ACUTE SURG Flashcards
Pathogenesis of acute appendicitis:
Lymphoid hyperplasia or faecolith obstructs the appendiceal lumen.
GI organisms invade the appendix wall causing oedema, ischaemia +/- perforation.
Strongest clinical indicator of appendicitis:
Migration of central umbilical / abdominal pain to RIF
What is the psoas sign?
Extension of the right hip causes pain if the appendix is retrocecal
Symptoms of appendicitis:
Migratory pain central to RIF
Some vomiting, not loads
Nausea
Mild pyrexia
Anorexia
Causes of acute pancreatitis:
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune e.g. SLE
Scorpion
Hypercalcaemia
ERCP
Drugs inc NSAID, azathioprine, mesalazine, diuretics, SV
What is meant by ‘third spacing’ in acute pancreatitis?
Inflammatory response increases vascular permeability and causes significant fluid shifting
How does acute pancreatitis cause hypocalcaemia?
Enzymes are released from the pancreas into the systemic circulation.
These cause autodigestion of fat, leading to fat necrosis.
Fat necrosis involves the breakdown of fat into free fatty acids, which bind with serum calcium to cause chalky deposits.
Discuss investigations in acute pancreatitis:
Serum amylase / lipase >3x upper limit of normal.
Lipase has longer half life and is more specific, more useful is presentation >24 hors.
FBC, CRP, ESR inflammatory markers
U+Es, eGFR for renal function
Diagnosis if enzyme >3x upper limit of normal, and typical pain
US for aetiology
CT for complications e.g. abscess
The Glasgow score is used to assess the severity of pancreatitis. What do the scores indicate, and what are the criteria?
0-1 mild
2 mod
3 severe
PaO2 <8
Age >55
Neutrophils - wcc >15
Calcium <2
uRea >16
Enzyme - LDH >600, AST/ALT >200
Albumin <32
Sugar >10
Use of antibiotics in acute pancreatitis:
Not recommended unless acute infection detected e.g. abscess, infected necrosis
4 supportive treatment options in acute pancreatitis:
Fluid therapy and balance, can cause significant third spacing
NG for nutrition but should encourage eating and drinking as soon as possible
Catheterisation for fluid balance
Opioid analgesia
Systemic complications of acute pancreatitis (4):
ARDS
Hypocalcaemia
DIC
Hyperglycaemia (islet of Langerhans dysfunction)
Which score assesses mortality of patients with pancreatitis?
Ranson score
Uses initial and 48 hour lab values to assess mortality in acute pancreatitis
Peritonitis is a symptom, and can be caused by many different things. What are the presenting features of peritonitis?
Abdominal pain and tenderness
N&V
Shock
Fever
Distension
Tachycardia
SOB
Diverticulosis vs diverticulitis is characterised by the presence of symptoms. What is the anatomical abnormality?
Herniation of colonic mucosa through muscular wall of the colon.
These herniations usually occur between teniae coli where the vessels pierce the muscles to supply the mucosa.
This is why the rectum is spared, because the rectum lacks teniae coli.
3 symptoms of diverticular disease:
Change in bowel movements e.g. constipation or diarrhoea
Intermittent abdominal pain
Bloating
?Blood in stool
Investigating acutely unwell abdominal pain imaging:
Plain abdominal films
Erect CXR, these assess for perforation
CT abdomen for abscess etc
Which classification is used to grade the severity of diverticulitis, and what do the stages indicate, including management of stage IV?
Hinchey classification
I paracolonic abscess
II pelvic abscess
III purulent peritonitis
IV faecal peritonitis - resection and stoma usually, HDU management as high risk of post op complications
Complications of diverticular disease inc symptoms:
Diverticulitis
Fistulae (pneumaturia or passage of stool through vagina)
Perforation peritonitis
Abscess
Haemorrhage
Why is urinary frequency, urgency or dysuria a fairly common complaint in diverticulitis?
Inflamed colon irritates the bladder
Symptoms of diverticulitis:
Low grade fever
LIF pain
Tachycardia
Tender palpable mass ?abscess
Guarding, rigid, rebound tenderness ?perf
Which nerve is most likely damaged in axillary node clearance?
Long thoracic
Which nerve is most likely damaged during carotid endarterectomy?
Hypoglossal
Which nerve is most likely damaged during posterior triangle lymph node biopsy:
Spinal accessory
Which nerve is always at risk during a parotidectomy?
Facial nerve
Why does ileus occur post GI surgery?
Fluid sequestration and loss of electrolytes
When are all men offered a Triple A screening US? What happens if the diameter is >3cm? >5.5cm?
Age 65 one off US screening.
3-4.4 = rescan every 12 months
4.5-5.4 = rescan every 3 months
Once an AAA has been found, CT contrast should be done as a follow up IF >5.5 CM.
Management of low rupture risk patients, and what counts as low rupture risk?
<5.5, no symptoms:
US surveillance
3-4.4 = rescan every 12 months
4.5-5.4 = rescan every 3 months
OPTIMISE cardiovascular risk factors:
Smoking cessation
Improve BP control
Commence statin and aspirin
Weight loss and increased exercise
Who counts as high rupture risk, and what is their management?
> =5.5cm, symptomatic or >1cm / year growth:
2ww referral
EVAR, or open if unsuitable - stent in femoral artery to stop blood from pooling into the aneurysm.
Complication = stent could leak, usually asx but seen on routine follow up.
Symptomatic AAA symptoms:
Abdominal pain
Back or loin pain
Distal embolisation resulting in limb ischaemia
?pulsatile mass felt in abdomen
When should DVLA be informed about an AAA?
> 6.5 cm
Disqualified from driving until repaired
Ruptured triple A risk is increased by (?) and symptoms are (?), indicating the classic triad:
Increased diameter, female, smoking and hypertension increase the risk of AAA rupture.
Symptoms:
Triad = hypotension, flank / back pain, pulsatile mass.
+ sudden onset, syncope, vomiting, etc
Direction of rupture of a triple A dictates prognosis to a certain degree. Discuss this.
Anterior rupture (20%) = very poor prognosis, ruptures into the peritoneal cavity
Posterior rupture into the retroperitoneal space = 80%, less bad
Immediate management of a suspected triple A rupture:
High flow oxygen
2x access, immediate bloods including FBC, U&Es, clotting, crossmatch 6 units.
Discuss BP control in suspected triple A rupture:
Permissive hypotension <100mmHg to minimise bleeding and to prevent the potentially formed clots from dislodging
Definitive management of triple A rupture:
Unstable = immediate surgical exploration and open repair
Stable = CT ANGIO to determine whether suitable for endovascular repair
4 types of AAA:
Supra-renal
Para-renal
Juxta-renal
Infra-renal
Risk factors for AAA:
HTN
Smoking
Age
Male
Ehlers Danlos Type I
Marfan’s syndrome
Syphilis
?Diabetes is protective?
Describe brief pathophysiology of AAA:
Failure of elastic proteins within ECM, usually degenerative.
Dilation of all layers of the arterial wall.
Primary event is loss of intima and elastic fibres from the media.
Timeframe for acute limb ischaemia:
<2 weeks counts as acute limb ischaemia
History taking in suspected acute limb ischaemia:
Acute changes and onset of new symptoms
Hx of previous PAD
Focused system review looking for embolic / thrombus causes.
6 Ps of acute limb ischaemia:
Pain
Pulseless
Pallor
+ poikilothermia, paraesthesia and paralysis
Discuss Rutherford Staging in acute limb ischaemia in terms of prognosis, sensory loss and muscle weakness.
I not acutely threatened, no sensory or motor changes
IIa prompt revascularisation, toes sensory affected, no muscle weakness
IIb immediate required, more than toes sensory, mild/mod limb weakness
III non-salvageable - anaesthetic sensory loss, paralysis
3 aetiological groups of acute limb ischaemia cause:
Embolus
Thrombus
Trauma e.g. compartment syndrome
Complete arterial occlusion will lead to irreversible damage in how long?
6 hours
Immediate management and investigation in suspected acute limb ischaemia:
High flow O2
IV access, bloods inc lactate for ischaemia, thrombophilia screen if <50 and have no other risk factors, group and save, ECG also.
Therapeutic dose heparin
Doppler US
CT Angiography!
Factors suggesting embolic vs thrombotic cause in acute limb ischaemia:
Embolus:
Recent MI / AF present
<24 hour onset
No Hx of PVD
Evidence of proximal aneurysm i.e. source of embolus
Important complication of revascularisation in acute limb ischaemia:
Reperfusion injury:
Compartment syndrome, fasciotomies are often done during the operation because of how frequent this is.
K+ and H+ release from damaged cells + myoglobin; acidosis + AKI
Definitive surgical management for a) emboli, b)thrombotic disease:
Embolus:
Embolectomy with Fogarty catheter
Intra-arterial thrombolysis
Bypass surgery
Thrombus:
Thrombolysis and bypass the same, but also angioplasty is an option.
Upper GI tract causes of perforation:
PUD
Stomach and oesophageal cancer
Boerhaave’s syndrome
Lower GI tract causes of perforation:
Diverticulitis
CRC
Foreign body
Appendicitis
Severe colitis e.g. Crohn’s
Toxic megacolon e.g. C.Diff / UC
