random goodies Flashcards
how do you treat pseudo-obs of large bowel
stop ca channel blockers, anticholinergics and opiates
give neostigmine and colonoscopic decomp
what test should you NOT do when testing for LBO
Barium-messes with colonoscopy
how can you confirm LBO
Abdo X-ray
what does sigmoid volvulus look like on water soluble contrast enema
birds beak
right sided colonic obs Rx
simple
right hemicolectomy via midline lap
anastomosis
left sided colonic obs Rx
COMPLICATED-high risk anastomotic leak
3 options
1. three stage procedure
2. 2 stage procedure (colostomy and closure)
3. one stage
what is 1 stage
subtotal colectomy and ileorectal anastom, good in young patients with good sphincter tone
or
segmental colectomy with washout and primary repair A segmental colectomy
what is a 2 stage
resect obs lesion and create colostomy
then close colost.
ideal for sigmoid carcinoma
what is 3 stage
EMERGENCY MANAGEMENT because little skill required
proximal stoma created to decompress colon
obs lesion removed
stoma closed
alternative to surg repair
endoscopic stent placement (SEMS)
palliative decompression or want to recover properly then do elective
duration of antibiotics to treat pyogenic liver abscess
4-6 weeks or up to 12 weeks (multiple abscesses)
how to treat a pyogenic liver abscess
antibiotics PLUS perc drainage/catheter
which antibiotics are used to treat pyogenic LA
Ceft and Ampi
add Metronidazole if Amoebic LA is suspected
which organisms are involved in Pyogenic LA
E coli
Klebsiella
Bacteroides
Enterococcus
staph and strep from hep artery
first line investigation for Pyogenic LA
U/S then CT
predominant symptom in amoebic LA
PAIN
also get SOB and cough
chronically ill
intermittent fever
where is an amoebic LA usually located
right lobe, solitary
how to treat amoebic LA
usually metronidazole tds 800mg for 5 days is good enough
BUT
U/S guided aspiration and drainage is indicated:
1. 10cm plus
2. inadeq response to Rx
3. impending rupture into NB cavities
4. serology is negative
definitive host for E. granulosus
dog (intermediate is sheep, ingests ova from dog poo whilst grazing)
humans get it when they accidentally eat dog poo
how does a hydatid cyst present
asymp
or compression sx such as RUQ pain, enlarged liver, rupture-shock
coughing up grape skins
diabetic foot: features of neuropathy
motor-muscles weak, foot becomes deformed, pressure at weird places
autonomic-cracks, skin fissures
sensory- not aware of trauma to foot
motor-claw foot syndrome, fat creeps up, ulcer commonly at head of metatarsals or FLAT FOOT
what does motor neuropathy lead to
callus, forms at pressure points
charcot’s foot, arch of foot collapses, bone destruction, tibia and metatarsals drive pressure on mid arch of foot and ulcerates
bony deformity leads to chronic osteitis and sepsis
NOT AS COMMON AS CLAW FOOT
what does autonomic neuropathy lead to
skin fissures-allows bacteria to enter
AV shunting-leads to relative ischaemia
what is most common cause of diabetic foot
COMBO of neuro, vascular and infection predisposition
diabetic vascular disease tends to be more distal-true or false
true
also multilevel
more thigh claudication
they have popliteal trifurcation
how does diabetes inhibit the immune system
polymorphonuclear leukocyte inhibition
does diabetic foot have multiple pathogens or single?
multiple-strep and staph is most dangerous
biggest risk factors for chronic venous disease
age
pregnancy
other risk factors for chronic venous disease
Female sex
* Familial
* Obesity
* Caucasian Race
are varicose veins palpable
yes
telanegctasia
intradermal, less than 1mm
deep blood vessels
below muscle fascia
iliac, femoral, popliteal and tibial veins and branches
subcutaneous superficial blood vessels
long and short saphenous vein
perforators
connects superficial and deep venous systems
direct and indirect(venous sinus in interrim)
3 layers in blood vessel
intima, media, adventitia
veins have wider lumen, thinner media, one way valves
which veins do not contain valves
central ones:
common iliac vein
IVC
Portal
Cerebral
how is venous blood flow mediated
muscle pump mechanism (calves)
Chronic Venous Disease 3 pathophysiology mechanisms
- Obstructed flow
Intrinsic: DVT
Extrinsic: Pregnancy - Refluxing valves
Absent valves (cong atresia)
1 valvular incomp
2 valvular incomp (previous DVT damage) - Dysfunctional muscle pump
neuro (spinal injury)
muscular and joint (arthritis)
outcome of mechanisms of CVD
venous insuff (entire system isnt working)
venous HPT (column of blood, increase pressure)
dilation-varicose veins
venous complications
sometimes step goes straight from venous HPT to venous complications (post-thrombotic)
how does CVD present
ASYMP
or discomfort (pain, aching, throbbing, itchy, heaviness, cramping, restlessness)
cosmetic
swelling-oedema Grade 1 (below ankle), Grade 2 (above ankle), Grade 3 (above knee)
when are symptoms worst for varicose veins
worse at end of day
improved by elevation and GCS (compression stockings)
examine standing and sitting
examination of varicose veins
standing
sitting
distribution (greater saph vein, pelvic etc)
ankle mobility (can calf muscle pump work)
preferred bedside exam of varicose veins
doppler handheld
acute complications of varicose veins
varicosity related
thrombophlebitis (thrombosis and subsequent inflam)-analgesia, Ibuprofen
extensive-anticoag
bleeding-pressure and elevation
chronic complications of varicose veins
venous HPT related
skin: dermatitis, hyperpig
lipodermatosclerosis (wine glass), atrophic blanche
skin ulceration, medial aspect
how to classify CVD
aetiology
primary venous insuff: weak vein walls, dilated walls etc (no underlying cause)
secondary: DVT but LESS COMMON, no varicose veins, just damage inside lumen
otherwise
CEAP classification
C: clinical (4,5,6-venous insuff)
E: Etiology (cong, primary, secondary, not known)
A: Anatomy (sup, deep, perforators, not known)
P: pathophysiology (reflux, obstruction, reflux and obs, not known)
most common CEAP
C2S
EP (primary)
AS (superficial)
PR
investigations for CVD
- Duplex U/S
looks at anatomy, physiology, causes - CT venogram
pelvic and abdo veins
contrast and radiation drawbacks
treatment indications for CVD
symptomatic
complications
cosmetic (private)
treatment for CVD
- Obstrcution-remove obstructing object
- Reflux-destroy/remove vein, replace or repair valves (deep vein)
- Improve musc pump-physio
dominant pathology that causes CVD
reflux
therefore
destroying or removing reflux vein is most common intervention
treatment for CVD
5 types
- compression-mainstay if symp
- sclerotherapy-reticular, spider and perf veins
- transdermal laser therapy-cosmetic, retic and telangectasia
- endovenous ablation-cannula, stim thromb and fibrosis, stop reflux (kill blood vessel), thermal or non-thermal
- open surgery-minimise reflux, complications are DVT and nerve injurt
contraindication to compression
mod to severe PAD
uses of compressive therapy
improves symptoms
confirms venous pathology
prevents progression
prevents complications
ulcer-multilayer compressive dressings
compressive stockings class ii
25-30mmHg at ankle
what causes phlegmasia
extensive proximal DVT
acute complication DVT
phlegmasia alba dolens
white-decreased arterial inflow but some patent venous outflow
phlegmasia cerulea dolens
blue leg
deep cyanosis
sup and deep systems
primary upper limb DVT
thoracic outlet syndrome
extrinsic comp of axillary vein
EFFORT THROMBOSIS
younger, active patients
needs catheter directed thrombolysis and decomp (remove 1st cerv rib)
secondary upper limb DVT
CVC
surgery
cancer
trauma
older patients
PEs
central vein filters
PE prevention
Lower limb: IVC
Upper limb: SVC
if anticoag contraindicated or ineffective
gold standard for PE investigation
CT Pulm Angiography
high risk dying from PE
BP below 90mmHg systolic more than 15 min
inotrope dependant
medium risk dying from PE
Cardiac injury
RV dysfunction
management PE
Anticoag
if not improving
1. thrombolysis (catheter, systemic)
2. endovascular
3. open
