DVT Flashcards
DVT SS, RX, Score Mnx and prevention
S+S: calf erythema, tenderness, swelling, warmth.
Risk factors: thrombophilia, synthetic oestrogen, obesity,
past DVT, trauma, ↑ age, pregnancy, surgery, cancer,
immobility.
Wells Score: 1 point – previous DVT, non-varicose collateral
superficial veins, pitting oedema, entire leg swollen, calf
swelling >3cm (measured 10cm below tibial tuberosity),
local tenderness, recently bedridden >3d, major surgery
<12w, immobilization of leg, active cancer (<6m). -2 points –
alternative diagnosis as likely.
0-1 points: unlikely, do d-dimer, if positive do USS and treat,
if negative DVT is excluded.
>1 point: do USS, if positive treat, if negative do d-dimer, if
d-dimer positive repeat USS in 1 week, if d-dimer negative
DVT is excluded.
Management: LMWH e.g. enoxaparin, DOAC e.g. apixaban.
Prevention: LMWH, mobilize early, stop OCP 4w pre-op,
intermittent pneumatic compression device, graduated
compression stockings, fondaparinux.
PE
S+S: hemoptysis, syncope, dizziness, pleuritic chest pain,
acute breathlessness, ↑ JVP, pleural effusion, pleural rub,
AF, hypotension, cyanosis, right ventricular heave, loud P2,
pyrexia, tachypnoea, tachycardia, swollen calf (DVT).
Risk factors: HRT, OCP, post-partum, malignancy,
thrombophilia (anti-phospholipid syndrome), previous PE,
immobility, recent surgery.
Causes: usually from venous thrombosis in legs or pelvis,
right ventricular thrombus post-MI, amniotic fluid, parasites,
air, fat, neoplastic cells, septic emboli (right sided
endocarditis).
Prevention: heparin if immobile, stop HRT and OCP 4w preop.
Investigations: U&E, FBC, ABG, ECG (tachycardia, right axis
deviation, RBBB, right ventricular strain V1-3, SIQIIITIII –
deep S waves in I, Q waves in III, inverted T waves in III),
clotting, d-dimer, CTPA, CXR (atelectasis, small pleural
effusion, wedge shaped infarction, ↓ vascular markings).
Modified PE Wells score: <4 = unlikely, >4 = likely. If unlikely
= d-dimer. If likely/positive d-dimer = CTPA or LMWH if
delayed.
Management: oxygen (hypoxia), morphine (pain/distress)
and anti-emetic, LMWH/fondaparinux, fluid bolus (hypotension), thrombolysis e.g. alteplase
(hemodynamically unstable), LMWH/unfractionated
heparin 5d (hemodynamically stable) then switch to DOAC
or warfarin.
Pancreatitis
Pathology: pancreatic enzyme autodigestion, oedema and
fluid shifts.
Causes GET SMASHED: Gallstones, Ethanol, Trauma,
Steroids, Mumps, Autoimmune, Scorpion venom,
Hyperlipidaemia, Hypothermia, Hypercalcemia, ERCP and
Emboli, Drugs.
S+S: severe epigastric/central abdominal pain relieved by
sitting forward, radiates to back, ileus, jaundice, fever, shock,
rigid abdomen, tachycardia, Cullen’s and Grey Turners.
Investigations: serum amylase (↑), serum lipase, glucose,
U&E, ABG, CRP, AXR (no psoas shadow, sentinel loop), erect
CXR (excludes perforation), CT, US (gallstones), ERCP.
Management: NBM, IVI, catheterize, analgesia, hourly
observations, daily bloods, ERCP and gallstone removal,
?antibiotics, CT monitor, assess severity (PANCREAS: PaO2
<8, Age >55, ↑Neutrophils, ↓Calcium, Renal function
↑urea, ↑Enzymes, Albumin <32, Sugar >10).
Complications: early – shock, ARDS, renal failure, sepsis, DIC,
↑glucose, ↓calcium. Late – pseudocyst, pancreatic
necrosis, abscesses, bleeding, fistulae, thrombosis, recurrent
oedematous pancreatitis.
gallstones
S+S: colicky RUQ pain, after meal, worse if fatty (high CCK
and ↑ gallbladder concentration), more symptoms if
smoking, parity.
Investigations: LFTs, USS, MRI cholangiography, intra-op
imaging.
Management: cholecystectomy, endoscopic retrograde
cholangiopancreatography (risks: pancreatitis, cholangitis,
duodenal perforation, bleeding).
Complications: gallstone ileus, obstructive jaundice,
cholangitis, pancreatitis, empyema, carcinoma, mucocele,
cholecystitis, colic, Mirizzi’s syndrome.
biliary colic
Pathophysiology: gallstones symptomatic with cystic duct
obstruction/ passed into common bile duct.
S+S: radiates to back, ± jaundice.
Investigations: urinalysis, ECG, CXR.
Management: analgesia, NBM, rehydrate, elective
laparoscopic cholecystectomy.
acute cholecystitis
Pathophysiology: follows stone/sludge impaction in neck of
gallbladder, inflammation.
S+S: mildly deranged LFTs, local peritonism, gallbladder
mass, Murphy’s sign, vomiting, fever, RUQ/epigastric pain,
can radiate to right shoulder.
Investigations: FBC (↑ WCC), USS (thick walled, ↓ size
gallbladder, ↑ fluid, stones, ± dilated common bile duct),
abdominal x-ray (± stones, ± porcelain gallbladder).
Management: NBM, pain relief, IVI, co-amoxiclav,
laparoscopic cholecystectomy, perforation = open surgery.
chronic cholecystitis
CHRONIC CHOLECYSTITIS
Pathophysiology: chronic inflammation ± colic.
S+S: vague abdominal discomfort, nausea, fat intolerance,
flatulence, distension.
Investigations: MRCP, USS.
Management: cholecystectomy, ERCP and sphincterotomy
(if dilated CBD and stones).
cholangitis
CHOLANGITIS
Pathophysiology: bile duct infection.
S+S (Charcot’s triad): jaundice, fever, RUQ pain, severely
septic/unwell.
Management: fluid resus, tazobactam, correct
coagulopathy, early ERCP.
acalculos cholecystitis
Pathophysiology: gallbladder inflammation in absence of
any stones.
S+S: high fever, intercurrent illness (diabetes, organ failure,
systemically unwell).
Management: cholecystectomy.
gallbladder abscess
S+S: prodromal illness, systemically unwell, swinging
pyrexia, no generalized peritonism.
Investigations: USS, CT.
Management: percutaneous drainage, cholecystectomy
Post cholecystectomy syndrome
Pathophysiology: abdominal symptoms remain postgallbladder removal. Gallstones escape from the gallbladder
during surgery through CBD, ampulla of Vater and block at
the sphincter of Oddi. Back-up of pancreatic enzymes and
liver bile. Distention and inflammation of ducts, pancreatitis.
S+S: jaundice, deranged LFTs, upper abdominal pain,
epigastric pain radiating to back.
mnx - ERCP
intestinal obstruction
Adynamic: pseudo-obstruction, no clear obstruction, ↓
findings on examination. Examples – mesenteric vascular
occlusion, paralytic ileus.
Dynamic: clear blockage, absolute constipation, ↑
peristalsis. Intraluminal – foreign body, fecal impaction,
gallstones, bezoar. Intramural – inflammation, strictures,
malignancy. Extraluminal – volvulus, malignancy, obstructed
hernia, intussusception, adhesions, and bands.
Pathophysiology:
Proximal: ↑ peristalsis, dilation/distention of gas and fluid,
reduces strength of peristalsis, alters motility,
leads_to_flaccidity_and_paralysis.
Distal: normal bowel motility.
Cardinal S+S: vomiting, constipation, central abdominal
pain, tinkling bowel sounds.
General management: NG tube, NBM, IV fluids, laparoscopy.
Investigations:erect_AXR.
Small bowel obstruction: no/minimal gas, central and
transverse, straight segments, ileum is featureless, jejunum
has_ladder(valvulae_conniventes).
Large bowel obstruction: haustral folds (incomplete lines),
caecum is a large, rounded gas shadow in the RIF.
Investigation_clues:
Strangulation: ↑ amylase, ↑ LDH, ↑ WCC, hyperkalemia.
Dehydration: ↑ urea, ↑ hematocrit, 2O polycythemia.
Fever causes: abscess, ischaemia, perforation, inflammation.
Hypothermia causes: septicemia.
volvulus
Pathophysiology: larger mesentery in sigmoid so easily
twists on own axis.
Management: pass flexible or rigid sigmoidoscopy and flatus
tube, keep for 24h, consider elective sigmoid colectomy if
fails.
intussuception
Pathophysiology: proximal bowel enters the distal lumen,
typically a lead point – lipoma, polyp, tumour.
S+S: severe colicky pain, sausage lump, empty RIF, red
currant jelly stool, blood-stained finger on PR.
Management: hydrostatic reduction with enema, manual
push.
upper gi haemorrhage
Causes: malignancy, peptic ulcer, oesophageal varices,
Mallory-Weiss tear, duodenitis, gastritis/gastric erosions,
drugs (NSAIDs, steroids, aspirin, anticoagulants,
thrombolytics).
S+S: ↓ GCS, hematemesis, melaena, weight loss,
tachycardia, ↓ urine output, clammy/cool, encephalopathy,
hypotension.
Investigations: FBC, LFT, U&E, clotting, crossmatch, ABG,
CXR, ECG, urgent endoscopy.
Management:
Acute: high flow oxygen, 2 large-bore cannula, correct
clotting abnormalities (FFP, vitamin K, platelets), fluids,
transfuse if Hb <70, catheterize, calculate Rockall score,
endoscopy and if fails surgery or mesenteric angiography/
embolization.
General: monitor hourly (CVP, BP, pulse), assess rebleed risk
(high = NBM).
gastrooesophageal varices
Pathophysiology: submucosal venous dilation secondary to
↑ portal pressures.
Causes:
Pre-hepatic: thrombosis (portal/ splenic vein).
Intra-hepatic: cirrhosis, schistosomiasis, congenital hepatic
fibrosis,_myeloproliferative,_sarcoid.
Post-hepatic: veno-occlusive disease, right heart failure,
constrictive pericarditis, Budd-Chiari.
Risk factors: variceal wall, ↑ portal pressure, advanced liver
disease, large variceal size.
Management: IV terlipressin and broad antibiotics.
Primary prophylaxis: propranolol (selective β-blocker),
endoscopic_banding_or_sclerotherapy.
Secondary prophylaxis: banding, non-selective β-blocker,
transjugular intrahepatic porto-systemic shunt.
peptic ulcer bleed
PEPTIC ULCER BLEED
Management: treat H. pylori if positive, PPI. If high risk –
endoscopic hemostasis.
lower GI haemorrhage
Investigations: mesenteric angiography, colonoscopy.
Management: 2 large-bore IV cannula, IV fluids/bloods,
withhold anticoagulants, correct coagulopathy, hemostasis
via colonoscopy
Pathophysiology: disrupted and dilated anal cushions
(usually contribute to anal closure) which are attached by
smooth muscle and elastic tissue. Become painful when they
thrombose or when venous return is blocked. Can protrude
(piles), and if anus is too tight can lead to increased
congestion, hypertrophy and further protrusion, eventually
strangulates.
S+S: bright red PR bleed, anaemia, pruritis ani, mucous
discharge.
Causes: constipation with prolonged straining, congestion
(portal hypertension, pregnancy, congestive cardiac failure,
pelvic tumour).
Investigations: flexible sigmoidoscopy, colonoscopy, rigid
speculum.
Classification: 1st degree = in rectum, 2nd degree = only
prolapse when defecating, 3rd degree = prolapse when
defecating and manually reduce, 4th degree = persistently
prolapsed.
Management:
General: ↑ fluid and fiber intake, topical analgesic,
short_term_topical_steroid.
Prolapsed and thrombosed: analgesia, ice packs, stool
softeners,_self-resolves_in_2-3w.
Non-surgical: rubber band ligation (ulcer to anchor to
mucosa, low recurrence, SE: bleeding, infection, pain),
sclerosants (injected to get fibrotic reaction, SE: prostatitis,
impotence), infra-red coagulation (coagulates vessels and
tethers mucosa to subcutaneous tissue), bipolar diathermy
and direct current electrotherapy (coagulation and fibrosis).
Surgery: excisional hemorrhoidectomy (most effective),
stapled hemorrhoidopexy (↓ pain, ↓ stay, quicker return to
normal, higher recurrence). Complications – infection,
stricture, bleeding, constipation.
neoplastic lower gi haemorrhage
Pathophysiology: mucosal defects on tumour surface, colon
polyps, colorectal cancer.
S+S: occult, painless, intermittent
intra abdominal abscess
Causes: acute appendicitis (pelvic), sigmoid diverticulitis
(paracolic), severe acute cholecystitis, upper GI perforation
(subphrenic), post-anastomotic leakage, infected acute
pancreatitis (parapancreatic), post-trauma.
S+S: malaise, anorexia, constant localized abdominal pain,
tachycardia, localized mass, swinging fever (peaks BD).
Investigations: CRP, U&E, FBC, G&S, helical CT scan, pelvic
USS.
Management:
Emergency: IV morphine, IV antibiotics if septic, large bore
IV access, if hypotensive catheterize and fluid balance.
Definitive: Causes: acute appendicitis (pelvic), sigmoid diverticulitis
(paracolic), severe acute cholecystitis, upper GI perforation
(subphrenic), post-anastomotic leakage, infected acute
pancreatitis (parapancreatic), post-trauma.
S+S: malaise, anorexia, constant localized abdominal pain,
tachycardia, localized mass, swinging fever (peaks BD).
Investigations: CRP, U&E, FBC, G&S, helical CT scan, pelvic
USS.
Management:
Emergency: IV morphine, IV antibiotics if septic, large bore
IV access, if hypotensive catheterize and fluid balance.
Definitive: radiologically guided via uss or ct, open surgical drainage
cellulitis
CELLULITIS
Pathophysiology: acute infection of dermis and
subcutaneous tissue.
S+S: pain, erythema, oedema, warmth, well-defined border,
temperature, tachycardia, typically lower limb.
Investigations: USS, swab, FBC, U&E.
Management: antibiotics, elevate affected part.
Complications: infectious myositis, osteomyelitis,
necrotizing fasciitis, soft-tissue abscess
nec fasc
Pathophysiology: rapidly progressive necrotizing soft tissue
infection, spreads along fascia, typically fatal, rare.
Organisms: polymicrobial, staphylococcus aureus,
clostridum difficle.
S+S: foul grey dish water exudate, friable superficial fascia,
hypotension, crepitus, fever, skin necrosis and bullae, acute
onset severe pain, erythema, oedema.
Investigations: FBC, U&E, swabs, MRI.
Management: broad spectrum antibiotics (clindamycin,
benzylpenicillin), prompt surgical fasciotomy, aggressive
debridement of necrotic tissue, amputation.
