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YEAR 3 - SEMESTER 2 > Case 9 - Acute Abdomen > Flashcards

Case 9 - Acute Abdomen Flashcards

1
Q

Name the 3 most common causes of an acute abdomen from the VINDICATE acronym

A

VIT - vascular, infection/inflammation, trauma

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2
Q

Name 3 gastrointestinal causes of acute abdominal pain

A
  • Appendicitis
  • Biliary disease
  • Pancreatitis
  • Diverticular disease
  • PUD
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3
Q

Name 3 genitourinary causes for acute abdominal pain

A
  • UTI
  • Nephrolithiasis
  • Ovarian torsion
  • Ruptured ovarian cyst
  • PID
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4
Q

Name 6 common causes of abdominal distension

A

Fluid, fat, faeces, flatus, foetus, filthy big tumour, organomegaly

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5
Q

What is the significance of rigidity?

A

Rigidity is the constant involuntary contraction of abdominal muscles in response to an injury.

It is an important sign of peritonism.

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6
Q

Hyperresonant percussion note across a distended abdomen indicates which cause of distension?

A

Hyperresonance = air

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7
Q

What is the most common cause of hyperactive bowel sounds? What are 2 other causes/DDx?

A

Most common: bowel obstruction

DDx: gastroenteritis, IBD

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8
Q

What do ‘tinkling’ bowel sounds indicate?

A

Bowel obstruction

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9
Q

Name 2 causes of absent bowel sounds

A
  • Ileus

- Later stages of intestinal obstruction

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10
Q

Give 2 differentials for each of the following causes of RUQ pain:

  • Liver
  • Biliary
  • Other
A

LIVER: infectious (acute viral hepatitis, liver abscess), non-infectious (CHF/hepatic congestion, non-infectious hepatitis e.g. alcohol & medication, Budd-Chiari syndrome)

BILIARY: infectious (ascending cholangitis, acute cholecystitis), non-infectious (gallstones, choledocholithiasis)

OTHER: RLL pneumonia, sub diaphragmatic abscess

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11
Q

Name 3 causes of acute abdominal pain that is DIFFUSE / POORLY-LOCALISED

A
  • IBD
  • Spontaneous bacterial peritonitis
  • Secondary peritonitis (e.g. bowel perforation)
  • DKA
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12
Q

What type of abdominal pathology causes pain to radiate to the back?

A

Pyelonephritis

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13
Q

What type of abdominal pathology causes pain to radiate down the groin?

A

Nephrolithiasis

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14
Q

What type of abdominal pathology causes pain to radiate to the shoulder?

A

Hepatic & biliary pathology

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15
Q

What type of abdominal pathology causes pain to radiate straight backwards?

A
  • AAA
  • Pancreatitis

https://www.youtube.com/watch?v=_PDOXlVGeuY

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16
Q

Name the 2 layers of peritoneum and the types of pain they cause

A

PARIETAL PERITONEUM: lines the abdominal cavity and causes SOMATIC (well-localised) pain

VISCERAL PERITONEUM: lines the abdominal organs and causes VISCERAL (poorly-localised, can cause referred) pain

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17
Q

Where does foregut, midgut, and hindgut pain refer?

A

FOREGUT: epigastric
MIDGUT: umbilical
HINDGUT: suprapubic

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18
Q

What is the most common type of peritonitis?

A

Secondary peritonitis; other structures are infected, causing the infective organism to be introduced to the peritoneum

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19
Q

Name 4 INFLAMMATORY causes of secondary peritonitis

A
  • ITIS: appendicitis, diverticulitis, acute pancreatitis, cholecystitis
  • Small bowel ischaemia
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20
Q

Name 3 PERFORATIVE causes of secondary peritonitis

A
  • PUD perforation
  • Appendicitis
  • Diverticulitis
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21
Q

Use the ‘I GET SMASHED’ pneumonic to list the causes of pancreatitis

A

I - idiopathic

G - gallstones
E - ethanol
T - trauma (post-ERCP)

S - steroids
M - mumps virus
A - autoimmune
S - scorpion stings / spider bites
H - high cholesterol / calcium levels
E - ERCP
D - drugs (azathioprine, diuretics)
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22
Q

Outline the pathophysiology of gallstones leading to acute pancreatitis

A
  1. Stone lodged in distal common bile duct, blocking the ampulla of Vater
  2. Increased pressure in the pancreatic duct / bile reflux into the pancreas
  3. Inflammation & injury to pancreas
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23
Q

List 4 common symptoms of acute pancreatitis

A
  • Rapid onset of epigastric pain (may radiate to the back)
  • Nause/vomiting
  • Anorexia
  • Malaise
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24
Q

The pain of acute pancreatitis may be relieved by what positional changes?

A

Leaning forward or sitting up

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25
Q

Name 2 scoring systems used to evaluate the SEVERITY of pancreatitis

(note that this is separate from the PAIN severity)

A
  • APACHE
  • Modified Glasgow score (PANCREAS: pO2, age, WCC, Ca2+, raised urea, elevated LFTs, albumin, sugar)
  • Atlants
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26
Q

Name the 4 components of SIRS (TTTW)

A

Temperature/Fever (>38 or <36)
Tachycardia (>90)
Tachypnoea (RR>20)
WCC (>11 or <4)

Presence of 2 or more features indicates SIRS

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27
Q

What is the progression of illness when someone has SIRS?

A

Organ dysfunction –> organ failure –> multiple organ failure (MOF) –> Death

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28
Q

Describe the presentation of acute pancreatitis

A
  • Burning epigastric pain (may radiate to the back, worsen with food and when supine)
  • NV
  • Fever
  • Possible pulmonary complications (chest pain, dyspnoea)
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29
Q

List 3 of the most common causes of acute pancreatitis

A
  • Alcohol
  • Gallstones
  • ERCP
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30
Q

Describe the Atlanta scoring system for the classification of acute pancreatitis

A

MILD: no local complications, no organ failure

MODERATE: transient organ failure (<48 hours), +/- local complications

SEVERE: persistent organ failure (>48 hours)

  • local complications = acute peripancreatic fluid accumulation, pancreatic pseudocyst, acute necrotic collection, pleural effusion
  • organ failure = failure of 3 main organs (cardio, respiratory, renal) + OTHER organ systems
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31
Q

What is shock?

A

Tissue hypo perfusion

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32
Q

Name the 6 types of shock

A
  • Hypovolemic
  • Septic
  • Haemorrhagic
  • Anaphylactic
  • Neurogenic
  • Cardiogenic
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33
Q

Metabolic acidosis + abdominal pain should be treated as WHAT CONDITION until proven otherwise?

A

Bowel ischaemia

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34
Q

Which laboratory studies may be deranged in a patient with small bowel obstruction? Explain why.

A

Hypokalaemia - due to vomiting

Hypo/hypernatremia - due to vomiting (retention of sodium and discharge of potassium can occur in the later stages of obstruction, leading to HYPERnatremia)

High urea & creatinine - dehydration, kidney hypoperfusion, AKI

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35
Q

Which anatomical feature distinguishes the small intestine on abdominal X-ray?

A

Valvulae conniventes / plicae circularis

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36
Q

What is the most common cause of small bowel obstruction?

A

Adhesions (related to previous surgical procedures)

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37
Q

What are the 3 most common causes of small bowel obstruction? (ABC)

A

Adhesions, hernias, neoplasms

ABC = adhesions, bulge/hernia, cancer

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38
Q

Use the acronym SHAVIING to list the causes of small bowel obstruction

A 
S - strictures
H - hernias
A - adhesions
V - volvulus
I - infection (e.g. TB, parasites)
I - intussusception / IBD
N - neoplasm
G - gallstones
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39
Q

Describe the clinical presentation of small bowel obstruction

A

Abdominal pain in the umbilical area, colicky in nature

Nausea / Vomiting (more severe in proximal SBO)

Constipation/obstipation

Abdominal distension

Possibly: fever, tachycardia

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40
Q

Describe the clinical presentation of small bowel obstruction

A

Abdominal pain in the umbilical area, colicky in nature

Nausea / Vomiting (more severe in proximal SBO)

Constipation/obstipation

Abdominal distension

Possibly: fever, tachycardia

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41
Q

Passing wind and stool 6-12 hours within symptom onset suggests what type of SBO?

A

PARTIAL small bowel obstruction (as opposed to complete)

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42
Q

Which investigation is used to diagnose a SBO?

A

Abdominal X-ray (supine and erect)

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43
Q

What features must be present on the abdominal X-ray in order for a diagnosis of SBO?

A
  1. Dilated bowel loops with air-fluid levels !
  2. Proximal bowel dilation w/distal bowel collapse
  3. Gasless abdomen
44
Q

Outline the NON-SURGICAL approach to a SBO. How long are these procedures utilised for?

A

72 hours:

  1. NG tube decompression
  2. Fluid resus
  3. Analgesia
  4. Anti-emetics

Continued clinical assessment. If symptoms of SBO persist, surgery is indicated

45
Q

How are adhesive vs. nonadhesive causes of SBO diagnosed?

A

ADHESIVE SBO is often a diagnosis of exclusion, as adhesions cannot be visualised by imaging. A past surgical history + absence of other known causes is suggestive of adhesions.

NON-ADHESIVE causes of SBO can usually be diagnosed with imaging studies

46
Q

When is immediate surgical management indicated for SBO?

A
  1. Signs of bowel compromise (ischaemia, perforation, necrosis) which may manifest as systemic signs (e.g. fever, leukocytosis, tachycardia, metabolic acidosis, SIRS)
  2. Surgically correctable cause of SBO (except adhesions)
46
Q

When is immediate surgical management indicated for SBO?

A
  1. Signs of bowel compromise (ischaemia, perforation, necrosis) which may manifest as systemic signs (e.g. fever, leukocytosis, tachycardia, metabolic acidosis, SIRS)
  2. Surgically correctable cause of SBO (except adhesions)
47
Q

During shock, blood redistribution occurs to protect the brain and heart. What are 2 clinical manifestations of redistribution?

A
  • Cool, clammy peripheries (blood diverted away from skin)

- Low urine output (blood diverted away from kidneys)

48
Q

Shock exceeding compensation is an emergency. List 4 clinical manifestations of this.

A
  • Tachycardia
  • Hypotension
  • Cool, clammy peripheries
  • Low urine output

(septic shock will also present with fever)

49
Q

Describe the supportive management approach for an acute abdomen

A
  1. ESCALATE: MET team, ICU, transfer
  2. AIRWAY/BREATHING: sigh-flow O2 15/L per hour
  3. CIRCULATION: 2x large-bore IV cannula (fluid + Abx if needed)
50
Q

Describe the 7 interventions that should be performed WITHIN 3 HOURS in someone who is suffering from septic shock (https://www.sccm.org)

A
  1. Measure LACTATE level
  2. Blood tests (to be cultured)
  3. Broad-spectrum Abx (if needed - often will be)
  4. FLUIDS: 30mL/kg of IV crystalloid fluids for hypotension or lactate >4mmol/L

Critical care territory / less relevant for med students:

  1. Vasopressors (e.g. noradrenaline)
  2. If persistent hypotension: more detailed assessment of volume status
  3. Re-measure lactate if initial lactate was elevated
51
Q

Which other systems would you consider reviewing in someone who presents with abdominal pain/abdominal pathology?

A
  • GIT
  • Gynaecological
  • Urological
  • Vascular
  • MSK
52
Q

Pyramid of abdominal examination findings in the ACUTE setting

A
  1. Soft, non-tender: normal
  2. Soft, tender: abnormal
  3. Tender, guarding: local peritonitis
  4. Tender, rigidity: generalised peritonitis

Increasing levels of abnormality/pathology which will affect your management

53
Q

What is the pathophysiology behind rebound/percussion tenderness?

A

Peritonitis –> inflammation of the peritoneum –> percussion or letting go of the abdominal wall quickly –> irritates peritoneum –> pain

Sign of peritonitis

54
Q

Localised vs. generalised peritonitis?

A

Localised = signs of peritonism (rigidity, guarding, tenderness) in one section/quadrant of the abdomen

Generalised = signs of peritonism across the entire abdomen

55
Q

How can a small bowel obstruction lead to bowel ischaemia and infarction?

A
  1. Small bowel obstruction
  2. Accumulation of GI contents (gas, fluid, food) proximal to the obstruction
  3. Continued accumulation over time and worsening distension proximal to the obstruction
  4. Increased luminal size & pressure
  5. Pressure compresses intestinal arteries
  6. Decreased bowel perfusion –> ischaemia, infarction, necrosis
56
Q

How can a small bowel obstruction lead to dehydration?

A

GI contents (salts, active solutes) osmotically draw water out of the vascular system and into the GI tract –> lower effective arterial blood volume –> dehydration

Also they’re probably not eating or drinking much

57
Q

How does a small bowel obstruction lead to pain?

A
  1. Small bowel obstruction
  2. Accumulation of GI contents (gas, fluid, food) proximal to the obstruction
  3. Continued accumulation over time and worsening distension proximal to the obstruction
  4. Continued peristalsis pushes against GI contents
  5. Colicky abdominal pain, tenderness, guarding, rigidity
58
Q

Describe the physical exam findings that may be present in someone with acute pancreatitis

A
  • Inspection: possible jaundice, skin changes (e.g. Cullen’s sign, Grey Turner’s sign)
  • Palpation: epigastric tenderness, rigidity, distension, guarding
  • Auscultation: reduced bowel sounds

VITALS: signs of shock (tachycardia, tachypnoea, hypotension, oliguria)

59
Q

Which lab tests would you order for someone with suspected acute pancreatitis and WHY?

A
  1. CBE: leukocytosis supports the diagnosis
  2. Iron studies: raised haematocrit indicates haemoconcentration due to third-spacing and/or inadequate fluid resuscitation
  3. LIPASE: 3x normal limit is diagnostic for acute pancreatitis
  4. AMYLASE: will rise, but is a bit less sensitive and specific for acute pancreatitis and has a short half-life
  5. LFTs: may be deranged due to the disease process, but can also indicate aetiology (raised ALP, GGT suggests biliary cause)
60
Q

Why are calcium levels important in acute pancreatitis?

A

HYPERcalcemia can cause acute pancreatitis, which THEN causes HYPOcalcemia

61
Q

Acute pancreatitis can be diagnosed when 2 out of 3 criteria are met. Name these criteria.

A
  • Consistent clinical findings
  • Lipase 3x normal
  • Supportive findings on imaging
62
Q

Name the 4 steps taken to evaluating and treating acute pancreatitis

A
  1. Evaluate SEVERITY (several scoring systems exist)
  2. Initiate acute treatment
  3. Assess local complications
  4. Assess aetiology
63
Q

Describe the acute treatment for acute pancreatitis

A
  1. Fluid resuscitation w/isotonic crystalloid!!! (fluid replacement is the most important measure)
  2. Analgesia
  3. Nutritional support
  4. Anti-emetics

(if gallstone pancreatitis –> cholecystectomy)

https://www.youtube.com/watch?v=RvYS2RFz4LU

64
Q

Name 4 local complications of acute pancreatitis

A
  • Pseudocyst
  • Abdominal compartment syndrome
  • Bacterial superinfection of necrotic tissue
  • Pleural effusion
65
Q

Name 4 SYSTEMIC complications of acute pancreatitis

A
  • SHOCK
  • SIRS, DIC
  • Hypocalcemia
  • Respiratory failure, ARDS
  • Paralytic ileus
66
Q

Gallstones block which structure to cause acute pancreatitis?

A

Sphincter of odd / hepatopancreatic duct / ampulla of Vater

67
Q

How does acute pancreatitis lead to SIRS?

A

Acute pancreatitis –> blockage of pancreatic secretions –> increased pressure –>

tissue ischaemia due to compression of pancreatic blood vessels + activation of enzymes

–> necrosis, digestion of pancreatic tissue –> inflammation –> SIRS

68
Q

What is the most useful initial test in someone with acute pancreatitis?

A

Ultrasound

69
Q

Describe the ultrasound findings of a patient with gallstones

A

Acoustic shadowing

Dilation of the biliary tract

70
Q

Use the acronym PANCREAS to list the treatment of acute pancreatitis

A

P - perfusion (FLUID REPLACEMENT w/electrolytes)
A - analgesia
N - nutritional support
C - clinical observation
R - radiology (imaging)
E - ERCP for gallstones
A - antibiotics (if there is infected necrosis)
S - surgery/cholecystectomy for biliary pancreatitis

71
Q

What is metoclopramide, and how does it work?

A

An anti-emetic.

It is a dopamine antagonist and has 2 actions:
1. Dopamine antagonist in the chemoreceptor trigger zone (medulla), inhibiting the chemicals that trigger NV

  1. Dopamine antagonist in the LOS, increasing tone and antral + SI contractions
72
Q

What is third-spacing and why does it occur in acute pancreatitis? What are the consequences?

A

DEFINITION: Third-spacing is the movement of intravascular fluid to interstitial spaces. May manifest as raised haematocrit.

Occurs as a result of:

(a) Altered hydrostatic/oncotic pressure
(b) Inflammation/injury to the epithelium.

Can result in hypovolemic shock.

73
Q

Which crystalloid solution is preferred for acute pancreatitis?

A

Lactated Ringer’s / Sodium lactate / Hartmann’s solution

Contains electrolytes

74
Q

Ultrasound findings of pancreatitis

A
  1. Pancreatic oedema: indistinct pancreatic margins
  2. Peripancreatic fluid buildup: area corresponding to pancreas will be hypoechogenic /dark
    - Maybe evidence of necrosis, abscesses, pseudocysts
75
Q

Anti-emetics

A

.

76
Q

Name 7 parameters that can be used to assess severity of hypovolaemic shock

A
  • Pulse (tachycardia)
  • Pulse pressure (weak)
  • Systolic BP (hypotension)
  • Respiratory rate (tachypnoea)
  • Capillary refill
  • Cool, clammy skin
  • Mental status
  • Urine output
77
Q

Name 4 differentials for RUQ pain

A
  • Biliary colic
  • Choledocholithiasis
  • Acute cholecystitis
  • Acute cholangitis
  • R LL pneumonia
78
Q

Name 4 differentials for EPIGASTRIC pain

A
  • PUD
  • Acute pancreatitis
  • GORD
  • MI
  • Gastritis
79
Q

Name 4 differentials for LUQ pain

A
  • PUD
  • Splenic infarct
  • Splenic abscess
  • Splenic rupture
  • LLL pneumonia
80
Q

Name 3 differentials for flank pain

A
  • Pyelonephritis
  • Nephrolithiasis
  • Perinephric abscess
81
Q

Name 5 differentials for umbilical pain

A
  • Early appendicitis
  • Gastroenteritis
  • PUD
  • Bowel obstruction
  • Ruptured AAA
  • Mesenteric ischaemia
82
Q

Name 5 differentials for RIF pain

A
  • Appendicitis
  • Ovarian torsion
  • Testicular torsion
  • Ectopic pregnancy
  • Ruptured ovarian cyst
83
Q

Name 5 differentials for LIF pain

A
  • Diverticulitis
  • Ovarian torsion
  • Testicular torsion
  • Ectopic pregnancy
  • Ruptured ovarian cyst
84
Q

Name 3 differentials for suprapubic pain

A
  • UTI
  • PID
  • Ectopic pregnancy
85
Q

Why is urinary output measured in acute abdo?

How much urine output is desirable?

A

Assess hydration status

0.5mL/kg/hour

86
Q

Name 4 causes of SBO

A
  • Adhesions
  • Hernias
  • Volvulus
  • Intussusception
87
Q

Name 4 causes of SBO

A
  • Adhesions
  • Hernias
  • Volvulus
  • Intussusception
  • Strictures
88
Q

What is Courvoisier’s law?

A

In a patient with painless jaundice and an enlarged gallbladder (or RUQ mass), the cause is unlikely to be gallstones and therefore presumes the cause to be an obstructing pancreatic or biliary neoplasm until proven otherwise

89
Q

What is Murphy’s sign?

A

Murphy’s sign is elicited in patients with acute cholecystitis by asking the patient to take in and hold a deep breath while palpating the right subcostal area. If pain occurs on inspiration, when the inflamed gallbladder comes into contact with the examiner’s hand, Murphy’s sign is positive.

90
Q

State the definitions for cholelithiasis, choledocholithiasis, acute cholecystitis, and ascending/acute cholangitis

A

Cholelithiasis: gallstones in the gallbladder

Choledocholithiasis: gallstones in the common bile duct

Acute cholecystitis: acute inflammation of the gallbladder

Ascending/acute cholangitis: bacterial infection of the biliary tract

91
Q

State the CLINICAL MANIFESTATIONS of cholelithiasis, choledocholithiasis, acute cholecystitis, and ascending/acute cholangitis

A

CHOLELITHIASIS: symptomatic biliary colic <6 hours (RUQ pain), but usually asymptomatic

CHOLEDOCHOLITHIASIS: biliary colic <6 hours (RUQ pain), possible jaundice

ACUTE CHOLECYSTITIS: RUQ pain, positive Murphy’s sign, fever

ASCENDING CHOLANGITIS: Charcot’s triad (RUQ pain, fever, jaundice), Reynold’s pentad (Charcot’s triad PLUS hypotension & mental status changes)

92
Q

Which biliary tract disorders are more likely to have abnormal LFTs? Name the markers which could be raised.

A

Choledocholithiasis: elevated GGT, ALP, AST, and ALT

Ascending cholangitis: elevated ALP, AST, ALT, and total bilirubin

93
Q

Describe the pain of acute pancreatitis

A
  • Epigastric
  • Burning
  • Sudden onset
  • Worsens with food and when supine
  • Improves on sitting up or leaning forward
94
Q

Describe the components of the modified Glasgow score (PANCREAS)

A

Modified Glasgow Score is used for assessing the severity of acute pancreatitis. The components are:

P - (spO2)
A - age >55 years
N - neutrophils (WCC) >15
C - calcium <2mmol/L
R - raised urea >16mmol/L
E - LDH >600
A - albumin <32
S - sugar (BGL >10)

3 or more points (1 point each): severe pancreatitis

95
Q

Outline the initial management of acute pancreatitis

A
  1. IV FLUIDS: 250-500mL of isotonic crystalloid solution
  2. Analgesia: IV morphine or fentanyl
  3. Anti-emetics if needed
  4. Oral intake may not need to be ceased if the patient only has mild pancreatitis and is tolerating PO intake
96
Q

State the following information for metoclopramide:

  1. Drug class
  2. Route of administration
  3. Precautions
  4. Side effects
A
  1. Drug class: dopamine ANTAGONIST
  2. Route of administration: PO, IM, IV
  3. Precautions: avoid in patients <20 years, Parkinson’s patients, and when stimulation of GIT is dangerous (e.g. bowel perforation, obstruction)
  4. Side effects: EPSE (tardive dyskinesia, acute dystonic reaction), akathisia, drowsiness
97
Q

3 complications of bowel obstruction

A
  1. Perforation
  2. Bowel ischaemia
  3. Sepsis (either from necrotic cells or bacterial dissemination d.t. perforation)
98
Q

Most common cause of death in acute pancreatitis?

A

Acute respiratory distress syndrome

99
Q

Mechanism of ARDS in acute pancreatitis

A

Acute pancreatitis –> circulating pancreatic enzymes –> increase in pulmonary vasculature permeability –> transudation of fluid into alveolar space

100
Q

How does acute pancreatitis lead to diminished bowel sounds?

A

Acute pancreatitis –> autodigestion of pancreatic tissue –> necrosis –> inflammation / SIRS –> irritation of intestines –> ileus

101
Q

How does SBO lead to SEPSIS?

A

SBO –> bowel distension –> compression of intestinal lymphatics & veins –> bowel wall oedema –> compression of intestinal arterioles & capillaries –> ischaemia –> increased permeability –> translocation of intraluminal bacteria –> SEPSIS

102
Q

How does SBO lead to peritonitis?

A

SBO –> bowel distension –> compression of intestinal lymphatics & veins –> bowel wall oedema –> compression of intestinal arterioles & capillaries –> ischaemia –> necrosis –> perforation of bowel wall –> PERITONITIS

103
Q

The presence of which 3 clinical features precludes oral intake in acute pancreatitis?

A
  • Ileus
  • Nausea
  • Vomiting
104
Q

Simple vs. complicated vs. red flag bowel obstruction

A

SIMPLE: no evidence of complications (e.g. bowel ischaemia, bowel perforation, or red flag symptoms)

COMPLICATED: strangulation, ischaemia, necrosis

RED FLAG: pain out of proportion, peritoneal signs, SIRS, haemodynamic instability, lab abnormalities (++leukocytosis, metabolic acidosis, lactate)

105
Q

What is the 3-6-9 rule for abdominal X-rays?

A

Transverse diameter greater than the following indicates dilation:

  • Small bowel >3cm
  • Large bowel >6cm
  • Caecum >9cm
106
Q

Results of the following investigations when complicated SBO is present:

  1. CBE
  2. Iron studies
  3. EUC
  4. Lactate
  5. ABG
A
  1. CBE: leukocytosis (e.g. due to SIRS)
  2. Iron studies: raised haematocrit (third-spacing)
  3. EUC: hyponatremia, hypokalaemia, hypochloraemia d.t. vomiting. Hyperkalemia if there is bowel ischaemia.
  4. Lactate: raised (bowel ischaemia)
  5. ABG: metabolic acidosis (bowel ischaemia)

YEAR 3 - SEMESTER 2 (12 decks)

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