GIT Flashcards

1
Q

Discuss formation of cholesterol stones

A

Usually occur as a consequence of an elevated concentration of cholesterol in bile relative to the other principle constituents. Bile acids and lecithin act in conert to solubilze cholesterol as cholesterol levels rise bile acids and lecithin reduced increasing the tendenecy of cholesterol to form crystals. - These crystals particulary in a non complete emptying gallbladder serve as a nidus for stone formation.

Risk factors for cholesterol stone formation include

  • increased age
  • female gender
  • massive obesity
  • rapid weight loss
  • CF
  • parity
  • Drugs
  • Family history
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2
Q

Discuss the fomration of pigment stones

A

Two varients black and brown. Black stones occur exlcusively in the gallbladder contain a large amount of calcium bilirubinate. Seen in older adults and those with haemolytic disease

Brown stones are associated with infection and can form in the fallbladder and intra and extrahepatic duct systems. Bacteria are usually the cause but parasites ( ascaris lubricoides, clonorchis sinensis)

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3
Q

Discuss the clinical finding in bilary colic

A

Patient usually report steady pain rather than colic. Is associated with passage of stone through the cystic duct into the common bile duct.

RUQ pain cramping associated with nausea and vomting which can be severe and lead to electrolyte imbalances.
Usually have had self limited episdoes in the past and can be associated with oral intake

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4
Q

Discuss investigations for choliethiasis

A

Raised ALP, alk phos, bilirubin, ALT and AST can be raised due to hepatitis

Ultrasound diagnositic test of choice can be performed bedside

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5
Q

Discuss management of bilary colic and complications it can give rise

A

Supportive care with correction of fluid balance and electrolyte
Pain relief - antispasmodics, NSAIDS and opiates if needed.

Defomotove treatment is cholecystectomy

Complications

  • dehydration
  • electrolyte imbalance
  • malloryweis tear
  • infection

Bilary colic is uncommon in children and usually associated with an underlying haemolytic disease (sickle cell, spherocytosis)

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6
Q

Discuss disposition bliary colic

A

Patient with uncontrolled pain, vomiting, severe dehydration or electrolyte imbalance should be admitted for monitoring and supportive care

Otherwise if symptoms can be controlled discharge home with surgical OPD

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7
Q

Define cholecystitis

A

Sudden inflammation of the gallbladder. Risk factors are generally those for cholethiasis

Obstruction fo the cystic duct appears to be the critical factor in the development of gallbladder inflammation. Stones are identified in approxmiatly 95% of patients and may be located in the CBD in many cases of äcalculous cholecystitis

The ensuring inflammatory response may eb related to mucosal ischaemia from increased hydrostatic pressure or to the action of cytotoxi procts of bile metabolism

Bacteria is isolated from the gallbladder in most cases of cholecystitis however the role of infection is not completly understood

Choleforms are the most common isolates (e.coli, klebsiella, citrobacter) - anaerobes have been identified in as many as 40% of cases

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8
Q

Discuss causes of cystic duct obstruction not related to choleliathisis

A
  • Tumor
  • firbosis
  • parasites
  • lymphadenopathy
  • kinking of the duct
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9
Q

Discuss clinical finding in Cholecystitis

A

Similar to bilary colic –
severe right upper qaudrant pain to palpation murpheys +ve

Fever and tachycardia are oftn absent in cholecystitis

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10
Q

Discuss DDX cholecyctitis

A
Bilary cholic 
cholangitis 
hepatits 
right lower lobe pathology 
pancreatitis
PUD
appendicitis
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11
Q

Discuss ultrasound finding of cholecystitis

A

Most commonly impacted stone seen
Gall bladder wall >3mm
pericholecysitic fluid

PPV of >90% with the above findings

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12
Q

Discuss CT in cholecytistis

A

Not modality of choice as ultrasound less complicatiosn and readily available with high spec and sens

It is particularly valuable in ephysematous or haemorrhagic cholecystitis

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13
Q

Discuss management of cholecystitis

A

Supportive care as per bilary cholic

Antibiotics – Triples

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14
Q

Discuss acalculos cholecystitis

A

More common inelderly patient and patients who are recovering from non bilary tract surgery.

Commonly seen in advanced immunodefiency syndrome usually secondary to CMV or cryptosporidium

Has a more acute and malignant course than calculus cholecystitis

In patients with acalculous cholecystitis, endothelial injury, gallbladder ischemia, and stasis, lead to concentration of bile salts, gallbladder distension, and eventually necrosis of the gallbladder tissue

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15
Q

Discuss Epmhysematous cholecystits

A

This is an uncommon variant characterized by the presence of gas in the gall bladder wall presumable due to invasion of gas forming organisms (e.coli, klebsiella, C perfringens)

More common in diabeteics has a male preponderance and is acalculis in 50
% of cases. Due to high rates of gangrene and perf surgery is indicated immediatly

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16
Q

Discuss disposition of cholecysitis

A

Admission for supportive care and ABs
Surgery is indicated in most cases – timing usually occurs when symptoms are resolving and the patient is still in hospital.

Immediate surgery is reserved for those in shock or preforation/gangrene

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17
Q

Discuss cholangitis

A

Acute cholangitis is a clinical syndrome characterized by fever, jaundice, and abdominal pain that develops as a result of stasis and infection in the biliary tract.

The key factors contributing to cholangitis are a obsturction, elevated intraluminal pressure and bacterial infection INcomplete obstuction occurs more commonly than a complete obsturction

Bacteria may gain acccess to the obstructed CBD in a retrograde manne from the duodenum or by way of the lyphatics or from the portal vein

Organisms are similar to those of other biliary tract disease - e.coli, klebsiella, enterococcus and bacteroids

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18
Q

Discuss clinical features of cholangitis

A

Most patient experience fevers, chills nausea and vomiting and abdominal pain

The class finding described by Charcto consists of RUQ pain, fever and jaundice . These finding are not only compatable with chalngitis but with hepatitis and cholecystitis

Sepsis is common with chalangitis evidenced by hypotension, tachycardia, tachypnoea and frank hypotension,

The presence of Charcot triad with clinical signs of sepsis, hypotnesiona and altered sensorium is reffered to as Reynolds Pentad.

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19
Q

DDX of cholangitis

A

Although patient with cholangitis generally have a higher fever than those with cholecysitis there is considerable overlap between the two condition

The presence of jaundice however is common in chlangitis and uncommon in cholecysitis

Ultrasound evidence of dialted common and intrahepatic ducts usually is required to differentiate the two.

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20
Q

Discuss diagnosis of cholangitis

A

Bloods – left shift leukocytosis, hyperbilirbuinaemia, elevated alkaline phosphatase and moderately increased aminotransferase levels. ABG to identify base excess as an early sign of abcess

US as above can show stones, intrahepatic or CBD dilatation

CT percutaneous transhepatic cholangiography and ERCP (endoscopic retrograde cholangiopancreatography) – THese offer the benefit of being able to offer therapeutics including sampling and culture of the bile, removal of impacted stones and decompression of the bilary tree.

TOKYO GUIDELINES can be used as a guide for the diagnosis of acute cholangitis : Guidlines include

  • Part A(systemic inflammation) - fever and or chilld, + labs CRP and WBC
  • Part B (cholestasis) Jaundice and abnormal liver enzymes
  • Parct C (imaging) bilary dilation or evidence of the eitology
  • Grading -system dysfucntion
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21
Q

Discuss management and disposition of cholangitis

A

Resus – with fluid and vasopressors as needed (ABC)
Broad spectrum coverage
Prompt decompression of the bilary tree is key for success

Disposition
Hospitalization

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22
Q

Discussing primary sclerosing cholangitis

A

idiopathic inflammatory disorder affecting the bilary tree characterised by diffus fibrosis and narrowing of the intrahepatic and extrahepatic bile duccts.

Commonly associated with IBD and particularly ulcerative collitits - is an isolated condition only 25% of the time

Patient report weight loss, lethargy, jaundice and pruritus

ERCP is often needed for diagnosis

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23
Q

Discuss AIDS cholangiopathy

A

Manifestation of sever HIV with CD4 counts under 200. AIDS cholangiopathy include bile duct stricutre, papillary stenosis and sclerosing cholangitis

Primary pathology is not well understood but infection with CMV, cryptosporidum, microsporidia or mycobacterium avium are related

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24
Q

Describe pancreatitis

A

Pancreatitis is an inflammatory condition that occurs with enzymatic autodigestation and inflammatory cascade that results in desctruction of pancreatic tissue.

It can range from a mild selflimiting disease to sepsis, to MOF

Overall mortality is 4-10% although in severe cases can be as high as 30%

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25
Q

Discuss causes of pancreatitis and list the three most common

A

Three most common

1) Gall stones (40-70%) - more common in females
2) ETOH 25-35% ( more common in men)
3) ERCP

Toxic-metabolic

  • ALcohol
  • drugs
  • hyperlipidaemia
  • hypercalcaemia
  • Uremia
  • Scorpian venom

Mechanical or obstuctive

  • Bilary stones
  • Congenital - pancreas divisum, annula pancreas
  • Tumors- umpullary, neuroendorcrine, pancreatic carcinoma
  • Post ERCP
  • Ampullary dysfunction or stenosis
  • Duodenal diverticulum
  • Trauma

Infection

  • Viral (CMV, mumps, coxsackie, HIV, EBV, varicella)
  • Bacterial - TB, salonella, Campylobacter legionella, mycoplasma,
  • Parasitic - ascaris

Vascular

  • Vasculitis
  • embolic
  • hypoperfusion
  • hypercoagulability

Other

  • idiopathic
  • herediatry
  • DM-DKA
  • Autoimmune
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26
Q

Describe the pathophysiology of pancreatitis

A

Begins with an exciting event wether that be toxic or metabolic such as ETOH, hyperlipidaemia or obstruction from gall stones

Cellular injury disrupts usual trafficking of enzymes and leads to activtion of trypsinogen and other digestive enymes

This in turn leads to autodigestion of the pancreatic tissue initiating both local and systemic inflammatory cascades

Locally cytockines cause increased vascular permeability which can results in complications such as oedema, haemorrhage and necrosis

Systemic inflammation may lead to SIRS, shock and sepsis.

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27
Q

Discuss disease classification in pancreatitis

A

Cna be classifed by type (interstitial odematous or necrotic) and be local complictions

Most patient will have interstial odematous disease which usually resolves within a week

About 5-10% of patient will develop necrotising pancreatitis which can involve pancreatic parenchyma and surrounding tissues,

Local complications as defined by the revised 2012 Atlanta Clssification are categorised based on which type of pancreatitis has occured

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28
Q

Discuss local complications of pancreatitis

A

Interstitial oedematous type

  • Acute peripancreatic fluid collection – within 4 weeks of infection no wall
  • psuedocyst formation more than 4 weeks after infection – well formed wall

Necrotic pancreatitis

  • Acute necrotic collection – heterogenous collection of fluid and necrosis: intrapancreatic and/or extrapancreatic
  • walled off necrosis- heterogenous collection of fluid and necrosis with well defined wall: intra or extrapancreatic seen > 4 weeks from symptom onset

Other local complications

  • bowel necrosis
  • splenic or portal vein thrombosis
  • GIT bleed
  • Gastric outlet obstruction
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29
Q

Discuss systemic complciations of pancreatitis

A

Related to progression of local inflammation. If persistant can lead to fluminant sepsis, shock and organ failure.

Pulmonary

  • ARDS - due to microvascular damage and increase permeability, also can have direct surfactant degradating affect
  • Atelectasis
  • Pleural effusion in up to 50% of cases usually on the left

CVS
- hypovolaemic shock secondary to fluid shift

Coagulopathy

  • DIC
  • Thrombocytopenia

Metaboic

  • hyperglycaemia
  • hypocalcaemia from low albuin and magnesium levels
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30
Q

Discuss clinical features of pancreatitis

A

Rapid onset of contant epigastric or left upper quadrant pain.
Usually moderate to severe in nature having nil correlation to severity of disease
Vitals reflect patient discomfort and inflammation with tachycardia, tachypnoea and hihg temp

Respiration can be shallow due to splinting
jaundice if obstruction present

Abdomen can be distended
Cullens and gray turners are rare but in cases of necrotic haemorrhagic pancreatitis are signs of poor prognosis

Tender epigastrium with gaurding and rebound

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31
Q

Discuss DDX of pancreatitis

A

Abdominal

  • GUD
  • Bilary colic
  • cholecysitis
  • cholangitis
  • Gastroenteritis
  • ureteral stone
  • bowel obsturction
  • mesenteric ischaemia
  • AAA
  • ectopic pregnancy
  • perf
Cardiopulonmary 
-ACS
-Pneumonia 
pericarditis 
-pleural effusion 

Systemic disorders

  • DKA
  • SIckle cell disease
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32
Q

Discuss amylase vs lipase

A

Lipase more specific and sensitive 96%,99%
Amylase less sensitivity with 78 and 99% respectively

Amylase is produced in both pancreas and salivary and is raised for a range of resions including

  • malignancy,
  • trauma, burns , salivary and liver disease, cholecystitis, renal failure, HIV and pregnancy
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33
Q

Discuss use of CT in pancreatitis

A

Rarlely needed as a routine investigation in pancreatitis
Reasons for CT include
1) diagnostic uncertainty
2) to excude other suscpected DDX
3)to assess for complications in patient who fail to respond to treatment within 48 hours

The evaluation of complications with CT is best performed 3-7 days after onset of illness. DUring the first few days it doe not accuratley identify the degree of pancreatic necrosis. Complications such as abcess or pseudocust do not occur for several weeks

Ct finding include

  • enlargement of the gland
  • loss of typical texture and borders
  • surrounding fluid and fat straning
  • areas demonstrating nil enhancing with contrast are likley necrotic
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34
Q

Discuss the Atlanta classification of pancreatitis

A

Criteria used to classify severity of pancreatitis – severe pancreatitis cannot be classified until 48 horus

MILD

  • no organ failure
  • no local or systemic complications

Moderate

  • Transiet organ failure (<48hours)
  • Local or systemic complications

Severe
Persistant organ failure >48 hours

35
Q

Compare the various severity scoring systems

A

Ransons 84% sens and 90% spec for severity of pancreatitis, 100% sens and 77% spec for mortality (best)

APACHE 2 (ICU) Model 70% sens and 72% spec for severity of pancreatitis, 100% sens and 66% spec for mortality

CTSI (CT findings) Model 86% sens and 71% spec for severity of pancreatitis, 100% sens and 59% spec for mortality

BISAP (bedside index) Model 38% sens and 92% spec for severity of pancreatitis, 57% sens and 88% spec for mortality

36
Q

Discuss Ransons criteria

A
AT admission 
Age> 55
WBC >16
Glucose >11.1
AST >250
LDH 350

At 48 hours

  • haemtocrit drop >10%
  • BUN rise >1.79mmol
  • Calcium <2mmol
  • Pao2 <60mmhg
  • Base deficit >4mg/dl
  • Fluid needs >6litres

1-2 points at admission is 1% mortality
2-4 15% mortality
5 40% mortality

37
Q

Discuss management of acute pancreatitis

A

Mainly supportive
Voume replacement in the first 24 hours is improtant and reduces SIRS and organ failure at 72 hours. Fluid should be targeted at reducing hypotension and haemoconcentration and preserving urine output. Hartmans is probably the preferred choice to reduce hyperchloremic acidosis
Haematocrit, BUN and creatanine can be surragate markers of effective fluid resus

Hypocalcaemia is usually due to low albumin and should not be corrected unless the ionized calcium is low or there is neurlogical signs of low calcium (chvosteks (face twitch) or trosseau’s sign (blood pressure hand))
If hypomag present fix this and it may fix the hypoca

Hyperglycaemia occurs due to reduced insulin production and patient may need this supplemented

Analgesia as needed

Dont with-hold enteral feeds as this has detrimental effects including GIT mucosal atrophy and permeabiity and amplifies bacterial overgrowth and translocation of gut floura. In mild cases can take PO in moderate to severe NG or NJ feeding. Low fat solid diet is as safe as clear fluids

Antibiotics are not routinely reccomended and should only be used for infected necrotizing pancreatitis or extrapancreatic infections such as cholangitis and bacteraemia. IF indicated a quinalone such as cipro and metronidazole or a single carbapenum are indicated due to coverage and pancreatic tissue penetration

ERCP is indicated in patient with cholangitis or an obstructed stone within 24 hours of admission. Due to the complications of ERCP it should not be performed unless the above are indicated (bilirbuin, jaundice, signs of sepsis). Dilated CBD on CT itself is not an indication need MRCP or Ultrasound in these cases

Acute surgery rarely indicated- cholecystitis once disease passed if due to stone, necrosis is not operated on until four weeks when is walled off

Early ERCP is indicated for patient with cholangitis or bilir

38
Q

Discuss chronic pancreatitis

A

Presents with either prolonged recurrent abdominal pain, signs of local complciations such as bowel obstruction or thrombosis or signs of pancreatic endocrine or exocrine dysfucntion (hyperglycaemia, steatorrhoea, malasopriton)

Nature of pain is similar to acute. It has been proposed that as disease progresses pain reduces due to reduced number of funcitonal acinar cells

DDX same as acute

39
Q

Discuss diagnosis chronic panc

A

Made with either CT, MRCP or EUS.

Serum lipase and amylase may not rise as they normally do. Hypocalcamiea and hyoalbuminemia are comm as is hyperglycaemia

40
Q

Discuss treatment of chronic pancreatitis

A

Mainly supportive – preferred analgesia are paracetamol and NSAIDs +- opiod if needed

If above fails various other option including oral enzyme rpalcement, octreotide, antioxidants and celiac plexus block. Referral to pain specialist early may be beneficial

41
Q

Discuss pancreatis cancer

A

Particulalry lethal as often goes undetected until the later stages. Survival rate is less than 10% with only about 5% surviving 5 years from the time of diagnosis.

Most deaths are related to metatstatic diseaer

Ampullary masses which make up a small percentage of cases are associated with a better prognosis because they tend to cause obstruction and are found earlier. Also 50% amneable to resection

Typical clincial features includinf abodminla pina, back pain, anorexia, nausea, weight loss and weakness. Tumours may cause obstruction leading to cholestasis, jaundice and pancreatitis.

Surgical resection can be curative but otherwise treatment is palliative.

42
Q

Describe causes for mechanical bowel obstruction

A

Extrinsic

  • post-operative adhesions
  • hernia
  • volvulus
  • compressing massess (tumor, haematoma, abscess)

Intrinsic

  • Primary neoplasms
  • Inflammatory (chrons disease)
  • Infectious
  • Traumatic
  • intraluminal
  • bezoars
  • foreign bodies
  • gallstones
  • ascaris infection
43
Q

Discuss closed loop obstruction

A

Obstruction at two points caused impaired bloods supply both proximally and distally- usually seen when twist in the mesentery are seen, or in the case of an internal hernia when a loop of bowel is trapped inside a defect in the mesentary

44
Q

Discuss Ileus causes and compare and contrast clinical features to bowel obstruction

A

Occur in the absence of physical blockage

Causes of adynamic ileus

  • metabolic (hypokalamemia)
  • medications (opiates
  • Infection
  • Abdonimal trauma
  • laparotomy

Clinical features

  • vomiting rarely present in ileus - marked in obstrcution
  • bowel sounds decreased in ileus - tinking and increased in obstruction
  • dehydration not prominent - prominent in bowel obstruction
  • bowel upper normal in ileus - distended in bowel obstruction
  • US decreased peristalisis, back and forth on US
45
Q

Discuss the pathophysiology of mechanical SBO

A

Interrupiton of normal flow thorugh the intestinal lumen triggers a cascade of physiological changes that correlate to the progressive development of symptoms.

In the presence of mechanical obstruction the proximal bowel becomes dilated by the accumulation of food stuffs and intestinal secretions. Increased intetinal dilation causes an increase in peristalsis thorughout the intestines which can trigger frequent loose bowel movement in the early phases of the obstruciton.

AS the process continues further wall oedema leads to loss of normal absorptive function leading to futher accumulation of contents on the intestinal lumen. Bacerital overgrowth begins to occur, IT is this overgorwht of bacteria in a portion of the bowel taht is usually sterile which explains the faeculent nature of the vomiting.

As obsruction continus there is a transudative fluid loss into the peritoneal cavity leading to worsening hypovolaemia and dehydration. In addition constant bouts of emesis can lead to electrolyte abnormalities, metabolic alkalsos severe hypovolaemia and shock.

46
Q

Discuss the pathophysiology of closed loop obstruction

A

In a closed loop obstruction the increase in intraluminal pressure occurs much more rapidly. Intestinal venous congestion and then arterial obstruction can also progress quickly to intestinal ischaemia and infarction. If not promptly relieved necrosis and intestinal perforation can occur.

47
Q

What are the three most common causes of SBO

A

1) Adhesions – occur in 93-`100% of people with previous abdominal surgery and 25% of these will have a SBO
2) Tumors
3) Hernias- similar to their relative frequency in general ventral and inguinal hernias are encounted most but femoral, para stomal, lateral ventral and internal hernias may all be encountered – Internal hernias are much more commonly seen with gastric bypass and up to 5% patient with Roux-en-Y will develop these

48
Q

Discuss gallstone hernia as a cause of SBO

A

Rare but important cause of SBO. Occurs in 1-4% of cases usually seen in the elderly with bilary enteric fistula formation.

The formation of the fistula is often seen in inflammatory conditions such as cholecystitis

As the stone enters and trafvers the small bowel it often grows in size as bowel sediment is attached to it
Eventually the gallstone gets lodged usually in the Ileum the narrowest portion of the small bowel

49
Q

Small bowel volvulus as a cause of SBO

A

Infrequent but is potentially catastrophic. 3-6% of SBO cases in the west much more common in afriva india and the middle east. Primary volvulus occurs in an otherwise normal abdominal cavity, secondary occurs when congential or acquired abnormality leads to the develpoement.

Always close loop

50
Q

Discuss Clinical features of SBO

A

Crampy abdominal pain, abdominal distenstion, nasuea and vomiting, constipation and/or the inability to pass flatus.

Pain is often described in the peri-umbilical region and typically has a crescendo decresecndo pattern.

Distal obstruction typically cause symptoms over a slower period of 1-2 days and are frequently accompanied by a greater abdominal distention

The colon requires 24 hours to empty after the formation of a SBO and thus faltus and stool can continue for this period even with full osbturciton,

Examination

  • Vitals and hydration status
  • abdominal exam for distention and hernias
  • Bowel sounds are described as high pitched and tinling in nature studies have also found decreased or absent sounds.
  • Peritonitis usually indicates late obstructive complicationsn
51
Q

Discuss IX sbo

A

Bloods for dehydration and lactate
AXR - diagnosistic in only 50-60% of acses, equivocal in 20-30% and normal, nonspecific or misleading in 10-20% of cases
CT - high degree of sensitivity and specific – will pcik up strangulation which AXR will not

US becoming a diagnositic tool with increasing sensitivties of probes

52
Q

Discuss MX and disposition of SBO

A

Resus
NG for decompression – little effect in duration fo SBO.
Can delay NG if vomiting can be contolled with antiemetics

SBO merit admission universally. Simple SBOs related to adhesions will resolve with conservative treatement in the next 48-72 hours

53
Q

Discuss Acute mesenteric ishcaemia

A

Involves the sudden reduction or loss of blood flow to the small bowel and may involve the right colon. THe left colon has a much greater supply of collateral and is not as commonly involved

Needs to be diffentiated from chronic mesneteric ischaemia “gut angina”In which there is recurrent episodes of abdominal pain post prandially when there is an increase in o2 demand

There are four main aetiologies of mesenteric ischaemia

1) arterial mesenteric emboli – most common
2) aterial mesenteric thrombos
3) Non occulsive mesenteric ischemia
4) Venous thrombosis

54
Q

Discuss the anatomy and physiolgy of supply to the guy

A

Mesenteric vessels arise from the primitive vental segmental arteries. THese become the coeliac trunk, SMA and IMA

The ceoliac trunk arises anteriorly from the aorta. It gives rise to the splenic, hepatic and left gastric and supplies the distal oesophagus to the middle of the duodenum

THe SMA arises 1 cm inferior from the trunk and supplies the rest of the duodenum to the mid of the transverse colon

THe IMA arises 6-7 cm below the SMA and supplies the distal third of the transverse to the anus

Intetinal blood flow accounts for 25% of CO increasing to 35% postprandially. OF this 70% supplies the mucosa. Given the high demand for O2 damage is seen quickly with ischaemia structural damage to the intestinal villi cna be observed within 15 minutes and sloughing occurs at 3 hours. ^hours transmural necoriss is complete. COmplicated this process is a any re-establishments of blood flow at this point will lead to signifiant repulsion injury

55
Q

Discuss mesenteric arterial embolisms

A

Most common cause of AMI accounting for approximately 50% of cases. The median age of patients is 70 and two third are women. Most common source of emboli are left artrial or ventricular mural thrombos or valvular lesions.

AF is only responsible for 0.14% of cases compared to 2.3% of CVA

SMA is the most common vessle to be involved as it is the largest calbire. MOst commonly lodge 3-10cm distal to the origin

56
Q

Discuss mesenterial aterial thrombosis

A

Results from progressive atherosclerotic disease. Same risk factors for normal athero. Usually will have a history suggestive of chronic mesenteric ischaemia

57
Q

Discuss non occlusive mesenteric ishcaemia

A

Occurs as a result of mesenteric vasospasms in the absence of physical obstruction.

This vasospasm is tirggered by mesenteric hypoperfusion or excessive sympathetic activity.

Hypoperfusion can be caused by a number of condition

  • sepsis
  • severe dehydartion
  • pancreaitis and third spacing
  • haemorrhagic shock

Excessive sympathetic drive

  • CCF
  • Drugs such as vasopressors, cocaine or digoxin

Once intiated the vasospasm tends to continue even when the initiating insult has been addressed leading to intermittent ischaemia and reperfusion thought to be more deleterious than a prolonged ischaemia

58
Q

Discuss mesenteric venous thrombosis

A

Least common cause of AMI accounting for only 5-15% of cases.
Usually involved the SMA vein and its branches
The majority are underlying inherited thombotic disease or inhierited or acquried hypercoagubale state

Factor V leidon is the mot common cause

59
Q

Discuss causes of mesenteric venous thrombosis

A

Hypercoaguable states

  • Factor V
  • Polycythemia vera
  • Sickle cell disease
  • antithrmobin 3
  • protein c or s defiency
  • malignancy
  • myeloproliferative disorders
  • OCP
  • Pregnancy

Inflammatory condition

  • Pancreatitis
  • diverticulitis
  • appendicitis
  • cholangitis

Trauma

  • Operative venous injury
  • post splenectomy
  • Blunt or abdominal truama

Miscellaneous

  • CCF
  • Renal failure
  • Decompression sickness
  • portal hypertension
60
Q

Discuss clinical features of acute mesenteric ischaemia

A

THe classic history is of Sudden onset of poorly localized abdominal pain, gastric emptying (vomiting or diarrhoea) in a patient with known cardiac disease

In cases of venous thrombosis the symptoms are slower in onset and often have been present for several days by the time the patient seeks medical attention.
50% of patient that have an acute embolic event have a personal history of thromboembolic disease

The pain to exam is described as being out of proportion to the physical examination findings. THe patient may be writhing in pain but have a soft abdomen, As the parietal peritoneum becomes involved the abdominal finding progess. Hypotension tachycardia and tachypnoea are all signs of severe ischaemia and have a poor prognosis

61
Q

Discuss DDX of mesenteric ischemia

A
AAA
Perforated viscous 
bowel obstruction 
biliary disease 
atypical MI
62
Q

Discuss IX mesenteric ischaemia

A

Non specific findings on labs- d-dimer, lactate and interleukin 6 have been described as biomarkers. Serial lactate probs best

Plain AXR are usually non specific

Mesenteric angiography is the gold standrd and offer the benefit that diagnosis and intitial treatment can occur concurrently

CTA is the most common IX as angiography suites are not commonly available

DUplex US is very specific 92-100% but its sensitivity is reduced by limited evaluation beyond the proximal main vessel.

63
Q

Discuss management of acute mesenteric ischaemia.

A

–Aim of treatment is to restore blood flow as soon as possible., manage the underlying condition and reduce vasospasms.

–Initially fluid resus and HD stability. If pressors are required in these patient dobutamine, dopamine or milrinone are recommeneded as they have the least vasoconstrictive effect on the mesenteric vasculature.

–Cover with IVABs if evidence of infarct peroration or peritonitis - triples ‘

–Pain management

–Urgent laportomy +- preoperative conventional angiography may be beneficial to attempt rapid revascularization.

–Papaverine a phosphodiesterase inhibitor may be infused directly into the effected vessels via angiography. THis results in elevated CAMP which results in profound smooth muscle relaxation.

–IV heparin should be administered to prevent thrombosis in vasospastic vessels.

In mesenteric venous thrombosis heparin infusion may be sufficient by itself

64
Q

Discuss the anatomy of the anorectum

A

Supported by three muscle groups , levator ani and the internal and external sphincters
Bloods supply is via the inferior, middle and superior haemorrhoidal arteries which arise from the inferior mesenteric, internal iliac and internal pudendal arteries

Lymphatic drainage is to the inferior mesenteric nodes superior to the dentate line and to the inguinal region below

Involuntary sphincter is supplied via parasympathetic nerves from the S2-4 nerve route. Volunatary control of the external is via nerve roots from s2-3

65
Q

Discuss Haemorrhoids + clinical features

A

Occur when the three anal vascular submucosal cushions become engorged. Blood supply is from the arterial system leading to bright red blood.

Haemarhoids are not varicose veins, they are normal structures that manifest symptoms whne the muscularis submucosa weakens and the cushions are displaced.

Bleeding is the chief complaint, and unless the haemorrhoid is thrombosed it is usually painless.

Blood on toilet paper is usually due to fissure or external haemorrhoid, dripping into the bowl is from internal, can have mucoid discharge, mixed with stool is from higher in the GIT than the anus and melena from the upper GIT

66
Q

List the types of haemorrhoid

A

External - inferior to the haemorrhoidal plexus, proximal to the dentate line - modified squamous

Internal superior to the haemorrhoidal plexus, distal to the dentate line - transitional or colunar

Mixed

67
Q

Discuss classification of internal haemorrhoid by severity

A

First degree – nil prolapse, medical treatment

Second degree - prolapse during defecations, medical treatment

Third degree - spont prolapse or during defecation, manual reduction, can be treated medically or surgical repair

Fourth degree- permanent - irreducible, require surgical repair

68
Q

Discuss surigcal management option of haemorrhoids

A

Thrombosed external – excision in emergency department – can be complicated by rebleeding, swelling and formation of skin tags – resolves spontaneously within 72 hours not often done

Second and third degree internal - electival surgical repair, banding, sclerotherapy, haemorrhoidectomy

Fourth degree non thrombosed - nonurgent haemorrhoidectomy

Fourth degree thrombosed or gangrenous – emergent haemorrhoidectomty

69
Q

Discuss management of haemorrhoids

A

Nonthrombosed external and non prolpasing internal use WASH (warm water, analgesics, stool softener, and high fibre diet)

Anal canal pressure reduces in warm water

Second and third degree internal haemorrhoids WASH but may need surgery

Thrombosed and gangrenous fourth degree haemorrhoid require surgical intervention

70
Q

Discuss Anal fissures

A

Most common cause of painful rectal bleeding of sudden onset.

Most commonly encountered anorectal problem in children.

Most occur along the posterior midline where the skeltal muscle fibers that encircle the anus are the weakest.

patient report sudden searing pain during defecation accompanied by a small amount of bright red blood in the stool or on the toilet paper.
This is followed by a nagging burning sensation cuased by internal sphincter spasm.
Subsequent bowel motion are excruciating

MX

  • WASH protocol
  • GTN ointment BID
  • Nifedipine gel
  • Surgical excition ]
  • Anal dilation performed with the patient under general anaethesia
71
Q

Discuss anorectal abcesses

A

Can occur in otherwise healthy adults when the mucous producing glands at the base of the anal crypts occlude - can be a herald of IBD, trauma, cancer, rdation or infection

Common organisms include (e.coli, staph, bacteroides, strep, proteus

Natural disease progression is to fistula formation in the body’s attempt to drain the infection spontaneously

Some can be mangemed in the ED however all anorectal abcesses have been associated with fistulae formation and definitive treatment of the fistula network at the time of I&D is needed for resolution

72
Q

Discuss management of perirectal and perianal abscesses

A

Account for 40-45% of anorectal abscesses. They produce painful swelling at the anal verge worsened on sitting and defecation.

Most paitent are afebrile and have localized tenderness eryhtema swellign and fluctuance. ED management with i&D is possible if patient is able to tolerate the procedure and they have nil co-morbidities.

WASH protocal

73
Q

Discuss ischiorectal abcess

A

20-25% of abcesses form outside the pshncter muscles in the buttocks, patient usually present with severe pain.

Most require surgical intervention

74
Q

Discuss intersphincteric abscess

A

25% of abcess from in the space deep to the external sphincter and inferior to the levator ani. The infection tracks cephalad and may appear to be a mass in the rectum.

Report continous rectal pressure and throbbing pain on sitting and defecation. They may have fever and leukocytosis. Inguinal lymp0hadenopathy are common

May be associated with fistulae formation

75
Q

Discuss supralevator abcess

A

rare accounting for less than 5% of abcess they cause perianal and buttock pain associated with fever and leukocytosis. External evidence is usually absent which often delays the diagnosis. Many patient are obese or have diabetes, IBD, PID or diverticulitis.

76
Q

Discuss pilonidal disease

A

Abcesses containing hair and pus in the lidline of the sacrococygeal area afflict young adults with a 4:1 male predominance and are more common in obese and hirsute people

Treatment ranges from aspiration to full surgical debridement - aspiration and AB with surgical OPD in week may promote faster healing than I&d

77
Q

Discuss hidradenitis suppurativa

A

is an infection of the apocrine glands. It is most common in young adults and is associated with poor skin hygiene, hyperhidrosis, obesity, acne, DM and smokling.

Occluded glands may be infected with strains of staph, strep, e.coli or proteus.

Extension through the dermis spreads the infection to neighboring ducts and a network of sinus tracts, leading to extensive scarring.

Found in the perianal region + axillae

Treatment begins with careful attention to hygiene warm compresses, ABs (cefalexin) and dietary modifications (avoidance of dairy products and foods with high GI)

78
Q

Briefly discuss pathogenesis of appendicitis

A

1) appendicieal obstruction prevents egress of mcuous and bacteria from the appendix
2) continued mcuous proudction and bacterial proliferation result in luminal distension which stimulates the T10 visceral afferent nerves creating periumbilical pain typically lasting 4-6 hours
3) intraluminal pressure eventually exceeds local cappillary pressure in the appendiceal wall preventing arterial perfusion and resulting in tissue ishcemia and inflamamtion
4) this causes trans-murral inflammation that extends into the surrounding tissues resulting in somatic localised pain typically focaused in the right lower quadrant.

Causes of obstruction

  • faecolith most common
  • appendicoliths
  • lymphoid hyperplasia
79
Q

Describe stump appendicits

A

Very rare

results from inflammation of the appendiceal remnant that may persist after the appendix has been removed surgically.

80
Q

Discuss history finding in appendicitis

A

Moderately useful

  • RLQ pain
  • migration of pain
  • presence of pain prior to vomiting
  • no history of similar pain

Mildly usfule

  • vomting
  • male gender
  • pain worsened when driving over speed bumps

Not useful

  • anorexia
  • nauea
  • pain worse with cough or movementb
81
Q

Discuss Exam finding in appendcitis and eponymous examinatios

A

Useful

  • RLQ tenderness
  • abdominal wall rigidity
  • Mcburneys point

Mild

  • Reboudn tenderness
  • garding
  • temperature >38.3
  • percussion tenderness
  • psoas sign

Psoas sign - increased abdominal pain with patient lying on left side while provider passively extends the patietns right leg at the hip with both knees extended
-Sens 42% spec 79-95%

Rovsigns - abdominal pain in the RLQ while palpating the lower left Sens 7% and spec 58-96%

Obturator sign - increased abdominal pain in the supin patients as the provider internally and externally rotates the right leg as it is flexed at the hip sens 8% and spec 94%

82
Q

Discuss ix of appendicits

A

WBC -
CRP -

Combined raised CRP and WBC has an Postive likelihood ratio of 23 and a -ve ratio of 0.03

Urinalysis - pyruis, haematuria and/or bacteria in up to 48% of patients with appendicitis

Graded compression utrasound (sens 75-90%, spec 83-95%) - criteria include

  • Require appendiceal diamter >6-7mm and noncompressible appendix
  • fat stranding and peritoneal fluid

CT (sens 94-100% and spec 91-99%)

  • Appendiceal diameter >6 with surrounding inflammation or >7 without
  • Appendiceal circufmernetial wall thickening >2mm with mural enhancement
  • calcified appendicolith
  • signs of periappendical inflammation
83
Q

Discuss management of appendicitis

A
  • Triple antibiotics or piptaz if perfed
  • Perforated or complicated appendicits (those with abscess formation) should be treated with either lap removal or percutaneous drainage
  • For non complicated appendicitis conservative management with supportive care and antibiotics can be considered

Conservative treatment has risk of failure or need recurrent appendicitis. This is countered by a negative appendectomy rate of 3.6-10% and a complication rate as high as 18% including SBO, adhesions surgical site infection and abscess formation