Session 9 Flashcards

1
Q

What is peritonitis?

A

Inflammation of the serosal membrane that lines the abdominal cavity

•The peritoneal cavity is normally a sterile environment (no bacteria)

Two types:

  • Spontaneously (primary)
  • Breakdown of the peritoneal membranes leading to ‘foreign’ substances entering cavity (secondary)
  • Subsequent inflammation follows a fairly uniform pattern
  • Peritonitis can be infectious or sterile
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2
Q

What is primary peritonitis?

A

Spontaneous bacterial peritonitis (SBP)

Most commonly seen in patients with end stage liver disease (patients with cirrhosis)

SBP is an infection of ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory, or surgically correctable condition

  • Arises from ascites, and ascites is a pathological collection of fluid within the peritoneal cavity
  • In cirrhosis it is caused by a combination of portal hypertension causing increased hydrostatic pressure in the veins draining the gut; and decreased liver function resulting in less albumin production causing decreased intravascular oncotic pressure. The result is the net movement of fluid into the peritoneal cavity
  • Symptoms of abdominal pain, fever and vomiting
  • Commonly symptoms are mild
  • Diagnosed by aspirating ascitic fluid- neutrophil count >250 cells/mm³
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3
Q

What is secondary peritonitis?

A

Secondary (surgical) peritonitis is a result of an inflammatory process in the peritoneal cavity secondary to inflammation, perforation, or gangrene of an intra-abdominal or retroperitoneal structure

•If a viscera perforates then the contents will enter the peritoneal cavity

Common causes of secondary bacterial peritonitis include: • Peptic ulcer disease (perforated) • Appendicitis (perforated) • Diverticulitis (perforated) • Post surgery

Non bacterial causes: • Tubal pregnancy that bleeds (the peritoneal cavity is not enclosed in females) • Ovarian cyst • Blood is highly irritant to the peritoneal cavity

Blood can move up under diaphragm which can irritate the diphragm and cause shoulder pain (phrenic nerve supplies diaphram, C3,4,5 refers pain to shoulder)

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4
Q

How does peritonitis present and how is it treated?

A

Abdominal pain is the most common symptom - patient will often be rigid.

  • This may come on gradually or acutely
  • Diffuse abdominal pain is common in perforated viscera •Patients often lie very still as any movement makes the pain worse
  • Often have knees flexed
  • Shallow breathing
  • Treatment approaches
  • Control the infectious source
  • Surgery
  • Eliminate bacteria and toxins
  • Antibacterial therapy
  • Maintain organ system function
  • Intensive care
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5
Q

What is bowel obstruction and what are its common causes?

A

Bowel obstruction is a mechanical or functional problem that inhibits the normal movement of gut contents

  • This can affect the large and small intestine
  • All ages can be affected
  • Common causes in children include: • Intussusception • Intestinal atresia
  • Common causes in adults include: • Adhesions • Incarcerated hernias
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6
Q

What is intussusception? What causes it? How is it treated?

A

Intussusception is when one part of the gut tube telescopes into an adjacent section

  • The cause is not well known
  • Potential motility issues
  • ‘Lead point’ (a mass that precipitates the telescoping action) - Meckel’s diverticulum or Enlarged lymph node
  • The intussusception can extend quite far (even prolapse out of rectum)
  • As soon as the lymphatic and venous drainage is impaired you get oedema
  • Enough oedema can impede arterial supply (infarction) so can lead to ischaemia
  • Classically you get abdominal pain, vomiting and haematochezia
  • Treatment - Air enema or Surgery
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7
Q

How does small bowel obstruction present? What causes it?

A

Nausea and vomiting (bilious) are most common symptom (early) as it has shorter distance to travel.

  • Abdominal distension •Absolute constipation (late) so no faeces or air.
  • Caused by:
  • Intra-abdominal adhesions (abnormal fibrous bands between organs or tissues or both in the abdominal cavity that are normally separated). These arise after more than 50% of abdominal surgeries - Greater omentum involved in 80%, bowel in 50%
  • Damage to mesothelium can also cause adhesions (direct trauma, post operative infection) - Capillary bleeding leads to exudation of fibrinogen
  • Other consequences of adhesions are Abdominal pain and secondary infertility
  • Hernias can narrow lumen enough to cause obstruction - Incarcerated groin hernias most common
  • Inflammatory bowel disease -Crohn’s causing repeated episodes of inflammation/healing also causes narrowing
  • Diagnosis
  • History- abdominal pain is crampy, intermittent due to movement of small bowel (more frequent compared to biliary colic)
  • Physical examination- abdominal distension, increased/absent bowel sounds, presence of hernia
  • Imaging
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8
Q

Large bowel obstruction?

A

Typically affects older generation

  • Common causes include:
  • Colon cancer (60% of mechanical obstructions) • Diverticular disease (20%) • Volvulus- Sigmoid, Caecal (5%)
  • Symptoms often appear gradually if caused by cancer but are abrupt with volvulus
  • Change in bowel habit (cancer) • Abdominal distension • Crampy abdominal pain • Nausea/vomiting (later) due to distane from obstruction.

If you have a competent ileocaecal valve then you will get less vomiting/nausea as its more difficult for gut contents to back track however this si more ofan emegency as pressure will rise more rapidly and will eventually lead to perforation so this is a surgical emergency.

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9
Q

What is a volvulus?

A
  • Part of the colon twists around its mesentery
  • Most common in sigmoid colon (60%) and caecum (but can technically occur anywhere) as these are more mobile.
  • Results in obstruction
  • Can result from overloaded sigmoid colon (constipation) - Extra mass predisposes elongates the sigmoid (relatively smaller mesenteric attachment) - High fibre diets can also lead to sigmoid overload and twisting
  • Caecal volvulus results in small and large bowel obstruction

On x-ray will look like a coffee bean.

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10
Q

How does age factor into prevalence of small vs large bowel obstruction? How are the symptoms different between the two conditions?

A

Age: Small bowel obstruction more common in younger age group - Large bowel obstruction older age group

• Causes explain this: (often large bowel obstruction will develop over time) •Competence of the ileo-caecal valve is of great importance - If it is competent then the colon cannot decompress proximally - Closed loop obstruction- ischaemia and perforation are more likely

For small bowel obstruction abdominal pain will be colicky (every3-4 minutes) whereas it will still be colicky in large bowel obstruction but every 10-15 minutes.

In sbo vomiting will be relatively early compared to lbo which will have vomiting relatively late

In sbo constipation will be relatively late whereas in lbo it will present relatively early.

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11
Q

How does the imaging differ between small and large bowel obstruction?

A

Often CT scans will be used to determine cause of obstruction

Howver X-ray still sometimes used:

Large bowel will have haustra (partial folds) whereas small bowel will have full folds (plicae circulares)

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12
Q

What is acute mesenteric ischaemia?

A

Symptomatic reduction in blood supply to the GI tract

  • More common in females (75%) and if you have a history of peripheral vascular disease
  • Acute occlusion (70% of cases) - Arterial embolism in SMA (50%)
  • Non occlusive mesenteric ischaemia (20%) - Low cardiac output - watershed areas- areas at risk of hypoxia when blood flow is limited - e.g splenic flexure (large bowel)
  • Mesenteric venous thrombosis (5-10%) - Systemic coagulopathy, malignancy (increases resistance so more diffcult for arterial blood to get through)

Most cases are in more elderly patients with a cardiovascular risk factors

  • Can be difficult to diagnose because the symptoms can be fairly non-specific
  • Abdominal pain (if present) is disproportionate to the clinical findings
  • Classically pain comes on 30 minutes after eating (and last 4 hours) as this is when blood flow increases to bowel
  • Nausea and vomiting are often present
  • Pain can often left sided because the blood supply to the splenic flexure is most fragile
  • Investigations
  • Blood tests
  • Metabolic acidosis/increased lactate levels
  • Erect chest x-ray (to check for perforation)
  • CT angiography is used (sensitivity is >90%) –intravenous contrast

Treatment

  • Surgery- resection of ischaemic bowel
  • bypass graft
  • Thrombolysis/angioplasty if caught early
  • Mortality is high (arterial thrombosis up to 70% mortality) - Often older patients with comorbidities
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13
Q

What can cause major upper GI bleeding?

A

peptic ulceration leading to perforation causing damge to slenicartery or gastroduodenal artery - duodenal ulcers mostcommon

Oesophageal varices - portosystemic anastomoses - often as a result of portal hypertension. portal drainage normally into left gastric vein which drains into portal vein - can reverse. Systemic drainage into azygous vein which drains into SVC

Splenomegally also caused as portal vein is normmaly contributed to by splenic vein so can acktrack to spleen.

Both cause Haematemesis (vomiting blood)

To treat oesophageal varices:

Band ligation

If bleeding not controlled by banding:

  • TIPS (Transjugular intrahepatic portosystemic shunt) • An expandable metal is placed within the liver • Bridges the portal vein to an hepatic vein • Decompresses the portal vein pressure • Reduction in variceal pressure • Reduction in ascites
  • Drug treatment • Terlipressin • Reduces portal venous pressure
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14
Q

What is an abdominal aortic aneurysm?

A

Abdominal aortic aneurysm (AAA) is a permanent pathological dilation of the aorta with a diameter >1.5 times the expected anteroposterior (AP) diameter of that segment, given the patient’s sex and body size.

The most commonly adopted threshold is a diameter of 3 cm or more.

More than 90% of aneurysms originate below the renal arteries.

  • Usually due to the degeneration of the media layer of the arterial wall
  • Media- smooth muscle cells with elastin and collagen
  • AAAs form due to degradation of elastin and collagen
  • Lumen gradually starts to dilate
  • Risk factors • Male • Inherited risk • Increasing age • Smoking
  • Most AAAs are asymptomatic

Most AAAs are infrarenal (>90%)

Normally asymptomatic until acute expansion or rupture

  • Can cause symptoms by compressing other nearby structures • Stomach, bladder, vertebra • Nausea, urinary frequency and back pain
  • Usual presentation of rupture: • Abdominal pain (+/-flank and groin pain) • Back pain • Pulsatile abdominal mass • Transient hypotension • Syncope
  • Retroperitoneum can temporarily tamponade the bleed
  • Sudden cardiovascular collapse (65% of ruptured AAAs die before hospital)
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15
Q

How do we diagnose abdominal aortic aneurysm?

A
  • Physical examination - Presence of a pulsatile abdominal mass (less than 50% of cases)
  • Ultrasonography - Non invasive and in the right hands very sensitive and specific - Can also detect free peritoneal blood
  • Computed Tomography (CT) - Can detect a lot of surrounding anatomy that may be relevant - Planning for elective surgery
  • Plain x-rays - If aneurysm has calcified then can be seen on plain x-rays
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16
Q

How is an abdominal aortic aneurysm treated?

A

Non surgical

  • Smoking cessation
  • Hypertension control
  • Surveillance of AAA - Less than 5.5cm (most grew slowly enough to not need treatment) - More than 5.5 cm- refer to vascular surgeons
  • Surgery
  • Endovascular repair- relining the aorta using an endograft (an exoskeleton of metallic stents over a fabric lining)
  • Inserted through the femoral artery (seals below renal arteries and above common iliacs)

Open surgical repair:

  • Clamp aorta
  • Open the aneurysm (remove thrombus and debris)
  • Suture in a synthetic graft to replace diseased segment
17
Q

Define microbiome and define microbiota

A

Microbiome – refers to all the genome within the gut environment

Microbiota – refers to the organisms within the gut environment

18
Q

Functions of the gut microbiota

A

Function:

  • Pathogen inhibition - Heavily colonised with stable diverse microbiome so not enough space or nutrients for any other pathogenic organisms to take over
  • Immune protection - Interacts with immune system by communicating with gut associated lymphoid tissue so they will grow tolerate their existence but have an immune response to pathogens
  • Nutrient metabolism- Helps to metabolise and synthesise short chain fatty acids and synthesis of vitamins B and K
  • Drug metabolism - Not well understood
  • Gut brain axis - Not well understood , could be related to depression and parkinsons
19
Q

GI infections – approach to history taking and examination

A

Presenting complaint & history of presenting complaint:

  • Diarrhoea – onset, duration, frequency, consistency (Bristol Stool Chart 1-7 from separate hard lumps to watery, no solid pieces), mucous/blood
  • Vomiting – onset, frequency
  • Pain – site, radiation, intermittent/continuous

Past Medical History:

  • Immunodeficiency/immunocompromised state - HIV, steroids, transplant???
  • Other GI conditions - Inflammatory bowel disease, crohns, coeliac?

Travel history:

  • Where, when, how long
  • Activities
  • Food and drink
  • Animal contact
  • Travel companions & household contacts

Drug history:

  • Recent antibiotics
  • Proton pump inhibitors
  • Laxatives
  • Immunosuppressant medications

Social History:

• Occupation - e.g farmer has igher risk of salmonella and e.coli - also public health like are they going to spread their pathogen to the food then distribute it?

20
Q

GI examination – things to look out for

A

Volume status - do they need fluid resuscitation

  • Mucous membranes
  • Blood pressure
  • Pulse
  • JVP

Abdominal examination

  • Ileus - lack of movement somewhere in the intestines
  • Peritonitis
21
Q

Investigations that can be done on a stool sample

A

Stool culture - use selective antiiotics to only allow pathogen growth - history can help with which agar to use.

E. Coli 0156

Salmonella

Shigella

Campylobacter

Enzyme immunoassay - need to know what were testing for

Cryptosporidium

Giardia

Clostridioides difficile

PCR

Clostridioides

Entamoeba histolytica

Norovirus, rotavirus

Other bacterial

Microscopy - parasites - stool sample needs to be concentrated so takes a long time and must be done by specialists - only done when history points towards speciic organism.

Ova, cysts and parasites

22
Q

Causes of acute infectious diarrhoea

A

Watery diarrhoea - generally large volume and from small bowel origin - accompanied by adbominal bloating and cramping

• Norovirus, rotavirus • Clostridioides difficile • Enterotoxigenic E. coli • Giardia lamblia • Cryptosporidium parvum

Inflammatory Diarrhoea - normally from invasive bacterial infections - can be bloody - tends to be smaller volume and have associated pain

• Non-typhoidal salmonella • Campylobacter • Clostridioides difficile • Shigella • E. coli O157 • Entamoeba histolytica

23
Q

Salmonella

A
  • Broad range of infections: gastroenteritis, enteric fever, bacteraemia, endovascular infections, osteomyelitis.
  • Generally divided into:

Typhoidal salmonella (Salmonella typhi and Salmonella paratyphi) which causes enteric fever.

Non-typhoidal salmonella (Salmonella enteritidis, Salmonella virchow etc) which causes primarily gastroenteritis.

24
Q

Non-typhoidal salmonella

A
  • Incubation period : 8-72 hours
  • Transmission route: food, faeco-oral, animals
  • General features: diarrhoea, nausea, vomiting, abdominal cramps (non specific features so stool culture needed)

Gram negative bacteria

  • Usually self limiting - so rest normally sufficient unless bacteraemic.
  • Complications include bacteraemia, endovascular infections, abscesses, osteomyelitis and septic arthritis (patients with sickle cell disease are more susceptible to bone and joint infections from salmonella (normally from gram-positive so this is different and so requires different treatment))
  • Treatment: ciprofloxacin, azithromycin, ceftriaxone. Sensitivity testing warranted if bacteraemic.
25
Q

Campylobacter

A

Gram negative bacteria looks spiral shaped

  • Found in GI tract of animals especially poultry.
  • Campylobacter jejuni and Campylobacter coli most common cause of infection.
  • Incubation period: ~3 days
  • Transmission route: food, water, animal contact
  • General features: abdominal cramping, diarrhoea, may have prodrome of fever and malaise. May have transient bacteraemia before diarrhoea.
  • Usually self limiting. Immunocompromised patients, elderly or severe infections may warrant treatment.
  • Treatment: Macrolides or fluoroquinolones
  • Complications: Reactive arthritis, Guillain-Barré syndrome (GBS) (ascending paralysis, diarrhoea has ceased so serology needed to confirm campylobacter cause)
26
Q

Shigella

A

Gram negative bacteria

  • Spectrum of disease depends on infecting serogroup
  • Shigella dysenteriae 1 or Shigella flexneri can cause dysentry (bloody diarrhoea)
  • Incubation period: 1 to 7 days
  • Transmission: faeco-oral, food and water. Person-to-person transmission can occur due to low infective dose.
  • General features: fevers, frequent low volume bloody stools, tenesmus. Nausea and vomiting usually absent. • Usually self limiting in immunocompetent host.

Complications:

  • Intestinal (rare): proctitis, rectal prolapse, toxic megacolon, perforation, obstruction
  • Systemic: bacteraemia, seizures (children), reactive arthritis and Haemolytic Uraemic Syndrome

Treatment: Ciprofloxacin, azithromycin, ceftriaxone. Special considerations: immunocompromised, food handlers, healthcare and childcare workers as its so infectious.

27
Q

E. Coli O157

A
  • Shiga toxin-producing E. coli (STEC)
  • Causes painful bloody diarrhoea and haemolytic uraemic syndrome (HUS).
  • Children <10 years and elderly particularly vulnerable
  • Incubation period: 1-10 days
  • General features: painful, bloody diarrhoea. Often NO fever.
  • HUS characterised by nonimmune-mediated hemolytic anemia, thrombocytopenia, and acute kidney injury (most common cause of acute renal failure in children in west europe and USA - tiny clots block renal vasulature)
  • Worsened by antibiotics.
28
Q

Clostridiodes difficile

A

(formerly Clostridium difficile)
• Anaerobic gram negative bacilli. One of the most common nosocomial infections. Cause of antibiotic associated colitis.

  • Colonisation of GI tract through faecal oral route. This is exacerbated by antibiotic therapy which disrupts normal gut microbiota so common cause of hospital acquired infection.
  • Produces spores which are very resistant and remain in the environment for a long time.
  • Risk factors: age>65, antibiotic therapy, PPI therapy, prolonged hospitalisation • Complications: toxic megacolon, colitis, perforation

Tested for using enzyme immuno assays

• Treatment: metronidazole, oral vancomycin (stays in gut as too large to spread), fidaxomicin (good against when recurrent), faecal microbiota transplantation

29
Q

Norovirus

A
  • Winter vomiting virus
  • Causes profuse diarrhoea and vomiting
  • Incubation period: 12-48 hours
  • Transmission: faeco-oral, direct contact, aerosol
  • Self-limiting, resolves within 1-2 days. Can excrete for longer.
  • Highly infectious (infective dose 10-100 particles).
  • Causes outbreaks in hospital wards, nursing homes, nurseries, schools, cruise ships.

Might do pcr in hospital setting to decide on shutting ward.

30
Q

Rotavirus

A
  • Important cause of gastroenteritis in young children.
  • Incubation period: less than 48 hours
  • Transmission: faeco-oral. Highly infective.
  • General features: diarrhoea, vomiting and fever. Young children have more severe disease than adults.
  • Usually self limiting, treatment is supportive.
  • Complications (rare): seizures, encephalopathy, acute encephalitis
  • Oral rotavirus vaccine introduced in UK in 2013. 2 doses (8 & 12 weeks old). Cases have fallen 69% since the introduction of the vaccine.
31
Q

Cryptosporidium

A
  • Intracellular protozoan parasite.
  • Cryptosporidium parvum main species causing human infection.
  • Associated with sporadic, water associated outbreaks like in swimming pools (not killed by chlorine), can last for months outside of host. also found in cattle.
  • Usually self limiting within 10-14 days but can cause debilitating, chronic illness in immunocompromised patients.
  • Affects all age groups but most frequently in children.
  • Incubation period: 7-10 days
  • Transmission: water, food, faeco-oral, person-to-person, animals
  • Treatment: nitazoxanide. Rarely indicated in immunocompetent host.
32
Q

Giardia

A
  • Caused by Giardia duodenalis, a protozoan parasite.
  • Associated with sporadic or epidemic infection linked to water, food, childcare settings and international travel.
  • High risk groups: infants, children, immunocompromised, travellers and cystic fibrosis patients
  • Transmission: food, water, faeco-oral
  • General features: malaise, steatorrhoea, abdominal cramps and bloating. Can be asymptomatic. Can persist as chronic infection leading to malabsorption and weight loss.
  • Treatment warranted for symptomatic patients: metronidazole or nitazoxanide.
33
Q

Entamoeba histolytica

A
  • Protozoan parasite. Can cause amoebic dysentery or infection at extraintestinal sites e.g. amoebic liver disease. Majority of infection are asymptomatic.
  • Risk factors for severe disease: young age, corticosteroid therapy, pregnancy, malignancy, malnutrition and alcoholism.
  • Incubation period: 2 weeks to years (Long travel history important)
  • Transmission: food, water, faeco-oral. Highly transmissible.
  • General features: diarrhoea (can be bloody) and abdominal pain. Fulminant colitis with necrosis and perforation can occur. Can mimic inflammatory bowel disease.
  • Treatment: high dose metronidazole followed by intraluminal agent e.g. paromomycin
34
Q

Infection prevention and control

A
  • Contact Precautions—used for infections or diseases that are spread by touching the patient or items in the patient environment.
  • Involves patient isolation and use of personal protective equipment (PPE).
  • Hand hygiene with soap and water essential in diarrhoeal illness. (alcohol doesnt kill spores of c.diff)
  • Terminal cleaning of patient environment after discharge with chlorine based disinfectant
35
Q

How is the periotoneum divided into infra and supra colic compartments

A

above the transverse mesocolon is supra colic and everything below is infra colic

36
Q

Describe the development of the gut microbiome in a neonate

A

Infant gut doesn’t have much diversity but after baby is born, depending on mode of delivery, vaginal flora for vaginal delivery or skin flora for surgical delivery will be the first exposure the baby has. Breast milk will then contribute the human milk microbiome (formula milk has slightly different additions) and then as the baby starts to have more solid foods and then go onto more traditional diets they will add more to their gut flora. By age of three, gut microbiome resembles that of an adult.

37
Q
A