), diverticula disease 20%, volvulus - sigmoid/ caecal 5% (Part colon twists around. Mesentery can be from overloaded sigmoid constipation)

❌gradually if cancer or abrupt if volvulus - change in bowel habit (cancer), abdo distension, crampy abdo pain, nausea/ vomiting (later)

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11
Q

Compare small and large bowel obstructions

A

Small - younger population,
abdo pain colicky 3-4mins (colicky but 10-15mins LB),
Vomiting relatively early (late Lb),
Constipation relatively late (early lb)

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12
Q

What is acute mesenteric ischaemia? Who is affected? Causes

A

Symptomatic reduction in blood supply to the Gi tract

More common females (75%) + history of peripheral vascular disease, elderly, CVS risk factors

Acute occlusion (70%), arterial embolism in SMA (50%).
Non-occlusive mesenteric ischaemia (20%)- low CO.
Mesenteric venous thrombosis (5-10%)- systemic coagulopathy, malignancy.

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13
Q

Symptoms, investigations, treatment for acute mesenteric ischaemia

A

Difficult to diagnose - symptoms fairly non-specific: abdo pain if present disproportional to clinical findings (classically 30mins after eating for 4hrs, left sided splenic flexure blood supply most fragile), nausea, vomiting

Investigations: blood tests (metabolic acidosis/ increased lactate), erect chest X-Ray (perforation), CT angiography with IV contrast sensitivity >90%

✅surgery- resection of ischaemia bowel (bypass graft), thrombolysis/ angioplasty
Mortality high (arterial thrombosis 70%), often older with co-morbities
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14
Q

How can peptic ulceration causes major upper Gi bleeding?

A

20-50% acute upper Gi bleeding

Disruption in gastric/ duodenal mucosa usually >5mm diameter going through to submucosa (through muscularis mucosa)

Duodenal ulcers most common - first part, gastro-duodenal artery behind first part

Gastric ulcers- lesser curve and antrum common sites - May erode into splenic artery

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15
Q

what are oesophageal varices? How can oesophageal varices lead to major upper Gi bleeding?

A

Porto-systemic anastomosis (venous drainage through portal and systemic veins) portal drainage - oesophageal veins -> L gastric -> portal. Systemic - oesophageal -> azygous -> SVC

12-14% acute upper Gi bleeding

Portal hypertension >10mmHg caused: pre-hepatic (portal vein thrombosis), hepatic (cirrhosis/ schistosomiasis), post hepatic (hepatic vein thrombosis, RHF)

Spontaneously rupture

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16
Q

Treatment of oesophageal varices

A

endoscopic Band ligation - tiny elastic bands tie varices off at ends first line

  • TIPS (transjugular intrahepatic portosystemic shunt) - expandable metal placed within liver, bridges portal v to an hepatic vein -> decompresses portal vein pressure ->reduction in variceal pressure and ascites
  • terlipressin (reduces portal venous pressure)
17
Q

What is an abdominal aortic aneurysm? Cause, risk factors

A

Permanent pathological distension of the aorta with a diameter >1.5 times expected anteroposterior diameter of that segment for sex and body size (normally _>3cm) >90% originate below renal arteries

Usually: degeneration of medial layer of arterial wall (smooth muscle cells, elastin, collagen)

Risk factors: Male, inherited, older, smoking

18
Q

Symptoms of abdominal aortic aneurysm (unruptured and ruptured)

A

Normally asymptomatic until acute expansion or rupture - but can get pulsating feeling/ madd stomach, compress other nearby structures (stomach, bladder, vertebra) e.g. nausea, urinary frequency, back pain

Ruptured: abdo pain (+/- flank/ groin), back pain, pulsation abdo mass, transient hypotension (syncope), retroperitoneum can temporarily tamponade the bleed, sudden CVS collapse (65% die before hospital)

19
Q

Abdominal aortic aneurysm diagnosis and treatment

A

Physical examination - pulsatile abdo mass (<50%)
Ultrasonography - non invasive, v sensitive and specific, also detects free peritoneal blood
Computed tomography - detect surrounding anatomy, planning for elective surgery
Plain X-rays - if aneurysm calcified

Treatment:
Non surgical
- smoking cessation
- surveillance (<5.5cm May never need treatment) >5.5 refers to vascular surgeons

Surgery

  • endovascular repair relining aorta using endograft (exoskeleton metallic detects over fabric lining) inserted through femoral artery
  • open surgical repair (clamp aorta, open aneurysm, remove thrombus and debris, suture in synthetic graft to replace diseased segment)