AIP Flashcards
C difficile management - gram positive rod - on colooscpy will see pseudomembranous colitis *yellow plaques, do ct for severe disease)
isolate to side room, strict hand washing and barrier nrusing - own toilet
stop laxatives and abx and antimotility drugs like codeine due to toxic megacolon risk (inflammation causes destruction of ganglion cells->paralysis)
review need for PPI (is a risk factor for CD)
metronidazole or
vanomycin or fidaxomicin in more severe cases
fluids as needed
acute severe may require surgery
fecal transplant may be needed for refractory or recurrent
no test of cure is needed
effect of eating on ulcers
eating worsens gastric ulcers
improves duodenal
eradication therapy for H pylori
7 days - all twice daily
PPI twice daily
amoxicillin 1g twice daily
and either clarithromycin 500mg twice daily or metronidazole 400mg twice daily
PACM
NB if associated with NSAID use as well then do PPI therapy for 2 month then do the eradication therapy
migraine prophylaxis e.g. occur >once a week on average or are prolonged or severe despite optimal treatment
propranolol
amitryptyline
topiramate (CI in preg)
GCA management (symptoms = unilateral headache, tender artery, hurts to comb hair, rest on pillow, fever, fatigue, weight loss, night sweats, anorexia, jaw (or tongue), visual blurring or loss, 30% have nerve problems eg carpal tuneel or cn6 palsy causing double vision, PMR >45min stiffness)
oral prednisolone - 60mg for claudication symptoms, 40mg without - response in 48 hours
once sympotms resolve, reduce by 10 every 2 weeks
osteroporosis prophylaxis for long term treatment
aspirin 75mg daily to reduce risk of thrombotic event with PPI
can be on steroids for several years - a small proportion for life
if visual disturbances - iv methylprednisolone
review reguarly to monitor BP and blood glucose
also monitor bloods then taper once in remission (inflammatory markers have resolved)
give a blue steroid card
avoid live vaccines like yellow fever
SAH management
ct scan - if neg then LP for xanthochromia
determine origin via CT, MR or traditional angiography
supportive care w intubation/ventilation/ng tube in patients w depressed conscious level. analgesia and antiemetics for conscious pts
endovascular catheter coiling (causes a blood clot in it which obilterates the aneurysm), clipping via craniotomy
nimodipine for 21 days - reduces vasospasm
can treat htn but only if severe - should be kept below 180
secondary prevention - stop smoking and treat HTN
CD induction of remission
if a single exacerbation in 12 month period -
prednisolone
(consider enteral nutrition in children with concern about growth or SE)
consider budesonide if steroids CI or not tolerated
or mesalazine and sulfalazine if steroids are CI and not tolerated (but explain to person that not as effective as steroids or budesonide)
if 2 or more exacerbations in a 12 month period -
consider adding azathioprine or mercaptopurine to steroid ( or methorexate if CI or TPMT deficient)
severe
then IV hydrocortisone, consdier need for parental nutrition, Abx, if not improving try infliximab or adalimumab
but if improving than transfer to oral prednisolone
pericarditis management
restrict physical activity until symptoms resolve or CRP, ECG resolve
aspirin or nsaid (like ibuprofen) for 4 weeks + PPI (aspirin over nsaid if recent MI)
colchicine for 3 months
steroids if refractory pain
majority as an outpatient unless fever, large effusion, cardiac tamponade, immunosuppressed, due to trauma, on anticoagulation, poor response to treatment
and treat cause - anti-tb for tb, antibiotics if bacterial
pericardiocentesis for symptomatic effusion
aortic dissection management
oxygen, analgesia, cross match 4u, BP monitoring with arterial line, monitor urine ouput
IV BB to reduce the force on the already-thinned walls of the false channel
keep SBP 100-120 - if hypotensive give fluids then escalate to vasopressor support with noradrenaline
type A - emergency open surgery - removal then graft
type B - medically with BB and analgesia if uncomplicated, surgery for dissections that are leaking, ruptured or compromising vital organs with TEVAR (or open if not)
patients will need lifelong antihypertensive and should be imaged 1, 3 and 12 months post discharge with CTA or MRA
PE management - outpatient anticoagulation amy be considered provided they are given all necessary info
analgeisa as necessary and resusicate as necessary
rivaroxaban or apixaban
LWMH for 5 days then dabigatran or edoxaban
LMWH for 5 days with warfarin until INR normal then warfarin alone
LMWH for pregnant women
3 months for provoked, 3 months provoked with cancer then 3-6 months, 6 months for unprovoked
haemodynamically unstable - continuous UFH infusion and consider thrombolytic with streptokinase or alteplase - systemic or catheter-directed +/- mechanical devices to break/aspirate the clot
IVC filter for recurrent or when anticoagulation is CI
CD maintenance
stop smoking
azathioprine or mercaptopurine
methotrexate is second line
management of central venous sinus thrombosis
elevation of head to 30-40 degress to reduce ICP
anticonvulsants for seizures
heparin (UFH or LMWH during stay) followed by warfarin - duration usually around 3 months but if no clear cause then 6-12 months
fibrinolytics like streptokinase via catheter may be used
surgery rarely if marked neuro deterioration
CAP management
low severity - amoxicillin 5-7 days
immediate - oral amoxicillin and clarithromycin 5-7 days
high - IV co-amoxiclav and oral clarithromycin 7-10 days but may be extended
hospital acquired - co-amoxiclav oral in mild, tazocin in severe
management of colonic angiodysplasia (note is most common in right colon - causes upper or lower gi bleed - either acute haemorrhage, occult pr bleed or asymptomatic) can investigate w wireless capsule endoscopy as well as other imaging
stable - fluids and potential tranexamic acid
persistent/severe - endoscopy with argon plasma coagulation or mesenteric angiography with catherisation and embolisation of the vessel
sugery for a minority with resection and anastomosis
assessing risk for an upper GI bleed
glasgow-blatchford score at first assessment - includes blood urea, Hb, SBP, pulse, comorbidites - predicts need for medical intervention
rockall score after endoscopy - age, BP, pulse, comorbidity, diagnosis post-endoscopy, signs of recent haemorrhage on endoscopy - predicts risk of re-bleeding and death and whether they can be discharged or need observing
meningitis management
BACTERIAL
IM benzylpenicillin if meningococcal is suspected
>3 months - ceftriaxone (add ampi or amoxi if >60)
<3 months - cefotaxime + ampicillin or amoxicillin
dexamethasone if >3 months, 4x a day for 4 days if bacterial suggested or confirmed especially if pneumococcal only - to reduce severeity and frequency of any hearing loss and neuro damage
fluids, analegisia, antiemetics as required
contact prophylaxis w cipro or rifampicin if prolonged contact in 7 days before illness onset
notifiable disease
VIRAL
no specific treatment - usually self limiting - aciclovir IV in herpetic
oesophageal varices management
REMEMBER TO MEASURE UREA IN AN UGIB
cxr to exclude pneumoperitoneum
initial resuscitation - oxygen, fluids, stopping anticoags, catheter, transfuse
endoscopy immediately if unstable, if not then within 24 hours
IV terlipressin prior to endoscopy in those with suspected variceal bleed (causes splanchnic vasoconstriction)
prophylactic antibiotics
band ligation
TIPS if not controlled by band ligation
stent insertion if not
balloon tamponade for temporary salvage treatment for severe bleeding
surgery is v rare
ischaemic stroke management (remember atrial myxoma and mural thrombus as cause of embolism)
investigate - a-e, cv exam, while awaiting ct do full set of bloods inc glucose to exclude hypo, lipids a risk factor, lfts clotting…
ecg to exclude af as a cause
non-enhanced ct head
ct or mr angiography if thrombectomy might be indicated
carotid us after
general - oxygen, blood glucose, swallow assessment (consider NG tube for poor swallow), nutrition screen with MUST, consider for carotid endartectomy - >50% on US (but defo for >70%)
<4.5 hours - alteplase infusion, 300mg aspirin for 2 weeks then clopidogrel long term (all after haemorrhagic stroke ruled out)
> 4.5 hours - aspirin 300mg for 2 weeks then clopidogrel long term
indications for thrombectomy to be used AS WELL (mechanical thrombectomy via femoral catheter +/- stent) - <6 hours confirmed occlusion of proximal anterior circulation demonstrated by CTA or MRA - AND later than this if potential to salvage brain tissue
manage comorbidites such as lipids etc
then rehabiliation, phsyiotherpay, barthel’s index to assess AoDL
note - dont anticoagulate for 2w after ischaemic stroke due to risk of haemorrhagic transformation
UC induction of remission
topcial +/- oral mesalazine or sulfalazine
add steroids if failing to respond
then hospital for biologics (like infliximab)
severe
fluids, Abx if needed, VTE prophylaxis
IV steroids
add IV ciclosporin if no improvement in 72 hours (or start on this if CI to steroids)
other options if poor response include infliximab
surgery if fail to repsond or develop complications like perforatin
GIST management
surgery and imatinib - tyrosine kinase inhibitor
DKA management
exam for signs of dehydration, check obs, GCS
blood glucsoe, ABG for bicarb and ph, test urine and blood ketones
FBC for infection, UE dehydration, plasma osmolality HHS, blood cultures and other investigatons depending on suspected cause
- Fluids <90mmHg - 500ml saline bolus - repeat if still <90
- Fluids >90 - 1L over 60 minutes, then 1L over 2 hours, and so on (table in guideline)
- At any point add 10% glucose to the fluids if glucose <14
- Fixed rate insulin at 0.1 units/kg/hour with actrapid - can increase this by 1 unit per hour if not reaching targets-Ketones decrease by 0.5/hour, glucose by 3/hour
- Potassium replacement if 3.5-5.5 with 40mmol/L - if <3.5 then senior review
- Continually monitor glucose and ketones
- Treat cause
(resolved when ketones <0.3 and pH <7.3)
MG management
- Pyridostigmine - acetylcholinesterase inhibitor
- Oral atropine to reduce muscarinic SEs
- Relapses/poor response with prednisolone +/- azathioprine
- Or can try other immunosuppressants such as ciclosporin, cyclophosphamide, methotrexate, tacrolimus…
- Thymectomy if thymoma OR hyperplasia with positive AChR and <45
myasthenic crisis management
immunoglobulins - first line
plasma exchange
steroids
(pyridostigmine should generally be avoided during an acute crisis due to the increase in respiratory secretions and risk of aspiration)
most common subtype of GB vs MND
GB = AIDP, acute inflammatory demyelinating polyradiculoneuropathy
MND = ALS, amyotrophic lateral sclerosis
MND management
- Riluzole - glutamate-release inhibitor - blocks muscle ACh receptors - prolongs by 2-4 months
- Hyoscine (anti-cholinergic) for drooling
- Quinine for muscle cramps
- Baclofen for stiffness /spasticity
- Physical, occupational and speech therapy
- Wheelchair services when needed
- Voice output communication aids for speech
- NG or gastrostomy for dysphagia
- NIV for respiratory impairment - consider opioids to relieve breathlessness or benzo for breathlessness exacerbated by anxiety
- Cough augmentation techniques
AMA is specific to
PBC
is notably absent in PSC
Ig in PBC vs PSC
IgM raised in PBC
IgG and IgM raised in PSC
triad in and treatment of haemolytic uraemic syndrome - triggered by shiga toxin which is produced by e coli 0157 (shigella can also produce this toxin)
this is why you dont use anti-diarrhoeals
microangiopathic haemolytic anaemic
thrombocytpenia
AKI
o Classic presentation is profuse diarrhoea that turns bloody 1-3 days later, then 5 days later has features of HUS like abdominal pain and vomiting, haematuria/dark brown urine, low urine output, confusion, HTN (because of the AKI), bruising
is an emergency has mortality of 10% - treat with fluids, antiHTN where needed, blood transfusions where needed to treat anaemia, dialysis where needed, plasma exchange is emerging
cause of HUS
shiga toxin producing E coli
investigations for autoimmune hepatitis - symptoms include fatigue, nausea, upper abdo, skin rashes, anorexia, amenorrhoea, weight loss, acne, hepatmogelay, jaundice
raised AST + ALT + bilirubin type 1 - ANA, anti-SMA type 2 - anti-LKM type 3 - anti-SLA, anti-LP raised IgG liver biopsy - gold standard
AIH management
prednisolone with azathioprine (either start together or start prednisolone first)
continue until 2 years after normalisation of LFTs - even then most will relapse
repeat biopsy may be neeeded to see if histological remission or longterm therapy is needed
osteoporosis prophylaxis
pred can be switched to budesonide if SE in non-cirrhotic patients
liver transplant needed in 10-20% in their lifetime
other drugs with specialist input include ciclosporin, rituximab….
PBC management
UDCA (obeticholic acid is 2nd option) cholestryamine for itching (rifampicin is 2nd option) fat soluble vitamins osteoporosis prophylaxis liver transplant
PSC management
cholestryamine for itching (rifampicin is 2nd option)
fat soluble vitamins
strictures causing recurrent cholangitis can be treated with balloon dilation +/- stents via ERCP
liver transplant
yearly colonoscopy and US due to cancer risk
insufficient evidence for UDCA
investigating steatosis and fibrosis
US can confirm steatosis
ELF (enhanced liver fibrosis) blood test indicates amount of fibroisis e.g. <7.7 = none-mild
when ELF isn’t available then NAFLD fibrosis score
if not then fibrosis (fib)-4 score
THEN a fibroscan should be done if ELF, NAFLD or fib-4 score indicates fibrosis
screening for cirrhosis
done every 2 years for…
- alcohol-related liver disease
- hep C
- NAFLD and advanced liver fibrosis
is done via fibroscan (transient elastography) or acoustic radiation force impulse imaging
HCC screening
done by US 6 monthly - and can do afp
alcoholic liver disease with cirrhosis
cirrhotic HBV carriers
HCV related cirrhosis
management of alcohol withdrawal
reducing dose of chlordiazepoxide over 5-7 days
pabrinex (thiamine) IM or IV once a day for 3-5 days (oral is poorly absorbed in dependent drinkers - but if well-nourished and uncomplicated then can do oral)
b12 as required
DKA resolution
when ketones <0.3 and pH <7.3
primary pneumothorax management (NB do CXR first, can also do CT to identify subtle pneumothoraces - increasingly used, and ABG)
Primary <2cm AND no breathlessness = discharge with outpatient x-ray - return if breathless, stop smoking
Primary >2cm OR breathless = 14-16G percutaneous aspiration and oxygen then 2nd x ray to confirm gone
secondary pneumothorax management - treat as secondary pneumo if >50 and smoker OR evidence of lung disease
Secondary <1cm = oxygen and admit for 24 hours
Secondary 1-2cm = 14-16G aspiration (if fails then chest drain)
Secondary >2cm OR breathless = chest drain (if fails then discuss with thoracic surgeon)
tension pneumothorax management
- Build-up of pressure within the pleural space eventually results in respiratory failure from compression of BOTH lungs
- AND will impair venous return to the heart compromised CO
investigations for pneumohtoaces = cxr, US may be used as part of FAST assessment and to guide chest drain, CT is being used more for subtle
needle compression in 2nd MC line
oxygen
chest drain in triangle of safety
in all pneumothoraces
- Air travel avoided until complete resolution - most advise at least 2 weeks after re-expansion
- Diving should be avoided if they have had any pneumothorax (unless they’ve had bilateral surgical pleurectomy)
heart failure management
REDUCED EF
ACEi and BB (if ACEi and ARB not tolerated then switch to hydralazine and isosorbide dinitrate)
spironolactone if they continue to have symptoms
NORMAL EF
furosemide to relieve fluid overload symptoms
SPECIALIST
digoxin - worsening HF with reduced EF despite first line treatment
ivabradine NYHA II-IV in sinus rhtyhm >75bpm, LVEF <35%
sacubitril valsatan - replace ACEi with this if EF <35%
hydralazine and nitrate
PLUS
antiplatelet in CAD, statin, CRT with defib or pacing (LVEF<35%), exercise-based rehab, vavle repair, heart transplant (or LV assist device while awaiting transplant)
stable angina management
avoid stressors
lifestyle
gtn for symptomatic relief - if not improved take another after 5 mins, then call 999 if pain not relieved 5 mins after 2nd
CCB (verapamil or diltiazem) or BB - switch if not working, then add the other in combo
then can step up to adding long-acting nitrate (isosorbide mononitrate), nicorandil, ivabradine or ranolazine
antiplatelet in all for seconday prevention
statin, acei
child pugh score vs MELD
child pugh score grades the severity of cirrhosis
MELD is recommended by NICE to use every 6 months in patients with compensated cirrhosis - it gives a 3-month mortality and helps guide referral for liver transplant
liver cancer management
nb remember do do some form of angiography - will show hypervascuarlisation
conservative in frail/ or decompensated end-stage - watchful waiting and monitoring AFP resection if <3cm (but higher chance of survival after transplant) ablative therapy for early-stage e.g. alcohol injection into tumour, radiofrequency ablation, microwave ablation liver transplant if meet Milan criteria (e.g. no metastatic disease) transarterial chemoembolisation (TACE) as a bridging for transplant
other radiotherapy immunotherapy advanced targeted radiotherapy sorafenib - tyrosine kinase inhibitor
courvoisiers sign
presence of a palpable gallbladder in the presence of painless jaundice
is saying that the mass is unlikely to be gallstones so presumes the cause to be an obstructing pancreatic or biliary neoplasm until proven otherwise
tumour marker in cholangiocarcinoma and pancreatic cancer
CA19-9
whipples
proximal pancreaticuduodenectomy with antrectomy
done in pancreatic cancer
prevention and management of encephalpathy
prevention - lactulose and rifaximin
management - raise bed, lactulose with neomycin, regular enemas
in more severe cases - IV mannitol and sedation with benzos to prevent seizures, therapeutic hypothermia
stress ulcer prophylaxis in shock/sepsis/trauma
use an H2 blocker or PPI
stress ulcers are erosions mainly in fundus and body of the stomach that develop after shock sepsis or trauma
types of obstructive shock
PE
cardiac tamponade
tension pneumothorax
SBP management
third generation cephalosporins such as cefotaxime
with human albumin solution to prevent development of AKI and hepatorenal syndrome
patients that are at risk can be started on long-term prophylactic abx such as rifaximin
how many Duke’s criteria for definite clinical IE
major = typical microorganisms from 2 separate blood cultures and echo evidence or new regurgitation
2 major criteria
1 major and 3 minor
5 minor
below this = possible and would do repeat echo/blood culture/cardiac CT/CT-PET
then next step down = rejected
infective endocarditis management
blind therapy after 3x blood cultures - native or late prosthetic with ampicillin, flucloxacillin and gent. Early prosthetic with vanc, gent and rifampicin
then treat depending on organism
staph aureus with fluxclox for 4-6 weeks (if prosthetic then add rifampicin and gent, ≥6weeks)
MRSA - vanc (if prosthetic add rifampicin and gent)
strep viridans and bovis - penicillin G or amox or ceftriazone for 4 weeks
surgery if new HF, uncontrolled infection (abscess or +ve blood culture), veg>10mm (risk of emboli) - remove infected tissue or valve repair/replacement
management of chronic limb ischaemia
note that pain is often worse at night - may have hair loss, poor healing
secondary prevention of CVD with smoking cessation, weight loss, statins, diet, exercise, anti-HTN, optimise diabetes management
all start on aspirin or clopidogrel
balloon angioplasty +/- stent when supervised exercise programme has not led to improved symptoms
bypass when angioplasty is unsuccesful
naftridofuryl oxalate (vasodilator) when supervised exercise not imrpvoed symptoms and does not want surgery - review progress with this in 3-6 months
management of critical limb ischameia (same as that for arterial ulcer as it suggests critical limb ischamia)
in critical - you see rest pain particuarly bad at night partially relieved by hanging foot out of bed
pale and cold
discuss at vascular MDT
revascularisation with angioplasty or bypass surgery
paracetamol for pain
amputation if revascuralisation not possible
criteria for grading chronic and acute limb ischaemia - note that acute limb ischaemia has sumptoms of less than 2 weeks duration
rutherford
management of acute limb ishcaemia
initial - heparin bolus then infusion UFH), morphine, NBM
conservative for early rutherford with prolonged course of heparin then surgery if no improvement
others, embolic - surgical embolectomy with a catheter or bypass or local intra-arerial thrombolysis with streptokinase or tPA
follow the first and last with heparin
others, thrombotic - intra-arterial thrombolysis, angioplasty or bypass suregry
irreversible limb ischaemia (mottled, hard woody muscle) - urgent amputation or palliatve approach
long term - secondary prevention inc aspirin or clopidogrel
diabetic foot management
footwear, insoles, daily feet checks, no barefoot walking
charcot - immobilise in a case for 3-6 months or realingment arthodesis
ulcers - off-loading - bed rest, therapeutic shoes, wound management, keep dry and debridement of dead tissue
infection - blood culture, swab, IV Abx/X ray for osteomyelitis
painful neuropathy - bed foot cradles, anaglesia like TCAs, contact dressing
treat fungal infections, manage PAD, optimise diabees control, surgery for amputaiton
treatment options for varicose veins - should treat any concomitant varicose veins when treating venous uclers in order to improve venous return and allow for better healing
endothermal ablation
sclerotherapy
open surgery - ligation or stripping
Well’s score outcome meaning in DVT and PE
DVT
>1 = likely - progress straight to US
PE
>4 = likely - progress straight to CTPA
unlikely - then do D dimer in both, then if this is positive then do respsective scanning
AAA screening
abdominal US offered to men at 65 (consider women >70 who have risk factors like high cholesterol, HTN or arterial diseae)
3-4.4 = yearly US 4.5-5.4 = 3 monthly US ≥5.5 = refer to vascular team within 2 weeks for surgery and confirm w CT w contrast (surgery should also be done if >4cm and expanding at >1cm/year or is symptomatic) >6 = same and inform DVLA but still drive >6.5 = same and cannot drive
NB can present w abdo or back pain, distal embolisation producing limb ischaemia, pulsatile masses found indictendally
management of AAA
<5.5 = monitoring and CV risk reduction (statin, antiplatelet where appropriate, BP…)
≥5.5cm - surgery (if unfit may be left until >6cm, if unsuitable then monitr every 3 months) via open (aorta is clamped then segment is removed) or endovascular (graft is introduced via femoral)
complications of endovascular include endovascular leaking due to incomplete seal therefore reagular US surveillance is needed
should offer open above endovascular due to less risk of rupture and reintervention
endovascular if co-pathology (stoma, adhesions, horshoe kidney), anaesthetic risk and/or medical comorbidities
management of AAA rupture
bloods - inc group and save and crossmatch
if strong supsicion go straight to theatre - can do ecg to rule out mi or portable us/ct/ct aniogram if uncertain and stable
oxygen
gather supplies like blood products, platelets and fresh frozen plasma
aim to keep SBP ≤100 = permissive hypotension
prophylactic Abx
If stable, CT angiogram to determine about the best management option for that patient
if unstable - immediate surgery via open or EVAR (endovascular aneurysm repair)
post EVAR will need surveillance via CT angiography or colour duplex US
when do you give adrenaline 1m IV and amiodarone 300mg IV in pulseless VT
after third shock
then repeat the adrenaline every 3-5 minutes during alternate cycles of CPR
a further dose of amiodarone 150mg may be given for recurrent or refractory VT
management of unstable VT
synchronised shock - up to 3 attempts
follow with amiodarone 300mg IV over 10-20 mins
then can repeat shock again
then 900mg amiodarone over 24 hours
for refractory cases - procainamide or sotalol may be considered
after restoraton of sinus - ICD insertion for those that had a cardiac arrest of significant haemodynamic compromise
management of stable VT
amiodarone 300mg IV over 10-20 minutes
then 900mg over 24 hours
if this fails then consider syndhronised DC cardioversion - or pacing if this doesn’t work or flecainiade
management of puselness VF
non-synchronised DC shock - no R wave to trigger shock in VF (would also do this in pulseless VT)
adrenaline 1mg IV and amiodarone 300mg after 3rd shock
repeat adrenaline 3-5 mins after
a further dose of amiodarone 150mg may be given for recurrent/refractory, followed by a 900mg infusion over 24hours
once stable - ICD insertion (if cause is ischaemia do revasculrisation first then ICD)
most common SVT
AVNRT
treatment of sinus bradycardia with adverse features e.g. shock, syncope, HF…
IV atropine 0.5mg
if poor response - can repeat this up to a max dose of 3mg OR transcutaneous pacing OR consider adrenaline infusion or isoprenaline infusion
other alternatives - aminophylline, dopamine, glucagon if caused by BB or CCB, glycopyrrolate
treat underlying condition - hypothyroidism, raised ICP etc.
chronic/severe cases with permanent pacemaker
management of acute SVT episode
haemodynamically unstable - DC cardioversion
stable
- vagal manoeuvres such as valsalva, carotid massage in young, or facial immersion in cold water
- if fails, 6mg IV adenosine (NB can use verapamil instead if severely asthmatic)
- if unsuccessful after 2 mins, give 12, then can give one further 12
- next step if DC cardioversion
focal atrial tachycardia treatment long-term - has abnormally shaped p waves before each qrs e.g. inverted or biphasic
(NB focal atrial tachy is not irregular like multifocal is)
balance the frequency, duration of episodes and risks associated (HF, sudden death) with the risks of long-term therapy
CCBs or BBs first line
(flecainide, sotalol or amiodarone may also be effective)
catheter ablation is an alternative
treat underlying cause (e.g. digoxin toxicity) or manage preciptating factors like caffeine, alcohol, recreational drugs
causes and LONG TERM management of multi-focal atrial tachycardia - will have at least 3 different p wave morphologies
asthma or COPD = classic - management is directed at managing this (otherwise with CCB, as BB CI due to pulmonary disease, and no role for cardioversion or ablation)
digoxin is an uncommon cause
short term management is same for all svts
AVNRT management
not treating if episodes are only v infrequent
radiofrequency catheter ablation of the slow pathway is generally successful
BB (or if not then CCB like diltiazem or verapamil)
valsalva can be taught to patients to do themselves
manage precipitating factors like caffeine, alcohol, recreational drugs, stress, smoking, medications (some asthma inhalers- albuterol)
management of atrial flutter
treat underlying conditions like hyperthyroidism then may not need further treatment except avoiding precipitating factors such as alchol and caffeine - after this they may not need further treatment
vagal maneouvres/adenosine wont work here - helps you diagnose
haemo unstable - DC cardioversion
recurrent or persistent flutter then radiofrquency catheter ablation is preferred
if not electrical cardioversion (fully anticoag for 3 weeks first if >48hrs - while awaiting can control w bb or ccb)
or pharmacological cardioversion with amioadarone, BB, CCB, digoxin, flecainide or quinidine
pacemaker if these have failed
anticoagulate with warfarin or DOAC - even after succesful catheter ablation
UC maintenance
mesalazine or sulfalazine - topical +/- oral
azathioprine or mercaptopurine may be consdiered if >2 inflammatory exacerbations in 12 month period, or remission can’t be maintained with 5-ASA alone
drugs that cause QTc prolongatoin
anti-arrhythmics - flecianide and amiodarone
antibiotics - ciprofloxacin, erthyromycin
ketoconazole
antidepressants - venlaflaxing, citalopram
methadone
atypical antipsychotics - olanzapine
ondansetron
sotalol
management of torsades de pointes
unstable - resuscitation and defibrillationi
stable - attach pads, discontinue offending drugs , IV magnesium sulphate over 10-15 minutes
refractory - speed up the heart to decrease QT with adrenaline (or dobutamine if normo or hypotensive)
if this fails - transcutaenous pacing or transvenous pacing
long term
congenital long QT - BB +/- permanent pacing is remain symptomatic +/- ICD if torsades STILL continues (rare to need this)
acquired - usually just remove predisposing factor, if not then pacemaker, if not ICD
2nd degree heartblock management
should be referred for cardiological assessment where investigations can be done such as 24-hour ECG, cardiac imaging, cardiac catheterisation
acutely symptomatic with low HR - atropine +/- temporary pacemaker insertion (e.g. this is indicated after an anterior MI with 2nd degree heart block)
permanent cardiac pacemaker may be required, particuarly for type II (risk of severe bradycardia and low CO - or could progress to 3rd degreE)
3rd degree heartblock
in acute setting - atropine (or noradrenaline or dopamine) or transcutanoeus pacing
treated moer permanently with pacemaker - but reversible causes should be ruled out before this is done
indications for CRT (aka biverntricular pacemaker/triple-chambered)
LBBB with QRS >150milliseconds
EF <35% in HF where QRS interval >120milliseconds
prevention of generalised tonic clonic seizures or tonic, atonic or myoclonic
sodium valproate
if not lamotrigine
prevention of absence seizures
sodium valproate or ethosuximide
prevention of focal seizures
e.g. temporal - motor things like lip smacking or chewing, deja vu, visual/auditory hallucinations, vertigo, automatism (wondering off)
or frontal - clonic movements including jacksonian march, todd’s paralysis
carbamazepine or lamotrigine
surgical management in epilepsy
must avoid driving until seizure free for >1 year
if drug-resistant epilepy = continuous seizures depsite trials of >2 drugs
vagal nerve stimulation
focal cortical resection if well-defined focus
more extensive surgery if the focus is not discrete
or can try ketogenic diet
management of status epilepticus
in commiunity can be buccal midazolam or rectal diazepam
call ambulance if continuing 5 minutes after medication has been given or has a history of status or this is first episode requiring emergency treatment
in hospital secure airway (e.g. npa or igel not oropharyngeal) and given oxygen, IV access IV lorazepam - maximum of 2 doses (buccal midazolam or diazepam PR if cannot secure access) - wait 10 mins before next dose
if seizure continues, IV phenytoin infusion (SE + heart block, hypotension, bradycardia) - requires BP and ECG monitoring
then refer to ITU for general anaesthesia with IV midazolam, propofol or thiopental sodium for a minimum of 12-24 hours
other - correct any cause like hypoglycaemia, thiamine for alcohol
once terminated - recovery position, repeat a-e, ecg, consider imaging to determine cause like ct
bowel obstruction management
remember to ask about any lumps
bloods = all baseline, group and save, cea, abg, culture if spiking
scans = axr, erect cxr for perforation then ct
things that increase chance of ileus - prolonged operation time, electrolyte abnormaliteis, hypothyeoridism, meds like opiates
conservative/initial
NBM, NG tube to decompress (helps relieve pain and prevent aspiration pneumonia), fluids, analgesia, anti-emetics, catheter to monitor fluids
adhesions = conservative, unless signs of strangulation or ischaemia - do early administration of gastrografin to see if evidence of resolving obstruction (this may also be therapeutic in some cases )- if not then surgery
volvulus - can try flatus tube to decompress then if not flexible sigmoidoscopy to decompress (=endoscopic detorsion) - may still require surgery after this (and surgery straight away if perforation or ischaemia or caecal volvulus more commonly needs surgery)
malignant obstruction - defunctioning stoma and resection with primary anastomosis
paralytic ileus - tends to settle with conservative
acute colonic pseudo-obstruction - treat any underlying cause, neostigmine to stimulate bowel, endocsopic decompression if failing to respond, or surgery if complications
closed loop obstruction (e.g. large bowel obstruction with competent ilieocaecal valve) will require surgery due to high risk of rapid necrosis and perforation
salter harris fracture vs greenstick
salter harris = fracture involving the growth plate - epiphyseal plate - 5 types (SALTR)
greenstick fracture = incomplete fracture of the immature bone - occurs when a bone bends and cracks instead of breaking completely
causes of complete white out
- Trachea pulled towards opacification - pneumonectomy, total lung collapse (ET tube misplacement)
- Tracheal central - consolidation, ARDS
- Trachea pushed away from opacification - pleural effusion
air bronchogram
where bronchi are made visible due to opacification of surrounding alveoli (something other than air fills the alveoli)
will not be visible if the bronchi themselves are opacified by fluid and thus indicate patent proximal airways
usually due to consolidation but could also by pulmonary edema
causes of lung collapse/atelecatsis
o This is commonly due to obstruction from e.g., a tumour, foreign body, or mucus plug
o Although could also see atelectasis in the lower zones if someone is in a lot of pain because it is too painful to take full breaths in (diaphragm splinting)
left lower lobe collapse = sail sign
lytic vs sclerotic lesions on xray
lytic lesions will be blacker e.g. myeloma, lung, breast, renal, thyroid
sclerotic will be white e.g. prostate, osteosarcoma
when is cpap vs bipap used
cpap = t1rf because is failure of oxygenation - recruites more alveoli to increase amount of oxygen entering blood
cpap is also used for CHF (increases intrathoracic pressure which decreases preload) and OSA
bipap = t2 beacsue is failure to ventilate
oxygen therapy
nasal cannulae
24-30%
2-4L
hudson
30-40%
5-10L
reservoir
60-80%
15L
venturi
oxygen cylinders are white - medical air is black and white
normal urine output
0.5ml/kg/hour minimum
oliguria is anything less than this
how much water and glucose is needed per day
water - 25-30ml/kg/day
roughly 2.5L
50-100g - 5% dextrose contains 50g/1L
when to switch from maintenance fluids to NG or eneteral feeding
when maintenance needs are >3 days - is much less likely to cause salt/fluid overload or electrolyte abnormalities and no infection risk from cannula
threshold for transfusion
70
consider 80 in patients with acute coronary syndrome
management of acute haemolytic transfusion eraction (ABO incompatibility)
o Stop the transfusion, resuscitate, IV saline
o Treat DIC appropriately - seek early advice regarding platelet transfusion /fresh frozen plasma
transfusion related acute lung injury /TRALI
sudden development of dyspnoea, severe hypoxaemia, hypotension and fever that develop within 6 hours after transfusion and usually resolve with supportive care within 48 to 96 hours
give high-concentration oxygen, IV fluids and inotropes (as for ARDS)
ventilation may be required - discuss with ICU
febrile non-haemolytic transfusion reaction
fever during blood transfusion with no associated haemolysis
fever will be slow rising - roughly 60 minutes after onset of transfusion
stop the transfusion
treated with paracetamol, and leukoreduction of future transfusions is sometimes done
although, fever often resolves in 15-30 minutes without any specific treatment
then you can recommence the transfusion, at a slow rate, if possible other causes have been excluded like TRALI or an acute haemolytic reaction
post transfusion purpura
antibodies against platelets
leads to thrombocytopenia
presents 5-12 days after transfusion
treat with high dose IV Ig
normal range for MAP
65-105
indications for arterial line
real time bp measurement
frequent abg analysis
types of eneteral nutrition
nasogastric
peg
nasjejunal
non shockable rhythm management
give adrenaline 1mg IV as soon as there is venous access
continue cpr
repeat adrenaline every 3-5 minutes during alternate cycles of cpr
shockable rhythm management
Give adrenaline 1 mg intravenously (IV) and amiodarone 300 mg IV after the third shock
Repeat the adrenaline every three to five minutes afterwards (during alternate cycles of CPR)
Additional 150mg amiodarone IV can be given after the 5th shock
investigations and management of cardiogenic shock
bloods, cardiac enzymes, abg, bnp (low may rule out in setting of hypotension but high isn’t diagnostic as also rasied in sepsis, af etc)
ECG
CXR - tension pneumo, wide mediastinum, signs of hf
CTPA or v/q for PE
echo - tamponade of valvular
manage with oxygen, boluses then infusion
cardiac monitoring, arterial line for bp, catheter, cvp (should be 5-10 - greater than this indicates cardiogenic shock and fluid overload, less than this indicates hypovolaemia)
analgesia
treat cause e.g. revascularisation
inotropic/vasopressor support
IABP - systolic deflation decreases afterload through a vacuum effect
diuretics for overload once CO is stablised
haemorrhagic shock management
- Direct pressure and elevation where possible
- Tourniquet where the pressure is ineffective
- Oxygen
- Venous access and fluids boluses
- Use of tranexamic in trauma is off label
- Group and save and cross match for transient/non-responders to the fluid boluses - blood transfusion may be needed
o Cross match takes 40 minutes - so if needed, a O- blood can be ordered via 2222 - Vasopressors may have a part to play if there is no response to fluids - but evidence is inconclusive
- Resuscitative endovascular balloon occlusion of the aorta
o It involves introducing a balloon via the femoral artery into the aorta, which is then inflated and in effect cuts off blood supply above the haemorrhaging point
management of inguinal hernia
if small or asymptomatic can be conservative - safteynet if really painful then could be strangulation
surgeyr if symptomatic (e.g. discomfort, dragging sensation, pain on lifting) - can be open or laparoscpic (open mesh repairs preferred for primary, laparascopic for bilateral or recurrent or risk of chronic pain e.g. young and active or female due to increased risk of femoral - studies show risk of chronic pain is less with lap)
note - will disappear with minimal pressure or when lying down, direct goes through weakness known as hesselbachs triangle
investigations for bowel obstruction
FBC, CRP, U+Es (important to monitor due to third spacing), LFTs, G+S
VBG or ABG for signs of ischaemia metabolic derangement
CT with IV contrast = modality of choice
AXR are less sensitive (but are often done prior to CT) - can differentiate between mechanical and pseudo-obtstruction - bowel dilation, air fluid levels, no distal gas
CXR if pneumoperionteum suspected
contrast study with gastrografin e.g via ng
MRI or US - US becoming more popular
what is acute mesenteric ischaemia
almost always involves small bowel
due to embolus or thrombus (usually SMA - main cause), venous thormbus or non-occlusive (NOMI - systemic hypotension, blunt trauma, surgey, coke)
>50, or younger if AF
causes colicky or constant poorly localised pain out of proportion to clinical signs (no guarding or peritonism - abdo SOFT)
may also have loose and bloody stools (may see red currant jelly stools)
ischaemia can become infarction in around 12h - can lead to sepsis via breaks in epithelial lining - and can lead to peritonism AND infarction will cause an ileus
investigations fo acute mesenteric ischameia
abg - metabolic acidosis
other baseline bloods (may see raised hb due to dehydration)
axr to rule out other causes - may show bowel obstruction in later stages secondary to infarction causing ileus
CT may show pneumatosis interstinalis, mesenteric oedema and bowel dilation
CT angiography is gold standard (or MR)
or classic angiogrpahy
ECG may show AF
intraoperative fluoresceine administration may be needed to higlight areas of bowel that need resection
management of acute mesenteric ischaemia
NBM, analegia, fluids, oxygien, ng tube for bowel reset, IV abx (ischaemia predisposes to increased bacterial translocatoin)
iv UFH
thrombolytics may be infused locally if angiography is done
surgery is indicated if perforation, peritonitis or impending perforation
prompt laparotomy if overt peritonitits with peritonal washout
resection of non-viable bowel
revascularisation procedures may have a role with partial arterial occlusion - may involve surgical embolectomy or mesenteric artery bypass or ballon angioplasty and stenting
further management involves reducing further risk of atherosclerosis w antiplatelet and statins and treat underlyign cause e.g. if AF present
mortality rate = 50-90%
presentation of chronic mesenteric ischaemia (a chronic atherosclerotic disease of usually all 3 mesenteric arteries aka intestinal angina)
weight loss due to fear of eating
postprandial pain - intestinal angina - moderate to severe colicky or constanta poorly localised pain
usually a history of cv disease
non-specific symptoms - n, v or bowel irregularity
+/- PR bleeding
malnourished state can lead to things like osteoporosis
investigations for chronic mesenteric ischaemia
may have abdomainl bruit
bloods may reflect malnutrition
angiography is gold standard - CT and MR angiography may be replacing standard angiography
plain CT to rule out other abdominal disorders
duplex US - but is more influenced by external factors like obestiy or resp movements
management of chronic mesenteric ischaemia
asymptomatic can be managed conservatively w smoking cessation and antiplateelet because is rarely lifethreatening in itself
being symptomatic is an indication for open or endovascular revascularisation - bypass or graft or stent - symptomatic patients have an increased mortality rate
nutiriton is important as may be malnourished e.g. TPN may be required both pre and post-op
what is ischaemia colitis aka chronic colonic ischaemia
the most common type of the 3 intestinal ischameias and also has best prognosis
usually due to low flow in IMA which has been shunted away - splenic flexure and rectosigmoid junction are at high risk because they are watershed areas
often a cause isn’t found - could be due to arrythmias or decreased co or trauma or vasculitits
presentation of ischaemic colitits
acute onset abdominal pain - this is useful in distinguishing from inflammatory or infective colitits (more subacute thant acute mesenteric ischaemia w lesser degree of pain)
most frequently at the left iliac fossa where the rectosigmoid junction is
n+v
damaged mucosa - dehydration, shock and metabolic acidosis
in later stages may have loose motion containing dark blood - bloody diarrhoea is a prominent sign
A classic case of ischaemic colitis is a patient who presents with bloody diarrhoea and severe abdominal pain after an abdominal aortic aneurysm repair
investigations for ischaemic colitits
abg - metabolic acidosis
bloods - may show dehydration
colonoscopy +biopsy - may show blue or erythematous swollen mucosa - biopsy would show mucosal atrophy/necrosis
axr quite unspecific
barium enema shows thumb printing (mucosal oedema)
CT may be helpful - but colonoscopy w biopsy is gold standard
management of ischaemic colitisi
medical - most managed conservatively w fluids, broad spec antibiotics, NG tube if ileus
if symptoms do not improve in 24-48 hours repeat colonscopy or ct angiogram to evaluate
then can do surgery for complications
management of viscus perforation
a-e resucictation broad spec antibiotics nbm and consider ng fluids surgery e.g. perforated peptic ulcer with omental patch, or perforated diverticulum w hartmann's plus surgical washout
investigations and management for acute cholecystitis
examine - may have mass or murphys sign
fbc, crp, amylase, lfts, ue
US - may see radiological murphys or thickened gallbladder and rule out cbd stone - if no stones seen but strong suspicions then go on to do mrcp or eus (uses us rather than video)
CT abdomen if complications suspected
manage - analgesia like nsaid, para, diclofenac suppository, morphine or pethidine
IV fluids
antiemetic
nbm for bowel rest
iv anitbiotics
lap chole acute or delyed - if delayed repeat us and lfts to make sure no cbd stones
investigations and management for cholangitis
bloods inc amlylase, blood culture if bile fluid is available e..g if bilairy drainage has occured or from ercp can send for culture US mrcp ercp
manage with fluids, analgesia, IV antibiotics, ERCP (may dilate w balloon first to dilate then uses intrsuments to extract the stone), larger stones may require extracorporeal shock wave lithotripsy before removal
narrow areas bridged w stent if stricturing occured
if too ill then percutaneous biliary drainage
later - cholecystectomy
treatment of gallstone ilieus
enterotomy then stone extraction
then cholecystectomy
will see riglers triad on imaging = small bowel obstruction, a gallstone (RIF opacity), and pneumobilia (presence of gas in biliary system)
investigations for kidney stones
urinalysis - haematuria, low ph can suggest uric acid stoens, WCC/nitrites for differential
mistream urine for microscopy, culture and sensitiviities
bloods - fbc, UE, crp, creatinine, bone profile (total protein, albumin, calcium, ALP), PTH (due to high prevelance or primary hyperparathyroidism in people with renal stones)
non-enhanced CT KUB
US if radiation risk - e.g. in children and pregnant woman
AXR KUB useful in watching passage of radio-opaque stones
stone analysis for first timers, recurrent stones, early recurrence after stone clearance, late recurrence after long stone free period (stone composition may change)
management of kidney stones
analgesia - NSAIDS, paracetamol or opioids - if in hospital can do IV para, IM diclofenac or OR then opioids if needed
antiemetics and rehydration as needed
<5MM
watchful waiting
majority will pass in 1-3 w - after 3w should try something else
try to catch stone for stone analysis
<10MM
medical expulsive therapy with an alpha blocker like tramsulosin (CCB like nifedpine as alternative)
can also consider watchful waiting after discussing risks and benefits
SURGERY/OTHER - approx 1 in 5
if ureter is blocked or could potentially become blocks, a JJ stent can be inserted using a cystoscopy (prevents ureter from contracting thus reducing pain and buys time)
nephrostomy - if evidence of obstructive nephropathy - tube is inserted into kidney to drain the urine as a temp solution
ESWL - outpatient procedure reserved for stones <20mm performed under radiological guidance (US or Xray) but CI in pregnany or stones positioned over a bony landmark like the pelvis
flexible uretero-renoscopy - passes scope retrograde into ureter then breaks up stones with a laser (10-20mm in size or where ESWL has failed)
percutaneous nephrolithotomy (PCNL) for large stones >20mm or others failed - a neprhoscope is passed into renal pelvis vis abdo wall then stones are fragmented down in theatre
open surgey where others failed
prevention of kidney stones
avoid excess salt
good oral hydration
potassium citrate in adults with recurrent stones that are >50% calcium oxalate
thiazide diuretics can also be given for this reason (works by reducing urinary calcium)
risk factors for diverticular disease
low fibre diet - increases intestinal transit time and decreases stool volume age genetics smoking obesity drugs like nsaids, opiods, steroids
weak factors - western diet
symptoms of deiverticular disease vs diverticulitits
DIVERTICULAR DISEASE
LLQ abdominal pain - colicky and intermittent
pain may be triggered by eating and relieved by passage of stool or flatus
constipation or diarrhoea
occasional haematochezia- diverticular occur at point of vessels where wall is weaker
bloating
passage of musus
DIVERTICULITIS
constant abdo pain usually severe starting in hypogastrium then localises to LLQ
N/v
may have fever
may have palpable mass or distenstion
tachycardia
inflammation will often resolve but may progress to fistula (faecaluria, pneumaturia or pyruia), abscess (abo mass), perforation/peritonitis (rigidity, guarding and rebound tenderness), sepsis, obstruction
investigations for diverticulosis/diverticular disease/diverticulitis
INITIAL DIAGNOSIS
usually barium enema, colonoscopy, CT or direct visualisation at surgery (colonoscpy should never be performed in someone w suspected diverticulitis due to risk of perforation)
ACUTE FLARE
contrast CT within 24 hours of admission to all with raised inflammatory markers and suspected complicated diverticulitis
FBC, CRP (WCC and bleeding may cause anaemia)
group and save
sigmoidoscopy or colonoscopy if having to locate an acute bleed
AXR
CXR if pneumperitoneum
blood culture if acutely unwell w diverticulitis
angiogram in acute bleeding if bleeding is too profuse to enable identification using colooscpy
criteria for admission w kidney stones
fever - worried about concomitant pyelonephritis is an emergency (will have renal angle tenderness!) pain not relieving sepsis solitary kidney anuria pregnancy AKI inability to take adequate fluids due to N+V known non-functioning kidney
management of diverticulosis
if asymptomatic found incidentally - no futher investigations needed - just recommend healthy diet, increased fibre
management of diverticular disease
healthy diet with increased fibre
drink adequate fluids
bulk forming laxatives if high fibre diet insufficient
analgesia - avoid NSAIDs and opiods due to increased risk of perforaiton
arrange to review in 1 month to see how managing
hospital may be needed in significant bleeding
surgery can be done to resect sigmoid in severe cases
management of diverticulitis
arrange urgent admission if suspected complications, peritonitic, significant pain or significant co-morbidities
IV co-amoxiclav
fluid replacement
analgeisa - avoid NSAIDs and opiods due to increased risk of perforaiton
surgery for people with acute complicated diverticulitis and for people who do not improve with antibiotics or complications - usually hartmann’s
manage in primary care if mild, uncomplicated - prescribe 7 days co-amox or consider watchful waiting if person is systemically well
analgesia - paracetamol
follow up in 48 hours
management of a diverticular bleed
- Usually-self limiting - 70-80%
- Management is supportive
- If well – send home with oral antibiotics if unwell
do a follow up colonoscopy to rule out malignancy
more bleeding
If unwell, admit & monitor bleeding & Hb
If continues to bleed, may need X-match and transfusions
can do intra-arterial vasopressin w aniography
if not may need radiological embolisation
If that fails –> surgical resection
NB rectal bleeding is LESS common with diverticulitis because the inflammation can lead to scarring of the blood vessels so that they don’t actually bleed
prescribing insulin for dka
say 50 units in 50ml normal saline
then rate is 7units/hour (if 70kg)
investigations and management for appendicits
obs
bloods - raised WCC, CRP, amylase to rule out pancreatitis, group and save, clotting
urine dip to exclude UTI and ectopic
US for gynae complications + may or may not identify appendicitis is user-dependent
CT and MRI if diagnostic uncertaining
IV fluids if needed, analgesia, anti-emetics as needed
antibiotics prior to surgery and continued for 7 days if pus or perforation is noted intra-operatively
lap appendicetyom
a small abscess may be treated with antibiotics alone, larger ones may benefit from percutaneous drain
if there is no abdominal pain, pelvic tenderness/cervical motion tenderness then what do you do in suspected ectopic
> 6 weeks - refer to EPAU
<6 weeks repeat pregnancy test in 7-10 days or return if worsen
managment for ectopic
EXPECTANT
serum hCG every 48 hours until repeated fall in level then weekly until <15IU
MEDICAL
methotrexate IM single dose
measure hCG 4 and 7 days after then another dose may be needed if drop in hcg <15%
will need contrception for up to 6m after cos is teratogenic
SURGICAL
laparascopic salpingectomy - if not salpingotomy
anti-D
AXR in pancreatitis
no psoas shadow due to increased retroperitoneal fluid from oedema
may see sentinal loop line - isolated dilation of a segment of the gut due to inflammed pancreas making it unhappy -> ileus
calficiations
4 conditions associated with a moderatly raised amylase
DKA
ectopic
ischaemic colitis
ruptured AAA
glasgow’s score
- P – PaO2 <8kPa
- A – age >55
- N – neutrophils, WCC > 15 x 109L
- C – calcium <2mmol/L
- R – renal, urea >16 mmol/L
- E – enzymes, LDH >600 IU/L or AST >200 IU/L
- A – albumin <32 G/L
- S – sugar/glucose >10mmol/L
if >3 then severe pancreatitis is likely and should refer to HDU
score gives indication of mortality
pancreatitis management
pancreatitis can cause metabolic acidosis - for multiple reasons that include lactic acidosis resulting from shock, renal failure, or late in the course of disease because of loss of bicarbonate-rich pancreatic secretions
renail failure is another cause of raised anion gap acidosis
remember to do an axr in pancreatitis
oxygen, anti-emetics as required
pain relief w pethidine - morphine is CI due to spastic effect on sphincter of oddi
IV fluid resuscitaiton
nutritional support - enteral feeding usually via NJ is thought to prevent bacterial translocation (TPN if ileus or where nutritional support not being met)
when pain resolves and bloods are normal - oral then solids can be reintroduced
treat cause e.g. ERCP
severe cases treat in ITU
IV abx if pancreatic necrosis after percutaneous aspitation of fluid for culture
surgery if necrosis
pseudocysts that are symptomatic or large need endoscopic, radiological or surgical management
types of insulin
rapid - novorapid
short acting - actrapid, humulin S (s for short)
intermiedate acting - humulin I (i for intermediate), insulatard, insuman basal
long - lantus, levemir
insulin in DKA - how is it given
50 units (0.5ml) of insulin in 50ml 0.9% saline
use a Y connector to attach it to the IV fluids already running
insulin and surgery
- Should be around 6-10 mmol before surgery
- Reduce basal insulin to 80% usual dose if major elective procedure then start on a variable rate infusion (continued until the patient is eating/drinking and stabilised on their previous glucose-lowering medication)
o IV fluids containing glucose must also be given to maintain basal glucose levels and hydration
o Capillary glucose should be checked 1-2 hourly and variable rate modified accordingly
o A variable rate infusion can be stopped once patient is eating and drinking - give their usual rapid acting at usual mealtime then wait 30 minutes before stopping variable aate - Omit SU on day of surgery
- with metformin - if only one meal is missed overtime of surgery you may be able to continue it
insulin changing - how much by
hypo - decrease basal insulin by 20%
hyperglycaemia - increase basal insulin by 10%
general rule for fast acting - 1 unit for a 3mmol drop in glucose
INR 5-8 - what to do with the warfarin
no bleeding - withold 1 or 2 doses
bleeding - stop warfarin and give vitamin K
major bleeding - stop warfarin, give vit k and prothrombin complex concentrate (FFP can be given but is less effective)
restart warfarin when <5
vit k = PHYTOMENADIONE
presentation, investigations + management for chronic pancreatitis
severe pain - chronic and recurrent
endocrine (diabetes) and exocrine insufficiency (malnutirtion)
steatorrheoa
weight loss
malnurition - may have fear of food due to pain
ADEK deficiency
n, v
low fecal elastase, CT for calcification, atrophy, blood glucose, axr for calcification, endoscopic ultrasound, other bloods (not amylase)
management
pain, ercp for strictures, surgery if pseudocysts, annual DM screening, annual DXA, low-fat diet, creon, treat high lipids and high calcium, treat DM
