Acute abdomen Flashcards
Which fibres carry visceral pain information? Provide extra info on visceral pain
- C- fibres
- slow conduction
- hijack somatic pain afferents
- pain in dull and vague, poorly localised
- C-fibres are stimulated with stretch, inflammation, ischemia
- located in organs and hollow viscera
- The bilateral sensory supply to the spinal cord means
visceral pain is generally felt in the midline
Which fibres carry parietal pain information? Provide extra info on parietal pain
- C and A delta fibres
A delta fibres are small, myelinated fibres with much faster speed of conduction than C fibres. They are
responsible for the transmission of sharp, acute sensations which are much more precisely localised.
The peritoneal lining of the abdominal cavity contains A delta fibres which can be irritated by the presence
of fluids including pus, bile, blood and urine. They can also be stimulated by inflammatory processes
spreading to involve the overlying peritoneum.
Parietal pain is transmitted unilaterally to the spinal cord and the cutaneous distribution corresponds to
spinal dermatomes. This ensures that parietal pain is more easily localised
3 most common causes of obstruction in the small intestine?
- intra-abdominal adhesions (~75% of cases)
- hernias -> therefore check for inguinal, femoral, and umbilical hernias.
- neoplasm
Review what a BO looks like on x-ray.
- plain x-ray of patient in supine and upright position can confirm the clinical diagnosis of SBO
- small bowel loops appear dilated proximal to the obstruction
- air-fluid levels increase within the colon
- evidence of complication such as:
- bowel perforation → pneumoperitoneum
- bowel ischemia → decreased or abnoral contrast enhancement
Outline management approach for bowel obstructions.
Conservative approach:
- patient needs to be nil by mouth
- need to ensure adequate fluids → IV fluid resuscitation
- patients often dehydrated due to decreased oral intake and vomiting
- electrolyte repletion as needed
- urinary catheter put in to to monitor urinary output
- gastrointestinal decompression with a nasogastric tube provides relief of symptoms, prevents further gas and fluid accumulation proximally, and decreases the risk of aspiration
Surgical intervention:
- nonviable segments of bowel should be resected → for strangulation and bowel necrosis
- laparoscopic adhesiolysis may be performed by skilled surgeons
- endoscopic intervention when there are no signs of strangulation → bowel isn’t removed, but can remove obstruction
- surgery is required for most mechanical large bowel obstructions
Describe the clinical presentation of appendicitis.
Clinical manifestation:
- begins with dull visceral pain in the epigastric area (for about 12-24hrs and progresses to more defined, sharp pain in the right iliac fossa. This is because the inflammation remained confined to the appendix (therefore visceral pain), and then it progresses to the peritoneum (becomes somatic/parietal pain).
- patient may look flushes, unwell, and often febrile
- will experience guarding and rebound tenderness
- pain upon coughing
- experience McBurney’s Point tenderness (the point on the lower right quadrant of the abdomen at which tenderness is maximal in cases of acute appendicitis)
Laboratory findings:
- raised WBC
- elevated CRP
Explain why shifting pain occurs in appendicitis.
Pain that “shifts” from the original site of onset to another location in the abdomen is most often associated with acute appendicitis where periumbilical or epigastric pain (visceral → C fibres) that is present early in the course of the disease is replaced with right lower quadrant (somatic → C and A-delta fibres) pain later in the illness when the parietal peritoneum becomes involved with the inflammatory process.
Hence, initially felt in the dermatomes of T10-11 as the C-fibres innervating the appendix ‘hijack’ the somatic pain efferents of the lesser splanchnic nerve.
Difference between cholecystitis vs cholangitis vs cholelithiasis
Cholecystitis = inflammation of the gallbladder and cystic duct
Cholelithiasis = gallstones
Cholangitis = inflammation of the bile ducts/biliary system
Essentials of diagnosis of acute cholecystitis
Essentials of diagnosis:
- steady, severe pain and tenderness in the right hypochondrium or epigastrium
- nausea and vomiting
- fever and leukocytosis
Aetiology of acute pancreatitis
I GET SMASHED
- Idiopathic
- Gallstones (60% → temporarily lodge at the sphincter of Oddi → pancreatic enzymes can be released and begin auto-digesting the pancreas)
- Ethanol (30% → leads to intracellular accumulation and premature activation of pancreatic enzymes.
- Tumours
- Surgeries → ERCP (endoscopic retrograde cholangiopancreatography)
- Microbiological
- Autoimmune → SLE, Crohn’s disease
- Scorpion venom
- Hyperlipidemia/hypothermia/hypercalcaemia
- Embolic/ischemia
- Drugs and toxins → e.g. corticosteroids
Essentials of diagnosis for acute pancreatitis
- abrupt onset of deep epigastric pain, often with radiation to the back
- history of previous episodes, often related to alcohol intake
- nausea, vomiting, sweating, weakness
- abdominal tenderness and distention and fever
- leukocytosis, elevated serum amylase, elevated serum lipase
Signs, symptoms and lab findings of acute pancreatitis
Signs and symptoms
- epigastric abdominal pain, generally abrupt in onset
- pain is steady and severe, and often made worse by walking and lying supine
- pain usually radiated to the back
- nausea and vomiting are usually present
- abdomen is often tender without guarding or rebound tenderness
- can have fever, tachycardia, hypotension, pallor
Laboratory findings:
- serum amylase and lipase are elevated → usually more than 3x the upper limit of normal
- leukocytosis often present
- elevated serum creatine level at 48hrs is associated with the development of pancreatic necrosis
Ranson criteria for assessing the severity of acute pancreatitis
What is Charcots triad and what is it associated with?
Fever, abdominal pain, and jaundice.
Associated with cholangitis.
What is Reynold’s pentad and what is it associated with?
Fever, abdominal pain, and jaundice + hypotension and confusion.
Associated with suppurative cholangitis (pus in the bile ducts)
Interpret investigation findings for jaundice. Include pre, intra, and post hepatic findings.
Consider:
UCB
CB
AST and ALT (transaminases)
ALP and GGT (cholestatic enzymes)
urinalysis (colour, urinary bilirubin and urinary urobilinogen)
Describe the classification and pathophysiology of hiatal hernias
Sliding:
- displacement of the GOJ above the diaphragm decreases the LOS pressure
- this decrease in pressure predisposes the patient to reflux, hence most common symptom is heartburn
- gastric fundus remains below the diaphragm
Rolling/para-oesophageal:
- twisting of the stomach into the thoracic cavity can produce strangulation with obstruction and ischemia
- can result in pain, vomiting and necrosis
Investigations for RLQ pain (suspected appendicitis)
How septic shock causes metabolic acidosis
