ACUTE SURG Flashcards by Eira Hegarty

Pathogenesis of acute appendicitis:

Lymphoid hyperplasia or faecolith obstructs the appendiceal lumen.
GI organisms invade the appendix wall causing oedema, ischaemia +/- perforation.

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Strongest clinical indicator of appendicitis:

Migration of central umbilical / abdominal pain to RIF

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What is the psoas sign?

Extension of the right hip causes pain if the appendix is retrocecal

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Symptoms of appendicitis:

Migratory pain central to RIF
Some vomiting, not loads
Nausea
Mild pyrexia
Anorexia

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Causes of acute pancreatitis:

Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune e.g. SLE
Scorpion
Hypercalcaemia
ERCP
Drugs inc NSAID, azathioprine, mesalazine, diuretics, SV

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What is meant by ‘third spacing’ in acute pancreatitis?

Inflammatory response increases vascular permeability and causes significant fluid shifting

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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.

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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

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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

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Use of antibiotics in acute pancreatitis:

Not recommended unless acute infection detected e.g. abscess, infected necrosis

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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

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Systemic complications of acute pancreatitis (4):

ARDS
Hypocalcaemia
DIC
Hyperglycaemia (islet of Langerhans dysfunction)

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Which score assesses mortality of patients with pancreatitis?

Ranson score

Uses initial and 48 hour lab values to assess mortality in acute pancreatitis

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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

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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.

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3 symptoms of diverticular disease:

Change in bowel movements e.g. constipation or diarrhoea

Intermittent abdominal pain

Bloating

?Blood in stool

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Investigating acutely unwell abdominal pain imaging:

Plain abdominal films
Erect CXR, these assess for perforation

CT abdomen for abscess etc

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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

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Complications of diverticular disease inc symptoms:

Diverticulitis
Fistulae (pneumaturia or passage of stool through vagina)
Perforation peritonitis
Abscess
Haemorrhage

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Why is urinary frequency, urgency or dysuria a fairly common complaint in diverticulitis?

Inflamed colon irritates the bladder

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Symptoms of diverticulitis:

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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?

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Long thoracic

Axillary node clearance regardless of nerve damage can lead to arm lymphoedema, also the nerve damage can cause functional arm impairment.

Which nerve is most likely damaged during carotid endarterectomy?

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Hypoglossal

Which nerve is most likely damaged during posterior triangle lymph node biopsy:

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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

ACUTE SURG Flashcards

(51 cards)