Acute Abdomen Flashcards
(144 cards)
1
Q
What type of pain would someone with appendicitis complain of?
A
central abdominal pain that moves into the right iliac fossa
2
Q
Typically, how does someone with appendicitis present?
A
- tends to be a young person (5 - 40 years old)
- acute onset within 12 - 24 hours
- present with umbilical pain that moves to the right iliac fossa
- nausea and/or vomiting
- diarrhoea or constipation
- fever
3
Q
What might be present on general inspection and palpation of someone with appendicitis?
A
- in the early stages there is general pain and peri-umbilical pain on palpation
- in the later stages, the person will often stay very still due to peritonitis
- this occurs after the appendix has ruptured, and the peritoneum has become inflamed
on palpation, there will be right iliac fossa pain
4
Q
What signs might be present in appendicitis?
A
- Rovsing’s sign
- Cope’s sign
- Psoas sign
- rebound tenderness
5
Q
What is Rovsing’s sign?
A
- pain is greater in the RIF than the LIF when the LIF is pressed
- this is specific to appendicitis
6
Q
What is Cope’s sign?
A
- there is pain on passive flexion and internal rotation of the hip
- it indicates irritation to the obturator internus muscle
- the appendix becomes inflamed and enlarged and may come into contact with the obturator internus muscle when this move is performed
7
Q
What is Psoas sign?
A
- there is pain on extending the hip
- pain indicates an inflamed appendix overlying the iliopsoas muscles
- this only occurs with retrocaecal appendix
- (as the iliopsoas muscle is retroperioneal)
- this indicates that the inflamed appendix sits behind the caecum
8
Q
When might rebound tenderness be evident in appendicitis?
What is this?
A
- this indicates that the infection is involving the peritoneum
- there is pain upon removal of pressure from the abdomen rather than application of pressure to the abdomen
- this is indicative of peritonitis
- there may also be abdominal guarding - the abdominal muscles tense up to avoid pain
9
Q
What are the investigations involved in appendicitis?
A
- first line investigation is CT abdomen
- USS can be done if CT is not available
- this will show increased appendix diameter and increased wall enhancement
- bloods - which will show leucocytosis and elevated CRP
10
Q
What is the most common cause of appendicitis in adults?
A
- appendicitis results from obstruction of the appendix lumen
- this may be due to a fecalith (hardened lump of faecal matter) that wedges itself within the lumen
- it can also be due to undigested seeds or pinworm infections
11
Q
What is a common cause of appendicitis in adolescents?
A
lymphoid hyperplasia
- this involves growth of the lymphoid follicles, which are dense collections of lymphocytes
- these reach their maximum size in adolescence and can obstruct the lumen of the appendix
- when exposed to viral infections or immunisations, the follicles can increase in size
12
Q
How does obstruction of the lumen of the appendix lead to pain?
A
- the intestinal mucosa secretes mucus and fluids to keep pathogens from entering the bloodstream and to keep the tissue moist
- even when obstructed, the appendix keeps secreting
- there is a build up of fluid and mucus in the appendix, which increases the pressure
- the appendix gets bigger and physically pushes on afferent visceral nerve fibres nearby, causing pain
13
Q
Why is there is an increase in serum WBC count in acute appendicitis?
What processes have to occur prior to this for it to occur?
A
- as there is an obstruction, flora and bacteria in the gut are trapped
- E. coli and bacteroides fragilis
- these bacteria are now free to multiply
- this causes the immune system to produce WBCs, which leads to the build up of pus in the appendix
14
Q
What happens if the obstruction in the appendix persists past the build-up of pus in the appendix?
A
- the pressure in the appendix increases even further
- it expands and begins to compress small blood vessels that supply it with blood and oxygen
- without oxygen, the cells in the wall of the appendix become ischaemic and die
- these cells were responsible for secreting mucus and keeping bacteria out, so now the growing colony of bacteria can invade the wall of the appendix
15
Q
What leads to rupture of the appendix?
What happens if the appendix ruptures?
A
- as more cells in the wall of the appendix die, it becomes weaker and weaker
- in a small proportion of patients, the appendix wall becomes so weak that it ruptures
- this leads to bacteria entering into the peritoneum and causing peritonitis
- this leads to abdominal guarding and rebound tenderness at McBurney’s point
16
Q
What is the most common complication of a ruptured appendix?
A
- formation of a periappendiceal abscess
- this is a collection of fluid and pus around the ruptured appendix
- sometimes smaller subphrenic abscesses can form
- these are below the diaphragm, but above the liver/spleen
17
Q
What is the treatment for appendicitis?
A
appendicetomy
- this is surgical removal of the appendix, followed by antibiotics
- if there is an abscess, this must be drained first
18
Q
What scoring system is used to determine the severity of appendicitis?
A
Alvarado score
- score of 1 to 4 is discharged
- score of 5 to 6 is observed
- score of 7 to 10 needs surgery
19
Q
Which antibiotics are given following appendicetomy?
A
- cefotaxime
-
metronidazole
- this is an anti-anaerobe antibiotic for the gut
20
Q
What are the 3 possible complications of appendicitis?
A
- perforation
- appendix abscess
-
appendix mass
- the inflamed appendix becomes covered in omentum and forms a mass
- this tends to occur in older men who avoid coming to the doctors when they get pain
21
Q
A
B-hCG test
- the first line investigation in any woman with an abdominal pathology should ALWAYS be a pregnancy test
22
Q
What is meant by diverticulosis?
A
- the presence of diverticulae
- these are outpouchings of the colonic mucosa and submucosa throughout the large bowel
-
high pressure in the bowel causes these outpouchings to form
- e.g. chronic constipation
23
Q
A
24
Q
What is meant by diverticulitis?
Which part of the bowel is more commonly affected?
A
- acute inflammation and infection of the diverticulae
- most commonly affects the sigmoid colon
25
What is the structure of the large intestine wall like?
What is the difference between a true diverticula and a pseudo-diverticula (false)?
* the wall of the large intestine is made up of **4 layers**
* mucosa
* submucosa
* muscle layer
* serosa
* a ***true diverticula*** involves **_all 4 layers_** of the intestine
* a ***false (pseudo) diverticula*** includes only the **_mucosa and submucosa_**
* these 2 layers are covered by serosa only, and the muscle layer is not involved
* these are more common
26
27
Why do diverticula form?
* they are formed by **_high pressure_** within the lumen of the large intestine
* **smooth muscle** in the intestinal wall contracts to push food along the bowel
* when it contracts, higher pressures are generated inside the lumen as it "squeezes" air inside
* **contractions** in someone with diverticula are **_abnormal_**
* instead of pressure being ***distributed evenly*** throughout the lumen, there are **_areas of very high pressure_** during abnormal smooth muscle contraction, which leads to diverticula formation
28
What is the most common location for diverticula to form and why?
**_sigmoid colon_**
* this has the **smallest lumen diameter**, and so it subject to the highest intraluminal pressures
29
Does rectal bleeding (haematochezia) occur in diverticulosis and/or diverticulitis?
Why?
* PR bleeding **_can_** occur in **_diverticulosis_**
* a diverticulum can form where blood vessels traverse the muscle layer, as this point of the wall is weaker
* the blood vessel becomes separated from the intestinal lumen only by mucosa
* it is predisposed to rupture, meaning blood enters the large intestine
* PR bleeding does **_NOT_** occur in **_diverticulitis_**
* this is because the blood vessels become **scarred from inflammation**
30
What genetic conditions and lifestyle factors are associated with an increased risk of diverticular disease?
* anything that **increases the stress** on the intestinal walls or **decreases their strength** predisposes to diverticula
* **_Marfan syndrome_** & **_Ehlers-Danlos_** are genetic conditions that affect **connective tissue**
* diverticula can form in the absence of strong connective tissue supporting the intestinal wall
* diets **_low in fibre_** and **_high in fatty foods_** and **_red meat_** increases risk of symptomatic diverticular disease
31
What symptoms may be present in diverticulosis?
* this is the presence of diverticula and usually has **_no symptoms_**
* sometimes there will be **vague stomach pain** and the diverticula can **bleed**
* they are often found incidentally on **colonoscopy** or **CT scan**
32
What are the 2 reasons why diverticula may become inflamed and cause diverticulitis?
* if a faecalith becomes lodged in the diverticula (less common)
* due to erosion of the walls of the diverticula from higher luminal pressures
33
What is the most severe complication of diverticulitis?
* if the diverticula become **distended enough**, they can **rupture** and form a **_fistula_**
* this is a connection with an adjacent organ or structure
* a **_colovesicular fistula_** between the **large intestine** and the **_bladder_** might form, leading to **air or stool** in the **urine**
34
How does someone with acute diverticulitis typically present?
* **_left iliac fossa pain +/- bloating_**
* anorexia
* this refers to not eating much
* fever
* nausea & vomiting
* may have bloody stools
* may have urinary symptoms if colovesicular fistula has formed
* e.g. brown urine due to the presence of faeces in the urine
35
What are the risk factors associated with diverticulitis?
* tends to present in **_50 - 70 year olds_** who have previously been asymptomatic
* **_low dietary fibre_**
* **smoking**
* **chronic _NSAID_ use**
36
What would someone look like on general inspection and palpation in acute diverticulitis?
What if they had peritonitis?
***_Acute diverticulitis:_***
* tachycardia
* low-grade pyrexia
* **_LIF tenderness_** on palpation
***_Peritonitis:_***
* this may occur if they have a **_perforated diverticulum_**
* they will be **_lying very still_** to not aggravate the pain
* on palpation, there will be **_guarding_** and **_rebound tenderness_**
37
What is the primary investigation for acute diverticulitis?
What other investigation might be performed if perforation is suspected?
**_CT abdomen with contrast_**
* an **erect CXR** may be performed if there are signs of perforation
* the presence of **air under the diaphragm** confirms perforation
* inflammation is shown as hyperdense tissue
38
What investigation might be performed once someone has recovered from diverticulitis?
**_barium enema_ +/- flexible sigmoidoscopy / colonoscopy**
this is to confirm the presence of **chronic diverticulosis**
39
What is the treatment for mild and severe diverticulitis?
***_Mild / Uncomplicated:_***
* oral antibiotics (in more severe cases, IV antibiotics are given)
* fluids
* bowel rest (no food / water orally)
***_Severe:_***
* bowel resection is performed if there is recurrence / severe cases
* this usually involves Hartmann's procedure
40
What is involved in Hartmann's procedure?
Why is this performed to treat acute diverticulitis?
* this involves **emergency / acute removal** of a piece of bowel
* this usually involves removal of the **sigmoid colon**
* this results in formation of an **_end colostomy_** and **_anorectal stump_**
* an immediate ***primary anastomosis*** is **_not possible_** due to ***inflammation*** and ***oedema***
* when the oedema starts to settle down, gaps will appear in the anastomosis and it will become leaky
41
What is the treatment for diverticulosis?
* encourage the patient to have a soluble, high-fibre diet
* once the inflammation has settled down from diverticulitis, a primary anastomosis can be formed
42
What other operation may accompany formation of an anastomosis in distal large bowel cancers (e.g. rectal carcinoma)?
**_defunctioning loop ileostomy_**
* this **diverts bowel contents** away from a distal anastomosis
* this allows it **time to rest** prior to reversal of the loop ileostomy
43
What are the possible complications of diverticular disease?
* acute diverticulitis
* faecal peritonitis
* this tends to occur if there is rupture of a diverticulum
* fistula formation
* peri-colic abscess
* colonic obstruction
* perforation
44
C - diverticulitis
* presence of bloody stools
* she has had blood in the past - bleeding diverticula
* fever
* tenderness in left iliac fossa
* this is the location of the sigmoid colon
* low fibre diet
45
A - Hartmann's procedure
* the presence of air under the diaphragm shows perforation
* a primary anastomosis cannot be performed in the acute presentation
46
What is the definition of a hernia?
What are the 2 major types?
a condition in which part of an organ is **displaced** and **protrudes** **through the wall** of the cavity containing it
* this is often involving the intestine at a weak point in the abdominal wall
* the 2 main types are **inguinal** and **femoral**
47
In what 2 different ways can abdominal hernias be classified?
* **_midline hernias_**
* epigastric hernias
* umbilical hernias
* **_groin hernias_**
* femoral hernias
* inguinal hernias (much more common)
* can also get **_incisional hernias_** when abdominal contents herniate through a scar from a previous abdominal surgery
48
What are the layers of the abdominal wall?
What could cause something to protrude through these layers?
* deepest layer is the **visceral peritoneum**
* this covers many abdominal organs and lines the peritoneal space
* this layer wraps around to form the **parietal peritoneum**
* extraperitoneal fat
* **transversalis fascia**
* muscle layer containing **external oblique**, **internal oblique** & **transversus abdominis aponeurosis**
* fascia
* anything that **_increases the pressure_ in the abdominal cavity** may result in a **sac** that forms in the abdominal wall through which **_organs might protrude_**
49
What are the 2 different types of midline hernias and when do they occur?
* a midline hernia occurs when organs protrude **_through the midline_**
* an ***epigastric hernia*** occurs when organs protrude through the **_linea alba_**, between the xiphoid process and the umbilicus
* an ***umbilical hernia*** occurs when organs protrude through the **_umbilicus_**
50
What is meant by an inguinal hernia?
What are the 2 openings of the inguinal canal?
* an inguinal hernia occurs when abdominal contents protrude through the **_inguinal canal_**
* the **_deep inguinal ring_** is an opening in the ***transversalis muscle fascia***
* the **_superficial inguinal ring_** is an opening in the ***external oblique muscle aponeurosis***
51
Why are inguinal hernias much more common in males?
* the **inguinal canal is much _larger_** and **more prominent** in males, which creates a **_site of weakness_** in the abdominal wall
* this is due to the testes having to descend further than the ovaries during development, meaning that the **processus vaginalis** (now obliterated) may remain open
52
What is meant by an indirect inguinal hernia and why does it occur?
Who tends to be affected by these?
* occurs when the **_processus vaginalis fails to close_** after the testes have passed through it
* sometimes called a ***congenital hernia***
* when the processus vaginalis remains open, intestinal contents herniate through **_BOTH_** the **_deep_** and **_superficial inguinal rings_** and into the scrotum
* think *"contents herniate INDIRECTLY through the inguinal canal"*
* this is more common in **_infants and children_** but can be discovered in adulthood
53
What is meant by a direct inguinal hernia and why does it occur?
Who tends to be affected by this?
* this results from **_weakness of the transversalis fascia_**
* sometimes called an ***acquired hernia***
* the abdominal wall gets **weaker with age**, so these tend to occur in **_middle-aged_** and **_elderly people_**
* the intestinal contents pass through the **_external inguinal ring_** ONLY
* think *"contents are herniating DIRECTLY through the abdominal wall"*
54
In which location is a direct inguinal hernia most likely to occur?
When does this happen?
* the transversalis fascia weakens most commonly in the p**osterior wall** of the inguinal canal
* this region is called **_Hesselbach's triangle_**
* hernia through Hesselbach's triangle occurs as a result of **increased abdominal pressure**, usually through **_coughing_** or **_heavy lifting_**
55
What happens in a femoral hernia?
* occurs when abdominal contents herniate beneath the inguinal ligament and into the femoral canal
* these are less common than inguinal hernias
56
What is the difference between an uncomplicated hernia and an incarcerated hernia?
* in an ***uncomplicated hernia***, the hernia can be reduced back into the abdomen by **_pressing on the hernial sac_**
* this is a pouch of peritoneum that covers the herniating organ
* if the contents of the hernia **_cannot be pushed_ back inside the abdomen** then this is ***incarceration***
* there is reduced venous and lymphatic flow
* this leads to **swelling and oedema** of the incarcerated tissue
57
What is meant by a strangulated hernia?
* if a hernia is **incarcerated**, eventually the tissue will **swell so much** that the **_arterial blood flow_** to the hernial contents is **_completely cut off_**
* this is strangulation and it leads to **_ischaemia**_ and _**tissue necrosis_**
58
How would someone with a hernia typically present?
* small hernias are often **asymptomatic**
* **_palpable lump_** in groin
* **_pain_** in the groin
* **scrotal swelling** (inguinal hernia)
* **nausea & vomiting** / **fever** are signs of **_incarceration_**
* incarceration may interrupt passage of contents through the intestines and lead to symptoms of **bowel obstruction**
* if the hernia appears **red**, it is likely to be **_strangulated_** and there is blood trapped in the hernial sac
* (groin pain and vomiting are red flags)*
59
What are key features to pick up in the history of someone who could have an inguinal or femoral hernia?
* **increasing age**
* **obesity**
* history of **chronic constipation**
* history of **chronic cough**
* recent **heavy lifting** (e.g. gym)
* (obesity, constipation, cough and lifting all increase intra-abdominal pressure)*
60
Who tends to be more affected by femoral and inguinal hernias?
Which is more likely to become strangulated and which is more likely to need surgery?
* inguinal hernias are the most common hernia in both sexes
* but femoral hernias occur more often in women
* ***femoral hernias*** are ***more commonly _strangulated***_ and _***surgery_ is recommended***
* **femoral hernias** affect **_older people_** and inguinal hernias affect younger people
61
What is the defintion of a strangulated hernia?
the compression around the hernia **prevents blood flow** into the hernial contents causing **_ischaemia to the tissues_** and **_pain_**
62
Where is a femoral hernia located and what is often contained within it?
* located **_lateral_** and **_inferior_** to the **pubic tubercle**
* often contains **_omentum_**
63
What is the location of the inguinal hernia?
What is often contained within it?
* located **_superior_** and **_medial_** to the **pubic tubercle**
* often contains **_bowel_**
64
What are the features that are common to both femoral and inguinal hernias?
What are the signs that they might have become strangulated?
* **swells / appears** **_on coughing_** and may **reduce on supination**
* both may be **_reducible on pressure_**
* signs of strangulation include:
* **redness / tender**
* **colicky abdominal pain**
* **distension**
* **vomiting**
65
What are the borders of Hesselbach's triangle?
What type of hernia is this associated with?
* **rectus abdominus**
* **inferior epigastric vessels**
* **inguinal ligament**
* associated with a **_direct inguinal hernia_** that will protrude through this weakness in the abdominal wall
* this tends to occur in **older people, weight-lifters** and **manual labour workers**
66
How can you make a clinical diagnosis of an inguinal hernia and distinguish an indirect from a direct hernia?
* ***reduce** the hernia*
* *place your finger over the **_deep inguinal ring_***
* just above the midpoint of the inguinal ligament
* *ask the patient to **cough***
* *if the hernia **reappears**, it **_CANNOT_** be an **_indirect hernia_** (must be **direct**)*
* your finger is blocking the deep inguinal ring so the indirect hernia could not pass through
* if still unsure, an **USS** can be done to **locate the hernia** and decide whether it is composed of **bowel or omentum**
* femoral = omentum
* inguinal = bowel
67
Which type of hernia is more likely to need surgery?
* **femoral hernia** needs **_urgent surgery_** due to risk of strangulation
* for inguinal hernia, surgery is less urgent
* this tends to be mesh repair or more conservative measures like wearing a corset
68
What is meant by inflammation of the pancreas?
What are the 2 different types?
* **_inflammation_** of the pancreas
* leading to **_autodigestion_** of pancreatic tissue by the pancreatic enzymes, resulting in **_necrosis_**
* this can occur in either an **_acute_** or **_chronic_** setting
69
What is the definition of acute pancreatitis?
sudden **_inflammation_** and **_haemorrhaging_** of the pancreas due to destruction by **its own digestive enzymes** (autodigestion)
70
What are the endocrine and exocrine roles of the pancreas?
***_Endocrine:_***
* alpha and beta cells release hormones like insulin and glucagon into the blood
***_Exocrine:_***
* acinar cells secrete digestive enzymes into the duodenum
* these break down carbohydrates, proteins and lipids that are also found within the cells of the pancreas
71
How does the pancreas protect itself from autodigestion normally?
* the acinar cells manufacture **inactive forms** of digestive enzymes (**_zymogens_**)
* zymogens are stored in vesicles (**_zymogen granules_**) with **_protease inhibitors_**
* this allows for extra protection if the zymogens were to become prematurely active
* the zymogens are released into the **pancreatic duct** and delivered to the **duodenum**, where they activated by **_trypsin_**
* trypsin comes from the pancreatic zymogen **trypsinogen**, which is activated by **_enteropeptidases_** in the **duodenum**
72
What are the 2 main causes of acute pancreatitis?
What is the mechanism behind this?
* **early activation** of trypsinogen or zymogens causes acute pancreatitis
* this can occur due to **_injury to the acinar cells_**
* or due to anything that **_impairs secretion of zymogens_** into the duodenum
* the 2 main causes are **_alcohol_** and **_gallstones_**
73
What is the mechanism behind how alcohol can cause acute pancreatitis?
* alcohol **_increases zymogen secretion_** from acinar cells
* it also **_decreases fluid and bicarbonate secretion_** from ductal epithelial cells
* the pancreatic juices become very thick and **_viscous_**
* this leads to a **_plug forming_**, which blocks the pancreatic ducts
* plug formation leads to pancreatic juices **backing up**, **increasing the pressure** within and **_distending the pancreatic ducts_**
74
How can a blocked and distended pancreatic duct lead to acute pancreatitis?
* distended ducts make **membrane trafficking** become more **chaotic**
* **zymogen granules may fuse with lysosomes**, bringing trypsinogen into contact with digestive enzymes
* trypsinogen is converted to **active trypsin**, which starts the **cascade of enzyme activation** within the pancreas
* this leads to **autodigestion** of pancreatic tissue
75
In what other ways can alcohol contribute to the development of acute pancreatitis?
* alcohol stimulates release of **_inflammatory cytokines_**, stimulating an immune response
* **neutrophils** arriving at the scene release **proteases**, making the problem worse
* high consumption of alcohol can produce enough **_reactive oxygen species_** to overwhelm cellular defences and damage the cells
76
How can gallstones lead to acute pancreatitis?
* gallstones can **_block the sphincter of Oddi_**
* this blocks the release of pancreatic juices
77
What is liquefactive haemorrhagic necrosis?
How does it occur?
* autodigestion / pancreatic tissue destruction can cause **tiny blood vessels** to become **_leaky_** and **_sometimes rupture_**
* extra fluid causes **_swelling and oedema_** of the pancreas
* this can **_activate lipases_** which **digest the _peripancreatic fat_**
* this is the fat surrounding the pancreas
* digestion and bleeding can **liquefy** pancreatic tissue
* this is liquefactive haemorrhagic necrosis
78
What is a pancreatic pseudocyst and how does it form?
What symptoms might be seen with this?
* **fibrous tissue** surrounds the **liquefactive necrotic tissue** of the pancreas
* this forms a **cavity** that fills with **pancreatic juices**
* typical symptoms include **_abdominal pain_**, **_loss of appetite_** and **_palpable abdominal mass_** following a bout of pancreatitis
* **serum amylase, bilirubin** and **lipase** may be raised
* the best way to image a cyst is with abdominal CT
79
What happens if the pancreatic pseudo-cyst becomes infected?
* it forms a **_pancreatic abscess_**
* it is usually infected by ***E. coli***
* this presents with the same symptoms, with additional **fever** and **high WCC**
80
How does someone with acute pancreatitis typically present?
* intense **_epigastric pain_** that may **radiate to the back**
* pain is **_worse on movement_**
* pain is **relieved when** **_sitting forwards_**
81
What is the mnemonic to remember the causes of acute pancreatitis?
I GET SMASHED
* I - idiopathic
* G - gallstones
* E - ethanol
* T - trauma
* S - steroids
* M - mumps infection
* A - autoimmune
* S - scorpion venom
* H - hypercalcaemia, hyperlipidaemia, hyperparathyroidism
* E - ERCP
* D - drugs (thiazides)
82
On examination, what signs might be present in acute pancreatitis?
* epigastric tenderness
* fever
* reduced bowel sounds
* shock, tachycardia, tachypnoea
* Cullen's sign & Grey-Turner's sign
83
What are Cullen's sign and Grey-Turner's sign and why do they occur?
* they occur due to **intra-abdominal bleeding** from pancreatic inflammation
* ***Cullen's sign*** is bruising around the **_umbilicus_**
* ***Grey-Turner's sign*** is bruising in the **_flanks_**
* remember "you have to TURN over to see it"
84
What blood tests will be deranged in acute pancreatitis?
* increase in serum digestive enzymes, including **_amylase_** and **_lipase_**
amylase is not very specific
* it will be raised in any cause of acute abdomen, including pancreatitis
lipase is more specific
* **_hypocalcaemia_** occurs in acute pancreatitis
* this occurs as **fat necrosis consumes calcium**
85
What other investigations may be performed in acute pancreatitis?
* **serum amylase**
* should be \> 3x upper limit of normal
* **serum lipase**
* **USS** to look for the cause (i.e. gallstones)
* erect CXR and **CT abdomen**
* CT will show inflammation, necrosis and pseudocysts
86
Why can acute pancreatitis lead to hypovolaemic shock and bleeding?
What is the most severe complication of acute pancreatitis?
* **_haemorrhage_** from a damaged blood vessel can lead to shock
* there may be systemic activation of blood coagulation factors (**_DIC_**)
this leads to **small blood clots** forming all over the body, **using up clotting factors** and making it easier to bleed
* massive pancreatic inflammation can lead to **_acute respiratory distress syndrome (ARDS)_**
* this makes it difficult to breath
87
How can the Modified Glasgow Score be used to determine the severity of pancreatitis?
* a score of \> 3 indicates severe pancreatitis
* P - pO2 \< 7.9 kPa
* A - age \> 55 years
* N - neutrophils \> 15 x 109 / L
* C - calcium \< 2 mmol / L
* R - renal function
* measured by urea \> 16 mmol / L
* E - enzymes
* LDH \> 600 U / L or AST \> 200 U / L
* A - albumin \< 32 g / L
* S - sugar \> 10 mmol
88
How do you expect serum calcium to change in acute pancreatitis?
What would normal calcium suggest?
* **serum calcium _drops_** in acute pancreatitis due to sequestering of free Ca2+ by free fatty acids
* **_very low_ Ca2+** has **_worst prognosis_**
* **_normal_ Ca2+** supports an aetiology of **_hypercalcaemia_**
89
What is involved in the medical and surgical management of acute pancreatitis?
* supportive management with fluids and analgesia
* enzyme supplementation
* diabetes medications
* if someone becomes insufficient (i.e. cannot produce sufficient insulin)
* ERCP may be performed to remove a gallstone if present
90
What is meant by chronic pancreatitis?
How is it different to acute pancreatitis?
***_Acute pancreatitis:_***
* involves **_sudden_ inflammation** of the pancreas caused by digestion by its own enzymes (**autodigestion**)
* generally is **_reversible_**
***_Chronic pancreatitis:_***
* involves **_persistent_ inflammation** of the pancreas caused by **_irreversible_ changes** to pancreatic structure
* this involves **fibrosis, atrophy** and **calcification**
* usually caused by recurrent bouts of acute pancreatitis
91
What are the most common causes of chronic pancreatitis?
* it is caused by **_recurrent bouts of acute pancreatitis_**
* this is most commonly due to **alcohol**
* **trauma** to the pancreas
* pancreatic **tumours**
* **_cystic fibrosis_**
* **__**this is the most common cause of chronic pancreatitis in children
92
How can cystic fibrosis cause pancreatitis?
* there is a mutation in the **_CFTR gene_**, which encodes an **ion transporter**
* there is **disruption to ion transport**
* this leads to **pancreatic secretions** becoming **_thick / sticky_**
* viscous secretions will **_obstruct / block pancreatic ducts_**
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How can repeated bouts of acute pancreatitis progress to chronic pancreatitis?
* with each bout, there is potential for **_duct dilatation_** and **_damage_ to pancreatic tissue**
* as part of the subsequent healing process, pancreatic **_stellate cells**_ lay down _**fibrotic tissue_**
* fibrotic tissue causes **_stenosis (narrowing)_** of the ducts
* there is also **_acinar cell atrophy_**
* **_calcium deposits_** of various sizes can accumulate on the protein plugs that have already formed within the ducts
* this only happens in some causes - such as alcoholic acute pancreatitis
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Why can early diagnosis of chronic pancreatitis be challenging?
What is the most common presenting symptom?
* continuous or intense **_intermittent epigastric pain_** that may **radiate to the back**
* this is usually related to **eating meals**
* it tends to last for several hours
* the pain is **relieved on sitting forwards**
* in acute pancreatitis, there would be elevated serum amylase and lipase
in chronic pancreatitis, there may not be enough healthy pancreatic tissue to make these enzymes
***_serum amylase / lipase is NORMAL_ in chronic states***
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What imaging investigations are performed to diagnose chronic pancreatitis?
* **abdominal X-ray** may show **_calcifications_** within the pancreas
* **ERCP** can be performed to **visualise the pancreatic ducts**
* this will show a **_"chain of lakes" pattern_** due to alternating stenosis and dilatation of the ducts
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What marker can be used to distinguish acute and chronic pancreatitis?
**_faecal elastase_**
* faecal elastase will be **raised** in **_chronic_ pancreatitis**
* it will be normal in acute pancreatitis
* ***serum _amylase***_ will be raised in _***acute_ pancreatitis***
* it will be normal in chronic pancreatitis
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As chronic pancreatitis progresses, what signs might someone with pancreatic insufficiency show?
Why does this happen?
* **acinar cells** become impaired and produce **fewer digestive enzymes**
* patient has **trouble absorbing food / dietary fats**, leading to **_weight loss**_ and _**deficiency of fat-soluble vitamins_**
* the fat-soluble vitamins are A, D, E and K
* fat passes through the intestines without being digested, leading to **greasy, foul-smelling stools**
* this is **steatorrhoea**
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What condition can develop as a long-term consequence of chronic pancreatitis?
**_diabetes mellitus_**
* recurrent inflammation begins to damage the alpha and beta cells of the pancreas
* this impairs insulin secretion
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What is involved in the treatment of chronic pancreatitis?
* treatment mainly involves **controlling pain / risk factors**
* drinking less alcohol
* eating less meat
* losing weight
* pancreatic **enzyme replacement** / **nutritional supplements** are given in pancreatic insufficiency
* **diabetes medications** are given if necessary
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What is meant by bowel obstruction?
What are the 2 categories of causes?
* when the normal flow of contents moving through the intestines is interrupted
***_Mechanical Causes:_***
* there is an **_actual blockage_** in the large or small intestine
* this blockage can be **partial** or **complete**
***_Functional Causes:_***
* this is causes by **_disruption to peristalsis_**
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What is the difference between partial and complete bowel obstruction?
***_Partial obstruction:_***
* **gas** or **liquid stool** can pass through the point of narrowing
***_Complete obstruction:_***
* absolutely **nothing** can pass through the point of narrowing
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What are the mechanical causes of small and large bowel obstruction?
***_Small bowel obstruction:_***
* post-operative adhesions
* scar tissue that forms after surgery can form fibrous bands that cause organs to attach to the surgical site or other organs
* the lumen of the bowel can become pinched tight in some locations
* hernias
***_Large bowel obstruction:_***
* volvulus
* a loop of intestine twists around on itself, kinking off the lumen
* a volvulus can occur around a mass - e.g. colorectal cancer
***_Both:_***
* ingestion of a foreign body
* intussusception
* inflammatory bowel disease - which causes strictures & adhesions
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What are the potential functional causes of bowel obstruction?
* anything that **_reduces smooth muscle contractility / peristalsis_**
* post-operative ileus
* transient paralysis of the smooth muscle following surgery
* hypothyroidism
* inflammation and infection
* electrolyte abnormalitites
* e.g. hypokalaemia, hypercalcaemia
* some medications - e.g. opioids
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How can oedema and ischaemia result from bowel obstruction?
* proximal to the obstruction, gas and stools start to **accumulate**
* this leads to **_dilatation of the bowel_** and **_abdominal distension_**
* as pressure within the bowel lumen increases, intenstinal contents will **compress blood and lymphatic vessels** within the intestinal wall
* **veins and lymphatics** are compressed first as they have weaker walls
* **increased pressure** within these vessels **pushes fluid** into the surrounding area causing **_mucosal oedema_**
* if the pressure in the lumen continues to increase, the **_arteries can become compressed_**
* this leads to **reduced blood flow to the intestinal wall** (ischaemia)
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How can bowel ischaemia and hypoxia lead to damaged capillaries?
* hypoxia is accompanied by production of **_reactive oxygen species_**
* these **damage mucosal cells**, leading to **_cell death / mucosal infarction_**
* capillaries within the intestinal wall **rupture**, leading to blood entering the intestinal lumen
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What happens once blood enters the intestinal lumen?
* the presence of **blood and stool** in the lumen acts as a **_nutritional supply for gut bacteria_**
* gut bacteria **multiply rapidly**
* gut bacteria enter the **intestinal wall**
* **macrophages** rush into the intestinal wall and release **inflammatory cytokines**
* cytokines **increase blood vessel permeability**, which increases **_mucosal oedema, inflammation and damage_**
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What are the consequences in bowel obstruction when inflammatory cytokines have increased blood vessel permeability?
* there is increased mucosal oedema, inflammation and damage
* the overall result is **_compromised ability_** of the mucosa to **_absorb food and water_**
* this leads to **_dehydration_** and **_loss of electrolytes_**
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How can perforation result from bowel obstruction?
* if pressure within the bowel lumen becomes high enough, it can lead to **compression of large arteries**
* bowel ischaemia / infarction extends from just the mucosa to **all layers of the bowel wall**
* this is **_transmural infarction_**
* transmural infarction can lead to **perforation**
* bacteria within the bowel lumen leak into the peritoneal cavity and cause **_peritonitis_**
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How can peritonitis lead to sepsis?
* the layers of the peritoneum are highly vascularised
* large numbers of bacteria **enter the bloodstream**, causing a **_massive inflammatory response_**
* this is sepsis
* blood vessels throughout the body become **"leaky",** allowing cells and fluid to leak into the interstitial space
* this **reduces blood volume** and **_blood pressure_**
* there is **less blood and oxygen** reaching vital organs, which is **_shock_**
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What are the typical symptoms of bowel obstruction?
* **vomiting**
* this is more common in small bowel obstruction
* **abdominal distension**
* **constipation**
* **diffuse / cramping abdominal pain**
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How can you tell the difference in symptoms of complete and partial bowel obstruction?
***_Partial obstruction:_***
* symptoms come on more **gradually** and are **milder**
* e.g. abdominal pain after meals, constipation
***_Complete obstruction:_***
* symptoms tend to come on **very suddenly**
* there is **_absolute constipation_**
* absolutely nothing can pass - not even gas / liquid stool
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How are the symptoms different in small and large bowel obstruction?
How might you know if there has been a perforation?
***_Small bowel:_***
* **_vomiting_** is more common
* pain tends to be **_periumbilical_** (around bellybutton)
* bouts of **crampy intermittent** abdominal pain that last for a **_few minutes_** at a time
***_Large bowel:_***
* vomiting is less common
* pain tends to be **_lower down_** in the abdomen
* bouts of pain tend to be **_less frequent_**, but **_last for longer_**
***_Perforation:_***
* when there is progression from **vague / crampy pains** to more **_constant / focal pains_**
* this indicates **peritoneal irritation** due to perforation
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What are key things to pick up in the history of someone with a bowel obstruction?
* **malignancy** history
* colorectal cancer can cause volvulus
* **hernia** history
* **surgical** history (risk of adhesions)
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How can bowel obstruction affect breathing?
* abdominal distension can **_push on the diaphragm_** and make it more difficult for the lungs to expand
* this leads to **_respiratory distress_**
* patient may present with **shortness of breath**, **tachypnoea** and **cyanosis**
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What might you see on general inspection and auscultation in bowel obstruction?
* **_high-pitched, tinkling bowel sounds_** suggest ***mechanical obstruction***
* complete **_absence of bowel sounds_** suggests ***functional obstruction***
* **abdominal distension**
* **pyrexia / sweating** - this is more prevalent if there is a perforation
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What investigations are performed if bowel obstruction is suspected?
* **abdominal X-ray**
* looking for signs of **volvulus** and/or **Rigler's sign**
* **CT abdomen with contrast**
* abdominal USS if CT is contraindicated
* e.g. in pregnancy / contrast allergy
* bloods
* FBC and crossmatch - in case of perforation
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How can you tell the difference between large bowel and small bowel on AXR?
* **_valvulae conniventes_** are seen in the ***small bowel***
* these are lines that **transect the entire bowel**
* **_haustra_** are seen in the ***large bowel***
* these do not transect the entire bowel
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How do you tell the difference between caecal and sigmoid volvulus on AXR?
* ***caecal volvulus*** is represented by the **_"embryo"**_ or _**"comma" sign_**
* formed from the caecum folding up in RIF
* **sigmoid volvulus** is represented by the **_coffee bean sign_**
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What is Rigler's sign?
* if there is **air present on _both sides_ of the bowel wall** then this indicates **_perforation_**
* also known as the ***double-wall sign***
* there is gas outlining both sides of the bowel wall
* gas within the bowel lumen and gas within the peritoneum
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What are the treatment options for bowel obstruction?
* generally, bowel obstructions resolve on their own so treatment focuses on **relieving symptoms**
* IV fluids
* nasogastric suction
* **"drip and suck"** to remove gas / liquid from the stomach that has accumulated
* if symptoms do not improve, or there is perforation, then surgery is performed
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What is meant by intestinal ischaemia?
What are the 2 different types?
* **_reduction in blood flow_** to the intestine, resulting in **ischaemia of the _bowel wall_**
* if it affects the ***small bowel***, it is **_mesenteric ischaemia_**
* if it affects the ***large bowel***, it is **_ischaemic colitis_**
* this leads to **_infarction_** when part of the intestinal wall necroses/dies
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What is the main source of blood to the small intestine?
What type of blood supply exists to try and prevent small bowel ischaemia?
* blood supply mainly comes from the **_superior mesenteric artery_**
* branches of this artery spread through the mesentery (**_mesenteric arteries_**)
* mesenteric arteries penetrate the submucosa and branch into arterioles
* small intestine has a **high demand for oxygen and nutrients** to sustain digestion, so it is **_susceptible to ischaemia_**
* mesenteric arteries **branch and reconnect at points** forming a **_collateral circulation_**
* if blood flow is reduced in one pathway, the tissue can still receive blood via another pathway
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When does small bowel infarction occur?
* when there is **_significant reduction in blood flow_** to the small intestine
* this **reduces the blood pressure** meaning that there is **_insufficient blood flow_ throughout the _collateral circulation_**
* this initiates **ischaemic injury** in a **_wide region_** of tissue
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What is meant by reperfusion injury?
* reperfusion injury occurs when **_blood flow returns to ischaemic tissue_**
* influx of oxygen into an already damaged cell can **increase oxidative stress** and cause **further cell damage**
* damaged /ischaemic cells release **_reactive oxygen species_**, which stimulate an **immune response**
* immune cells remove damaged/dead cells and release **cytokines**
* cytokines cause blood vessels to become more **permeable**, resulting in **_bowel oedema_**
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What layers of the bowel are affected in mesenteric ischaemia?
How do symptoms range in severity?
* mesenteric ischaemia becomes more severe as it extends from a **_mucosal infarct_** to a **_transmural infarct_**
* it goes from only affecting the mucosa to affecting all the layers of the bowel wall
* early-on, ischaemia causes **_ileus_**
* this is where the bowel stops working
* food lingers in the bowel and doesn't get pushed along
* severe damage can cause a **_break in the epithelial lining_** of the bowel, allowing **bacteria in the lumen** to enter **blood vessels** within the bowel wall
* bacteria can pass through the wall into the **peritoneal space**, causing **_bacterial peritonitis_**
* they can also pass from the peritoneal space into lymphatics and blood vessels
* if bacteria enter the bloodstream, this can lead to **_septic shock_**
* this involves hypoperfusion of organs throughout the body
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What are the occlusive causes of mesenteric ischaemia?
What type of infarct does this usually cause?
* this involves a **_physical blockage_** that prevents blood flow through the vasculature
* usually causes a t**_ransmural infarct_**
* **_thrombus formation_** in superior mesenteric artery or vein
* this leads to thrombosis and occlusion of the vessel
* **_thromboembolism_** occluding superior mesenteric artery
* part of a blood clot has broken off, travelled through the bloodstream and lodged in SMA
* **tumour, hernia, volvulus or intussusception** (telescoping of bowel) can physically **_compress the vascualture_** and occlude blood flow
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What are the non-occlusive causes of mesenteric ischaemia?
What type of infarct does this usually cause?
* non-occlusive causes are related to **_systemic decreases in blood flow_**
* this usually leads to **_mucosal infarcts_**
* **_hypovolaemia_** due to **severe haemorrhage** or **dehydration**
* **_low cardiac output_** state
* e.g. after an MI
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What is the key triad of symptoms associated with mesenteric ischaemia?
* sudden, diffuse abdominal pain
* shock
* normal abdominal examination
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What are the typical symptoms of mesenteric ischaemia?
* ischaemia causes **_sudden, severe abdominal pain_**
* the abdomen is **normal on examination** and soft
* infarction develops after 12 hours and causes **vomiting** and **bloody diarrhoea** (sometimes)
* over time, the abdomen **becomes distended** and **bowel sounds stop** as the bowel stops moving
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What are the signs that mesenteric ischaemia has lead to sepsis or peritoneal inflammation?
* signs of sepsis include **hypotension, tachycardia, tachypnoea** and **fever**
* fluid accumulating in the abdomen leads to signs of peritoneal inflammation
* these are **_rebound tenderness_** and **_guarding_**
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What is involved in the investigations for mesenteric ischaemia?
* AXR and CT abdomen
* to look for perforation, megacolon and dilation of intestine
* **ABG** shows **_lactic acidosis_**
* CT angiography
* ECG to look for signs of AF
* colonoscopy
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Does mesenteric ischaemia tend to be more occlusive or non-occlusive?
What are key risk factors to pick up from the history?
* tends to be more **_occlusive_** with **sudden, severe symptoms**
* risk factors include **old age** and **cardiovascular disease**
* risk factors for occlusive causes include
* **_AF_**
* **cocaine use**
* **smoking**
* risk factors for non-occlusive causes is **trauma**
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What might be seen on abdominal CT and angiography in mesenteric ischaemia?
* abdominal CT shows **bowel dilatation** and **bowel wall thickening** from oedema/inflammation
* it can also show **_intestinal pneumatosis_** (air in bowel wall)
* CT angiography is used to **visualise blood flow** through the small intestine
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What is involved in the treatment for occlusive and non-occlusive causes mesenteric ischaemia?
* occlusive causes require **thrombectomy** or **thrombolysis**
* this involves dissolving a blood clot or re-establishing blood flow through surgery
* non-occlusive causes are treated with **fluid resuscitation**
* if there is **_gangrene_** (***ischaemic death of the bowel***) then a **_laparotomy_** is required
* this requires surgical resection of the infarcted tissue
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What are the common symptoms of ischaemic colitis?
* this presents with a much more **chronic picture**
* **transient gut claudication**
* **PR bleeding**
* **post-prandial abdominal pain** (after eating)
* **weight loss**
* less calories are being absorbed from food
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What is the blood supply to the large intestine?
Which location is most commonly affected by ischaemic colitis?
* the **_superior mesenteric artery_** supplies from the ***2nd part of the duodenum*** up to the ***splenic flexure***
* the **_inferior mesenteric artery_** supplies the rest of the colon from the splenic flexure
* if there is **hypovolaemia**, the **_splenic flexure_** will be affected first
* this is due to crossover of blood supply from SMA to IMA
* this is known as **Griffith's point**
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Does ischaemic colitis tend to be more occlusive or non-occlusive in nature?
* it is more commonly **_non-occlusive_**
* symptoms typically involve **transient claudication**
* treatment is usually **conservative** with fluids and bowel rest
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What are key factors to take from the history of someone presenting with ischaemic colitis?
* old age
* cardiovascular disease
***_Occlusive causes:_***
* atrial fibrillation
* smoking
* cocaine use
***_Non-occlusive causes:_***
* history of trauma
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What is involved in the management of ischaemic colitis?
* management is mainly supportive with **_IV fluids_**
* **_drip and suck_** is performed if there is an **ileus**
* ****an ileus occurs when the bowel stops moving
* this can cause an obstructive picture (**pseudo-obstruction**)
* if it is more severe and there is gangrene (areas of infarction) then **_laparotomy_** is performed
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