Clinical Skills Flashcards
resp?
rate, sound regularity
12-20 breaths per min
SpO2?
- scale 1: 94-100
- nails: acrylic, nail polish (probe sideways)
- check cap refill
- only put in on their fingers
Recording BP on a NEWS chart?
- systolic: arrow up, diastolic arrow down, diagonal line in between
- is this normal for the patient
pulse?
- manual for an AF patient
ECG = ?s per big square?
0.2 sec per big square (1 small sq is 0.04s)
ECG sticker placement
- 3rd iCS right and left
- left, 5th ICS and one in between the 2
- shoulder or wrist
- ankle
v4 placement?
5th ICS
ECG sticker placements
limb lead placement
- red right arm
- yellow left arm
- green left leg
- black right leg
RIDE YOUR GREEN BIKE
which type of hernias are more common in men?
inguinal
which type of hernias are more common in women?
femoral
test for appendicitis?
speedumb, almosy always lost their appetite
guarding?
tense their abd muscles when you’re about to palpate
rebound?
Rebound tenderness involves tenderness with the sudden withdrawal of manual pressure
what are the signs of peritonitis?
Blumberg’s sign (rebound tenderness) and guarding
air under D on a CXR?
perforation
PR interval should be?
5 small squares
Q wave?
LEFT DEPOLARISES B4 RIGHT SIDE
S wave?
purkinje fibres at the base going off
ST?
isoelectric line, not depolarsing, refractory period
aVR?
negative p and T bc directly opp direction of current
First degree HB?
BBs cause prolonger P-R interval
AF ecg?
no P wave, squiggly baseline and irregularly regular
p mitrale?
double P wave, L artrium enlargement or MS
tall P wave?
RA enlargement (P pulmonale - copd, PE)
which 2 drugs can’t be given together?
DON’T GIVE BBS and CBS together bc can cause 3rd degree HB
priceton heartblock poem
flattened p wave?
hyperkalaemia
RBBB?
2 R waves - r down then r again
ventricular tachycardia?
wide qrs and no p waves
tall tenting T waves?
hyperkalemia, widended qrs needs urgent tx
torsaides de points?
w Mg (key Tx for this), type of VT
LBBB?
axis deviation, septum activated right to left meaning depolarisation vector is not straight down (towards left)
V fib ecg?
should never be a 12 lead - unconcious patient - very random looking
v parkinson white?
p launches straight into qrs without the PR int of the isokinetic line
Breast exam - inspection?
- inspect - arms in neutral
- inspect - arms pressed into hips leaning forward - contracts pecs muscles
- arms raised above head
palpation in a breast exam?
- 45 degree angle
- arm behind head
- start w normal breast
- use flats of fingers
- axillary tail, axillary, supraclavicular and cervical LNs
Method of examining the breast?
- quadrants, clock face methods
describing masses?
- location (to nipple)
- size and shape - round, oval, irregular
- consistency
- margins - smooth or irregular
- mobile, fixed
- tenderness
- skin colour
- note discharge
masses/ skin changes need triple assessment:
- clinical
- imaging - US or mammography
- histology
Signs of breast pathology?
- irregular lump and skin tethering
- asymmetry
- nipple inversion
- discharge
RF for BC?
female, age, oestrogen exposure. BRCA, chest wall radiation
Breast cysts?
- rounded smooth fluctulant lumps
- sometimes tender
fibroadenoma?
- develop from excessive division of a single lobule
- mobile, non tender breast lump
- doesn’t vary in size w menstrual cyccle
* discrete, smooth,very mobile, rubbery swelling
who are fibroadenomas common in?
under 20s
which type of tumours can present similarly to fibroadenomas?
phyllodes tumours
fat necrosis
- due to trauma with rupture of fat cells -> inflammation and calcification over time
- signs - history of trauma, presents similar to cancer
BPH occurs in?
- bph: transitional zone
- sulcus in the middle flattens out
cauda equina?
- bilateral leg weakness, inability to pass urine
position for PR exam?
- lie on their LHS, knees to chest
asking them to cough in a PR exam?
- cough - rectal prolapse, int haemorrhoids - dilated vascular cushions in anal canal
PR - palpation?
- anal tone - 360 degrees
- masses, stool, tenderness
- prostate - walnut sized w palpable midline sulcus
- rubbery but firm with smooth surface
BPH vs PC
bph - symmetrical enlargement
PC - HARD AND IRREGULAR LUMPS
What can falsely raise PSA?
PR exam
which lymph nodes drain the testis?
para-aortic lymph nodes for the testis due to embryological origin
peyronie disease?
fibrous scar tissue on penis, causing curved shape during erection + pain during erection
cemasteric reflex?
L1/L2 loss w torsion
palpation - prehn’s test?
lifting the painful testes reduces the pain in epididmymitis but not testicular torsion
palpation for a PR exam?
- scrotum and scortal wall
- testes - check both prrsent in the scrotum
- inguinal canal and lymph nodes
- abdomen - including para-aortic lymph node
- reassess after getting the patient to stand (hernia at iC - mass that u can’t get above)
hydrocele?
when fluid builds up in tunica vaginalis of the testes
causes of scrotal masses?
- hydrocele - non painful fluctulant swellling that transilluminates
- usually idiopathic but can be 2’ to tumours, trauma, inflammation, pancreatitis, peritoneal dialysis
- should be able to feel it sep from the testes
varicocele?
- varicosires of the pampinoform plexus
- normally on the left
- if occurs suddenly exclude renal cancer
- bag of worms in scortum when standing
RF for testocular tumours?
undescended testes
testicular tumours?
- non tender solid mass in testes, irregular surface to the testes
- assoc w abn sensation
- haematospermia
- secondary hydrocele
- spread via PA LN not inguinal to lngs
markers of testicular tumours?
- markers: B-HCG, LDH and a-FP
presentation of a testicular torsion?
- unilateral severe testicular pain or abd pain
- swollen, red hot testis
- may lie high and transverse in scrotum
what can be lost w TT?
- cremasteric reflex may be lost
treatment of torsion?
bilateral orchidopexy +/- orchidectomy if testis not viable
6 Ps of ischemia?
which nerves are first to become ischemic?
- sensory nerves are small and unmeylinated so they’re first to become ischemic
- first they get tingling from this - parasthesia without paralysis is reversible
why does paralysis occur later on in ischemia?
- paralysis much later bc motor nerves are affected
ALI timeline?
- 6 hour timeline
- 2 hours: parasthesia
- 4 hrs: paralysis from nerve damage
- muscle tenderness indicated muscle damage = poor sign
saddle embolus?
- saddle embolus: aorta blocked at the bifurcation
- can present several hours later with completely rigid legs
rhabdomialysis?
- condition where skeletal muscle breaks down rapidly releasing breakdown products into BS
- myoglobin is harmful to kidneys
causes of rhabdo?
- causes: extensive muscle damage e/g/ crush injury, prolonged immobilization, 3rd degree burns
medications that can cause rhabdo?
statins, propofol
toxins that can cause rhabdo?
snake venom, mushroom poisoning, bee stings, wasp stings
process of rhabdo?
- influx of EC sodium and calcium into muscle cells
- influx of water
- sustained contraction and ATP deletion
- inflammatory process leading to muscle necrosis and release of breakdown products
signs of rhabdo?
- muscle pain
- muscle weakness
- dark urine
- elevation in creatine kinase
most common ALI pres?
- arrythmia - very high pulse
- decompensate - low blood pressure
- blockages can cause thumps higher up
where do blockages occur more?
- blockages can cause thumps higher up
- blockages occur more at the birfurcations - most common is at the common femoral artery - into superficial and deep arteries
what can cause a secondary ischemic episode?
Warm foot and pain -> compartment syndrome from reperfusing quickly after ischemia -> swelling -> reduced perfusion -> secondary ischemic episode
PVD features?
- calf pain in both legs
- come on when exercising
- PVD claudication is alleviated by stopping activity and standing still
- obs to BF of muscle during times of high demand
PVD clinical signs?
- absent pulses
- bruit - turbulent flow usually at the point of stenosis
PVD stents?
- arteries are ballooned at the same time to avoid one artery occluding the other - kissing stents
Rf of PVD?
- smoking
- hypertension
- IHD
- hypercholesterolemia
- diabetes
- male
- age
Spinal claudication?
- spinal claudication also comes on when walking but it typically relieved by sitting down or flexing the spine
- causes the same referred pain down the same leg muscles
critical limb ischemia?
- defined as tissue loss either in the form or gangrene or an ulcer or rest pain for more than 2 weeks
burgers test for ischemia?
With the patient supine, elevate both legs to an angle of 45 degrees and hold for one to two minutes. Observe the color of the feet. Pallor indicates ischaemia. It occurs when the peripheral arterial pressure is inadequate to overcome the effects of gravity.
sunset foot?
critically ischaemic foot may appear red and ‘healthy’. This is known as a ‘sunset’ foot and occurs due to maximal skin capillary dilatation and is often mistaken for cellulitis
what causes sunset foot in critical ischemia?
- due to SNS activiation to get blood to peripheries so there is perm vasodilation -> hot foot - sleeping in chair with foot hanging out
APBI values?
Peripheral arterial disease (PAD) is present if the ABPI is less than 0.95
APBI greater than 1?
in diabetes bc of arterial calcification or arteries can’t be compressed
chronic limb ischemia is ?
end stage PVD
Venous ulcers?
- swelling, discoloration around it
- AVPI >1.4 - inflexible arteries due to diabetes
- elderly
venous ulcers respond to?
compression
Things that would make u consider a venous rather than arterial ulcer?
- DVT history - causes scarring of valves in veins which increases pressure in veins
- varicose veins - inc pressure (reflux)
- palpable pulses excludes arterial disease
appearance of a venous ulcer?
- shallow wet appearance of a venous ulcer
- rusting of skin - hemosiderin deposition
- capillary perfusion drives RBCs into subcutaneous space where they become brown caused by venous hypertension
venous ulcer - scarring?
- proteins in ECM of blood and become hard and scar which causes the leg to shrink - lipodermatossclerosis (upside down champagne bottle)
how does venous hypertension cause ulceration
- venous hypertension -> protein exudate leaks into capillary bed -> ischemia -> ulceration
what impairs ulcer healing?
diabetes
mixed aetiology ulcers?
- 10% are venous ulcers
- 10% are mixed
mixed ulcers signs?
- edematous feet
- monophasic signals on doppler - should be triphasic or biphasic (this requires resistance)
- varcicose veins and hemosiderin depositon
- absent pulses
what causes monophasic signals on doppler?
- monophasic signals on doppler - should be triphasic or biphasic (this requires resistance)
what do we treat first w mixed ulcers?
- treat arteries first - can’t compress bc there is limited circulation so treating veins would cause more ischemia
arterial vs venous ulcers?
diabetic foot ulceration?
- often younger patients
- diabetes and microischemia causes poor healing from injury
- microischemia kills nerves causing misshapen foot (clawed toes) as muscle groups imbalance due to lack of proprioception
diabetic foot ulcer pres?
- swollen foot, swollen lymph notes
- boggy foot that feels like a balloon filled w water
- toe has become black
Tx of DFU?
- emergency - will require amputation within 1 day
- Tx - drainage of pus
Pathogenesis of atherosclerosis?
- Inflammation and accumulation of “foam cell” macrophages
- Fibrosis and progressive luminal narrowing
- Plaque rupture or ulceration
- Thrombosis or thromboembolism
athero steps
non mod athero RF?
- Age (risk increases with advancing age)
- Sex (M>F)
- Family history/ genetics / Race
Modifiable athero RF?
- Smoking
- Hyperlipidaemia
- Hypertension
- Diabetes
- Sedentary lifestyle
Intermittent claudication?
- Cramping muscular pain, which is brought on by exertion, relieved by rest and reproducible on walking that distance again.
- It is due to inadequate oxygen delivery to the muscles.
definition of CLI?
- Defined as ischaemic rest pain for more than 2 weeks, despite analgesia, or the presence of tissue loss (ulcers / gangrene)
recognising intermittent claudication: history
- Site: symptoms evident distal to the level of disease (e.g. calf pain = SFA disease)
- Onset: occurs during exertion e.g. walking; often worse on inclines
Type of pain in intermittent claudication?
cramping, muscular pain
assoc factors w IC?
- Ask about skin changes and ulceration (critical limb ischaemia!)
relieving factors in IC pain?
- Relieved by rest within a few minutes. Unlike spinal stenosis it is not relieved by leaning forwards/bending over.
Leriche Syndrome:
- Aortoiliac occlusion manifesting in:
- buttock & thigh claudication
- impotence
core feature of CLI?
- The core feature of CLI is rest pain.
- This pain is felt in the toes/forefoot as this is the most distal site.
Pain in CLI often?
- Pain often wakes the patient up at night, because of the loss of gravity’s help in perfusing the foot.
- Patients typically hang their legs from the side of the bed, or just resort to sleeping in chairs.
Examination in ischemia?
- Inspection of the legs, comparing both sides, looking for pallor, mottling, skin changes, loss of hair, ulcers (active or healed), gangrene.
- Palpation of temperature, comparing both legs/feet with the back of your hand, and checking the capillary refill time distally.
- Pulses: for the lower limb, this begins with the abdominal aorta, moving distally.
femoral bruit?
sign of occult aortoiliac disease.
Buerger’s test?
- Reported as the angle at which the leg becomes pale when you elevate it against gravity (which healthy limbs don’t do). You then swing the patient’s leg over the side and watch out for a “sunset foot” (arteriolar vasodilatation with foot reperfusion).
falsely high APBI?
diabetes or CKD
+ of computed tomographic angiography
- rapid image acquisition (seconds)
- Relatively high radiation dose
- of CTA?
- Uses iodinated contrast
- risk of causing/ worsening renal injury or failure
- risk of allergic reaction
Magnetic Resonance Angiography – aka MRA -?
- Can take up to 40-60mins
- claustrophobia sometimes an issue
- the contrast used (gadolinium) can very rarely cause Nephrogenic Systemic Fibrosis in patients with existing renal impairment
MRA is not possible in patients w?
pacemakers, ICDs
+ of MRA?
- No iodine-based contrast, therefore lower renal risk
- No Radiation dose - uses magnetic excitement of water molecules
PTA?
- Percutanous Transluminal Angiography / Angioplasty – aka PTA
- catheter in arterial tree
- injection of contrast
DSA?
- “Digital Subtraction Angiography” (DSA) removes all background structures, such as bone, from the image to allow a more detailed view of the arteries
- The “gold-standard’
PTA uses?
- Uses iodinated contrast – risk of causing/ worsening renal impairment
- CO2 can sometimes be used as an alternative
risks of pta?
- Risks of damage to vessels, bleeding, emboli, dissection, pseudoaneurysm
+ of PTA?
balloon angioplasty or stenting) - can be performed at the same time
Tx for PAD?
- Antiplatelet
- statin
- BP control
- diabetes screening
lifestyle for PAD?
- smoking cessation advice +/- nicotine replacement therapy / further intervention
Limb revascularisation in CLI?
- An open surgical procedure (bypass, endarterectomy)
- Autologous vein (e.g. great saphenous vein) is preferred to prosthetic (dacron/PTFE) graft wherever possible, particularly for below-the-knee disease
- An endovascular procedure (angioplasty, stenting)
- A Hybrid procedure (combination of both open and endovascular techniques)
Indications for amputation:
- PAD/ diabetes
- Trauma and Military injuries: one of the most common causes worldwide, especially young men
- Neoplasm
- Venous ulcers
- Congenital deformity
- Chronic pain
- Neurological injury resulting in a non-functional limb
Minor amputation?
major amputation?
post op management for amputations?
- psychological impact considered
- risk of infection, ischemia, prevention of slump trauma, pressure injury
- social input and home adaptations
prognosis for amputation
- major amputation reflects end stage PAD
- mortality double for AKA than BKA
thrombotic ALI?
- Rupture of atherosclerotic plaque
- Bypass graft thrombosis
- Prothrombotic e.g. malignancy
- Arteritis
- Infection
- States of low flow e.g. shock
Embolic ALI?
- Mural thrombus
- Atrial fibrillation
- Thoracic / abdominal aortic Aneurysm
- Bacterial endocarditis
- Cardiac tumour
Rare causes of ALI?
- Compartment syndrome
- Dissection
- Trauma
Sx of ILA
- Sudden onset painful, numb, weak and cold limb
- atherosclerosis is predominant cause but can manifest in both thrombotic and embolic presentations
Signs of ALI - 6 PS?
Assessment of ALI?
- sensory and motor function of the leg
- assess muscle tenderness (late sign)
- doppler US
ABPI for PAD
Test for ALI?
- ABPI
- ECG – arrhythmia may precipitate an embolic event.
- creatine kinase - marker of rhabdomyolysis
Rutherford classification of acute limb ischemia?
Initial Mx of ALI?
- oxygen
- UF heparin
Categories of ALI?
compartment syndrome?
- Acute increase in pressure within a compartment which endangers the perfusion of tissues, requiring emergency decompression
Causes of compartment syndrome?
- Reperfusion injury post revascularisation in acute limb ischaemia
- Other causes include fractures, crush injuries, burns
symptoms of CS?
- Disproportionate ’Crescendo pain’, unresponsive to analgesia
Pathophys of CS?
- Ischaemia-reperfusion injury
- Release of free radicals, K+, Ca++, Toxins etc
- Vascular leakage causing tissue swelling within fixed fascial compartment
- Decreased perfusion pressure
Signs of CS?
- Pain on passive movement
- Paraesthesia
- Pulselessness (late)
- Paralysis (late)
Management of CS?
- Urgent fasciotomy
- remove constrictive dressings
Rare causes of ALI
CS most commonly affects the ?
- CS most commonly affects the lower leg
- most common causes: soft tissue injury and fractures
what to be careful of in a fasciotomy?
saphenous nerve and vein
chronic exertional compartment syndrome ?
- higher resting intra-compartmental pressure
- pressure rises steeply after intiation of exercise
- burning, cramping or aching pain within 20 mins of exercise
aortic aneurysm?
- A permanent, focal dilation of an artery with at leasta 50% increase in diameter compared to normal
AAA high risk group?
- Highest incidence is in Caucasian men aged >65 years: 5%
- The risk of rupture increases exponentially with increasing size
AAA screening programme?
- There is a screening programme in place in the UK NHS: the NAAASP
RF for AAA?
- PREV 4-5x higher in men
- atherosclerosis predominant cayse
Rare causes of AAA
- rare causes: mycotic aneurysm (infection), CT disorders (Marfans and Ehlers-Danlos), arteritis
- diabetes had a protective effect
Risks for AAA
National Abdominal Aortic Aneurysm Screening Programme (NAAASP)?
- First invitation is at 65yrs of age for men
- Abdominal USS, measures the anteroposterior (AP) infrarenal aortic diameter
AAA clinical pres?
- Generally asymptomatic until rupture
- Some patients may report back or hip pain if large or rapidly expanding AAA
- May compress surrounding structures – vague GI symptoms, DVT
common features of an AAA rupture
- abd pain radiating to back
- shock
management of an AAA rupture?
- Urgent CT scan
- proceed to either open or endovascular repair
chronic venous disease?
- Superficial venous incompetence
- Deep venous disease
- Which may manifest as obstruction or incompetence
anatomy of leg veins
normal physiology - veins?
- Blood in deep veins returns to the heart due to pressure generated by the calf muscles.
- 80% of venous return from the legs is via the deep veins.
superficial and deep veins?
- blood collected from superficial venous capillaries is directed upward and inward via one-way valves into superficial veins.
- These in turn drain via junctions & perforator veins, which pass through muscular fascia into deeper veins
pathology - veins?
- unlike deep veins which are thicker and confined by fascia, superficial veins cannot withstand high pressure and eventually become dilated and tortous
superficial venous incompetence?
- men = women
- more women present w symptoms
RF for superficial venous incompetence?
- Obesity
- Increasing age
- Family history / genetics
- Pregnancy
- hormonal factors increase the laxity of venous walls and valves
Sx of superficial venous incompetence?
- Itching, aching discomfort and heaviness of the legs
- Leg swelling
- “Restless” legs
when are symptoms worse for SVI?
- Symptoms typically worse after prolonged standing / towards end of day
- Bleeding varicosities (typically after minor trauma)
Aggrevating factors for SVI?
- occupation: prolonged standing, lifting e.g. factory production lines etc
- pregnancy
- hormonal changes – endogenous or exogenous
- menstruation
Exam - varicose veins?
- Varicose veins will typically empty when lying down or with application of pressure, and then refill when pressure is released or patient stands up
Small vs great saphenous vein varicosites?
- Great saphenous vein varicosities may run the whole length of the leg and are generally distributed medially
- Varicosities of the small saphenous vein are seen below the knee and are distributed posterolaterally
signs of advanced venous insufficiency?
include (healed) ulcers, lipodermatosclerosis, haemosiderin pigmentation, telangiectasia or eczema / atrophie blanche.
typical site for change w venous insufficiency?
- the typical site of skin change is around the ankle, the so-called “gaiter area”, particularly around the medial malleolus
CEAP classification system?
- clinical, aEtiologic, anatomic and pathophysiologic
examples of venous insufficiency?
management of varicose veins?
investigations for varicose veins?
Duplex ultrasound (combination of Doppler and B-mode ultrasound) is the gold standard
Tx for superficial venous incompetence - first line?
- endovenous thermal ablation - sealing of the lumen of the incompetent vein by delivering thermal energy via catheter using US guidance
2nd line for varicose veins?
- Ultrasound-guided foam sclerotherapy - This is recommended if endothermal ablation is unsuitable. It involves injection of a sclerosant chemical into the veins.
- Offered as 2nd line treatment to patients unsuitable for Thermal Ablation
3rd line for varicose veins?
- Conventional surgery: (junctional ligation, stripping and avulsions)
- 3rd-line option if the above treatments not feasible
mechanism of endovenous thermal ablation?
*Thermal injury to venous endothelium
* Luminal obliteration
* Contraction & fibrosis
features of endovenous thermal ablation
- daycase procedure performed under LA
- lesser complications and lower recurrence rates comp to conventional surgery
Ultrasound-guided Foam Sclerotherapy mechanism?
- Chemical injury to venous endothelium
- → Luminal obliteration
- → Contraction & fibrosis
featurs of UGFS?
- Walk in procedure
- local anaesthetic
side effects of UGFS?
- higher risk of DVT than surgery or EVTA
- can cause transient migraine/ visual aura from bubbles in circ
- higher failure and reccurence rates than EVTA/ surgery
Surgery for venous insufficiency mechanism?
- ligation of the saphenofemoral (or saphenopopliteal junction)
- Stripping of the incompetent superficial vein (GSV/SSV)
- Avulsion of the varicosities through stab incisions
- of surgery?
- DVT/ PE, wound infection
- delays at work
causes of chronic leg ulceration?
leg ulcers =
- breach in epithelial integrity of the skin
- chronic: present for > 6 weeks
majority of chronic ulcers have a…
- majority of chronic ulcers have a vascular cause
- chronic venous hypertension is a primary cause
venous ulcers?
- very painful
- relieved slightly by elevation
appearance of venous ulcers?
- most commonly affect medial perimalleolar (gaiter) areas
- Ulcer is large, shallow and irregular with an exudative and granulating base
venous insufficiency
assoc features w VI?
- warm skin
- normal peripheral pulses
- varicose veins
- leg oedema
- haemosiderin pigmentation (leaching of iron from blood into the soft tissues)
- venous eczema
- lipodermatosclerosis and atrophie blanche
risk factors for venous ulcers
- Superficial venous incompetence (e.g. Varicose veins)
- Previous deep vein thrombosis in the affected leg
- Phlebitis in the affected leg
- Previous fracture, trauma, or surgery to leg
symptoms of venous incompetence?
include leg pain, aching, itching, swelling, pigmentation and eczema and ultimately ulceration.
arterial ulcer features?
- Painful and worse when legs are elevated
- Most commonly affect pressure and trauma sites (pretibial and supra-malleolar) and distal points e.g. toes
arterial ulcers appearance?
- Lesion is typically small, deep, sharply defined (developing a “punched-out” appearance with time), often with a necrotic base
Features associated with arterial ulcers?
- Associated features: cold skin, weak or absent peripheral pulses, shiny pale skin, loss of hair
- Represent advanced PAD – Critical Ischaemia
RF for arterial ulcers?
- Peripheral arterial disease.
- Coronary heart disease.
- History of stroke or transient ischaemic attack.
- Diabetes mellitus.
- Obesity and immobility.
appearance of venous vs arterial ulcers?
- shallow irregular exudative gaiter ulcer = venous
- smaller punched out deep ulcers = arterial
which areas are more affceted by diabeteic ulcers?
- usually foot rather than leg
- affects pressure sites more: soles, heels, toes, metatarsal heads
- often painless with abn or absent sensation
diabetic ulcers are caused by
- caused by peripheral neuropathy secondary to diabetes
Appearance of diabetic ulcers?
lesion usually punched out w variable size and depth with a granulating base
features of DU?
warm skin, peripheral neuropathy, normal peripheral pulses
Ix for a venous ulcer?
- Venous: Venous duplex ultrasound to look for venous incompetence
Ix for arterial ulcer?
- Arterial: Arterial imaging – usually multilevel disease
Ix for diabetic ulcers?
- Diabetic: Assess sensation – monofilament test. Check HBA1C & optimise
- Foot x-rays to look for underlying osteomyelitis.
APBI >1.3?
- > 1.3: generally indicates calcified, stiff arteries.
- This may be seen with advanced age, diabetes or chronic kidney disease
APBI which represents PAD?
- < 0.8: PAD very likely
- < 0.5 indicates severe PAD and should be referred urgently
Management of venous vs arterial ulcers?
- Venous: If ABPI >0.8 apply compression bandaging
- Arterial: vascular reconstruction
management of a mixed ulcer?
- Mixed arterial/ venous: initially modified strength compression w close obs (+ revascularisation if needed)
what is Raynaurd’s?
- Episodic vasospasm of the arteries of the extremities resulting in digital ischaemia, can be induced by cold or emotional stress
- idiopathic in 95% of cases
who does Raynaurd’s affect?
- older age, M=F
aetiology of RS?
- Associated with connective tissue disease especially Scleroderma,
- Also SLE, RA, Sjogen’s Syndrome
Drugs causing raynaurds?
amphetamines, cocaine, beta blockers, chemotherapy, COCP
Vascular occlusive disease causing RS?
Buerger’s, Atherosclerosis, Thromboembolic
Haematological
Haematological causes of RS?
- Haematological e.g. polycythemia, leukaemia, Protein C, S or antithrombin III deficiency.
Environmental/occupational causes of RS?
- vibration, frostbite, ulnar aneurysm
Anatomical cause of RS?
CTS
infections causing RS?
- Infections e.g. Hep B & C (cryoglobulinaemia), mycoplasma (cold agglutinins), parvovirus B19
Endocrine causes of RS?
hypothyroidism, phaeochromocytoma, carcinoid syndrome
Symptoms of RS?
- Pallor of distal part of fingers
- Numbness
- Pain
- Blue fingers (cyanosis)
- Hyperaemic phase – red and warm fingers
Symptoms assoc w RS?
- Migraines
- Dry Eyes etc (Sicca syndrome)
- Joint/muscle pain
- Gastro-oesophageal reflux
- Weight loss
- Rashes
Signs of RS?
- blanching then cyanosis (hyperamia can occur after)
Imaging for Raynaurds?
- Infrared thermography (cold provocation test)
- Laser doppler flowmetry
- Digital plethysmography
diagnosis of RS?
- At least one colour change e.g. cyanosis/erythema
- Identified cold/emotion triggers
- Exclude cervical rib/ thoracic outlet syndrome
when to suspect secondary Raynaurds?
- Onset >30yrs
- Asymmetrical, Intense or painful episodes
- Features of underlying condition
- Digital ulcers
- Positive autoimmune tests
Tx of raynaurds?
- Calcium channel blockers esp. Nifedipine
- Consider antiplatelet
- Consider immunosuppression for autoimmune associated raynaud’s
3 management options for ALI?
- analgesia
- heparin
- revascularisation
Thrombolysis?
- usually alteplase
- percutaneous technique that involves obtaining vascular access with a catheter
percutaneous mechanical thrombectomy/thrombo-aspiration ?
- removal of thrombus
- can be combined w catheter directed thrombolysis
surgical thrombectomy?
- vessel opened and thrombus removed
surgical bypass?
- bypass involves placing a graft connecting the vesse; proximal to the obstruction to the vessel and distal to it
rehab following amputation?
- exercises whilst sitting or lying
- taught transfer techniques from wheelchair to bed
- encouraged to move around ASAP using wheelchair
- physio and OT
- physio will teach them how to use prosthetic limb
mobility aids post amputation?
- OT: for adaptations required to home
- e.g. wheelchair ramp or stairlift
side effects of arterial reconst?
- thrombosis
- sepsis
- disruption
initial Tx of ALI?
The initial management of acute limb ischaemia includes analgesia, IV heparin and vascular review
All ppts w PAD should take…
All patients with peripheral arterial disease should take clopidogrel and atorvastatin
femoral vs iliac claudication?
Claudication affecting the femoral vessels is likely to present with calf pain rather than iliac claudication which causes buttock pain
