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
management of coeliac
gluten free diet - dairy, fruit and veg, meat and fish, potatoes, rice, gluten-free flours (avoid some sausages - may have wheat for flavouring, avoid beer)
vitamin replacement if deficienct e.g. iron, vit b12, folate
consider annual blood testing for fbc and ferritn, tfts, lfts (autoimmune hep), vit d, electrolytes for addisons
patients with coeliac have functional hyposplenism - need pneumococcal vaccine and yearly influenza
peptic ulcer disease investigations
h pylori carbon 13 urea breath test or stool antigen test
fbc for anaemia
upper gi endoscopy - get a biopsy - can do urease testing (CLO test) on this and histology for neoplasm as cancers can look similar to ulcers
ensure all people w proven ulcer have a repeat endoscopy to confirm healing w re-testing if appropriate 6-8w after starting therapy
e.g. via urea breath test - repeat treatment if still positive, if not then offer PPI as needed
management for peptic ulcer disease
in peptic ulcer bleed - coffee ground vomit
lose weihgt, avoid trigger foods like caffeine, chocolate, tomatos, spicy foods, eat smaller meals, eat eve meal 3-4 hours before bed, stop smoking, reduce alcohol, sleep with head of bead raised
review meds - ssris, steroids, bisphosphonates, cocaine
h pylori eractivation for 7 days - if associated w nsaid use then do ppi for 2 m, then h pyrloi eradication
if nsaid associated then ppi for 4-8w
absence of both - exclude rare things like zollinger ellison
surgery for refractor e.g. antrectomy
(NB for GORD - full dose ppi for 4w then if symptoms return and long term needed then step down strategy to lowest efective dose - if severe oesophagatits then ppi for 8w and longterm
can add in h2 receptor antagonist like ranitidine if recurrent
then fundoplication)
active bleeding peptic ulcer
a-e
fluids/transfuse
oxygen
glasgow-blatchford then rockall after endoscopy
endoscopic therapy w adrenaline and one other - mechanically w clips, thermal coagulation or fibrin/thrombin
continued bleeding after first endoscopy should be treated with repeat endoscopic therapy but subsequent bleeding by transarterial embolization or surgery
patients who have ulcers with high risk lesions (active bleeding, visible vessel, adherent clot) should receive high dose proton pump inhibitors for 72 h
o Only offer PPI to patients with non-variceal bleeding and stigmata of recent haemorrhage shown on endoscopy
notes on CD presnetation and histology
skip lesions, terminal ileum, transmural, fat wrapping, cobblestoning, fissures, thick wall, non-caeseating granulomas
abdo pain diarrhoea 4-6w - inc nocturn \+/- mucus and blood weight loss fatigue, anorexia, fever mouth ulcers mass in RLQ (temrinal ileal inflammmation) recurrent UTIs and passing gas or faeces in urine or vagina bowel obstruction if strictures
erythema nodusum
arhtritis <5 joints
episcleritis
bone disease
histology of uc
mucosa only
crypt abscesses
thin wall or normal thicnkess
note - will see a hypokalaemic metabolic acidosis in diarrhoea, vs an aklalosis in vomiting
skin disorder associated w cd vs uc
CD = erythema nodusum
UC = pyoderma gangrenosum - deep ulcer
drugs to avoid in UC
loperamide - increases risk of toxic megacolon
nsaids - may aggrevate colitis symptoms
opiates may increase risk of toxic megacolon
types of reflex syncope vs orthostatic syncopr
REFLEX
vasovagal - triggered by emotional distress or prolonged standing
situationall - coughing, sneezing, defecating, exercising
carotid sinus hypersensitivity - (hypersensitive baroreceptors) sudden head turning, wearing a tight collar, shaving
^ will have blurring or clouding of vision before event
ORTHOSTATIC
hypovolaemia - haemorrhage, diarrhoea, vomiting
drugs - bb, diuretisc, alcohol, antidepressants
autonomic - diabetic nephropathy, PD, spinal cord injury
don’t forget Todd’s paralysis as a differential
and subclavian steal sybdrome - working with arms above head
ask about exposure to rapidly flickering light source at time
fall to ground in vasovagal vs CV
vasovagal = slow, controlled collapse CV = sudden
ask - do you remember hitting the floor and did they vomit when unconscious - any history of sudden death in family e.g. long qt syndrome
investigations for syncope
- Measure HR - transient bradycardia may occur straight after
- Measure BP - transient hypotension may occur straight after
- ECG - e.g. look for arrythmias
- Holter monitor if thinking of a transient rhythm disturbance
- Tilt table test for orthostatic hypotension
- EEG for seizures
- Echo for structural heart disease
- U+E for arrythmias
- Blood glucose for diabetes - autonomic nephropathy
- FBC for anaemia
TIA investigations
raised BP after cerebral ischaemic veent listen for carotid bruit do bloods exlude hypo difference in brachial pressure in subclavian steal ECG for AF (+ echo if heart disease)
refer to specialist centre in 24 hours (but if >1 week ago then in 7 days)
can be admitted to hosp based on ABCD2 score but no longer recommended by NICE (predicts liklihood of further CVA)
MRI is preferred imaging - enables detection of small infarcts
carotid doppler US - >70% stenosis then consider carotic endarctectomy
TIA management
admit if cresecendo, bleeding disorder or vulnerable patient
aspirin 300mg for 2w
then clopidogrel 75mg after
carotid endartectomy
treat AF
secondary prevention w lifestyle factors, statin 80mg, anti-HTN, stop driving for 1 MONTH
safteynet - they now have susbequent increased stroke risk - so be aware of signs
TACS vs PACS
TACS all of hemiparesis/hemiplegia higher mental function - aphasia, apraxia, inattention homonymous hemianopia
PACS is 2/3
NB anterior circulation - anterior and middle cerebral artery (or carotid - which leads to these 2)
posterior circulation stroke
basillar, posterior cerebral, vertebral
causes cerebellar or brainstem signs, LOC, homonymous hemianopia, contraleteral motor/sensory defect AND cranial nerve palsy,
visual agnosia - not able to name visually presented objects
what will a lacunar stroke not have
any cortical signs e.g. neglect, aphasia, hemianopia
investigations for ischaemic stroke
a-e, histroy, CV exam, FAST for reapid assessment
bloods - lipids, glucose, clotting, serum toxicology (may mimic stroke), FBC, antiphospholipid syndrome, FBC, UE (exclude electrolyte distrubances)
ECG bedside
non-enhanced CT head within 24 hours but immediately if risk of bleed, GCS<13, severe headache, progressive symptoms, papilloedema
CT or MR angiogram if thrombectomy might be indicated
CT perfusion scan can differentiate penumbra - useful in assessing for thrombolysis - is there still salveagble tissue (or MRI but in many centres is not easily accessible)
carotid US for stenosis, transcranial doppler
recomend that a 24 hour ecg should be done to exclude AF
severity tool for UC
truelove and witts criteria
CI for thrombolysis
previous allergy
previous haemorrhagic stroke
active internal bleed, excluding menses
previous ischaemic stroke <3m
relative - IE, anticoagulatn therapy, peptic ulcer, known coag disorder
management of haemorrhagic stroke
oxygen if needed BP control blood glucose control swallowing assessment - NG if needed minimise falls risk early mobilisation nutrition screen with MUST REVERSE/DISCONTINUE ANTICOAGS
decompressive hemicraniectomy if needed - should be done within 48 hours of onset - use national institues of health stroke scale to determine - basically may be needed
then rehabilitation, physiotherapy
treat any underlying conditions
barthel’s index to assess AoDL
consider statin, anti-htn as needed
macro vs microangiopathic anaemia
macro = calcific aortic valve micro = platelet clumps e.g. dic, ttp, hellp
investigations for meningitis
assess conscious level w GCS or avpu
LP if no signs of raised ICP
CT to rule out if signs of brain shift like focal neurology or reduced GCS
bloods - whole blood PCR for n meningitidis, blood culture, blood gas, coag
other - urine culture, cxr if tb, serology for hiv, throat swabs for bacteria and viruses
on LP - proteins will be high in fungal/tb/bacterial - mildly raised in viral, neutrophils in bacterial, cloudy in bacterial
investigations for encephalitis
contrast-enhanced ct - will show oedema, focal bilateral temporal lobe enhancement in HSV encephalitis LP once rasied ICP been ruled out viral serology specific viral PCR tests bloods inc culture throat swabs stool cultures EEG - may show changes but not always routinely required MRI may show sublte changes that ct cant
manage w abx for meningitis, IV aciclovir to cover herpes
other viral causes are supportive (be careful w fluids not to aggravate oedema)
anticonvulsants (e.g. phenytoin) if seizures, dexamethasone to treat raised ICP, and sedatives (to reduce agitation)
rehabilitation
addisons diagnosis and management
serum cortisol at 8am - low
synacthen test to confirm - measure cortisol 30m after (low in all 3 types cos adrenal glands will have atrophied over time)
ACTH levels
plasma renin and aldosterone - renin will be high and aldosterone low (but in secondary will be normal because RAAS still functions)
serum electrolytes - high K, low Na
ABG - metabolic acidosis (aldosterone excretes H)
autoantibody levels - 21 hydroxylase
CT or MRI if haemorrhage or neoplastic disease suspected
TB acid fast bacilli
glucose - low
manage w hydrocortisone 3x/day (10, 5, 5,), fludrocortisone 1x, only some specialists will prescribe androgens
medicalert bracelet
have to adjust in times of illness + stenuous exercise, take extra if travelling + emergency hydrocortisone kit, warn against abruptly stopping
high fever or broken bone then double for 2 days, LA surgery then double dose on that day only
elevated TSH with normal t3, t4
subclinical hypothyroidism
treat if >10 - this is to avoid hyperlipidaemia and CVD
40% will revert spontaneously
antibodies in hashimotos
TPO
thyroglobulin antibodies
after levothyroxine and TSH levels normalised - 10% still have persistent symptoms
graves vs toxic nodular goitre
- Graves = exophthalmos, lid lag and retraction, MNG = only lid lag and retraction
- Graves may have pretibial myxoedema, MNG = none
nodules = thyorid adenomas
management of thyroid storm
bb
antithyroid drugs
cooling
steroids - iv hydro
(myxoedema coma = active warming, IV fluids, levothyroxine)
(can give iodine after because can over correct and become hypothyroid)
treatment of hyperthyroidism
graves orbitopathy - steroids, prisms, orbital decompression surgery
prophylthiouracil or carbimazole (P is usually not first line due to small risk of liver injury - except if first trimester preg or for treatment of thyroid storm)
titration block regime
block and replace regieme
continue either for 12-18m then withdraw - 50% will relapse and require radioiodine or surgery
may also be presrcibed a bb becasue take 1-2m to work
risk of agranulocytosis - more so w carbimazole - seek help if sore throat, febrile illness - need blood test to exclude low WCC - can lead to a dangerous sepsis
radioiodine is not recommended for active orbitopathy - most will become euthyroid then hypothyroid within 6m - dont become pregnant for 6m after - will need to not share a bed, avoid children, no preg for 6m after
surgery w total or near-total thyroidectomy e.g. if large goitre causing compression, in pregnancy, patient preference, if graves’ orbitopathy
treat subclinical if <0.1 to avoid osteoporosis and CVD
investigations and management for CO poisnoing
COMA - cohabities (anyone else in house affected), outdoors (better outside), maintenance (are vents properly maintained, fuel burning appliances), alarm (do they have one)
measure CO levels using a breath test done at the site
neuro exam
CO pulse oximeter or blood analysis
MRI may show cerebral abnormaliteis
low-level exposure manage via GP by removing source
high-level then 100% oxygen until levels <3% - takes about 6 hours (hyperbaric oxygen can be used - this accelerates process)
if cerebral oedema then mannitol, monitor ECG
investigations for alcohol dependence
dependence = withdrawlas, cravings, narrowing of repertoire, altered drinking habits, increased tolerance, drinking despite negative consequences, neglecting others
CAGE AUDIT C or full AUDIT questionnaires physical exam - may be signs of liver disease breath or blood alcohol levels FBC - rasied MCV LFTs, clotting glucose due to chronic pnacreatitis
management of alcohol dependence
total abstinence is advised in dependence (in misuse then can benefit from methods to decrease like counselling)
brief interventions in primary care and motivational interviewing
CBT
alcoholics anonymous
disulfiram/antabuse - inhibits ALDH so causes unpleasent symptoms like flushing, headaches, vomiting
naltrexone - decreases pleasurable effects
acamprostate - reduces cravings
oral thiamine if deficient and b12
alcohol withdrawal management
withdrawal symptoms -> hallucinosis -> seizures -> delirium tremens (hallucinations, gross tremor, autonomic instability)
admit if previous tremens or seizures from alcohol, autonomic overactivity, concerns about saftey, suspected Wernicke’s, inability to make regular appointments during withdrawal period - 5-7 days
treatment may not be required if drinking <15 units per day and no withdrawal symptoms
reducing dose of chlordiazepoxide over 5-7 days - ideally see pt and dispense daily - can check alcohol on breath to confirm abstinence - should not drive while undergoing detoxification
thiamine - pabrinex to prevent wernicke’s - given IM for once a day for 3-5 days (if healthy and well-nourished then oral is an alternative) - b12 as required
50% will relapse soon after treatment - so can use acamoprosate, disulfiram and naltrexone
delirium tremens triad and management
bloods, amylase, glucose
ecg may reveal arrythmias
ct head if seizures
remember to ask about mood in alcohol history
and repertoirs
deliruim hallucinations tremor DHT usually begins 24-72 hours after alcohol has been stopped
benzodiazpines
barbituates may be added in those that are refractors e.g. phenobarbital
IV pabrinex
fluid replacement
dextrose to avoid hypoglycaemia - give after thiamine as it increases thiamine demand
usually resolves after 3-4 days
wernicke-korsakoff - differences and management
wernicke = confusion, ataxia (unsteady walking), ophthalmoplegia (double vision, nystagmus) other = autonomic dysfunciton
korsakoff = a state of impaired memory after signs of wernickes has subsided - anterograde amnesia, confabulation (answer Qs promptly w inaccurate and sometimes bizarre answers), telescoping of events (something that happened yrs ago apparently happened recently)
do serum thiamine, serum or urine alcohol levels, UEs, FBC for MCV
treat w thiamine, alcohol abstinence, glucose if needed but after thiamine
oral thiamine in korsakoff to prevent progression w psychiatric and psychological therapy
PINCHES ME
pain infection nutrition constipation hydration endocrine and electrolytes stroke medical and alcohol (intoxication or withdrawal) environement - change in or sleep deprivation
risk factors = dementia, age, frailty, comorbidities, sensory impairement
3 types - hyperactive (inappropriate behaviour, agitation, hallucinations), hypoactive (lethargy, quiet, reduced concentration + appetite), mixed
worse at night = sundowning, hallucinations, altered LOC, personality changes, disorganised thinking, inattention, change in cognition, flutuating, acute
investigatinos/tools for delirium
history - baseline, any precipitating factors like new medications or previous stroke
GCS or AVPU
obs, glucose, dip urine
general exam - see if rectum is impacted, palbate badder for retention, MSK for fracture, sources of infection on skin
medication review
4AT (4 or above is possible delirium) or CAM or SQiD (do you think x has been more confused lately?)
investigations - bloods, urinalysis, cxr, ecg, ct may be useful to rule out sol or stroke
management of delirium
treat cause
hearing aids and glasses and dentures
enable the patient to do what they can for themselves e.g. independent washing, dressing, eating…
regular (at least three times a day) cues (for example explaining to the person who and where they are)
easily visible clocks and calendars
continuity of care from carers and nursing staff
encouraging visits from family or friends and exposure to familiar objects
avoid physical restraints such as cot sides
encourage walking at least 3 times a day (provide walking aids if needed) or, if the person is unable to mobilize, try active range of motion exercises
discouraging napping and encouraging bright light exposure in the daytime
encouraging uninterrupted sleep at night with a quiet room and low-level lighting
address any underlying causes for the behaviour (such as discomfort, thirst, or need for the toilet)
if these measures fail, seek advice from an elderly care psychiatrist, consultant or challenging behaviour team (if available locally)
short-term pharmacological therapy may be suggested but should be avoided if possible (more if harm to selves or others) e.g. haloperidol low dose for 1 week (CI in PD)
be aware that it may persist beyond the duration of the original illness - do not assume dementia - reassess 1-2 months later
tool to screen for dementia
mmse
stage 2 AKI
creatinine rises 2-2.9x baseline
<0.5ml/kg/hour for >12 hours
(stage 3 is <0.3 >24 or anuria >12, >3x baseline or need for renal replacement therapy)
investigations + management of AKI
investigations include bloods, monitor UO, VBG (metabolic acidosis), anaemia suggests CKD, UE (high K), creatinine, urea:creatinine ratio (high in pre-renal), culture, urinalysis, paraprotein screen, antistreptolysin O titre (post-strep AKI), ANCA, ANA, urine osmolaltiy (high in pre-renal - low in renal because kidney isnt concentrating well), US, ECG in hyperkalaemima
prevention w creatinine + urine output (be aware trimethoprim can cause false raised creat)
monitor UE daily, stop nephrotoxic drugs
treat hyperkalaemia
fluid challenge for dehydration
then maintenance fluids
consider urgent dialysis if overloaded (but if passing urine then can use furosemide while awaiting - nice say use diuretics w caution)
relieve any obstruction e.g. catheter for retention due to prostate (or urethral stenting, percutaneous nephrostomy)
dialysis for hyperkalaemia unresponsive, pulmnonary oedema unresponsibe, uraemic complications like pericarditis or enceph, severe metabolic acidosis, fluid overload
hyperkalaemia treatment
<6 w otherwise stable renal function may not need urgent treatment - may just need change in their meds
>6 and ecg changes urgent treatment
>6.5 treatment urgent regardless of ecg
stop any offending medications
10ml of 10% calcium gluconate over 10 minutes - will improve ecg in minutes, if no improvement give another 10ml dose every 10 minutes
use of calcium gluconate without ecg changes is controversial
10 units actrapid in 50ml 50% glucose IV infusion over 30mins (or 100ml 20%)
back to back nebulised salbutamol w total dose 10-20mg over 30 minutes
IV fluids are an option to increase UO which encourages K loss from kidneys - avoid in renal failure due to overload risk
RESISTANT
can give further insulin-glucose solution
sodium bicarbonate may be useful if acidosis
haemodialysis
CHRONIC
resins (resonium) can reduce potassium but take hours/days to take effect
presentation and investigations for addisonian crisis
presents w severe abdo pain, fever, myalgia, fatigue, n+v, dehydration (leading to hypovolaemic shock), confusion, LOC and coma can occur
investigate via plasma cortisol and ACTH (dont wait for this before giving steroids)
abg shows hyperkalaemic metabolic acidosis, ue, hypoglycameia is classic
then investigate for precipitating causes
management of adrenal crisis
4S
stabilise - saline or dextrose in hypo (1L over 60mins)
steroids - hydrocortisone im or iv - 100mg over 8 hours
sugar - may need iv glucose
search for cause
emergency administration of fludrocortisone is not required because high dose hydrocortisone has a mineralocorticoid effect
change to oral steroids after 72 hours if good condiiton after gradual reduction in iv dose
continually monitor electrolytes and ecg if high K
some investigations for poisoning
GCS
check eyes - e.g. dilated w anticholinergics (atropine, oxybutynin, ipratropium), TCAs, cocaine, weed, LSD
risk assess if deliberate
consult TOXBASE
toxicology levels
LFTs
glucose - risk of hypo w salicylate
ue
abg - metabolic acidosis seen in aspirin (will first see mixed resp alkalosis due to stimulating resp centres in brain), ethylene glycol
ecg - TCAs cause prolonged pr and qrs duration leading to vt (prolong qt)
cxr if vomiting in the unconscious patient
ct to exclude other causes of loc
poisoning management w examples
activated charcoal if <1 hour of ingestion - doesnt work w lithium, iron or ethylene glycol (can try gastric lavage for these)
alkalinisation of urine for salicylate w IV sodium bicarb (check urine ph hourly - aim for 7.5-8.5)
treat low glucose seen w aspirin - measure levels 2 hourly
manage seizures
haemodialysis may be needed (e.g. as well as alkalnisation of urine in aspirin)
flumazenil for benzos
BB - atropine or glucagon if that fails
cocaine w benzos
heparin w protamine sulphate
OPIOID OVERDOSE
remove source e.g. patch
a-e - may need ventilatory support e.g. bag mask
naloxone iv boluses tritrated to effect (half life is shorter than opioids)
can consider activated charcoal
there is no consensus about the management of patients if body packing of opioids is confirmed. Options include watchful waiting, with or without the use of laxatives, whole bowel irrigation, endoscopic removal or surgery
causes of hypernatraemia
HYPERVOLAEMIA
iatrogenic from saline
conns
cushings
EUVOLAEMIC diabetes inspidus (confirm via water deprivation test for 8hrs followed by desmopressin - central w have high urine osm, nephrogenic wont - this will also distinguish it from psychogenic polydipsia)
HYPOVOLAEMIA
burns, sweating, diarrhoea, vomiting
osmotic diuresis - HHS
levels >170 associated w DI, >190 exogenous gain
do urine osmol - if high - vomiting/burns, isotonic osmotic diuresis, hypotonis DI or conns, cushings
management of hypernatramia
OVERALL
increase oral fluids, increase oral fluids, IV glucose if euvolaemic, saline instead if hypovolaemic, dextrose and diuretics if hypervolaemic, haemodialysis if very high
HYPERVOLAEMIA
glucose 5% IV (basically like adding free water back)
can also give diuretics to ofload fluid
treat underlhing casue
EUVOLAEMIA
DI - desmopressin for central, for nephrogenic if <4L of urine not always necessary, high dose desmopressin may help - can do combo of thiazide and nsaid if not - and remove offendeding agent e.g. lithium
HYPOVOLAEMIA
saline
if extremely high then consider haemodialysis or filtration
aim is drop of no more than 10mmol/L correction per day to prevent cerebral oedema - should use oral means where possible with IV being last resort
causes of hyponatraemia
falsely low due to high lipids or proteins or severe hyperglycaemia (can use a vbg in this instance)
HYPERVOLAEMIC
CCF, cirrhosis, nephrotic syndrome
EUVOLAEMIC siadh psychogenic polydipsia severe hypothyroidism addisons
HYPOVOLAEMIC
diuretics
vomiting, diarrhoea, skin loss via sweat or cf
causes of siadh
small cell lung cancer
pneumonia
other things affecting lungs like cf, asthma, tb
brain damage affecting hypothalamus e.g. trauma or tumour or sah or meningitis
drugs like ssri’s, diuretics (thiazides, loop) and carbamazepine
management of hyponatraemia
correct any underlying cause e.g. ssris are biggest risk of hypo in elderly
patients w acute should be managed in hdu esp in prescence of neuro symptoms
HYPERVOLAEMIA
treat underlying failure
loop diuretics often beneficial
EUVOLAEMIA
in siadh - fluid restrict to 1L per day, can consider demeclocycline or vaptans (antagonist) however is expensive and can correct too quickly
HYPOVOLAEMIA
saline slowly as rapid overrcorection leads to central pontine myelinosis
if over-corection can give desmopressin
hyperkalaemia causes
addisons acidosis aki, ckd, rental tubular acidosis sprionolactone acei arbs nsaids herparin bb tumour lysis rhabdomyolysis digoxin toxicity
hypokalaemia causes
vomiting, diarrhoea, laxative abuse thiazide or loop diuretics low magnesium insulin and glucose administration cushings, conn's alkalsosis beta receptors - acute illness or salbutamol hypothermia anorexia/malnutrition
if on diuretics - raised bicarbonate is the best indication that hypokalaemia is likely to have been long-standing (potassium reabsorption at expensive of H loss in tubules via h/k atp)
ecg signs hyperkalaemia
prolonged pr tall tented t waves flattended p waves and eventual disappearance broad qrs sine wave pattern VF
ecg signs hypokalaemia
prolonged pr flat t waves prolonged qrs st depression prominent u waves
later arrythmias - premature ventricular contractions, torsades, vt, vf
management of hypokalaemia
mild >2.5 with sando k then review
severe <2.5 IV replacement at no more than 10 per hour
corrected calcium calculation
for every g less than 40 of albumin, mulitply by 0.02 and add result to measured calcium
presentation of hypercalcaemia
bones - painful
stones
thrones - hypercalcaemia causes DI - polyuria, polydipsia
abdominal groans - gi symptoms like constipation
psychic groans - is associated w depression , also fatigue
NB acidosis will cause more free calcium
causes of hypercalcaemia
primary hyperparathyroidism
cancer - bone mets, lytic lesions in bone like myeloma and release of PTHrp
(cancer causes higher calcium than primary hyperparathyroidism)
other causes = thiazides
what makes up a bone profile
albumin
calcium
alp - will be raised with bony mets
total protein
management of hypercalcaemia
ACUTE
0.9% saline
correct any hypokalaemia and hypomagnesia
loop diuretic may be used but is debated
after rehydration w fluids, IV bisphosphonates will further reduce calcium over a few days
calcitonin may also be given (but less effective than bisphosphonates)
steroids in resistant cases
haemoldialysis
for PTH mediated hypercalcaemia can reduced dietary calcium and have surgery (if asymptomatic can just have monitoring)
presentation of hypocalcaemia
ACUTE
paraesthesia
seizures
tetany = intermittent muscle spasms - trousseau’s (inflate bp cuff then see wrist and fingers flex and draw together)
chvosteks sign (tapping over parotid causes twitching of mouth corner)
prolonged QT
CHRONIC
papilloedema
cataracts
depression, extra pyramidal symptoms…
main causes of hypocalcaemia
CKD
hypoparathyroidism e.g. due to destruction to glands from surgery, radiation, autoimmune
pseudohypoparathyroidism (primary condition - body cannot respond to the pth)
vitamin d deficiency or malabsorption (CD, chronic pancreatitis)
resistance to vit d/mutations in receptor
hypomanaeasaemia decreases pth
following bisphosphonates
acute pancreatitis
tumour lysis (cells burst and release phosphate which bind to calcium)
treatment of hypocalcaemia
ACUTE
10ml of 10% calcium gluconate
repeat as necessary
monitor calcium reguarly to judge response
if likely to be persistent then prescribe vit d
correct magnesium
CHRONIC
calcium
vitamin d analogues w calcitriol
as of yet PTH is not available commercially to be able to treat
if due to alkalosis then correct
presentation and diagnosis of acute angle closure glaucoma
eye pain, halos around lights, blurred vision, headache, n and v, eye redness, fixed mid-dilated pupil and hazy cornea
may be a precipitating factor like watching tv in a darkened room
NB primary angle closure suspect = some angle closure but person has normal IOP and no signs of glaucoma
DIAGNOSIS
ophthalmoscopy + slit lamp
goinoscopy to examine the anterior chamber angle
humphrey’s visual field test
managment of angle closure glaucoma
PRIMARY CARE
lie flat, pilocarpine drops 2% blue 4% brown
oral acetazolamide
SECONDARY CARE IV acetazolamide pilocarpine drops other topical drops = bb (timolol), alpha aognist (brimonide), prostaglandin analogues (latanoprost) AND laser iridotomy also treat unaffected eye
diagnosis and treatment of open angle glaucoma
ophthalmoscopy + slit lamp
goinioscopy to differentiate from angle closure
goldmann applanation tonometry to detemrine IOP
visual field testing
cup to disc ratio > 0.4and notching of optic cup
scotomas on visual field testing
TREATMENT
lifelong once iop >24
topical prostaglandin - latanoprost
topcial bb - timolol
second line - pilocarpine, acetazolamide, brimonidine
laser procedures targeted at trabecular meshwork to improve dreainage
or surgery - insertion of drainage shunt or creation of a bled (small reservoir) on the sclera (= trabeculectomy)
presentation of open angle glaucoma
usually asymtpomatic and insidiuos in onset
- Usually affects both eyes - but one eye may be more affected than the other
- Visual loss noticed by patient only when condition is advanced - peripheral vision is affected first
presentation investigations management for raised icp (low pressure headaches have oppsite pattern of presentation)
headache (nocturnal, on waking, worse on coughing or moving), papilloedema, vomiting, constriction then dilation, peripheral field loss, CUSHING’S repsonse, 3rd or 6th nerve palsies, cheyne’ stokes
fundoscopy (blurring of disc margins), CT/MRI, ICP monitoring (can be diagnostic or therapeutic via csf removal), consider lp if safe to measure opening pressure
treat underlying cause e.g. burr hole or craniotomy
avoid pyrexia - increases icp - same w seizures
restrcit fluid <1.5l
csf drainage via icp monitor
elevate head of bed
analgesia and sedation e.g. propofol - causes reduction in cerebral blood flow
reduce muscle activity e.g. suxamethnoium
mannitol - but can lead to a rebound icp
hypertonic saline if not
hyperventilation
second line = barbituate coma, hypothermia, decompressive craniectomy
steroids to reduce icp if due to oedema around tumours
investigations and management for low pressure headache
investigate with mri, ct myelogram
manage w increased fluid intake, caffeine (increases csf production), epidural blood patch, rarely surgery is needed to fix the leak
auras with a migraine + investigations
Visual = zigzag lines and/or scotoma Sensory = unilateral pins and needles or numbness Speech = dysphasia
often the aura symptoms will only affect one eye
usually an hour before the headache
fundoscopy, CN exam, drug history (is there overuse), headahce diary
management of migraine
avoid triggers - choc, hangovers, cheese, caffeine, OCP, sleep changes, alcohol
restrict acute meds to 2 days a week to prevent medication overuse headache
analgesia - ibu, asp, para
offer a triptan alone or with - sumatriptan (at start of headache not start of aura) - if vomiting restrricts then can offer intra-nasal or subcut
can co-prescribe metoclopramide or prochloperazine in addition
consider prevention if >2 per month and having significant impact on qol or acute treatments not effective (review need after 1 year)
consider other therapies along side e.g. mindfulnes, acupuncture, riboflavin
during menstruation - mefanamic acid or combo of paracetamol, aspirin and caffeine
can NSAIDs be used in pregnancy
- NSAIDs can be used second line in the first and second trimester
o RCOG state they should be avoided unless clinically indicated like for severe migraine, within the first trimester and should not be taken after 30 weeks
o Avoid in 3rd due to risk of closure of fetal ductus arteriosus in utero and possibly persistent pulmonary HTN of the new-born
o They are safe for breastfeeding though
cluster headache presentation and management (most common type of trigeminal autonomic cephalgia)
one-sided pain always same side, around eye or temporal region, conjunctival injection, lacrimation, rhinorrheoa, sweating, flushing, same time of day
will be restelss, may pace the floor, may have a trigger like alcohol
MANAGEMENT
avoid tiggers, good sleep hygieen
acutely - 100% oxygen 15L (can can home oxygen if needed - up to 5x a day) and sumatriptan SC or intranasal if dont want injection
anti-emetic if needed
lidocaine can be given IN to affected side
anti-inflammatories can be used
PREVENTION verapamil - first line prednisiolone can be effective at breaking cluster lithium if verapamil not effected melatonin possible addition for nocturnal attacks ergotamine is sometimes prescribed DBS if intractable or ablation of part of trigeminal nerve
idiopathic intracranial hypertension - all
most common in obese women of childbearing age w COC, may be linked to first trimester of preg
headache - worse first thing in morning, relieved on standing, aggrevated by straining, coughing
visual field defects (blurring, scotoma), n, v, tinnitus
CT or MRI to assess ventricles, visual field charting, LP will show raised pressures (CI in raised icp but can do for therapeutic use)
manage w weight reduction, analgesia, acetazmolamide or other diuretics in mild cases
can try serial lp drainage
use of steroids is debated - main use is if pressure is due to oedema from tumour
surgery - csf diversion (shunt is placed in ventricles then threaded under skin), optic nerve sheath fenestration
cerebral venous sinus thrombosis risk factors/causes
pregnancy
coc
hypercoagulable states e.g. antiphoshpholipid syndrome, protein c and s deficiencies (tend to cause thrombosis in venous more than arterial)
infection like meningitis, sinusitis - immune-mediate vasospasm or thrombosis
dehydration
nephrotic syndrome - is associated with a hypercoagulable state
cirrhosis
fhx of DVTs
presentaiton of cerebral venous sinus thrombosis
headache w signs of raised ICP +/- stroke symptoms that don’t necessarily affect one side
e.g. vomiting, seizures, decreased vision, papilloedema, LOC
neuro signs= hemiparesis, aphasia, ataxia, CN palsies
cerebral venous sinus thrombosis investigations
fbc- dehydration, wcc in infection, thrombphilia screen, anti-cardiolipin screen in antiphospholipid syndrome, proteinuria for nephrotic, lfts cirrhosis, D dimer, ct with contrast (mri alternaive), CT OR MR VENOGRAPHY may show absence of a sinus, LP if infection
presentation of SAH - and some investigations
sudden thunderclap headache usually accompanied by n and v
may also have focal neuro signs
OR may just have sudden collapse and loc (whereas extra and subdural more likely to cause collapse after trauma)
after the headache there may be neck stiffness (signs of meningism), seizures, signs of raised icp
on admission, 2/3rds have depressed level of consciousness
there may be warning symptoms in the 3 weeks prior to SAH that represent small leaks = sentinel bleeds or expansion of the aneurysm
remember to do opthalm - intraocular haemorrhages in 15%
ct may show suprasellar cistern blood - lp if not (xanthrochromia - yellow), do ecg (changes are relatively common in sah)
after sah is confirmed then determine origin via catheter angiography (this offers possibility of coiling an aneurysm), ct angiography, MR angiography
presentation of epidural vs subdural - remember to ask if taking any anticoags as this is a risk factor as is liver dysfunction and coagulatophy
Epidural - trauma -> LOC -> lucid interval -> deteriorates with severe headache and then may lose consciosness (may take a few hours to few days for a bleed to declare itself from rising ICP)
may also have n+v, seizures, brisk reflexes, limb weakness, other focal neuro deficit like aphasia or visual field defects or ataxia, cushings triad (brady, hypo, deep/irregular breathing)
a later sign is unequal pupils of fixed and dilated if brain herniates
Subdural - trauma -> gradual deterioration - gradual headache and confusion (+/- lucid interval before this) (LOC may occur but not always)
may present Loc - same with epidural
can have drowsiness, personality changes, seizures, vomiting, headache
may have fluctuating levels of consciousness
4 ways stemi can be diagnosed
2 or more 2mm chest
2 or more 1mm continguous
new onset lbbb
st depression in 2 or more leads v1-v4 = posterior STEMI
stable angina investigatinos (NB usually lasts under 10 mins, pressure or squezing - may also have palpitaitons, syncope, sob)
ask about diamond classification
cv exam
ECG normal in majority - may see ishcaemia e.g. t wave flattenting or inversion, pathological q wave (>1 small box duration or >25% QRS amplitutde)
cxr to exclude other causes
echo (stress or nonstress) - gives info about left ventricular function and ventricular and atrial wall motion defects as a result of prev mi
then look at things that may worsen workload of heart like tsh, lipids, fbc
determine likelihood of angina based on age, sex and typicality of symptoms (diamond)
> 90% then treat as known angina
61-90 then invasvie angiography (50-70% considered obstruction) OR SPECT (myocardial perfusion scan - does not directly visualise arteries), stress echo, stress MRI
30-60 then spect, stress echo or stress mri
10-29% CT calcium scoring
an alternative to angiography is cardiac ct angiography - CTCA should be offered to patients deemed to be low risk as a way of excluding CAD. If obstructive CAD is identified, patients require further functional or invasive testing to determine the significance of obstruction
safteynetting to a patient w stable angina - when is it concerning
Chest pain lasts > 10 minutes
Chest pain not relived by two doses of GTN taken 5 minutes apart
Significant worsening/deterioration in angina (e.g. increased frequency, severity or occurring at rest)
The above features may be suggestive of ACS and patients need immediate medical attention
management of stable angina
patient education - explain tings can provoke like exertion, cold, large meals, emotional stress
lifestyle
GTN spray for symptomatic - 2nd dose after 5 mins, if after 5 mins of second dose pain not eased then 999
BB e.g. bisoprolol or CCB - switch to other if not tolerated - or do both
consider monotherapy or as add on to one of above if others not tolerated or CI 1 isosorbide mononitrate 2 nicorandil 3 ivabradine 4 ranolazine
review effects of treatment 2-4w after starting (+ review person 6m-1yr)
secondary prevention
asprin, acei, atorvastatin (3As)
refer to cardiologist if max dose of 2 drugs + lifestyle but still symptomatic - CABG or PCI
investigations for unstable angina/nstemi
bloods for risk factors like lipids, glucose
ecg- may be normal of have st depression, t wave inversion
troponins - at presentation and at 3 hours after presentation
cxr to exclude altenratives
echo - gives info about left ventricular function and ventricular and atrial wall motion defects as a result of prev mi
coronary angiography = gold standard
management of unstable angina/nstemi
MONAC morphine 10mg IV +10mg metclopramide oxygen <94% gtn aspirin 300mg clopidogrel 180mg ^ all done asap if ischaemic ecg changes or raised trops admit to CCU
risk asses via GRACE or HEART to see if they need revascularisation - if low risk then treat medically and discharge if repeat trop is negative (an exercise test can be performed as follow up)
medically with bb IV (e.g. atenolol) or ccb, and fondaparinux unless coronary angrioaphy in 24 hours then UFH
ongoing = continue dual antiplatelet in those w unstable angina or nstemi if admission to hospital regardless of treatment for 12 months AND bb (or ccb), acei, atorvastatin
if high risk then do OCI or CABG - time to do this wihtin depends on score
can drive after 1 week if successful revascularisation
stemi territories and arteries
inferior = right coronary artery
lateral = circumfelx artery
anteiror = left anterior descending artery
posterior = posterior descending artery
silent mi
o SOB, weakness, dizziness, syncope, PE, epigastric pain, vomiting, acute confusion, stroke, diabetic hyperglycaemia
o 30% of MI’s present WITHOUT chest pain
o Atypical presentations are particularly important in women, diabetes and the elderly
other causes of st elevation
high st segment take off = a normal variant - usually limited to v2-v3 (does not have same coved appearance tho) - often seen in LVH
acute pericarditis - concave
LBBB
management of stemi
morphine 10mg with 10mg metoclopramide oxygen gtn aspirin 300mg rest / relocation to cardiac clopidogrel unfractionated heparin during and after pci
pci within 90 minutes ideally if not 120 minutes - stents should be routeinly used ideally drug-eluting stent
IABP if needed if cardiac support needed
CABG if more severe CAD
fibrinolysis if pci cannot be delivered within 120 minutes w alteplase or streptokinase
post MI - ABARS (acei,bb for 3 years, anitplatelets for 12 months, rehabilitation, statin)
complications for safteynetting = dressler’s syndrome, mural thrombus, HF, arrythmias
provoked PE (NB w PE you see a widely split second heart sound)
WELLS SCORE >4 = likely
significant immobility surgery trauma pregnancy use or coc or hrt
in previous 3 months
(thrombophilia and cancer would come under unprovoked)
bloods to do in unprovoked pe
antiphospholipid
thrombophilia testing
ecg changes in pe (trops are elevated in 20-40% due to extra strain on RV)
large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III (S1, Q3, T3)
some notes on aortic dissection inc classifications and risk factors
tear in intima causing blood to go between layers of media - HTN most common risk factor - dont forget CT disorders
stanford or debakey (1 = all, 2 = ascending only, 3 = descending)
may have new aortic regurgitation murmur
other symptoms depending on if occlusion of smaller arteries like angina, paraplegia, limb ischaemia, anuria, neuro defect
investigations for aortic dissection
exam - aortic regurg murmur may be heard, difference in BP in 2 arms
basline bloods includ trop and d dimer to rule out pe
abg
ecg - distinguish from mi
ct angiography if haemodynamically stable
transthoracic or oesophageal US if unstable
CXR in low risk patients - widening of mediastinum but no specific
MRI angiogram if CTA isn’t conclusive or contraindicated to CTA
symptoms and triad for pericarditis and investigations
(in pericardial effusion - will additionally get softer heart sounds, light-headedness, sob, syncope - due to decreased co)
chest pain - sharp and relived by leaning forwards in tripod, is pleuritic and worse on swallowing/coughing, radiates to tranepzisus and neck
pericardial friction rub - hgih pitched and squeaky
serial ecg changes - widespread saddle shaped st elevation w pr segment depression in most leads
on ecg may see electrical alterans in effusion when heart swings back and forwath
may also ahve fever, cough, breathlessness
will have raised trops
should do blood culture when bacterial pericarditiis
fbc - leukocytes suggest bacterial
elevated creatinine may suggest uraemic cause
do cxe to exclude other causes (and in effusion will be enlarged)
echo if suspecting effusion
can do pericardiocentesisis in effusion - when tb, malignant or purulent effusion is suspected - CEA will be raised in malignant effusion
cardiac tamponade presentation and triad
beck’s triad = raised jvp, muffled heart sounds, hypotension
raised jvp that does not fall with inspiration = kussmaul’s = constrictive pericarditis and restrictive cardiomyopathy - not positive in cardiac tamponade
pulsus paradoxicus = >10 decrease in systolic bp with inspitation
e.g. 65 years old presents w decresed exercise tolerance and dyspnoea at rest for 3 days - also noted bilateral ankle oedema and raised jvp
OR 47 year old presents w decreased exercise tolerance after being diagnosed w metastatic breast cancer
(think HF symptoms
management of pericardial effusion vs tamponade
EFFUSION
treat cause e.g. cytotoxic drugs for malignany
most resolve spontaneously
if they reaccumulate due to malignancy - may require pericardial fenestration
oxygen if needed
perciardiocentesis can be diagnostic and therapeutic
surgery if not successful
TAMPONADE oxygen fluids leg elevation positive inotropic drugs like dobutamine perciardiocentesisi surgical drainage if not
constrictive pericarditis - all
complication of pericarditis but particuarly that of tb percarditis, also occurs after open heart surgery and rheumatic heart disease
most cases occur 3-12 months after pericardial insult
in healing process makes a scar
as these changes are chronic, it allows body to compensate so not as immediately life threatening as tamponade
is treatatable in contrast to restrictive cardiomyopathy
increased jvp, kussmaul’s,= (JVP doesnt fall w inspiration), pulsus paradoxus (>10 drop in bp in inspiration), quiet heart sounds
hepatosplenomegaly, ascites, oedema due to systemic venous congestion
reduced co causes fatigue, hypotension, reflex tachy
cxr - small ehart, calcification, ecg low voltage QRS, echo thickened pericardium, ct - thickened wall, endocardial biopsy can distinguish from restrictive cardiomyopathy, cariac cathterisation
manage w complete resection of pericardium (pericardectomy)
notes on oesophageal rupture
resp distress, chest pain, subcutaneous emphysema
do CXR pneumoperitoneum, ct cap
if high level suspicion then urgent ogd in theatre
abx, resus, surgery inc drainage of mediastinsum
need nj feeding after - will need a ct before starting oral again
time that you have to start treatment within for ramsay hunt, bells and shingles
72 hours of rash onset
in all - can also use steroids
notes with asthma - whats a saba, cut off for feno, symptoms, cut off for variability
worse at night or early morning, chest tightness
40 parts per billion 17+
20% variability for at least 2 weeks
saba = salbutamol or terbutaline
obstructive vs restrictive pattern
OBSTRUCTIVE
Reduced FEV1 (<80% of the predicted normal)
Reduced FVC (but to a lesser extent than FEV1)
FEV1/FVC ratio reduced (<0.7)
RESTRICTIVE
Reduced FEV1 (<80% of the predicted normal)
Reduced FVC (<80% of the predicted normal)
FEV1/FVC ratio normal (>0.7)
LABA example
salmeterol, formoterol
SAMA example
ipratropium
LAMA exampel
tiotropium
when to add on a steroid in asthma
3x a week saba or more
wake once at night or more a week
have asthma symptoms 3x a week or more
In addition, an ICS should be considered for adults and children over the age of 5 years who have had an asthma attack requiring treatment with oral corticosteroids in the past two years
people on long-term steroids are at risk of osteoporosis so should make sure they have a good supply of calcium in their diet
moderate vs severe vs life-threatning attack of asthma
Moderate asthma exacerbation: o PEFR >50-75% best or predicted o Oxygen saturations (SpO2) ≥92% o Speech normal o Respiration <25 breaths per minute o Pulse <110 beats per minute
Severe attack – any one of the following o Unable to complete sentences o RR > 25/min o PULSE >110 beats/min o PEFR 33-50% of predicted or best
Life-threatening attack – any one of the following o PEFR <33% predicted o Silent chest, cyanosis o SpO2 <92% o Bradycardia or hypotension o Confusion or coma o Altered conscious level o Low PaO2 (<8kPa), high/normal PaCO2, low pH
doses in asthma exacerbation - hospital
NB discharge if >50% predicted at 2 hours, or earlier if >75%
admit if lifethreatening <50% PEFR or ongoing feautres of severe asthma
oxygen via face mask venturi or cannuale
5mg salbutamol nebulised - ideally oxygen driven
100mg iv hydrocortisone (or can do pred PO - usually for 5 days (3 days in children <12))
neb ipratropium 500 micrograms
monitor PEFR in response to treatment
give up to 2g mangesium sulpahte over 20 minutes
if not improving - senior input for iv aminophylline or theophylline
then can escalate to ICU - strongest indicator is ph <7.35 because it represents co2 retention in a tiring patient
if improving - give neb salbutamol and oral pred for 5 days
need to be stable on discharge mediateion for 12-24 hours before discharge - then gp folow up in 48 hours
asthma exacerbation - home
4 puffs initially followed by 2 puffs every 2 minutes according to response - up to 10 puffs
repeat every 10-20 minutes according to clinical response
consider quadrupling ICS dose for up to 14 days or prescribing a short course of oral prednisolone
seek medical advice if symptoms worsen, or PEFR decreases
once symptoms have subsided, advise the person (or their parent/carer) to return to using their short-acting beta-2 agonist as required, up to four times a day (not exceeding 4-hourly)
cut offs in resp failure and cause of some
<8 O2
> 6 co2
type 1= pneumonia, fibrosis, shunt, high altitude, pneumothorax, pe (DIFFUSION)
type 2= COPD, asthma, CF, bronchiectasis, chest wall, GB, stroke, obesity
if type 1 –> type 2 if breathing so heavily they tire
signs of hypercapnia
headache due to cerebral vasodilation - often in morning because co2 builds up overnight
bounding pulse
flapping tremor
drousy
notes with copd therapy
saba and sama is for acute symtpoms
laba and lama are baseline
before stepping up to laba and lama - must switch from sama to saba
LTOT can be offered to non-smokers who have PO2 of <7.3 or those with a PO2 of 7.3-8 AND
secondary polycythaemia, pulmonary HTN or peripheral oedema
increased vs decreasde transfer conditions
INCREASED asthma pulmonary haemorrage left-to-right shunts polycythaemia
DECREASED fibrosis pneumonia pe pulmonary oedema emphysema
small cell lung cancer neoplastic syndrome
SIADH
ACTH - cushings
lambert eaton
azathioprine (DMARD) and allopurinol
bone suppresion
remember to do TPMT levels before giving azathioprine
LVH on ECG criteria and causes
S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm
Hypertension (most common cause) Aortic stenosis Aortic regurgitation Mitral regurgitation HOCM
anaphylaxis investigations and management
mast cell tryptase levels asap then second one ideally in 1-2 hours (no later than 4)
monitor sats and ecg
a-e
remove trigger if poss
place in comfortable position - sitting up may make breathing easeir, or lying flat in everyone else (helpful for low BP)
IM adrenalin 0.5mg 1 in 1000 (means 1g in 1000ml) - repeat at 5 minutes intervals (if multiple doses needed may benefit form IV adrenaline) (0.3 in 6-12, 0.15 <6)
high flow oxygen
if stridor can give neb salbut
rapid fluid challenge - up to 2L may be needed (20ml/kg in children)
following initial resuscitation
IM or IV chlorphenamie (10mg in adults), IM or Iv hydrocortisone (200mg in adults)
observe for 6-12 hrs since symptom onset depending on their response to treatment in case of biphasic
offer referall to a specialist allergy clinic - epipen w 0.3mg 1 in 1000 (0.3ml), 0.3ml in 1 in 2000 in children (0.15mg)
IPF all
mostly at basal zones
subset of idiopathic interstitial lung disease - but has UIP pattern
cause - smoking, male, wood dust, raising birds, farming, GORD (microaspiration)
median age = 70
SOB on exertion w dry cough and bilateral end inspiratory fine crackles (make patient cough - crackles would change in bronchiectasis), clubbing, weight loss, fatigue
spirometry can be normal or restrictive, do cxr (reticular opactictires), gas transfer test shows impaired exchange, HRCT shows honeycombing and tracion bronchiectasis and ground glass
still not sure then biopsy
can do autoantbiodies due to association w autoimmune disordsers like sle, RA
acute exacerbations w steroids
ONGOING pulmonary rehavilitation exercise and weight loss vaccines against influenza and pneumococcas smoking cessation consider PPI antifibrotics - pirfenidone and nintedanib oxygen - can have LTOT opiods for deliberating cough NAC - but benefits are uncertain lung transplant palliative care referral
monitor w spirometry and gas transfer
quick notes on hypersensitivity pneumonitis
can be acute (flu like), subacute (gradual cough) or chronic (weight loss, sob, clubbing, pulmonary htn)
avoid, oxygen, steroids for severe
sarcoidosis
chornic granulomatous disorder - non-ceseating granulomas
middle age black woman w dry cough, sob, nodules on shins (erythema nodusum)
can affect any organ but mianly lungs
Lofgrens = an acute form of sarcoid where triad of bilateral hilar lymphadenopathy, erythema nodusum and polyarhralgia (NSAIds, but colchicine and low dose pred may be used too)
bloods - raised ACE, high calcium, crp, raise Ig
CXR - bilateral hilar lymphadenopathy
HRCT in more details
MRI if CNS
PFTs
ECG - cardiac involvement e.g. arrhythmias, HF
urine dip/acr - renal nephritis
opthal
us abdo for liver and kidney
tissue biopsy - histology is gold standard
most people dont need treatment will resolve - 60% 6m
painkillers
steroids if lung disase, uveitis, high calcium, neuro
immunisuppressants second line e.g. methotrexate
symptoms and diagnosis of pleural effusion - and some causes of exudate v transudate
sob, pleuritic chest pain, cough (can be productive if due to pneuomnia), stongy dullness, decreased breath sounds
transudate if fluid protein <25, exudate if >35, LIGHTS if in middle
LIGHTS - exudate if = pleural protein to serum protein >0.5, pleural LDH to serum LDH >0.6, pleural LDH >2/3rds upper limit of normal for serum
d dimer, culture , SERUM LDH AND PROTEIN FOR FLUID SAMPLE, glucose, albumin (low in liver and nephrotic), amylase
CXR
pleural US useful if loculated or small effusion and guide aspiration
thoracentesis/aspirate - cytology, gram stain, culture, acid fast bacilli, ldh, ph, protein
CT malignancy suspected
if suspected empymea, chylo or haemo from appearance of fluid - additionally should centrigue, cholesterol levels, haematocrit
causes of exudates = parapneumonic effusion, empyema, malignancy, TB, PE, cancer
causes on transudates (pale yellow) = all failures
chylothorax = chyle e.g. due to cancer or trauma (disruption of thoracic duct) pseudochylothorax = accumulation of cholesterol crustals due to RA, TB
types of parapneumonic effusions
simple - common and usualy sterile (nothing on culture) and resolves without intervention
complex - pH <7.2, like gram stain or gulture positive, need intercostal drain (a complicated parapneumonic effusion is basically one that needs a procedure like drianage to treat vs uncomplicated which goes away w abx)
empyema - pus, needs intercostal drain
a parapneumonic effusion w ph <7.2 indicates empyema
management of pleural effusion
treat cause e.g. abx
transudate - avoid drainage just treat cause
manage small effusions w observation
thoracentesisi for symptomatic relief (insert just above a rib)
chest drain is an alternative
in malignant effusions can consider pleurodesis
or indwelling pleural drainage or pleurecotmy
systolic vs diastolic failure and severity score
LVEF <40 = systolic
> 50% = preserved, diastolic
new york heart association
investigations for heart failure
BNP - refer if >400 for echo
TTE
ECG
CXR - alveolar oedema, kerly b lines, cardiomegaly, dilated upper lobe vessels, effusion
measure bloods - what could worsen it
consider other imaging if poorly imaged via echo - angiogrpahy, cardiac mri, TOE, stress testing
management of HF
systolic - <40%
bb, acei
can offer spironolactone as well if still have symptoms
diastolic >50%
fuorsemide as necessary for symptom relief w overload
in all
consider statin and antiplaelet if atherosclerotis diseaes
weight loss, exericse etc, treat any high output states like anaemia
exercise based rehab
discussion on advance decisions
non-drug
valvular reapir, revascularisation
CRT for EF <35% (can to CRT w defib or ICD dependin gon NYHA class) - e.g. ICD if survived VT or VF cardiac arrest
heart transplant
specialist treatment - DISH digoxin ivabradine sacubitril valsartan hydralazine and isosorbid dinitrites
management of acute heart failure
oxygen IV diuretics furosemide ventilate if resp failure consider mechanical assist device if candiate for tranplant vasopressors if shock
for acute pulmonary oedema - nitrate infusion, IV furosemide and morphine
copd investigations (azithormycin for lots of exacerbations, resuce pack w pred and amox) (assess need for LTOT FEV1<30 or po2<7.3 - 15 hours per day w oxygen)
mrc dyspnoea scale post-broncho spinormetry sputum culture bloods inc alpha-1-antitrpysin cxr ecg and echo for cor pulmoanry prongostic score w BODE index
2 stop smoking drugs
varenicline
bupropion
copd exacerbation management
HOME increase saba 30mg pred for 5 days antibioitcs e.g. amox no improvement then send sputum culture
HOSPITAL oxygen via venturi saba 2.5 neb hydrocortisone iv or pred 30mg 5 days ipratoprium antibotics - low severity = amox, mod = amox + clarith, severe = co-amox + clarith NIV in resp failure
O SHIAN
CURB-65 and BTS follow up
confusion urea >7 rr >30 bp <90 SBP 65
hospital if 2 or more (0-1 consider outpiatnet)
BTS recommend CXR at 6-8w after if persistenitng symptoms and those at risk of maliannct (>50 and smoker)
lung tumours found may be incidental or causative; tumours may block parts of the bronchial tree which increases the risk of infective events
Qs to ask in lung cancer history
any clubbing any facial swelling - SVC compression any hoarseness any horners any shoulder pain any bone pain
remember to say - treatment involves an MDT discussion
management of lung cancer (NB CEA is raised in some cases)
surgical resenction - lobar resection (lobectomy) or pneumoectomy
if not tolerated can try limited resection
adjuvant chemo and radiotherapy should be considered
should have hilar and mediastinal LN sampling for all those undergoign surgical resection
stage 3 - may be treated with chemoradioation before surgery
not suitable for surgery then have radiotherapy or chemotherapy
palliation - tracheal stenting, radiotherapy, pleudeosis for recurrent effusions, morphine for breathlessness, steroids, cryotherapy or brachytherapy
dex for brain mets
megaloblastic anaemia
immature RBCs = megaloblasts - produced due to deciecnt b12 and folate - will see hypersegmented neutrophils
macrocytic anaemias without DNA replication problems = non-megaloblastic macrocytic anaemia e.g. seen in copd where lots of new reticulotcytes are produced - or alcohol
ferritin level, transferrin, TIBC and transferrin saturation in anaemia
remember haptoglobin low in haemolyssi, LDH high, direct coombs
remember h pylori as cause of ida
FERRITIN
ACD high - trying to keep all iron in cells
NOTE CAN BE HIGH IN IDA if infection also going on
TRANSFERRIN
ida - high - trying to transfer
acd - low
TIBC
same as transferrin
TRANSFERRIN SAT - iron/tibc
low in both
causes of bloody diarrhoea and cause of diarrhoea w bloating
shigella
campylobacter
salmonella
schisosomiasis
giardia lamblia can cause bloating and diarrhoea
gernal management for diarrhoea and public health
admit if unable to retain fluids or severe dehyration
IV fluids
loperamide after each loose stool or codeine phosphate - BUT in gastroenteritis then not recommended
antispasmodics like hyoscine butylbromide
public health need to be notifified for food poisoning
IBS crieteria - do a hydrogen breath test for bacterial overgrowth and carb malabsorpton (lactose, fructose malabsorption) and do giardia lamia as can cause bloating w diarrhoea and do CA125 in women
Make a diagnosis of IBS if a person has abdominal pain which is either:
o Related to defecation, and/or
o Associated with altered stool frequency (increased or decreased), and/or
o Associated with altered stool appearance (hard, lumpy, loose, or watery); and there are at least two of the following:
Altered stool passage (straining, urgency, or incomplete evacuation)
Abdominal bloating or distension
Symptoms worsened by eating
Passage of rectal mucus, and
Alternative conditions have been excluded
(rome says abdo pain for at least 3 days per mont in last 3 months associated w 2 of - relieved by defecation, change in frequency, change in consistency)
management of IBS
manage any anxiety and depression
adjust fibre - insoluble for consipation only (brown rice, fruit and veg)
soluble for both (oats, nuts)
consider OTC probiotics for at least 4 weeks for diarrhoea or bloating
adequate fluid intake and exercise
bulk forming laxatives like fybogel
loperamide for diarrhoea
antispasmodic for abdominal pain or spasm like peppermint oil or hyoscine bromide (buscopan) or mebeverine
TCA for refractorsy abdominal pain
dietician referral - FODMAP diet
CBT or hypnotherapy
notes on bile acid malabsorption
bile acid are secreted by liver, stored in gallbladder and 95% are reabosrbed by terminal ileum (enterohepatic circ)
if fialure of reabsopriton then escape in colon and stimulate electrolyte and water secretion
cause = ileal resection, CD, idiopathic/primary, post-cholecsystecotmy, coeliac, pancreatic insufficienciy, DM, bacterial overgrowth
presents with watery chronic non-bloody dirarhoea
idiopathic usually presents at 30-70
may also have bloating wind cramping
investigate with SeHCAT test - artificial bile acid is swallowed then scan a week later to see how much retained - normal is >15%
or can do trial of bile acid minder
manage w low-fat fiet and binder like colestyramine
may also need ADEK vitamines
avulsion fracture
hairline/stress
bone attachment of ligament/muscle is pulled off
barely visible w no diasplacement - repeated subclinical injiry e.g. runners
fracture examples
colles- distal radius w dorsal displacemenet via foosh - need to be reduced then back slab
smiths - distal radius w anteiror displacement - falling backwards onto palm of outstretched hand
often need surgical management - can give haematoma block for pain relief and put in slab while awaiting theatre
scaphoid - foosh or sterring wheel during rta (risk of non-union and avascular necrosis due to vulnerability of blood supply)
greenstick - reduction involves slow constant pressure to reduce over 5 minutes until intact cortex is broken - then put in cast
bartons - smiths or colles w dislocation
investigation and management notes for fracture
assess neurovascular function, assess ROM
X ray AP and lateral
scaphoid are missed on 20% so do mri and ct if still suspicious
use ottawa rules to determine if x ray is needed
can also do a bone scan - fractures will appear dark
MANAGEMENT
pre-hospital splinting e.g. vacuum splint or traction splint
analgesia (can do intranasal in children - but codeine and tramadol should be avoided in them)
for open - irrigate w saline, then cover w sterile moist dressing and give iv antibiotics-operative repair should ideally be within 6hours to reduce osteomyelitis risk (use gustilo classification - type 3 may require amputation - extensive soft tissue loss/exposed bone/vascular injury)
imobilise join above and below - avoid full cast initialy as swelling may impeded circulation and produce ischaemic contractures
so do back slab first held in place w bandages then few days later do x ray and apply full cast (scahpod is exception just go straight to case as doesnt usually swell)
if neurovascular compromsise then urgegnt closed reduction - any displacement or dislocation must also be reduced - anaesthesia is required (IV regional, conscious sedation or haematoma block)
if not possible then surgery - can involve plate and screws, intramedullary wires or intramedullay nailing
plaster or paris is recommended cast - warn pt may feel warm - dont use for torus/buckle as should heal by themselves
investigations and management for hip fracture
bloods, urine drip, ecg, bone profile (albumin, calcium, ALP, phosphate), CXR look for shenton’s line which should be continuous, mri or ct if plain films inconclusive
MANAGEMENT catheter- majority in retention asess cognition e.g. 6-CIT 4at for delirium falls risk assessment analgesia review meds in case of aki nbm conservative occassionally involving tractino, bed rest and restricted mobilisation but outcomes v poor e.g. chest infection or clots
SURGERY
intracapsular - minimally or non-displaced (gardens 1 or 2) = dynamic hip screw (all fracture ends to slide which promotes bone healing)
intracapsular - displaced = total hip replacement (replace socket as well) or hemiarhtroplasty (THR if able to walk independently w no more than a stick, not cognitively impaired, fit for anaesthesai/procedure)
extracapsular - dynamic hip screw or intra-medullary nail
POST-OP 4at for delirium vte prophylaxis w lmwh and ted strockings physio and ot ecnouge mobilisation day afer surgery screen for infections screen for osteoporosis
type a vs b vs c pelvic fractures
type a = rotationally and vertically stable - generally these do not need surgery
e.g. avulsion fractures or isolated pubic ramus fractures
type b = horizontally unstable but vertically stable - includes open book fracture
type c = both horizontally and vertically unstable - whole ring is disrupted at 2 or more points - associated w massive blood loss
investigations and management pelvic fractures
- Urinalysis for haematuria
- Serial haemoglobin and haematocrit measurements to monitor ongoing blood loss; group and crossmatch
- Check for pelvic stability
- Full neuro exam of lower limbs
- And LL vascular exam - iliac vessels can frequently be injured
- Assess for other injuries e.g. urethral injury - blood at urethral meatus, high-riding or non-palpable prostate, perineal swelling
- A minimum of 3 plain radiographs are required (anterior-posterior, inlet view and outlet view)
- However, in the trauma setting, often a CT scan is performed as part of the patient assessment, which usually negates the need for plain films
- Angiography for vascular injuries
- Retrograde urethrogram for determination of urethral injuries (catheter is inserted followed by contrast then a plain radiograph is obtained -leakage of the contrast suggests urethral injury)
- Cystography for haematuria but intact urethra, to check for bladder injury
MANAGEMENT
a-e
primary survery
add a pelvic binder (wings over greater trochanters - if not available then use a sheet)
fluid resuscitation
surgery with plates or screws
manage any associated urological injuries
conservative - stable fractures - short-term bed rest and pain adapted mobilisatino e.g. crutches, vte prophylaxis, physio
notes on spinal column injury
american spinal injury association impairement scale
o A - Complete
o B - Sensory incomplete - sensory function is preserved
o C - Motor incomplete - motor function is preserved and more of half of key muscles below that level have a grade <3
o D - Motor incomplete - motor function is preserved and more of half of key muscles below that level have a grade ≥3
o E - Normal
primary injury arises from the mechanical disruption, whereas secondary are msotly casued by arterial disruption or hypoperfusion due to shock (refers to a cascade of events that follow the injury that may worsen the primary injury)
antieor cord syndrome = paralyysis below level and loss of pain and temp
posteiror cord syndrome = loss of proprioception and vibration sense
brown-sequard = ipsilateral spastic paresis, ipsi loss of proprio and vibration sense, contralateral loss of temp and pain
neurogenic shock occurs with injuries above t6 where htere is distributive shock as a result of sympathetic fibre disruption (triad of hypotension, brady, hypothermia)
AMPLE history
allergies medicaton past medical histroy last meal or orther intake events leading to presentation
canadian c spine rules
detemrine whetehr high low or no risk of c spine injury and whether they need imaging - ct
e. g. fall from height, paraesthsia in limbs, >65, can they walk, any midline cervical spine tenderness, pre-exicisnt spinal pathology like osteoporosis
- Ask patient if in any pain - if no, then feel along spine - if still no pain then ask them to move 45 degrees either side
management of a spine injury
extrication where needed
CAcBCDE (catastrophic haemorrhage)
c spine immobilisation
+/- full in line immobilisatin of spine if high risk for c spine injury - strab to backboard
needs to be strapped so that in the case of vomiting, the patient can be rapidly rotated while remaining in the neutral position
IV morphine
get to major trauma centre
clear aiway of sections - modified jaw thurst, oral airway (intubation may be needed in some - e.g. if lesion above c5)
oxygen and fluids as needed
treat bradycardia w atropine
monitor UO w catheter
ileus is common - ng tube and anti-emetics
protective padding to prevent pressure sores
monitor - GCS, neuro, temp (may be loss of thermoregulation), ecg
discuss with neurosurgeons
if no neuro deficit or displacement or instability can be managed conservatively w bed rest, cervical collar, traction then early mobilisation and rehab
surgery for dislocation type injiry, progressive neuro defect
physio, OT
w a cervical spine fracture, minor can be immobilised and traction may be used with a pulley, rope and weight for up to 12w while it heals
surgery if need to relieve pressure on cord w plates/screws/wires
GCS
Eye opening E4 = spontaneously E3 = to voice E2 = to pain E1 = none Verbal response V5 = conversation V4 = confused V3 = words V2 = sounds V1 = none Motor response M6 = obeys commands M5 = localises M4 = withdraws M3 = flexes - decorticate M2 = extends - deceberate M1 = none
criteria for CT scan w head injury
1 HOUR
gcs <13 initially, or <15 2 hours post injury
suspected open or depressed skull fracutre
any signs of basal skull fracutre (haemotympanum, panda eyes, rhinorrhea, battle’s sign, CSF from ear, CN palsy) - nb basal skull fractures usually heal without intervention if non-dsplaced (surgery if required)
seizure
focal neuro deficint
>1 episode of vomiting
8 HOURS >65 bleeding or clotting disorders dangerous mech of injury >30mins of retrograde amnesia
can also consider further imaging like ct angiography and venography to assess for vascular injry
MRI may be useful in evaluating CSF leak
send ‘csf’ fluid for analysis of beta transferrin (to check it is actually csf)
NB basal skull fracture is a break in at least one of temporal, occipital, sphenoid, frontal or ethmoid (temporal most common)
cause and vessels involved in brain bleeds
extradual = middle meningeal artery or vein (although any tear in the dural venous sinuses will also cause)
caused by trauma to pterion /temple
EDH in spinal column may follow trauma via epidural or lp
subdural = bridging veins
chronic is most common presentaiton - begins 2-3w after initial injury
typically sheared veins with a blunt injury or rapid acceleration-deceleration injury
shaken baby syndrome in babies
as due to veins - will present slower than epidural
may both be spontaneous due to av malformaiton, aneursym, clotting disorder
spike in age for extradural haematoma
less common over 60 due to dura being tightly adherent
less common in children due to plasticity (mouldable) of skull
peaks in 4th-5th decades
investigations and management for epidural and subdural haematoma
GCS FBC+ U+Es, LFTs, bone profile for calcium, coagulation, G+S, crossmatch, glucose to rule out hypoglycaemia as a cause neuro exam inc look for papilloedema CT MRI adds little benefit
MANAGEMENT
a-e w full trauma assessment (put out a trauma call)
correction of coag e.g. vitamin K and beriplex (dried prothrombin complex) for warfarin
abx if open skull fracture
IV mannitol may be used to decrease icp before surgery
small haematoma then observe
burr hole craniotomy
or larger haematomas may require decompressive craniotomy or craniectomy (bone not put back)
any bleeding source identified should be controlled w ligation or cauterisation
patients are then managed at intensive care often
ct in acute vs subacute vs chronic subrual
acute = blood hyperdense - more white subacute = may not see at all so will need CT WITH CONTRAST chronic = hypodense - more black
complex (major) vs non-complex (minor) burns
non-complex = <15% of total body surface area and does not affect a critical area
complex = any burn to a critical area like face, hands, feet, crossing join,s circumferential, genitals, + all chemical and electrical burns
investigations and management for burns
primary survery and CAcBCDE
wallace’s rules of nines to estimate % body surface area covered
bloods inc g+S, clotting, ck, bone profile, bm, ecg, abg, carboxyhaemoglobin
may need arterial line for invasive bp monitroing
trauma ct depending on mechanism e.g. electrocution with fall from height
MANAGEMENT
high flow oxygen - intubate if needed (smoke may cause oedema of airway)
escharotomy if circumferential
fluids via parkland’s formula (give half over first 8 hrs since burn, next half over 16 hours)
keep warm
iv morphine (in children intranasal diamorphine)
ng tube cos ileus potential complication
catheter
secondary survery - head to toe and AMPLE and tetanus
remvoe jewellery
debridement as needed- leave blisters intact due to infection risk
wound infection w fluclox
refer to specialist burn service if needed
wound care - dressing changes every 3-5 days - massage w emollient, high factor sunblock for 2years after
splenic rupture management
haemodynamiically unstable or grade 5 injury based on american association scale for splenic injury
- urgent laparotomy - if only peripheral rupture can do trial of splenic salvage - if hilar rupture tho must do splenectomy
- asplenic patients should be vaccinated against Strep Pneumoniae, Haemophilus Influenzae B (HIB) and Meningococcus
- in addition, prophylactic Penicillin V should be considered
haemodynamically stable w grade 1-3 o Can be treated conservatively with frequent US examination o Resuscitation with fluids o Bed rest o Repeat CT scan 1-week post-injury
ecg changes in tamponade
low-voltage qrs complexes
may see electrical alternana
in management - raise legs to improve venous return
GAVE
gastric antral vascular ectasia = dilated vessels in pyloric antrum
causes 4% of upper gi haemorrhage
autoimmune disorders are present in 60% of cases - caise is unknown - maybe a ct disease
edoscopy -looks like watermelon or honeycomb
histology if uncertain
mainly in women >70
haematemesis, anaemia, blood in stool
treat w endoscopic laser surgery or argon plasma cosgulation
screening for bowel cancer - remember to monitor cea - barium enema shows apple core lesion - do transrectal endoscopic us for rectal cancer
fecal immunochemical testing( FIT) - takes place every 2 years from 60-74
if abnormla - hb>120 then offered colonoscopy or imaging if colonocsopy is unsuitable
from colonoscopy -
low risk adenoma or no abnormalities = returned to routine regimen
intermediate or high risk adenoma invited for colonoscpi surveillance
cancer = referred for treatment
ie the polyp is removed and anlysed to see what risk
about 1 in 10 referred will have cancer
NB after treatment of cancer - nice recommend regular cea and a minimum of 2 ct afterwards
investigations for UGIB
- Regular observations and monitor urine output
- FBC - low Hb, platelets may also be low
o Be aware that Hb won’t necessarily initially be low because you are losing whole blood (compensatory haemodilation occurs in 24 hours) - Coagulation profile (INR/prothrombin time) - synthetic function of the liver
- Serum LFTs
o Be aware that LFTs can be paradoxically ok in cirrhosis - U+Es
- Urea > creatinine
- OGD - endoscopy is required within 24 hours of presentation - sooner if unstable after initial resuscitation
- Group and save and cross match
- Ascitic tap if ascites
- CXR should be arranged if possible, to evaluate for pneumomediastinum (oesophageal perforation) and free air under the diaphragm (perforation of abdominal viscus)
hypoglycaemia investigations and management (Remember t1dm need to inform dvla and need to measure bm before a long drive)
NB a reactive hypo is having a hypo after eating within 4hours due to too much insulin - to manage should increase meal frequency and reduce size
INVESTIGATIONS
cap glucose
blood glucose
insulin - if low could be alcohol, addisons, pituitary insuff, anti-insulin receptor antibodies. if high could be insulioma, SU, insulin injection
c peptide - high with SU ingestion or insulinoma
ketones
LFTs
cortisol for addisons’
sulphonyrea screen via blood or urine
anti-insulin antibodies suggest administration of insulin OR autoimmune hypo
can do 72 hour fast once acute phase over - in normal people should not lead to hypo - do all bloods after
MANAGEMENT
able to swallow then 10-20g e.g. 4 jelly babies, 4 glucotabs, if confused then buccal glucogel
recheck after 10 then repeat if needed, if still not then consider im glucagon or glucose 10% infusion
if improved then eat long-acting starchy carb like sandwcih or biscuits
if unconscious then im glucagon but avoid this if poor glycogen stores e.g. malnourised, liver disease or ON SU - then if not responding to 10% glucose 200mls over 15 mins - if reposnding have long acting carb
in alcoholic patients, also give thiamine as glucose increases thiamine demand
for people w recurrent - consider blood glucose awareness training porgramme
IF SU WAS CAUSE
IV glucose infusion
and octreotide
presentation of dka - as an investigation in dka say that you would do plasma osmolality and calculate anion gap and ecg monitor
potassium - low because shifts into cells and because large amoutn lost w osmotic diuresis
‘although normal - it is unlikely to represent the total body potassium which is usually low in dka)
- Develops within 24 hours
- Increased thirst and urinary frequency
- Weakness
- Weight loss
- Inability to tolerate fluids
- Persistent vomiting and/or diarrhoea
- Abdominal pain
- Lethargy and/or confusion
Signs include
o Fruity smell of acetone on the breath
o Acidotic breathing- Kussmaul’s respiration = rapid and deep respiration due to acidosis
o Dehydration
cut offs for HHS
hyperglycaemia >30
osmolality >320
ketones 1+ or trace
will be hypovolaemic
NB at presentation usually have low sodium and raised potassium and raised urea/creat due to dehydration
management of hhs
fluids 0.9% saline - usually 1L over first hour - risk of being too rapid and causing cerebreal oedema (if osmolality not decreasing then can switch to 0.45%)
0.05units/kg/hour insulin if glucose not falling by 5/hour with fluids alone
add glucose if levels <14
give potassium if 3.5-5.5
check glucose 2 hourly
resolution = osmolality <315, glucose <12.2 (normalisation may take up to 72 hours)
then transition to subcut insulin
high vs normal anion gap causes (metabolic acidosis)
high = lactic acidosis, salicylate poisoning
normal = diarrhoea (los HCO3), renal tubular acidosis (HCO3 reabsorption impaired), addisons…
NB in a normal person all of all the gap is due to unmeasured albumin which is an anion
GB presentation, investigations and management
ascending progressive weakness
facial wakness may develop
neuropathic pain
reduced reflexes
paraesthesia aand sensory loss - can be absent tho
autonomic symptoms like ileus, reduced sweating
diagnosed by LP - elevated protein w normal wcc
can also do an antibody screen
spirometry is a major determinant for need for icu
nerve conduction studies will be slowed
check immuobluin levels - pateints w iga def may experience anaphylaxis when given iv-ig
manage w iv immunoglobulin OR plasma exchange ITU if requried gapapentin pain relief splinting joints to prevent contracture dvt prophylaxis
notes on MG
antibody to ach receptor
or musk
or lrp4
or seronegative
often ocular symptoms first to appear - ptosis, double vision
more fatigue after exericse
more proximal muscles
tone, reflexes et all normal
myasthenic crisis = resp failure
diagnose with crushed ice - imrpvoes ptosis serum anti acetlcholeine ab mri brain thymus ct or mri tenislon test but rarely done now emg and nerve conduction studies count to 50 - will tire
some parts of liver screen
- LFTs
o AST>ALT in cirrhosis, alcoholic liver disease (S for Smirnoff)
o ALT>AST in chronic liver disease e.g. hepatitis
o GGT is sensitive for excess alcohol intake - Conjugated vs unconjugated bilirubin levels
- FBC including a reticulocyte count + blood smear for haemolysis
- ESR may be raised e.g. in PBC
- LDH raised in haemolysis
- Hepatitis serology
- ANAs and ASMA
o PBC hallmark = AMA (but notably absent in PSC)
o ANA, SLA and ASMA in autoimmune hepatitis - Serum immunoglobulins - IgG and IgM
o IgM is raised in PBC
o IgG and IgM may be raised in PSC - Alpha-1-antitrypsin levels - deficiency causes cirrhosis
- Ferritin will be high in haemochromatosis
- Low ceruloplasmin in Wilson’s
o Ceruloplasmin is the major copper-carrying protein in the blood - US for gallstones or hepatosplenomegaly
warm vs cold immune mediated anaemia
warm = igg - bind at body temp and treat w steroids/immunosuppressants
cold = igm mediated and low temps <4 - often accompanies renauds - keep warm
paroxysmal nocturnal haemoglobinuria = an acquired stem cell disorder with haemolysis especially at night + marrow failure + thrombophilia (increased risk of thrombosis)
nb microangriaophatic anaemias will cause schistocytes
haemosiderinuria
presence of haemosiderin in the urine = only seen in intravascular
haemoglobinuria is another indicator of intravascular haemolysis, but disappears more quickly than hemosiderin, which can remain in the urine for several weeks
oamotic fragility testing
if break easily then could be hereditary spherocytosis
can do a splenectom to treat this
other test - hb electrophoresis, blood film
symptoms of pbc/psc
25% asymptomatic fatigue pruritus hepatmogealy ruq pain jaundice, pale stool, dark urine sjogrens hyperpigmentaion xanthelsam
investigations for pbc vs psc - remember to say cholestyramine for treatment of these as well as treatment for cirrhosis
PBC fbc, esr, lfts ama m2 subtype (some may also have ana) raised igm us liver and fibroscan to evaluate degree of fibroisis liver biopsy can monitor afp, US and lfts
PSC
fbc, esr, lfts
no specific autoantibodies
us may show bile duct dilation
mrcp gold standard or ercp - beaded appearance
liver biopsy not needed for everyone but may be useful for staging
do yearly colonoscopy and us - bile duct, gallbladder, liver and colon cancers are common
surveillance in cirrhosis
offer gi endoscopy every 3 years
calculate MELD score every 6 months - helps decide prognosis and whether or not need liver transplant
mamangement points for cirrhosis
ASCITES fluid restric <1.5L low salt diet empirical antibiotics if >250cells/mm3 spirolocatone or furosemide daily weights paracetnesiss +/- human albumin solution to prevent circulatory dysfunction TIPS in refractory ascites
ENCEPHALOPATHY
lactulose to maintain bowel motion to clear harmful substances
rifaximin for prevention
SBP
antibiotics
human albumin solution
rifaximin for prophylaxis
OTHER
penicillamine for wilsons
transplant
saag
serum ascites-albumin gradient
>1.1 = transudate - raised portal pressure
<1.1 = exudate
tumour marker for cholangiocarcinoma
ca19-9
management of pancreatic cancer
- Surgical resection - only 10-20% are resectable
o Proximal pancreaticoduodenectomy with antrectomy (Whipple’s procedure - removal of head of pancreas, gallbladder, duodenum and pylorus)
o Distal pancreatectomy for tumours of the body and tail - Adjuvant chemotherapy (or radiotherapy)
- Unresectable
o Stenting of the bile duct or duodenum
o Chemotherapy
o Analgesia - oral paracetamol or could do coeliac plexus block (an injection of local anaesthetic into or around the coeliac plexus of nerves)
o Steatorrhea can be improved with pancreatin supplements e.g. CREON
o Slowed gastric emptying (due to compression of duodenum or stomach) causes N+V - prokinetic agents like metoclopramide or domperidone
MALT tumour
MALT - arises from mucosa associated lymphoid tissue (MALT) which appears in the stomach due to chronic inflammation, thought to be a result of H pylori infection (is not usually present in the stomach)
If a MALT is low grade, eradication of the H pylori is all that is needed
In high grade or atypical cases, chemo and/or radiotherapy may be required
however most gastric cancers are adenocarcinomas
notes on gastric cancer inc intestinal vs diffuse
intestinal = histology representative of intestinal epithelium - as a result of inflmmation from chronic gastritis (causes metaplasia) - more common and better prognosis - affect older
diffuse = arise from normal gastric mucosa - tend to be in younger patients
risk factors inc h pylori, high salt and preserved food, FAP
present w dyspepsia, anaemira, anorexia, difficulty swallowing, vomiting, melena, mass, virchow’s, early satiety , may be a succession splash on audsultation
investiagtions - endoscopy w biopsy and endoscopic us to see how far tumour has progressed through the wall, PET, HER2 testing, performance status w ecog, clotting
manage - distal antral tumours w subtotal gastrectomy, and proximal by total gastrectomy
ones involing GOJ will also require partial oesophageal resection
limited resection in elderly
pre or post chemo
or endoscopic techniques - mucosal resection or mucosal dissection for v early
lymphadenoectomy
palliatve via coeliac plexus block, stent, transfusions for anaemia, chemo
targeted cancer cells for her 2
investigations and management for liver failure
baseline bloods coagulation - INR >1.5 blood culture - susectpible to infection glucose can be v low high ammonia abg - can be raise dlactate raised creatinine amylase - pancreatitis is a complicatins liver screen - hep, tox, paracetamol, autoimmune markers and ig, ferritin, low caeruloplasmin us for cancer ct more detailed ct or mri head exclude other causes of distrubed mental function dopper us - hepatic vein in budd chiari eeg to define grade of enceph mc and s of ascites visual evoked potentials for enceph
MANAGEMENT
manage in itu
insert urinary adn central venous catheters to monitor fluid status
fluids
ascites = restrict fluid, low salt diet, weigh dailu, diuretics
10% glucose for low glucose
treat hepatorenal syndorme w terlipressin, TIPS for refractory
iv mannitol for icp
lactulose w neomycin for enceph , w regular enemas (rifaximin w lactulose is for prevention)
therapeutic hypothermia for cerebrela oedema
treat abnormal bleeding w ffp etc
liver transplant using kings college criteria
SIRS criteria - remember to implenet sepsis 6 within first hour
- Temperature >38 degrees or <36 degrees
- HR > 90
- RR >20 OR PaCO2 <32mmHg
- WBC > 12,000/mm³, < 4,000/mm³, or > 10% bands
septic shock = severe sepsis with persistent hypotension despite fluid correction and inotropes AND high lactate >2mmol/L
management points w sepsis
may see hypo due to depleted glycogen or hyperglycaemia due to sress response - so manage w insulin dosing
may require cvp measuring
may need vasopressors like noradrenaline or dopamine
dvt prophylaxis
cause and brief presentation of neurogenic shock
cervical spine injury above t6 leading to loss of sympathetic tone
or iatrogenic from spinal anesthesia
hypotension, no tachy, warm periphereis
organisms in infective endocarditisi and what sort of valves they affect
early prosthehtic = stpah - staph aureus or staph epidermis
late = strep = strep viridans, strep bovis (link w colon cancer)
strep viridans = poor dentition and dentral procedures
staph aureus = ivdu
presentation of IE
remember to do urinalysis in investigation
3 sets of blood cultures from 3 diff sites
repeat TTE/TOE should be performed 7-10 days later if both negative and the clinical suspicion of IE remains high
MRI in complications like abscesses
acute IE is associated with a rapidly progressive infection and can cause HF, valvular insufficiency with or without embolic events (emboli can be presenting feature in 30% - may also affect kidneys causing haematuria)
subactue presenst with fever, non-speicic features
new heart murmurs
systemic - weight loss, poor appeteie
spinter haemorrhages, roth spots on eyes, olsers painful, janeway, clubbing, splenomegaly due to splenic abscess formation (will cause abdo pain)
more so in acute, may have features of hf like raised jvp, bilateral crackles
A 31-year-old woman presents with a 1-week history of fever, chills, fatigue, and unilateral ankle pain. Her past medical history includes mitral valve prolapse and hypothyroidism. She admits to infrequent intravenous heroin use and has a 10-pack-year history of smoking. Physical examination reveals temperature of 39°C
managemnet of IE
IV antibiotics - first do blind therapy (all have at least gent in) then treat depending on organism like vancomycin for mrsa, fluclox for staph aureus
need for 4-6 weeks
up to 50% will need surgery - remove infected tissue or valve repair e.g. if new HF or uncontrolled infection or prevention of emboli in big >10mm vegetations
prevention for high risk patients (prosthetic valve, previous IE, CHD) e.g.before dentral procedure or cardiac or resp
with amoxicillin iv
should do followup blood cultures 1 and 2 weeks following therapy to ensure not bacteraemic
investigations for chronic limb ischaemia
full cv exam
fbc, glucose, lipids
ecg - 60% of patients w intermittent claudication have ecg evidence of pre-existing coronary diseaes
abpi (normal is 0.9-1.4, <0.3 critical - do not exclude a diagnosis of pad in people w diabetes w a normal abpi)
treadmill test - patient walks on slope until pain - a decrease in ankle systolic >30 or ABI >20% decrease is diagnostic
duplex US
offer CT or MR aniography for people that need further imaging before considering revascularisation
rutherford classificaion can be used to grade based on claudication pain
inevestigations for acute limb ischaemia
hand held doppler us ct angiography where time allows or catheter guided angiogrpahy fbc, glucose, lipids abg for lactate thrombophilia screen investigations to find source of embolus = ecg, echo abpi may be done after to establish if any risk of chronic pad
complications x2 of acute limb ishcaemia
comparemnt syndrome
release of substances from damaged muscle cells like k causing hyperkalaemia, h causing acidosis, myoglobin causing aki
some management points for leg ulcers
venous - leg elevation, increase exercise to improvem muscle pump, weight reduction, compression bandaging after abpi, emollients, treat any varicose veins (endothermal ablation, sclerotherapy or open surgery) to improve return, abx if infection
arterial - anyone w cirtical limb ischaemia(ie w ulcers) should be urgent referred for vascular review. conservative, cv modification w statin and antiplatelet and bp control. suregry w angiogplast +stent or bypss
ischaemic or necrotic tissue - surgical debridement
severe cases - amputation
neuropathic - optimise diabetes control, diet, execerise, cv modification, podiatry appointments w appropriate footwear
surgical debridement as needed
ampuation if severe
differentials for a dvt
ruptured bakers cyst cellulitis superifical thrombophlebitis calf muscle haematoma calf muscle tear achilles tednon teat post-thrombotic syndorme
investigations and management of dvt
examine
baseline bloods inc clotting screen
wells score - if >1 go straight to US, if less then d dimer
can use intermin anticoagulation
if unprovoked - do thrombphilia testing and investigate for any undiagnosed cancer w a physical exam
oral anticoagulant - rivaroxaban or apixaban first line, or LMWH then dabigatran, or LMWH w warfarin then just warfarin
for 3 if provoked, 3-6 if cancer, 6 if unprovoked
can consider catheter directed thrombolytic therapy for those w symptomatic ileofemoral dvt
or IVC filter where anticoag is CI or has failed or recurrent
post-thrombotic syndrome
chronic venous hypertension causing swelling, hyperpigmentaion, lipdermatosclerosis, venous grangrene
is a complication following dvt (other causes = phelbitis (when varicose veins get inflamed after a blood clot), congenital leaky valves, pregnancy)
causes and presentation of ventricular tachy
CAUSES
late phsae of MI
cardiomyopathy
electrolyte disturbances
caffiene or cocaine may stimulate vt in vulnerable hearts
drugs like flecainde
(with polymorphic vt - think ischaemia or things that prolong the QT interval - polymophic VT w twisting morphology in setting of qt prolongation = TdP)
PRESENTATION
hypotenison, collpase, acute HF, degeneration to VF
chest pain, sob, resp distress
management of non-sustanined VT <30 seconds
beta blocker or self-terminating so no treatment may be needed
ICD criteria for VT
cardiac arrest survivor (VT or VF)
have spontaneous sustained VT causing syncope or significant haemodynamic compromise
have sustained VT without syncope or cardiac arrest and also have LVEF <35%
familial syndomr w high risk of sudden death
4H and 4T - cause of PEA, VF, puslness VT, asytole
4Hs o Hypoxia (give oxygen) o Hypovolaemia (correct with IV fluids) o Hypothermia (especially consider in cases of drowning - check with a low-reading thermometer) o Hyperkalaemia (or hypokalaemia, hypocalcaemia, acidaemia, or other metabolic disorder)
4Ts
o Tension pneumothorax (consider if trauma or previous attempts to insert a central venous catheter)
o Tamponade (cardiac) - particularly in cases of trauma
o Toxins
o Thromboembolism (coronary or pulmonary) - consider thrombolytic drugs but these may take up to 90 minutes to work
differentials for a narrow wrs tachy but irregular
random note - any SVT w bbb can be mistaken for a wide complex tachy
AF or atrial flutter w variable block
bradycardia algorithm
a-e, give ocygen if needed
12 lead ecg and ecg monitor, bp monitor
adverse features - shock, syncope, MI or HF - if YES then 500mcg atropine IV
if NO but risk of astyole (recent asystole, mobitx II, complete heart block, ventricular pause >3s) then also give atropine
if not satisfactor response to atropine then can repeat up to 3mg, or adrenaline or isopernaline or alternatives like glucagon in bb or ccb overdose, dopamine… OR transcutanous pacing
presentation of svts
palpitations
fatigue
pre-syncope/syncope
chest pain
the time between episodes of SVT can vary greatly – in some cases, short bursts of SVT occur several times a day. Or at the other extreme, an episode may occur just once or twice a year
do you see p waves in avnrt - NB AVRNT involves the fast and slow circuit and is triggered by a prematural atrial contraction - i.e. there is no accessory pathway
either are not visible or seen immediately before or after the qrs - or can see retrograde p waves
avrt on ecg and name of accessory pathway and the main concern of wpw and management
bundle of kent - signal can then go back up this if avn is in refractory period
shortening of pr - ventricles are being stimuatled quicker than usual as there is no avn delay
wide qrs
presence of delta wave - indicatest that the ventricles are being stimulated over a longer amount of time
might also be right or left bbb
the main concern of wpw is development of AF which may be conducted to the ventricles giving a rapid ventricular response - this can deteriorate into vt or vf
management is with acessory pathway ablation - only if symptomatic - and avoid triggers
circuit in atrial flutter and some causes
re-enterant circuit that runs around annulas of tricsupid valve = typical flutter
in atypical, the origin is elsewhere in right or left atrium
CAUSES
age, structural abnormalities like atrial dilation due to septal defects
CHD
inciscional scars from prior atrial surgery
alcohol abuse
sick sinus syndrome
HTN
patients taking anti-arrhythmics for chronic suppression of atrial fibrillation may convert to atrial flutter
hyperhtyorid
alcohol
obesity
3 types of AF
paroxysmal = >30 secs but <7 days persistent = > 7 days or <7 days but requiring pharmacological or electrical cardioversion permanent = fails to terminate using cardioversion, relapses within 24 hours or >1 year adn cardioversion has not been attempted
anticoagulation in AF
using a doac or warfarin
2 or more on chadvas and consider 1 or more for males
hasbled>3 you are worried
be aware that DOACs have a very short half-life so need good adherence, whereas warfarin lasts up to 72 hours so may be better if someone is forgetful
DOACs have a reduced risk of haemorrhagic stroke than compared to warfarin
rate vs rhythm control in AF - and another option if they’ve failed plus pill in pocket
rate = beta blocker like atenolol or propranolol, or a CCB like diltiazem or verapmil
if these fail then can try digoxin - if sedentary
avoid verapamil in severe HF
can use combo if monotherapy fails
rhythm control = amiodarone if structural heart disease, flecaininde if not
advocated for new onset, younger, reversible cause, HF worsened by AF
can do electrictral conversion if unstable or in those not responding
left atrial catheter ablation is another option to try if other mails have failed
paroxysmal (>30secs but <7 days) = flecaininde or sotalol
acquired causes of long qt for tdp and presentaiton of tdp
antiarrhtymic drugs like flecainide and amiodarone
antibiotics like erythrmo
electrolyte abnormalites
episodes of tdp may be caused by stress exercise or fear
patients present with palpitations, syncope, dizziness, sudden death may occur
2 types of type 2 heart block - symtpoms inc low hr, fatigue, sob, syncope, dizziness, chest pain, palpitaitons, stokes adams attack in 2nd and 3rd degree
mobtiz type 1 = pr becomes progressively longer until qrs is dropped
type 2 = fixed unchanging pr then occassional loss of q wave usually in a regular ratio
heart block management
1st = no treatmen requied, is a relative ci to some drugs like flecainide, bb, ccb, digoxin, follow up ecg annually to monito progression
2nd type 1= atropine or temp pacemaker insertion and further investigations like 24 hour ecg, echo, cardic catheterisation. with type 2 - permanent pacemaker (could result in severe brady or progress to ype 3)
3rd = atropine (or adrenaline or dopamine), transcutanoues pacing n unstable, pacemaker more permently solution
management of bundle branch block
- Require complete cardiac evaluation
- Treat underlying cause if possible
- Those with syncope or near-syncope may require a pacemaker
- Some patients with LBBB, a markedly prolonged QRS (usually > 150 ms), and systolic heart failure may benefit from a biventricular pacemaker, which allows for better synchrony of heart contractions
investigations and management for paracetamol overdose
take paracetamol levels 4 hours after ingestion or asap if >4 hours ago or staggered overdose
U+E
LFTs, clotting screen, INR
ABG - acidosis in early stages
glucose - hypoglycaemia is common in hepatic necrosis so should check glucose hourly
MANAGEMENT
a-e
consider activated charcoal if presents within 1 hour
NAC if above treatment curve
3 bags over 21 hours
if staggered or taken 8-24 hours ago and >150mg/kg then can start immediately without waiting for levels
if pt is still in hepatic failure then bag 3 is conitnued
hypersensitivity is common and antihistamine may be needed (anaphylactoid reaction) - stop infusion and give chlophenamine if necessary (and neb salbutamol if bronchospasm is sig) - then restart treatment once reaction has settled - start slowly
prior to discharge, recheck inr and lfts
KCH criteria for consideration of liver tranplsant
triggers that push neuron excitement past the seizure threshold in epilpsy
and some causes of epilspey
and what bloods differentiate it from pseuoseizure
can do 24 hour ambulatory eeg or sleep depreivation eeg or video eeg telemtry
- Sleep deprivation
- Alcohol (alcohol intake AND alcohol withdrawal)
- Drug misuse
- Physical/mental exhaustion
- Flickering lights –e.g. on TV/video games – cause primary generalised epilepsy only
- Infection / metabolic disturbance
- Medications such as TCAs and phenothiazines (e.g. chlorpromazine)
epislepsy causes = idopathic, truam, after neurosurgery, infection, genetic, vascular e.g. stroke
bloods = ck and prolcatin
general measures of epilepsy management
advise family and carers to record further episodes
stop driving until 1 year seizure free and any potentially dangerous activties
sleep deprivation and allcohol may lower seizure threshold
shower instead of baths
acute
protect head from injury by cushioning head, remove glassess or harmful objects
recovery position after seizure stops
after first seizure attend first fit clinic
call ambulance if >5 mins
drugs are not recommended after one fit unless risk of recurrence is high e.g. structural brain lesion or pt wishes
what time of day is long acting insulin taken
last thing at night - 10pm
name some things that will increase insulin requirements
and what is variable rate insulin
sepsis
infection
steroids
pancreatitis
variable rate = cbg every 15 mins and changed accordinly
management of alcoholic liver disease
abstinance
chlordiazepoxide 5-7 reducing dose
alcoholics anonymous
weight reduction and smoking reduction
nutrition - pabrinrx
influenza and pneumococcal and hepatitis A and hepatitis B vaccine
steroids can imporve short term outcomes in severe alcoholic hepatitis - pred
liver transplant - but must abstain for 6m
SBAR
SITUATION
introduce self, grade and ward
confirms who they are speaking to - get their name
are you free to talk
states patients name and hospital number
states reason for cal - i would like your advise on management or i would like you to come and review the patient
BACKGROUND reason for admission how long ago PMH relevant SH, DH, FH describes course of events describe current event
ASSESSMENT what i think the prob is and why concerned describe exam findings state observations state investigations done
RECOMENDATION what you want done ask if anything can be done in meantime repeat back plan ask if i can document convo in notes thank them
COPD managmenet nots - inc most effective stop smoking stratedgy
INITIAL THINGS THAT SHOULD BE DONE AFTER INITIAL DIAGNOSIS
ask does he have his annual flu jabs
stop smoking
pulmonary rehab - lasts 6 to 8 weeks, with 2 sessions of about 2 hours each week. You’ll be in a group of about 8-16 people
inhaler review
most effective stop smoking stratedgy = combination of varenicline and behavioural support or a combo of a short and long acting nrt (patches, gums, inahalers, sprays)
patches release nicotine slowly, others act more quickly
E-cigarettes are also a form of nicotine replacement treatment. They are more effective than the other products but you need to buy them yourself and they may still carry some risk over long-term use. Other NRT products are risk-free
usually lasts about 8-12w before u gradually reduce the dose of nrt then stop - however if you use longer than this is still considerably less harmful than smokig
e cigarretes/vaping is 20x less harmful than smoking
Pick a date to stop and decide you’ll be a non-smoker from that day. Tell your family and friends and plan something fun to take your mind off it
get rid of everything from ur home that reminds you of smoking
call yourself a nonsmoker
A craving can last 5 minutes. Before you give up, make a list of 5-minute strategies - e.g. 5 min walk - evidence shows this helps cut cravings
toxic megacolon management
NBM NG tube decompression IV fluids IV steroids hydrocortisone antibiotics - broad spec e.g. meropenam IV ciclopsorin
correct any electrolyte abnormalieis - esp hypokalaemia, hypomagnesaemia
total colectomy may be required - no improvement after 72 hours
notes about stop smoking treatments
Most people using NRT products do not become dependent on them. In fact, one of the biggest problems with NRT is that people don’t use enough of it for long enough
E-cigarettes do not contain tar or carbon monoxide – 2 of the most harmful elements in tobacco smoke
the nicotine part does not cause cancer
antibiotic prescribing station/counselling
see doctor if blood in stools
stop taking if develop rash or feel like tongue/throat is swelling
must complete course even if feeling beteer
things to remember with UGIB history
ANY DARK STOOLS
ask about diet - has it changed, when was last time you ate
remember to say group adn save and cross match
