Emergency medicine Flashcards
What should you look for when assessing of breathing? (B)
signs of resp. distress
RR
Assess depth/quality of breathing
chest deformity, raised JVP abdominal distension
Record FiO2 and SpO2
Listen near face: wheeze, coughing, stridor
Palpate, percuss, auscultate
Trachea position
How can hyperventilation affect ventilation?
Reduces the level of ventilation achieved (just gets rid of CO2)
What signs may indicate resp. distress?
Increased RR (in SEVERE resp. distress - can become hypoventilation)
accessory muscle use, intercostal and subcostal recession
Agitation (untreated hyperaemia - cerebrally irritated)
Sweating
Pallor/redness/cyanosis
Wheeze
What RR indicates that pt. may be near death?
> 27
Or v. low
What may chest deformity tell you about pt?
Existing disease (eg. barrel chest, COPD)
Cause of breathlessness - abdominal breathing, broken ribs, restrictive disease etc.
Why is JVP important in resp.?
Cardiac cause of resp. problem (pulmonary oedema)
What things can cause tracheal deviation?
Large pleural effusions
tension pneumothorax
What treatments can you give breathless pt.?
Oxygen
Salbutamol nebs
GTN or furosemide (in pulmonary oedema - esp. if near arrest)
ABX and steroids (Later management, once pt. stable)
Flow rate of Oxygen that can be given when using nasal cannula. What percentage oxygen is delivered?
2-6L (usually 4L)/min
24-30%
Flow rate of Oxygen that can be given when using Hudson Mask. What percentage oxygen is delivered?
5-10L/min
30-40%
Flow rate of Oxygen that can be given with non-rebreathe mask. What conc. of oxygen is delivered?
12-15L
85% (ideally, would be 100%)
What is a benefit of a bag-valve mask?
Delivers positive pressure
What are CPAP/BiPAP?
Types of non-invasive ventilation
Should you prescribe O2 for someone who is breathless, but has normal-range O2 sats?
NO.
If they do not have oxygen requirement, THEY DO NOT NEED TO BE GIVEN SUPPLEMENTARY OXYGEN
What is normal range of sats in COPD pt.?
88-92%
What is normal range of sats in non-COPD pt.?
94-98%
62 yr M COPD SOB Productive cough, fever, pleuritic chest pain O2 sats 90%
Does he need Oxygen?
NO.
25 yr M Operative repair of femur # No PMH ABCDE confirms he's not critically unwell Sats 90%
Differentials What is his O2 target range? Does he need supplementary O2? What delivery system should you use? Why is ABCDE normal?
Fat embolism
Hospital-acquired pneumonia
O2 target range: 94-98%
Yes he needs O2
What delivery system? Nasal cannula (commencing on 1L/min up to max of 6L/min) - start small, increase!
ABCDE has shown he’s not critically unwell as he is ACUTELY unwell, not CRITICALLY unwell (critical means near-death). You have time to manage him before he turns critical.
What are features of fat embolism?
SOB, reduced sats, usually cerebrally confused
19Yr M Collapsed at home Vomiting Pyrexial Florid non-blanching purpuric rash Critically unwell Sats on 99% on face mask
Does he need Oxygen?
How should it be delivered?
Critically unwell - therefore even if sats in range, need to be on 15L
non-rebreathe reservoir mask
78 yr F COPD Long-term O2 therapy Collapse Reduced consciousness In extremis (about to have cardiac arrest) Slow-intermirrent gasping breaths Sats are unrecordable
O2 target range? Does she need supplementary O2? What O2 delivery system would you choose? What might her ABG look like? What do you need to consider?
88-92%
Yes
She needs a bag and valve mask - she isn’t breathing, therefore needs ventilation (+ve pressure of bag and valve mask)
Low O2, high CO2 - possible resp. acidosis
Whether she may have a DNACPR, therefore, what you do re. withdrawng care/ continuing resuscitation
48 Yr M Pneumonia on ward Increasing SOB On O2 (nasal cannula 6L/min ABCDE: not critically unwell Sats 93%
Does he need O2?
If so, via which O2 delivery system?
Yes
Simple fase mask (5L/min - although reduction, this would probably be enough via this method. If not working, titrate up)
28 Yr M CF Recovering from pneumonia ABCDE: not acutely unwell Sats: 86% on 60% venturi (V60) mask
What is his target range? Why?
Does he need O2?
Via which delivery system?
Who else might you want involved?
88-92
Yes
Non-rebreathe mask
Critical care review, if not HDU (as he is deteriorating and requiring high-flow Oxygen and aggressive treatment)
*in leeds, can’t be in normal ward if you’re on non-rebreathe
Who should get a blood gas?
ANYONE who’s Critically ill
Unexpected/inappropriate hyperaemia (Sp O2 <94%) Or requiring O2 to maintain normal sats
Deteriorating O2 sats
Increasing SOB with previously stable hyperaemia
Deteriorating pt. who now requires O2 to maintain constant O2 sats
RF for hypercapnia resp. failure, develops acute SOB, reduced O2 sats, drowsiness or other Sx of CO2 retention
SOB and thought to be at risk of metabolic conditions
Acute SOB or critical illness and poor peripheral circulation in whom reliable oximetry cannot be obtained
ANY OTHER EVIDENCE THAT WOULD INDICATE THAT BG WOULD BE USEFUL
Any reduction in O2 sats of 3% or more (even if within target range)
What are the benefits of ABG over VBG?
ABG is gold standard for determining the arterial metabolic parameters
Can determine PaO2 (can’t do this on VBG)
What is a normal pH range on a BG? What is it called if value is:
a) below range
b) above range?
- 35-7.45
a) acidaemia
b) alkalaemia
What is a normal PaO2 range on a BG? What is it called if value is:
a) below range
b) above range?
> 10kPA
a) hypoxaemia
b) hyperoxaemia
What is a normal PaCO2 range on a BG? What is it called if value is:
a) below range
b) above range?
4-6
a) respiratory alkalosis
b) respiratory acidosis
What is a normal HCO3 range on a BG? What is it called if value is:
a) below range
b) above range?
22-30
a) metabolic acidosis
b) metabolic alkalosis
What is a normal BXS range on a BG? What is it called if value is:
a) below range
b) above range?
- 2 to +2
a) metabolic acidosis
b) metabolic alkalosis
Outline the process of blood gas interpretation
How is pt. clinically O2 pH PaCO2 BXS or bicarb
Outline blood gas interpretation
How is pt. clinically - KNOW CLINICAL SCENARIO (incl. FiO2) O2 pH PaCO2 BXS or bicarb
Does your interpretation fit clinical picture
20 yr M Tachypnoea Abdo pain Vomiting Confusion
What are differentials?
vomit has to be suctioned from airway
RR 28 SpO2 99% on air AE L=R Pulse 128 BP 95/60 HS I + II + 0 No other obvious abnormal signs
Differentials:
DKA
Pneumonia
Sepsis
20 yr M Tachypnoea Abdo pain Vomiting Confusion
What are differentials?
vomit has to be suctioned from airway
RR 28 SpO2 99% on air AE L=R Pulse 128 BP 95/60 HS I + II + 0 No other obvious abnormal signs
Knowing this, What other differentials might you come up with?
GCS 13/15
ES V4 M6
can he have blood gas?
VBG: pH 6.9 PO2 11.5 PCo2 3.5 HCO3 8 BXS 12
What does this tell you?
Are the results a surprise?
Differentials 1:
DKA
Pneumonia
Sepsis
Differentials 2:
Septic shock
Hypovolaemic shock
He needs blood gas: shock and ?metabolic illness
Metabolic acidosis
No, results fit clinical picture
What are signs of C02 retention?
Cyanosis
Confusion
What is the definition of shock?
Clinical syndrome caused by inadequate tissue perfusion and oxygenation leading to abnormal metabolic function
What are the different types of shock?
Cardiogenic
Hypovolaemic
Obstructive
Neurogenic
Anaphylactic
Septic
What are the physiological effects of shock and re-perfusion?
Intracellular calcium overload leading to ↓myocardial contractility, ATP reduction & degradation of ion pumps via free radicals.
H+ excess causing ↓ catecholamine effect and ↓ myocardial function
Metabolism becomes glycolysis dependent leading to↑ FFA and
↑lactic acid
What are common causes of hypovolaemic shock
fluid loss eg. excess urination, reduced intake, vomiting, burns
haemorrhage (haemorrhage shock)
How should you treat hypovolaemic shock
IV access
IV fluids +/- blood
Treat cause (stop bleeding)
Monitor response
What is an anaphylactic shock?
Sudden onset generalised immune condition caused by exposure to a causative substance in a sensitised
person
How long after exposure to substance, do Sx of anaphylaxis begin?
depends what source is/route of contact (generally 30 mins)
topical 10-15 mins
eaten 30 mins
IV = matter of minutes
How would you treat anaphylactic shock?
1) Adrenaline (IM = thigh, elevate leg)
2) Crystalloid fluids (DO NOT GIVE COLLOID)
3) Hydrocortisone (prevent bi-phasic reactions)
4) Chloramphenamine (anti-histamine)
Ranitidine (H2 blocker)
May need to repeat IM adrenaline after 5 mins
Continue to deteriorate - IV adrenaline bolus (BY A SENIOR)
All anaphylaxis pts. are admitted - at risk of biphasic shock within around 6 hours
What is septic shock?
Sepsis accompanied by hypotension and perfusion abnormalities despite adequate fluid resuscitation
What is syncope?
transient loss of consciousness
(usually without warning)
Transient global cerebral hypotension
Rapid onset
WITH SPONTANEOUS COMPLETE RECOVERY (if you have lasting Sx, IT IS NOT SYNCOPE)
Can a pt. lose consciousness with TIA?
Unlikely that unconsciousness would occur TIA (as would need to effect both halves of brain blood supply at same time)
What are the main general categories of causes of TRUE syncope?
Cardiac
orthostatic
neurogenic
What are the San Francisco syncope rules? What do they help you decide?
CHESS - IF YOU THINK Pt HAS HAD SYNCOPE, helps you decide who is safe to go home.
Hx of congestive HF Haematocrit <30% Abnormal ECG SOB Triage systolic BP < 90
Any of these - high risk of having had cardiac event. Need to be admitted.
What is the OESIL risk score?
Risk score
Point score of following RF: Age >65 (1) Hx of Cv disease (1) Syncope with prodromes (1) Abnormal ECG (1)
Score of 2 or more implies increased risk of cardiac death
What are some more unusual Sx of syncope? How can each of these be told apart from a seizure?
Twitching (for about 5-10 seconds - convulsive syncope)
Tongue biting (at tip - unlikely to be seizure. Tongue biting at side, more likely to be seizure)
What should you include in a neurological assessment in a pt. with collapse?
Cranial nerves Peripheral nerves Cerebellar Gait AMTS - best done on first meeting Fundi NIHSS GCS Pupils Lateralising signs Capillary glucose
What is the NIHSS? What is it used for?
NIH stroke scale
Scale used to decide whether someone can be thrombolysed
What are common causes of hypoglycaemia in diabetic pts.
Hypoglycaemic agents
Decreased glucose intake
Increased glucose utilisation (increased exercise)
Increased insulin sensitivity (weight loss, increased exercise)
Reduced insulin clearance (renal failure)
Why would you do CXR if you think pt has PE?
May see wedge infarct
Rule out differentials (eg. pneumothorax)
What are the main two investigations for PE?
CTPA VQ scan (looking for VQ mismatch)
Which direction do shoulder dislocations most commonly occur in? What are two key things associated with anterior shoulder dislocation that you should make sure you assess/document?
Anterior dislocations
test regimental badge and document radial artery
What are people given when they have been poisoned (if this has occurred within the last hour)?
Charcoal (drink)
What are the classical features of an opiate toxidrome?
pin point pupils
resp depression
reduced GCS
What can be used to reverse benzo toxicity? Why might you not do this?
flumazanil
Why might you NOT give a full dose of naloxone to someone who has suffered a heroine overdose?
Naloxone could recover their RR before the heroin has worn off, therefore pt may leave before the effects of heroin have worn off and you’ve been able to treat properly
What is a common s/e of poppers?
methaemoglobinaemia
w
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What scoring system is used for PE? (other than Well’s score)
PERC
How should you approach a pt. who is acutely unwell?
Focussed Hx Collateral Hx Focussed examination Investigation Working diagnosis, initial treatment management plan (incl. referral to correct ward)
How should you approach a pt. who is critical unwell?
ABCDE approach (treat at each stage)
Investigations
Working diagnosis, further initial treatment
Once stable: focussed Hx
focussed Ex
Longer-term management plan (incl. referral to correct ward)
List what should be done in A of ABCDE?
Look for signs of airway obstruction
TREAT obstruction (adjuncts)
Give oxygen (if sats require it)
List what should be done in B of ABCDE?
Look for resp distress RR Quality of breathing Chest deformity FiO2 and spO2 Listen near face palpate, percuss and auscultate Tracheal deviation
Initiate treatment
List what should be done in C of ABCDE?
HR BP Fluids (if low BP/CO) Look at cardiac monitor Look/feel hands assess peripheral and central CRT Assess venous filling (cap. refill) Central and peripheral pulses Listen to heart Look for signs of poor cardiac output, haemorrhage
Treat cause of cardiovascular collapse
List what should be done in D of ABCDE?
Review and treat ABC - sats and BP esp.
GCS/AVPU Drug chart (drug-induced reduced GCS) Pupils Lateralising signs Capillary glucose Ensure airway protection
List what should be done in E of ABCDE?
Examine pt: bruising, breaks etc.
Temp
What should you do after you’ve done ABCDE assessment of pt.?
Take Hx Review notes Review results Consider which level of care required Reassess response Documentation Definitive treatment
How can causes of collapse be classified to help diagnosis?
Head
Heart
Vessels
Drugs
What are ‘head’ causes of collapse?
Hypoxia Hypoglycaemia Epilepsy Affective Dysfunction of brain stem eg. verterbrobasilar stroke, TIA or migraine
What are ‘heart’ causes of collapse?
IHD Emboli Aortic obstruction (eg. stenosis, HOCM) Rhythm disorders Tachyarrhythmias (VT, SVT, QT syndrome)
What are ‘vessel’ causes of collapse?
Vasovagal ENT: BBPV, labyrinthitis, meniere's Situational: micturition/cough syncope Sensitive carotid sinus Ectopic pregnancy Low vascular tone Subclavian steal
What are ‘drug’ causes of collapse?
Anti-Hypertensives eg. beta blockers
‘Street’ drugs
What questions do you want to ask a pt. who has come in with collapse?
What were you doing at time? Any associated Sx Witnesses Recent illness On-going illness Medication Previous episodes
What systems do you want to examine in pt. who has come in with collapse?
General appearance (sats, BP/HR/RR) CV resp neuro head and neck abdo and pelvis
What investigations might you want to do for pt. who has come in with collapse?
blood glucose
What is cariogenic shock?
Heart unable to pump enough blood to meet body’s needs
What is neurogenic shock?
Shock caused by disruption of autonomic pathways within spinal cord
What is hypovolaemic shock?
Fluid loss means heart cannot pump enough blood around body to meet its needs
What is anaphylactic shock?
Severe allergic reaction
mediators released in allergic reaction cause vasodilation, bronchial restriction, leaky blood valves, depressed HR
What is obstructive shock?
Physical obstruction of great vessels or heart itself
What is septic shock?
Inflammatory markers and organ damage lead to lowered blood pressure and abnormal cellular metabolism
What are some common causes of cariogenic shock?
MI
Malignant dysrhythmia
What are some common causes of obstructive shock?
tension pneumothorax
cardiac tamponade
What types of shock fall under the term ‘distributive shock’?
septic shock
anaphylaxis
neurogenic shock
What might you find on ABC examination of a pt. suffering from an anaphylactic shock?
A: swelling, hoarseness, stridor
B: rapid breathing, wheeze, fatigue, cyanosis, sats < 92%, confusion
C: pale, clammy, low BP, faintness, drowsy/coma
What ratio of adrenaline is given in anaphylactic shock?
1:1000
What dose (and volume) of adrenaline is given to adults in anaphylaxis?
500 micrograms IM
0.5 mL
What dose (and volume) of adrenaline is given to children over 12 in anaphylaxis?
500 micrograms IM
0.5 mL
What dose (and volume) of adrenaline is given to children 6-12 yrs in anaphylaxis?
300 micrograms IM
0.3 mL
What dose (and volume) of adrenaline is given to children under 6 in anaphylaxis?
150 micrograms IM (0.15 mL)
What volume of CRYSTALLOID fluid is given to a) adults and b) children?
a) 500mL-1000mL
b) 20 mL/Kg
What dose of hydrocortisone is given to pts (IM or slow IV) in anaphylaxis?
a) adult or child >12 yrs
b) child 6-12 yrs
c) child 6 mths - 6 yrs
d) child < 6 mths
a) 200mg
b) 100 mg
c) 50 mg
d) 25 mg
What dose of chloramphenamine is given to pts (IM or slow IV) in anaphylaxis?
a) adult or child >12 yrs
b) child 6-12 yrs
c) child 6 mths - 6 yrs
d) child < 6 mths
a) 10mg
b) 5 mg
c) 2.5 mg
d) 250 micrograms/Kg
What is BUFALO and what does it stand for? What timeframe should it be completed in?
Septic pt. management: Blood cultures and septic screen Urine output (monitor hourly) Fluid resuscitation Antibiotics IV Lactate measurement (ABG) Oxygen - to correct hypoxia
Try to complete within one hour (ASAP)
What are the problems with ABGs? (which might make you consider getting a VBG)
painful increased risk of bleeding and haematoma (compared to VBG) risk of pseudo aneurysm and AV fistula Increased risk of infection Nerve injury Digital ischaemia Can cause delays in care Serial exams may be needed
(some of these problems are still the case in VBGs)
Which elements of a VBG are usually adequate to aid decision making and have good correlation with ABG findings?
pH
PCO2 (if normocapnic - if PvCO2 normal in VBG, then PaCO2 is definitely normal)
HCO3
BXS
Other than hypercapnia, when might PCO2 from VBG not be as reliable as an ABG?
severe shock
What results on an ABG might indicate metabolic acidosis? What on the ABG might indicate respiratory compensation?
Metabolic acidosis: pH low, HCO3 low, Base excess high
Resp. compensation: CO2 low - pt. is blowing CO2 to try and reduce acidity of blood
What results on an ABG might indicate respiratory acidosis? What on the ABG might indicate metabolic compensation?
Resp acidosis: pH low, PaCO2 high
Metabolic compensation: HCO3 high - kidneys retain more bicarb in order to reduce acidity of blood
What results on an ABG might indicate respiratory alkalosis? What on the ABG might indicate metabolic compensation?
Resp alkalosis: pH high, PaCO2 low
Metabolic compensation: HCO3 is low - protein buffering in cells (acute) or kidneys excrete more bicarb to increase acidity of blood (chronic)
What results on an ABG might indicate metabolic alkalosis? What on the ABG might indicate metabolic compensation?
Metabolic alkalosis: pH high, HCO3 high, BXS low
Respiratory compensation: high CO2 - hypoventilation to increase acid in blood
What is included on an ABG?
pH paO2 paCO2 HCO3 BXC
Lactate Sodium Potassium Hb glucose CO Methaemoglobin
Flow rate of Oxygen that can be given with venturi mask? What conc. of oxygen is delivered? What is a benefit of the venturi?
Flow rate depends on what type (based on colour)
24-60%
More specific percentage of oxygen can be delivered to pt. (you can be more certain that pt. is getting prescribed %)
What are the different flow rates (and %O2 delivered) of the different types of venturi?
Blue: 2-4L/min = 24% White: 4-6L/min = 28% Yellow: 8-10L/min = 35% Red: 10-12L/min = 40% Green: 12-15L/min = 60%
When might you use a nasal cannula?
non-acute ward or if pt. mildly hypoxic
When might you use a Hudson mask?
Step up from nasal cannula
Doesn’t deliver specific % of oxygen like venturi
When might you use a venturi?
COPD
When you want to deliver a more specific amount of O2 to a pt.
When would you use a non-rebreathe mask?
acutely unwell pts.
When might you use CPAP?
sleep apnoea
heart failure
When might you use BiPAP?
COPD and atelectasis
What percentage oxygen is given in invasive ventilation? when might this be used?
100%
Used in theatre and in intensive care (when pt. in resp. arrest)
What should you do if O2 therapy is being use maximally and O2 levels continue to drop?
Involve ICU: view to use non-invasive ventilation, intubation and ventilation
Below what level O2 sats should you do an ABG?
92%
Why is an Oxygen saturation of below 90% such a big problem?
below sats less than 90%, the oxygen-Hb saturation curve drops significantly - therefore haemoglobin will rapidly become significantly less saturated with small changes in oxygen partial pressure
Which patients could be considered ‘CO2 retainers’? What happens to these pts?
severe obstructive lung disease (COPD, bronchiectasis and CF)
severe restrictive lung diseases (neuromuscular, severe kyphoscolliosis, severe obesity)
Respiratory drive is normally driven by CO2 levels, but CO2 retainers are desensitised to hypercapnia - rely on hypoxia to stimulate respiratory drive
What is the aim of oxygen therapy in CO2-retaining patients?
Increase oxygen level
WITHOUT
causing respiratory drive to decrease
(which will increase CO2, worsening resp. acidosis)
What is ACS (acute coronary syndrome)? What are the main classifications within ACS?
Range of heart conditions caused by lack of blood flow to myocardium
2 main divisions:
ST elevation ACS (STE-ACS)
Non-ST elevation ACS (NSTE-ACS) (which can be further divided in to unstable angina and NSTEMI)
What is the difference between unstable angina and an MI?
Unstable angina: blood clot or artery narrowing limits blood flow, but does not block it completely - therefore there is NO INFARCT in unstable angina
What is the difference between STE-ACS and NSTE-ACS?
STE-ACS: chest pain + ST elevation for >20mins. Most go on to develop STEMI
NSTE-ACS: chest pain WITHOUT persistent ST elevation
Other changes may be present on ECG
What features may be present on an ECG in NSTE-ACS?
persistent or transient ST-segment depression T-wave inversion Flat T waves Pseudo-normalisation of T waves no ECG changes at presentation
What are risk factors for ACS?
Non-modifiable RF for atherosclerosis: age, male, family Hx of premature coronary heart disease, premature menopause.
Modifiable RF for atherosclerosis: smoking, diabetes mellitus (and impaired glucose tolerance), hypertension, dyslipidaemia (raised low-density lipoprotein (LDL) cholesterol, reduced high-density lipoprotein (HDL) cholesterol); obesity, physical inactivity.
Consider non-atherosclerotic causes in younger patients or if there is no evidence of atherosclerosis: coronary emboli from sources such as an infected cardiac valve, coronary occlusion (secondary to vasculitis), coronary artery spasm, cocaine use, congenital coronary anomalies, coronary trauma, increased oxygen requirement (eg, hyperthyroidism) or decreased oxygen delivery (eg, severe anaemia).
How might ACS present/what might be important to ask about in the Hx?
Chest pain (>15 mins) at rest Pain in arms, back jaw sweating nausea vomiting fatigue SOB palpitations syncope tachycardia OR bradycardia extra heart sounds murmur hypotension pulmonary oedema narrowed pulse pressure raised JVP
Limitation of daily activities due to angina (pain on less exertion than previous, pain lasting longer etc.)
Hx of angina
Hx of MI
Cardiovascular RF: smoking, BP, FHx, exercise, diet/weight, kidney problems, Previous cardiac problems/investigations, diabetes
Which patients may be less likely to have pain or chest tightness during a STEMI or an NSTEMI? How might this present instead?
Elderly
Diabetic
Syncope Pulmonary oedema Epigastric pain Vomiting Acute confusional state Stroke Diabetic hyperglycaemia
What investigations do you need to do in ACS?
ECG
Echocardiography
CXR (cardiomegaly, pulmonary oedema, widened mediastinum)
Coronary angiography
Bloods: Troponin I&T (raised (2X) 3-6 hours post-infraction, remain raised for 14 days). Test at 6 and 12 hours after onset of pain. Levels usually raised for about a week. FBC Blood glucose Renal function Electrolytes TFTs CRP CK (raised in muscle trauma) Lipids
Diagnosis: 2/3 - Hx, ECG changes and raised troponin
How would you initially manage a patient presenting with symptoms of ACS?
ABCDE assessment (incl. BP, RR, HR etc.)
A: secure airway if necessary
B: Oxygen (if necessary, 15L non-rebreathe). Get ABG. GTN sublingual (unless BP<90 or HR<50)
C: Get IV access. Get ECG if not done already. Take bloods. Cardiac exam.
Anti-platelet/anti-coagulant - 300 mg aspirin + Ticagralor 180mg loading dose
Fondaparinux (unless angiography due within 24 hours, then give unfractionated heparin)
D: Pain relief - GTN spray (unless R ventricular infarct)
If that doesn’t work, IV opioid (+ anti-emetic)
5-10mg morphine + metoclopramide 10mg IV
STEMI: thrombolysis (best within 12 hours) - streptokinase
Beta-blocker - atenolol 5mg IV
ACEi (in STEMI)
Statin
What is a normal RR in an adult?
12-20 breaths/min
What might you see on an ECG during an episode of unstable angina?
T wave inversion
ST depression
Normal
What risk-scoring system is used to predict risk of pt. having future cardiovascular event and six-month mortality?
GRACE score
Global Registry of Acute Cardiac Events
What is an important factor to bear in mind at each stage of ACS management (particularly in terms of prescribing drugs)?
Bleeding risk
ask re medications eg. warfarin, NOACs etc.
When might you consider use of PCI OR CABG in a patient with unstable angina/risk of MI? What are the risks associated with this?
If pt. has a high risk of recurrence
Risk of procedure-related MI or bleeding
After stabilising the pt., what would your more definitive treatment be of a patient who had a medium risk GRACE score? When else might this intervention be offered?
early in-hospital coronary angiography
angiography may also be offered in pts. whose risk is low, but are having recurrent episodes
What other differentials might you consider for a pt with ACS-like symptoms?
Cardiovascular: acute pericarditis, myocarditis, aortic stenosis, aortic dissection, pulmonary embolism.
Respiratory: pneumonia, pneumothorax.
Gastrointestinal: oesophageal spasm, gastro-oesophageal reflux disease, acute gastritis, cholecystitis, acute pancreatitis.
Musculoskeletal chest pain.
What are features of acute severe asthma?
any one of: RR >=25/min HR >=110/min Inability to complete sentences in one breath PEF 33-50% best or predicted
What are features of life-threatening asthma? (symptoms and signs)
Any one of:
Resp distress/poor resp effort
Silent chest
Cyanosis
Collapse
tachycardia, Arrhythmia, bradycardia, hypotension
Exhaustion, altered conscious level, coma
What investigations would you want to do in pt. presenting with features of acute asthma attack?
Pulse oximetry
ABG (if pt has ANY life-threatening features or SpO2<92%)
PEF (not always necessary)
(ECG and CXR in very specific circumstances)
What results would you find from investigations in life-threatening/near-fatal asthma?
Pulse oximetry: Sp O2<92%
PEF <33% previous best or predicted
(severe: 33-50%, moderate: 50-75%)
ABG: PaO2<8kPa
PaCO2 > 6.0 (near-fatal)
Low pH
What is the immediate management for acute severe asthma in adults?
A: check airway patent
B: O2 sats, RR, listen to apices and bases, look for cyanosis, ABG, (if well enough: PEF)
Prescribe: Oxygen (15L non-rebreathe): SpO2<94%
Salbutamol (5mg) or terbutaline (10mg) nebuliser (oxygen-driven). Repeat at 15-20 minute intervals
Ipratropium bromide (0.5mg) nebuliser (4-6 hourly)
Write up:
Prednisolone tabs (40-50mg) OR IV hydrocortisone (100mg)
(depends on how ill pt. is)
C: check HR, BP, cap refill
Cannulate
Bloods: FBC, U&Es, glucose
?ECG
D: fingers, toes, eyes, GCS
E: CALVES, rashes, temp.
CXR (once stable)
If life-threatening: discuss with senior clinician/ICU (consider aminophylline infusion)
Consider IV magnesium sulphate (1.2-2g) infusion over 20 mins
salbutamol 10mg continuously hourly
REASSESS
What single investigation do you need in pts with life-threatening asthma?
ABG
No other investigations are necessary for immediate management
What are the key features of asthma?
SOB Cough (worse at night) Chest tightness WHEEZE (usually expiratory, but can also be inspiratory in severe asthma) Poor Hx of control/recent increase of inhaler use Possible resp. tract infection Respiratory distress: Cyanosis increased RR Accessory muscle use
tachycardia (increased salbutamol use)
prolonged expiratory phase
After initial management of severe acute asthma, what should you do?
REASSESS
Pt improving:
Oxygen to maintain SpO2
Prednisolone 40-50mg daily OR IV hydrocortisone 100mg 6 hourly
Nebuliser beta-agonist and ipratropium 4-6 hourly
Pt not improving after 15-30 mins:
Continue oxygen and steroids
Continuous nebulisation of salbutamol (5-10mg/hour)
Continue ipatropium 0.5 mg 4-6 hourly until pt. is improving
Pt still not improving: Discuss with senior and ICU, the use of: IV Magnesium sulphate 1.2-2g over 20 minutes IV beta agonist or IV aminophylline Non-invasive and mechanical ventilation
What monitoring should be done in pt. with acute severe asthma?
PEF 15-30 mins after starting treatment. Do one before and after B2 agonist treatment and QDS during hospital stay
Oximetry
ABG within 1 hour of starting treatment if:
PaO2 <8 (unless subsequent SO2>92%)
PaCO2 normal/raised
Pt deteriorates
When should you transfer a pt. with severe acute asthma to ICU?
Deteriorating PEF Worsening or persisting hypoxia or hypercapnoea Exhaustion Altered consciousness Poor resp. effort or resp. arrest
What should patients with acute severe asthma have in order to ensure they can be discharged from hospital safely?
Pt. should have been on discharge medication for at least 24 hours
Check inhaler technique
PEF > 75% of best or predicted AND PEF diurnal variability <25%
Oral and inhaled steroids (in addition to bronchodilators)
own PEF meter and written asthma plan
GP follow up arranged for within 2 working days
Follow up with respiratory clinic within 4 weeks
What (in basic terms) is the treatment for an acute asthma attack?
OSHITME
All together: Oxygen Salbutamol 2.5-5mg NEB Hydrocortisone 100mg IV (or prednisolone 40 mg PO) Ipratropium 500mcg NEB
With senior input:
Theophylline: aminophylline infusion 1g in 1L saline (0.5ml/Kg/h)
Magnesium sulphate 2g IV over 20 mins
Escalate care (intubation and ventilation)
What are the key features of life-threatening asthma?
33, 92, chest
33: PEF <33% best/predicted SpO2 < 92% Cyanosis Hypotension Exhaustion Silent chest tachycardia
What PEFR would indicate mild asthma?
> 75%
What PEFR would indicate moderate asthma?
< 75%
How would you treat an acute COPD exacerbation?
OSHIT
BUT
Give controlled oxygen: 24-28% venturi mask
Consider BiPAP if sats don’t improve (and in type 2 resp failure)
ABG after 15 mins
Regular ABGs
ABX: Doxycycline 100mg OD (200mg loading dose)
Chest physio
What investigations would you do in someone with exacerbation of COPD?
CXR
ABG
ECG
Bloods: FBC, U&Es, blood cultures
Sputum microscopy and culture
What symptoms might you expect from someone with exacerbation of COPD?
Increased cough/sputum production/SOB
Reduced exercise tolerance
Resp distress: accessory muscle use, tachypnoea, cyanosis, wheeze
Confusion
Upper airway symptoms: colds, coughs etc.
Fluid retention
Increased fatigue/malaise
Resp failure
How would you manage COPD?
A: check airway patent
B: sats, RR, ABG, auscultate (apices and bases)
Oxygen (venturi 24-28%)
Salbutamol (5mg) NEB 15-20 mins. Air driven.
Ipratropium bromide (500 mpg) NEB. Air-driven.
Hydrocortisone (100mg) IV and Prednisilone (30mg) PO
Theophylline: aminophylline
CXR
C: HR, Cap refill, BP, Cannula, Bloods (incl. blood culture) - FBC, U&Es and glucose.
ECG
D: fingers, toes, pupils, GCS
E: temp, CALVES, Sacrum
What should you ask a pt. with COPD in A&E?
Assess COPD severity: Oxygen/nebulisers at home No. of exacerbations a year/in winter Do you have a rescue pack Ever been in to hospital with exacerbation before Ever been admitted to ICU
When should you use the PERC (Pulmonary embolism rule-out criteria) score for PE? What is the aim of the PERC score?
Low-risk/pt. unlikely to have PE
Aim of score is to rule out PE.
Pt with score of 0 = rule out PE (<2% chance of PE). Its do not need a D-dimer.
CANNOT rule PE out safely if ANY of criteria are positive
What criteria are included in the PERC scale?
Age >= 50 yrs HR >= 100 SpO2 on rom air < 95% Prior Hx of DVT/PE Recent trauma or surgery Haemoptysis Exogenous oestrogen (OCP, HRT) Unilateral leg swelling
What are the symptoms of PE?
sudden onset SOB Shortness of breath Haemoptysis Syncope Cardiovascular collapse (tachycardia, hypotension) Raised JVP Hypoxia (CXR often normal)
What scoring systems can you use to help you decide on investigations and management in PE?
Don’t think pt. has PE: PERC
Think pt. might have PE: Wells score
What is included in the PE Wells score? (how many points are given)
DVT Sx (3)
PE primary diagnosis (no alternative diagnosis more likely) (3)
HR >100 (1.5)
Immobile > 3 days or surgery < 4 weeks (1.5)
Previous PE or DVT (1.5)
Haemoptysis (1)
Malignancy (1)
<2 = low probability 2-6 = moderate probability >6 = high probability
For what PE wells score range would you do D-dimer? What would you do after this?
4=> (PE unlikely)
D-dimer -ve: reassure
D-dimer +ve: LMWH (1.5mg/Kg)
CTPA when possible
CTPA -ve: stop LMWH
CTPA +ve: continue LMWH and start warfarin for 6 months
(Stop LMWH 5-7 days of dual therapy and when INR 2-3)
For what PE wells score would you NOT d-dimer?
5=< (PE likely)
Wouldn’t bother with D-dimer, JUST TREAT
LMWH (1.5 mg/Kg)
CTPA when possible
CTPA -ve: stop LMWH
CTPA +ve: continue LMWH and start warfarin for 6 months
(Stop LMWH 5-7 days of dual therapy and when INR 2-3)
If you can’t do a CTPA on a patient, what other scan could you do to confirm/exclude PE?
V/Q scan
What investigations can you do to check for severity of PE?
ECG (tachycardia, RV strain: T-wave inversion in R and inferior leads, RBBB, R axis deviation, S1Q3T3, RA enlargement: P pulmonale, RV dilation: dominant R in V1)
CXR (wedge infarcts, regional oligaemia, enlarged pulmonary artery, effusion)
echocardiogram (R heart strain/overload)
bilateral leg doppler (look for DVTs)
How would you manage a PE acutely?
A: check airway patent. Sit patient up.
B: RR, sats, ABG, auscultate
Oxygen 15L non-rebreathe
C: HR, BP, cap refill, cardiac monitor
Cannula
Fluid bolus
?inotropic support
D: fingers, toes, eyes
E: temp, CALVES
LMWH
Send for CTPA once stable
Call senior
Consider thrombolysis in:
Massive PE (SBP<90, puleslessness or persistent bradycardia) = STRAIGHT to thrombolysis
Submassive PE (RV dysfunction ot myocardial necrosis) = give LMWH and consider thrombolysis
What are some causes of pulmonary oedema?
Ischaemic heart disease: MI/ACS, LV failure
Murmurs: aortic regurg, mitral regurg, SEVERE aortic stenosis
PE
Arrhythmia
Cardiac tamponade
Cardiomyopathy
AKI or CKD
Iatrogenic fluid overload
High-output heart failure eg. sepsis, anaemia etc.
Liver failure, fat embolism, ARDS
neurogenic (after neurological insult e.g. status epileptics, head injury, stroke)
What are features of anaphylactic shock?
A: laryngeal/pharyngeal oedema, bronchospasm (stridor), hoarse voice
B: SOB, increased RR, wheeze
C: shock (pale, clammy), hypotension (dizziness, collapse), tachycardia
D: confusion, tiredness, agitation, LOC
E: rash/flushing urticaria angio-oedema hypotension and shock nausea, vomiting or diarrhoea
Three key criteria make anaphylaxis v. likely:
- Rapid onset and progression of symptoms
- life-threatening Airway, breathing or circulation problems
- Skin and/or mucosal changes
How would you manage anaphylaxis?
Call for help 2222 (at very least anaesthetist)
Lie pt. flat
Raise pt.’s leg (try to raise BP)
Adrenaline 0.5mg IM (0.5mLs of 1:1000). Repeat every 5 minutes.
A: establish airway (nasopharyngeal/LMA/intubation)
B: RR, Sats, auscultation, air entry
15L non-rebreathe (may need intubation)
Wheeze: salbutamol (as in asthma)
C: HR, BP, cap refill
Cannula
Attach cardiac monitor
1) Adrenaline (IM) 1:1000 - 500 micrograms (0.5mL)
2) IV fluid challenge: 500-1000mL (Hartmann’s or NaCl)
3) Cloramphenamine 10mg IM (or slow IV)
4) Hydrocortisone 200 mg IM (or slow IV)
Bloods: FBC, U&Es, LFTs, calcium and glucose)
May need inotropes/vasosupressors
D: GCS, pupils, fingers, toes, glucose level
E: Feel abdo
Calves
Temp
What would you do for a patient with anaphylactic shock, once they’re stable?
Mast cell tryptase (venom-related, drug-related, idiopathic): ASAP after emergency, 1-2 hours after onset, 24 hours after or in f/u.
Observe pt. for 6 hours (risk of another reaction)
WARN PATIENT
Some may need 24 hrs observation
Adrenaline injector as interim measure (before specialist appointment)
Anti-histamine and steroid therapy for up to 3 days
Reassure pt.
Info about how to manage anaphylaxis (incl. how to use adrenaline injector)
Info about biphasic reaction
What things would you need to write in the notes re. anaphylactic shock and its management?
Clinical features Time of onset Circumstances immediately before onset of symptoms Treatments administered Results of any tests Obs
What differentials might you think about in someone with anaphylaxis-like symptoms?
asthma (esp. in children)
septic shock
vasovagal episode
panic attack
breath-holding episode
non-allergic urticaria or angioedma
Which pts. may need observing for 24 hours
Severe reactions with slow onset severe asthma Hx of biphasic reactions Pts presenting at evening or night Pts where access to emergency care is limited
What are common features of pulmonary oedema?
Dyspnoea Orthopnoea Pink frothy sputum Pale, sweaty, distressed pt. Increased jugular venous pressure Inspiratory crackles Wheeze (cardiac asthma) Triple/gallop rhythm (S3 sounds - fluid overload)
What findings might you see on an X-ray?
Cardiomegaly
Fluffy bilateral shadowing with peripheral sparing (bats wings)
Kerley B lines
Pleural effusions
What is the CURB-65 score used for? What are its components?
estimates mortality for CAP
Confusion (1) Urea >7 (1) RR >30 (1) SBP >90 or DBP<60 Age 65 =
What are the differentials you might consider for someone with shortness of breath (in ED)?
Exacerbation of COPD Asthma PE Pneumothorax Pneumonia Pulmonary oedema
How would you manage a patient with pulmonary oedema?
A: sit pt. upright, check airway is patent
B: RR, sats, ABG (if in resp. distress), auscultate, tracheal deviation
O2 (15L NRB)
Salbutamol NEB if wheeze present
C: HR, BP, cap refill, cardiac monitor, CXR
Venous access, bloods - ?culture, FBC, LFTs, U&E, glucose
Treat any arrhythmias
2 sprays GTN or buccal suscard 2-5mg (if SBP>90)
Diamorphine 2.5mg IV (slowly)
Furosemide 40-80mg IV (slowly)
GTN IV 50mg in 50mls 0.9% NaCl 2ml/hr, titrate up to 20ml/hour. Maintain BP at 90
D: GCS, pupils, drug chart and notes
E: calves, abdo, temp
Reassess: no B improvement - CPAP
Senior/critical care outreach/anaesthetists/ICU
What are then different types of pneumothorax?
Spontaneous: primary and secondary
Traumatic: following penetrative chest trauma
Iatrogenic: following procedures eg. invasive ventilation, central line placement, biopsy etc.
Catamenial: pneumothorax around time of menstruation due to endometriosis
TENSION PNEUMOTHORAX
What are the different types of spontaneous pneumothorax?
Primary: no apparent underlying cause. Occur in young fit people.
Secondary: Associated with underlying lung disease - eg, COPD, TB, sarcoidosis, CF, malignancy, and idiopathic pulmonary fibrosis
Why is it important to establish whether a spontaneous pneumothorax is primary or secondary?
The consequences of a pneumothorax in patients with pre-existing lung disease are significantly greater and the management is potentially more difficult.
What are the BTS guidelines of working out whether pneumothorax is primary or secondary?
Age > 50 and significant smoking history
Evidence of underlying lung disease on exam or CXR?
What are symptoms of pneumothorax?
Primary spontaneous pneumothorax: Sx minimal or absent
Secondary spontaneous pneumothorax: greater than primary
Sudden onset pain
May be SOB
Can be Sx-less
Distressed and sweating
What might you find on examination of a pt. with pneumothorax?
A: airway may be patent
B: Resp distress
Reduced chest expansion on one side
tracheal deviation (towards side of pneumothorax)
Hyper-resonance on percussion over areas of collapse
breath sounds reduced/absent
C: Cyanosis
Tachycardia (>135 = tension)
pluses paradoxical (slows on inspiration)
HypoTN
How would you investigate a NON-tension pneumothorax?
CXR
CT in uncertain cases
ABG (if sats <92%)
What differentials might you consider in someone with pneumothorax-like symptoms?
Pleural effusion (slower onset and dullness to percussion)
PE (haemoptysis, more common in lower lobes)
Pleuritis
How would you measure the size of a pneumothorax on a CXR?
Measure the distance between pleural surface and lung edge (at level of hilum)
2cm or more = pneumothorax of at least 50% of hemithorax. This indicates need for drainage
What should you do in the following scenario?
Primary pneumothorax
Size >2cm and/or SOB
If this improves the situation (<2cm and breathing improves), what should you do?
If this does not improve the situation, what should you do?
Aspirate using 16-18g. cannula
Aspirate <2.5L
Consider discharge
R/v in OPD in 2-4 weeks
Chest drain
Admit pt.
What should you do in the following scenario?
Primary pneumothorax
Size <2cm and/or not SOB
Consider discharge
R/v in OPD in 2-4 weeks
What should you do in the following scenario?
Secondary pneumothorax
Size >2cm and/or SOB
Chest drain
Admit pt.
What should you do in the following scenario?
Secondary pneumothorax
Size <2cm (1-2cm) or not SOB
If this improves the situation (<1cm and breathing improves), what should you do?
If this does not improve the situation, what should you do?
Aspirate using 16-18g. cannula
Aspirate <2.5L
Admit
High flow oxygen
Observe for 24 hours
Chest drain
Admit pt.
What should you do in the following scenario?
Secondary pneumothorax
Size <1cm or not SOB
Admit
High flow oxygen
Observe for 24 hours
What are KEY features of TENSION pneumothorax?
Same Sx as above (reduced unilateral expansion etc.)
Hypotension
Trachea deviated AWAY from side of collapse
Distended neck veins
How would you manage someone with tension pneumothorax?
A: airway patent B: RR, sats, AUSCULTATION, CHEST EXPANSION, PRECUSSION, TRACHEAL DEVIATION 15L Oxygen NRB ?ABG C: HR, BP, cap refill Confirmed diagnosis: Needle decompression 14-16g cannula, 2nd intercostal space, mid-clavicular line, leave in place D: GCS, eyes, fingers etc. E: calves, abdo etc.
What is the definition of HAP?
Pneumonia developed 48 hours after hospital admission
Which type of pneumonia has worse prognosis? why?
HAP - generally more comorbidities
Bugs more resistant
What are the common organisms for CAP?
Streptococcus pneumoniae, haemophilus influenzae
Anaerobes are rare
What are the common organisms for HAP?
Gram negative bacilli, staphylococcus aureus
Drug resistant organisms are more common, and more dangerous
What are the rarer causes of CAP?
Chlamydia pneumoniae (common in institutions – e.g. collegues, military camps – mild)
mycoplasma pneumonia
legionella
What are common precipitating factors for pneumonia?
Strep pneumoniae infection often follows viral infection with influenza or parainfluenza. Hospitalisation Cigarette smoking Alcohol excess Bronchiectesis (e.g. in CF) Bronchial obstruction (e.g. carcinoma) Immunosupression IV drug use Dysphagia (both oesophageal and co-ordination disorders – leading to aspiration)
What are symptoms of a pneumonia?
Similar for HAP and CAP cases SOB Tachypnoea Reduced oxygen sats Tachycardia Cough (purulent sputum, can be dry in infants and elderly) Fever Riggers Vomiting Headache Loss of appetite Pleuritic chest pain, may radiate to shoulder (if diaphragm is involved) Upper abdo pain Increased secretions
What investigations might you do for someone you suspect has pneumonia? What might you see?
BTS guidelines: Pulse oximetry (may need ABG)
CXR: consolidation (may not be present for first 48 hours, but can be present for up to 6-weeks).
Repeat weekly as inpt, then 6 weeks after as f/u (community and hospital)
(may not need initial CXR if in community, if sure of diagnosis and no risk of underlying lung pathology)
ALL suspected CAP in hospital, should be investigated with CXR
Bloods: FBC WCC (raised) ESR and CRP (raised) LFTs Anaemia
Microbiological: Blood cultures (moderate to high severity - start empirical ABX) Sputum culture (in pts. who do not respond to empirical ABX)
Urine antigen investigations (if pneumococcal and legionella suspected)
Pleural fluid aspiration (if they have an effusion))
What scoring system would you use to assess the severity of pneumonia?
CURB 65
List some complications of pneumonia?
Sepsis: resp failure, hypotension pleural effusion empyema Lung absences Lobar collapse/pneumothorax
what should you do for a pt. with CURB-65 score of 0-1?
0-1: low severity
Other reason to admit = hospital
No reason to admit = home treatment
Amoxicillin 500mg TDS PO
(or doxycycline 200mg loading dose, 100mg PO)
Can have same dose IV if unable to do PO.
what should you do for a pt. with CURB-65 score of 2?
2: moderate severity
Hospital admission (short stay)
Supportive care: Oxygen, fluids, neb saline, chest physio, VTE prophylaxis, analgesia (NSAIDS or paracetamol)
ABX: amoxicillin 500mg-1g TDS PO + clarithromycin 500mg BD PO
Unable to use PO: amoxicillin 500mg TDS IV PLUS clarithromycin 500mg BD IV
(or doxycycline 200mg loading dose, 100mg PO)
what should you do for a pt. with CURB-65 score of 3-5?
3-5: high severity
Urgent hospital admission (and senior review)
Supportive care: Oxygen, fluids, neb saline, chest physio, VTE prophylaxis, analgesia (NSAIDS or paracetamol)
ABX: Antibiotics given as soon as possible
Co-amoxiclav 1.2 g tds IV plus clarithromycin 500 mg bd IV
(If legionella strongly suspected, consider adding levofloxacin)
Consider referral to critical care (if score 4/5)
What monitoring and follow up would you want to do in a patient with pneumonia?
Inpatient -
Repeat: bloods, X-rays etc after 3 days
24 hours after discharge, obs
6 WEEK FOLLOW-UP INCL. RPT.CXR.
What are the different types of aortic dissection?
Stanford classification: Type A (involving the ascending aorta, can extend ad infinitum) Type B (not involving the ascending aorta - aorta beyond subclavian artery only)
(less used) DeBakey Classification:
Type I: aorta, aortic arch, and descending aorta.
Type II: ascending aorta only.
Type III: descending aorta distal to left subclavian.
What are some risk factors for aortic dissection?
HTN smoking raised cholesterol pre-existing aortic diseases aortic valve disease FHx or aortic diseases Hx of cardiac surgery blunt chest trauma use of IV drugs
Marfan’s
Ehlers-Danlos syndrome
What is an aortic dissection?
Tear in inside of aorta
Blood flow between layers of wall of aorta, forcing layers apart
How might aortic dissection present?
Chest pain/back pain (ripping/sharp)... also groin. SUDDEN ONSET MAXIMAL AT ONSET MIGRATES (as dissection progresses) Proximal dissections: retrosternal pain Distal dissections: between scapulae aortic regurg
angina/MI: involvement of coronary arteries
CCF
Pleural effusions
Syncope
Neurological symptoms (acute paraplegia, U/L limb ischaemic neuropathy): involvement of spinal arteries or carotid or distal aortic involvement
AKI
Often presents in two phases:
1st event: severe pain, pulse loss
2nd event: rupture = cardiac tamponde, pleural space or mediastinum
What might be a typical presentation of someone with chest pain?
man in 60s HTN SUDDEN onset chest pain (also groin or back) retrosternal or between scapulae 'ripping' or 'sharp' Maximum pain at the beginning
What differentials might you think about in a patient with ?aortic dissection?
ACS (can occur with dissection) aortic regurg aortic aneurysms MSK pericarditis mediastinal tumours pleuritis PE cholecystitis
What investigations would you do on someone with ?aortic dissection?
ECG - MI, normal or non-specific ST-T segment changes
CXR (will not exclude, but may see widened mediastinum)
US echocardiography in unstable pt. (site and extent)
CT angiography is investigation of choice.
How is aortic dissection treated?
A and B as necessary
C: control BP and HR (prevent disease extension)
aim: SBP<120 and HR 60
Cannulate
Labetalol IV
analgesia eg. morphine
type a: surgery (stent or graft)
type b: not generally for surgery (managed just by BP) except:
Persistent pain, branch occlusion, leak, continues extension
*risk of paraplegia with surgery
What is type A more likely to end up malperfusing?
brain coronary artery spinal cord liver bowel kidneys legs
What is type B aortic dissection more likely to end up malperfusing?
JUST spinal cord liver bowel kidneys legs
What are risk factors for aneurysms?
Hypertension Smoking Age Diabetes Obesity High LDL levels Sedentary lifestyle Genetic factors Co-arctation of the aorta Marfan’s syndrome, and other connective tissue disorders Previous aortic surgery Pregnancy (particularly 3rd trimester) Trauma Male
How might AAA present?
Unruptured: no Sx Pain in back, abdo, loin, groin (*severe lumbar pain, recent onset = think ?impending rupture) pulsatile abdo swelling limb ischaemia ureterohydronephrosis
Collapse, syncope or shock (hypotension) epigastric pain: radiating to back (may also get pain in groin, iliac fosse and testicles) Constant or intermittent
rupture into peritoneal space: dramatic, death on arrival
rupture into retroperitoneal space: contained (temporary seal formed)
What clinical signs might you find on examination of someone with ?AAA?
Bimanual palpation of abdo: pulsatile
Abdo bruit
retroperitoneal haemorrhage: Grey Turner’s sign
What investigations might you do for someone ?AAA (non-urgent)?
Bloods: FBC Clotting screen renal function liver function cross-match (if surgery planned) ESR/CRP
ECG, CXR
US
CT
MRI angiography
What investigations might you do for someone ?AAA (urgent)?
Bloods:
FBC
Group and save/cross-match
U&Es
Plain abdo x-ray
US (may not need if emergency, may go straight to theatre)
CT angiography
How would you manage someone with ruptured AAA?
large bore IV access
group and cross-match
*SURGICAL REFERRAL IMMEDIATELY - emergency endovascular aneurysm repair
How would you manage a patient with uncomplicated AAA?
<5.5cm: monitor (US)
>5.5cm:surgery
manage risk factors: statins, anti-platelets (if not at risk of bleed)
Other indications for surgery: onset of sinister symptoms (back or abode pain), rapid expansion and RUPTURE
How might alcohol withdrawal present?
Hx of alcohol abuse
Collapse
Within a few hours: Tremor Nausea Sweating Agitation Tachycardia Palpitations Hypertension
after 24-48 hours: Delusions Confusion Diarrhoea convulsions auditory hallucinatinos
After 48 hours:
delirium tremens
How might delirium tremens present?
Someone (generally) with a v. long drinking history - can also occur after a few months of drinking
3-4 days after withdrawal
Sx: Restlessness Fear Paranoia Confusion/reduced consciousness Terror-stricken face Sweaty/tachycardia/pyrexia/flushing/pallor Visual hallucinations (lilliputian), formication Auditory hallucinations
How do you treat delirium tremens?
MEDICAL EMERGENCY: DEATH IN 10-15% (35% if untreated)
Benzo: sedation and anti-convulsant. Give up to 10 days, at night - avoid nightmares
B vitamins (pabrinex): reduce risk of encephalopathy
Fluid replacement
Dextrose (avoid hypoglycaemia)
Be aware of infection and head injury
On recovery: check for signs of alcohol brain damage, assess motivation for permanent change
what causes death in delirium tremens?
Epileptic seizure
self-injury
infection
How long does delirium tremens usually go on for?
3-4 days
Anxiety can go on for months
Why does delirium tremens occur?
Long term changes occur in the brain with long-term/excessive alcohol use: decrease in GABA receptors (as tolerance develops)
When alcohol is withdrawn, patient is left with a v. low number of inhibitory receptors and nothing acting on them
This is why there is over-activity of the CNS
What is Wernicke’s encephalopathy? what are the symptoms?
Acute syndrome (neurological symptoms) caused by thiamine deficiency
Ocular palsies (esp. abducens nerve)
Ataxic gait
Nausea
Memory problems
(can be caused by all types of thiamine deficiency, not just alcohol)
If someone presents with Wernicke’s, and it continues chronically, it becomes Korsakov’s syndrome. Can also present at same time as Korsakov’s = wernicke-korsakov syndrome
What is Wernicke’s triad?
eye signs: nystagmus and ophthalmoplegia
Ataxic gait
Confusion
What is korsakov’s syndrome and how does it present?
Chronic condition caused by thiamine deficiency (also called korsakov’s psychosis) - impaired memory function following signs of Wernicke’s encephalopathy.
Anterograde memory disorder (can’t consolidate new memories). Able to recall facts immediately, within a few minutes. No ability to get this info in to long-term memory.
Little/distorted sense of time
Make up events (confabulation)
Anser questions in a very laid-back manner
Memory recall for events before the syndrome are usually fine
No clouding of consciousness
Peripheral neuropathy
What are the differentials for alcohol/alcohol-withdrawal problems?
Withdrawal (no dangerous features)
Delirium tremens (more common than Wernicke’s - no neurological symptoms)
Wernicke’s encephalopathy
Korsakov’s syndrome
Acute brain syndromes of miscellaneous cause
Chronic brain syndromes (different pattern of memory loss - incl. long-term memory)
Chronic alcohol intake can lead to chronic brain syndrome due to atrophy of the cerebrum
How would you treat Wernicke’s encephalopathy?
Thiamine and other B vitamins (IM or IV) - PABRINEX
Sedation (benzodiazepines) - chlordiazepoxide
Fluids/electrolytes
How would you treat Korsakov’s?
Life-long chronic illness
No real treatment
Thiamine supplements don’t really help after acute phase
Eventually, patients will require care
What’s the prognosis of wernicke’s and other alcohol related brain syndromes?
Palsies: usually clear with appropriate treatment
Ataxia: usually resolve on its own over several months
Neuropathy: resolve slowly
Amnesia: 1/2 all patients recover from this
What are features of opiate withdrawal?
Dilated pupils High BP Sweaty Runny nose Cramps
What are features of benzo withdrawal?
Hypersensitivity
Hyper-reflexia
Depersonalisation
What are features of psychostimulant withdrawal?
Agitation
restlessness
What are features of heroin withdrawal?
Cold/shivery
flu-like symptoms
Body pain
CANNOT KILL YOU
What are symptoms of third degree (complete) heart block?
Light-headedness Dizziness Fainting Fatigue Chest pain bradycardia Palpitations
What is complete heart block?
Electrical signal can’t pass normally from the atria to the ventricles.
P and QRS waves conducted at different speeds, no connections between them
What are the features of complete heart block on an ECG?
P waves about 90/min (more P waves than QRS waves). Regular.
QRS about 36/min
Regular.
BUT NO LINK BETWEEN THE TWO.
Variable PR intervals
Abnormally shaped QRS due to abnormal spread of conduction throughout ventricles. Generally broad.
Right axis deviation.
What are different causes of complete heart block?
MI
Chronic - fibrosis of bundle of His or BBB in both branches (eg. old age)
Fibrosis more common than ischaemia
How would you investigate whether someone may have complete heart block?
ECG
If well enough to go home, 24 hour tape
How would you treat heart block?
Withdraw any medications that may be causing, aggravating condition eg.
Anti-hypertensives/anginal/anti-arrhythmic and heart failure medications cause AV block
Oxygen (if necessary)
Monitor ECG, BP, SpO2
Bloods: ABG, FBC, U&Es,
Identify and treat reversible causes (drug chart, electrolytes etc.)
if have adverse features (shock, syncope, MI or heart failure):
ATROPINE 500 mcg IV
If no response: repeat atropine 500 mcg IV to max of 3 mg
alternatives to this:
isoprenaline or adrenaline
Transcutaneous pacing
If successful: observe (unless risk of: systole, mobitz-type-2 block, broad QRS and ventricular pause >3 secs - then complete above)
Long term: pacemaker
What alternative drugs can be given to atropine in complete heart block?
isoprenaline and adrenaline
Glycopyrrolate
aminophylline
dopamine
GLUCAGON (if beta-blocker or CCB overdose)
What are the different classifications of hypoxia?
Hypoxic hypoxia - reduced O2 supply
Anaemic hypoxia - reduced haemoglobin function
Stagnant hypoxia - inadequate circulation
Histotoxic hypoxia - impaired cellular O2 metabolism (eg. carbon monoxide/cyanide poisoning)
What is the oxygen delivery equation?
delivery of oxygen = cardiac output x conc. of oxygen in the blood
How can you maximise oxygen delivery in trauma?
Increase cardiac output:
fluids
oxygen
BLOOD (reduce risk of coagulopathy)
What is the triad of death?
Coagulopathy (causes lactic acidosis) metabolic acidosis (causes decreased myocardial performance, causing hypothermia) hypothermia (halts the coagulation cascade = COAGULOPATHY)
What is clinically significant hypothermia?
Body temp <36 for 4 hours or more
What is cerebral perfusion pressure (CPP)?
pressure gradient causing cerebral blood flow (CBF) such that CBF=CPP/CVR
(CVR: cerebrovascular resistance)
OR MORE COMMONLY AS:
CPP = MAP-ICP
How do you work out MAP?
(2 x diastolic BP + systolic BP)/3
What is the Monro-Kellie Doctrine?
Cranial compartment volume is fixed
Cranium and its constituents (blood, CSF and brain) are in a state of volume equilibrium
Increased volume in one of the cranial constants must be compensated by a decrease in volume of another
What are the main buffers in the MKD?
CSF
(to a lesser extent) blood volume
If there is an increase in volume requirement (eg. extradural haematom), there will be downward displacement of CSF in to the spinal canal, reduction in cerebral venous blood and stretch of falx cerebri between hemispheres and the tentorium between the hemispheres and the cerebellum.
These compensatory changes able to maintain normal ICP for changes in volume of less than 100-120mL
What does the Monro-Kellie Doctrine tell us about changes in volume?
Small increases do not lead to an immediate increase in ICP.
Once ICP reaches about 25mmHg, small increases in brain volume can lead to marked increases in ICP as threshold for intracranial compliance is passed (CRITICAL VOLUME)
What are some features of raised ICP?
Changes in LOC
Eyes: papilloedema, pupillary changes, impaired eye movement
Posturing: decerebrate, corticate, flaccid
Changes in speech
Headache
Seizures
Impaired sensory and motor function
Changes in vital signs - cushion’s triad: High systolic BP, low pulse, irregular resp.
Vomiting
What is Cushing’s triad? Why does it happen? What does it tell you?
High systolic BP
Low HR
irregular breathing pattern
Body trying to increase CPP by raising BP and dilating cerebral blood vessels, but this increases intracranial haemorrhage, which raises ICP further
Very close to dying
Why is raised ICP associated with higher mortality rates in TBI?
Raised ICP = cerebral ischaemia = infarction
What can a very high ICP caused by a unilateral space-occupying lesion (eg. haematoma) result in?
Midline shift
Hydrocephalus or brain herniation
Herniation is usually uncle or tonsillar
Brainstem compressed = coning
What clinical signs might you begin finding in someone with raised ICP?
Dilated pupil - sluggish then fixed (CNIII palsy)
Aphasia
How would you manage a TBI clinically?
ABCDE - URGENT INTUBATION is first priority
Prevent secondary brain injury
How might you prevent secondary brain injury?
Prevent: hypoxia
hypocarbia
hypoglycaemia
hypotension
Who should you immobilise following a head injury/trauma? How long should they remain immobilised for?
GCS < 15 Neck pain or tenderness Focal neurological deficit Paraesthesia in extremities Any clinical suspicion of cervical spine injury
Remain immobilised until full risk assessment incl. clinical assessment and imaging (if necessary) have deemed it is safe to remove immobilisation device
What is the purpose of the Canadian C-spine rules?
Assessment tool used to RULE OUT cervical spine injury in LOW-RISK patients (obviating need for radiography)
Use for all alert (GCS 15) and stable trauma patients where cervical spine injury is a concern
What are the high-risk factors which mandate radiography of C-spine (according to C-spine rules)?
Age >= 65 years
Dangerous mechanism
Parasthesia in extremities
Yes to any one of these = radiography necessary
No to all of these, move on to consider low-risk factors
What are the low-risk factors which allow safe assessment of range of motion? (according to Canadian c-spine rules)
Simple rear-end motor vehicle collision
Sitting position in ED
Ambulatory at any time
Delayed onset neck pain
Absence of midline c-spine tenderness
If patient doesn’t have these features, they are at risk of having a cervical spine injury, radiography is needed.
If they do have one of these features, move on to consider whether they can actively rotate their neck
Does a patient need radiographic imaging if they are able to rotate neck 45 degrees L and R?
No (if other criteria have been fulfilled eg. no high risk and some low risk features)
Radiography needed if unable to move neck
Outline the Canadian c-spine rules.
- any high-risk factor which mandates radiography (age >=65 years, dangerous mechanism or parasthesia in extremities)
- any low-risk factors which allow safe assessment of range of motion (simples rear-end MVC, sitting position in ED, ambulatory at any time, delayed onset neck pain, absence of midline c-spine tenderness)
- Assess whether able to actively rotate neck 45 degrees L and R
How should you manage someone with a head injury?
ABC - stabilise these
GCS <8 - involve anaesthetist very urgently
Assess whether at high risk of brain injury or cervical spine injury - decide whether to image or not (using Canadian C-spine/NICE guidelines). Assess neck movement IF APPROPRIATE
If decide not to image, re-assess patient in one hour
Manage pain (as this can lead to raised ICP) - small doses of IV opioids
What are the criteria for performing a CT head scan in someone with a head injury?
Any of the following risk factors = perform a CT head scan within one hour of risk being identified:
GCS less than 13 on initial assessment at ED
GCS less than 15 at two hours post-injury
Suspected skull fracture
Any sign of basal skull fracture: haemotympanum, panda eyes, cerebrospinal fluid leakage from ear to nose, Battle’s sign)
Post-traumatic seizure
Focal neurological deficit
More than one (SEPARATE) episodes of vomiting
If patient is on warfarin treatment
OR any of the following risk factor with LOC or amnesia since injury:
65yrs or older
Any Hx of bleeding or clotting disorders
Dangerous mechanism of injury
more than 30 mins retrograde amnesia of events immediately before the head injury
What are the NICE criteria for performing a CT cervical spine in adults following a head injury?
Any of the following risk factors = CT should be completed within one hour
GCS < 13 on initial assessment Pt. intubated Plain X-rays technically inadequate Plain x-ray suspicious/abnormal Need definite diagnosis High risk Canadian c-spine factors
When would you admit someone with a head injury?
Patients with new, clinically significant abnormalities on imaging
Patients whose GCS has not returned to 15 after imaging, regardless of imaging results
Pt has indications for CT scanning, but this cannot be done within appropriate period
Continuing worrying signs eg. persistent vomiting, severe headaches)
Other causes for concern eg. drug/alcohol intoxication etc.
What are symptoms and key features of hyperglycaemic hyperosmolar state?
Generally T2DM v. high blood sugar levels increased urination, thirst nausea dry skin disorientation, drowsiness and LoC weakness, leg cramps, visual impairment
Key features:
Hypovolaemia (eg. confusion, sunken eyes, longitudinal furrows of tonge, extremity weakness, raised urea, tachycardia, hypotension)
Hyperglycaemia (BG 30 or more)
WITHOUT hyperketonaemia (<3) OR acidosis (pH>7.3, bicarb >15)
Osmolality usually >320
May get HHS and DKA at same time
what are the goals of treatment of HHS?
normalise osmolality Replace fluid and electrolyte losses Normalise blood glucose Prevent arterial/vnous thrombosis Prevent other complications Prevent foot ulceration
How do you calculate osmolality?
2Na + glucose + urea
How would you manage a patient with HHS?
A - ensure airway is stable
B - RR, sats, oxygen if desaturating. ?CXR if suspect chest infection
C - cannula, fluids, bloods, BP, HR etc. listen to heart sounds. ECG. Fluid output. urinalysis.
D - GCS, pupils, BLOOD GLUCOSE. Neuroexamination
E - full body exposure, looking for infection/rashes or abdo problems
Check for thyroid enlargement
Temp.
Address fluid balance, give 0.9% saline (with potassium if required)
Calculate osmolality every hour
Try to replace half of fluid (3-6L) loss within first 12 hours, and other half in second 12 hours
Aim for decrease in glucose of 4-6 mmol/Hr
Target glucose: 10-15.
Aim for normalisation within 72 hours
No ketonaemia = no insulin
Only start insulin if BG does not decrease following fluid replacement therapy.
Potassium over 5.5 = do not infuse saline with potassium
Potassium 3.5-5.5 = 40mmol/L infusion
below 3.5 = senior review/HDU
LMWH for full duration of admission
What investigations would you do for someone with probable HHS?
Bloods: FBC U&E ABG/VBG blood glucose CRP (looking for infective source) blood cultures
Urine: urinalysis
urine dip
CXR
ECG
What are common differentials for HHS?
delirium
Poisoning
Sepsis
Lactic acidosis or other causes of metabolic acidosis
What are some complications of HHS?
Ischaemia of any organ esp. MI or cerebral
DVT/PE
ARDS
SIC
Rhabdomyolysis
Fluid overload/hypoglycaemia (caused iatrogenically)
What are some causes of HHS?
MI Infections stroke/TIA Hyper/hypothermia PE AKI Acute abdo Burns
Medication: metformin, diuretics, beta blockers, H2 receptor antagonists CCB APs steroids Anti-convulsants Substance misuse
First presentation of diabetes
Poor diabetic control/non-compliance
What are some risk factors for seizures?
Fever
Head injury
Alcohol/drugs - excessive or withdrawal
Brain infection
Ischaemic stroke or intracranial haemorrhage
eclampsia
pro-convulsive drugs (tramadol, theophylline, baclofen)
Specific stimuli: strobe lights, reading, psychological stress or sleep deprivation
Following a suspected seizure, what examinations should you do for a patient?
cardiac
neurological
mental state
what are some features of a seizure?
Temporal lobe: feeling frightened, deja vu, strange taste/smell, rising sensation in stomach, staring, lip-smacking, confusion
Frontal lobe: moving head or eyes to one side, not being aware of surroundings, screaming/swearing/laughing, unusual body movements, repeated movements
Parietal lobe: numbness, tingling, sexual sensations, sensation of body distortion, feeling out of your body, feeling dizzy, seeing things, language difficulty
Occipital lobe: seeing things, visual changes, seeing image repeatedly, eye pain, uncontrollable sideways movement of eyes, nystagmus
Aura: focal seizures acting as a warning of generalised seizure
generalised seizure: rigid muscles Voilent muscle contractions Loss of consciousness Biting cheek/tongue Clenched teeth or jaw Incontinence Stopped/difficulty breathing Blue skin colour
After seizure: confusion drowsiness amnesia headache weakness on one side of body (mins-hours. Todd's paresis)
What are some differential diagnoses for
syncope (post-anoxic convulsion) TIA (although no LoC generally) Metabolic encephalopathy Night terrors Sleep-walking Migraines Arrhythmias Psychogenic non-epileptic seizures
How would you investigate a seizure?
Bloods: glucose, U&E, calcium, renal function, liver function, urine biochem)
12 lead ECG
CT/MRI
EEG - within 24-48 hours of first seizure or see-deprived
If to support diagnosis of epilepsy, do after second seizure
DO NOT PERFORM IN PROBABLE SYNCOPE because possible false-positive produced
How would you manage a seizure acutely?
Keep pt from falling, guide them to floor, move objects that might cause them harm
TIME THE SEIZURE
Try to get them on to their side, but don’t be too hard
Pay close attention to what is happening
(in community, after 5 mins, ring ambulance and give buccal midazolam if pt. has it)
Post seizure: get pt on side if not already, loosen clothing around neck and waist
move anything from front of mouth out
wait with patient until come around fully
What would you have to tell the patient/patient’s family?
How to recognise and manage seizures
Reporting further attacks
Stop driving
Avoid swimming or bathing without supervision
Driving is permitted after one year’s freedom from seizures after an unprovoked seizure and on a case-by-case basis on provoked seizures
Commercial driving not usually allowed for 10 years freedom from seizure with AED
How would you manage someone with a seizure in the long term?
investigations
refer to specialist in management of epilepsies
patient education
How do you manage status epileptics?
A - ?nasopharyngeal
B - oxygen 15L NRB
C - IV access, bloods: FBC, U&E, LFTs, calcium, magnesium, glucose
How do you manage status epileptics?
A - ?nasopharyngeal
B - oxygen 15L NRB
C - IV access, bloods: FBC, U&E, LFTs, calcium, magnesium, glucose, blood cultures if suspect sepsis
D - pupils, AVPU
E - injuries, temperature etc.
Time the seizure
After 5 mins: 1-2mg lorazepam IV
Repeat after 5 mins if necessary (max of 4 mg can be given).
If seizures continue: IV phenytoin 20mg/Kg (max 2g), give at 50mg/min. Monitor ECG and BP
Continues seizures: anaesthetic sedation.
What causes appendicitis? What happens if it is untreated?
Obstruction of appendical lumen - once obstructed, there can be: bacterial overgrowth, distention, ischaemia and inflammation
If untreated: necrosis, perforation, abscess formation and gangrene
What are the clinical features of someone with appendicitis?
‘classic’ symptoms only in about 50% of patients
Pain: usually Epigastric or periumbilical THEN localises to RLQ
Pain migration due to different innervation of layers.
Peritonitis: wash-board rigidity. Pain exacerbated by slightest movement.
Rebound tenderness at McBurney’s point (2/3 of way along imaginary line from umbilicus to R anterior superior iliac spine)
Rousing’s sign: pain in LRQ when LLQ palpated
Psoas sign: increased pain on passive extension of right hip
Obturator sign: pain felt on passive internal rotation of flexed hip
Nausea/vomiting Anorexia Low-grade fever Reduced bowel movements Urine dip may show WBC or RBCs
What investigations might you want to do for someone with ?appendicitis?
Bloods: FBC, U&E, LFTs, CRP
Pregnancy test
Urine dip
USS ( would see aperistaltic and non-compressible structure with diameter >6 mm)
Contrast CT (good sensitivity and specificity, able to diagnose other differentials BUT takes time to arrange)
Laparotomy
How would you manage a patient with appendicitis?
Pain relief!
Appendectomy under GA
Keyhole or open
Contraindicated in IBD involving the caecum and possibly elderly or severely ill.
Unable to have appendectomy: IV antibiotics (not curative, reduce mortality in 50%, therefore buy time).
May consider IV ABX and appendectomy a few weeks later if patient has an appendix mass (fatty mass around appendix)
What are the complications associated with appendicitis?
Perforation with/without peritonitis
Abscess formation
What are the differentials for someone with ?appendicitis?
Gastroenteritis IBS constipation bladder or urine infections Crohn's disease pelvic infection
ECTOPIC PREGNANCY
What are the two different types of appendicitis?
Simple appendicitis—Inflamed appendix, in the absence of gangrene, perforation, or abscess around the appendix
Complicated appendicitis—Perforated or gangrenous appendicitis or the presence of periappendicular abscess
what are some risk factors for cholecystitis?
GALL STONES or biliary sludge Female gender Age Obesity Rapid weight loss Pregnancy Crohn's disease Hyperlipidaemia
how might cholecystitis present?
epigastric or RUQ pain vomiting fever (high-swinging fever - riggers and chills) raised WCC Jaundice Murphy's sign
chariot’s triad: RUQ pain, jaundice, fever
What investigations might you do for someone with ?cholecystitis?
FBC - WCC raised
LFTs (often mildly abnormal)
U&Es
USS - thickened GB wall, pericholecystic fluid or air
(thickened GB wall, but no gallstones = calculus cholecystitis)
What are risk factors for gall stones?
Fair Fat Fertile Female Forty (increasing age) \+ve family history Sudden weight loss diabetes Oral contraception
How might someone present with gall stones?
biliary colic (most common presentation - cause by gallstone impacting in cystic duct or ampulla of Vater)
cholecystitis (second most common presentation, caused by distention of GB)
pancreatitis
obstructive jaundice
How does biliary colic present?
Sudden onset pain in epigastrium or RUQ, may radiate from back into intrascapular region
subsides spontaneously with analgesics
nausea or vomiting
What are differentials for biliary-tract obstructions/infections?
reflux
ulcers
IBS
pancreatitis
How would you manage biliary colic and acute cholecystitis?
Pain relief: morphine, pethidine parenterally or diclofenac suppository
IV ABX
Fluids (if electrolyte/hydration imbalance)
refer for laprascopic cholecystectomy
unfit for cholecystectomy: percutaneous cholecystectomy (surgical drainage of GB)
Which intestine is more likely to become obstructed? Large or small?
Small bowel
What are some risk factors for small intestinal obstruction?
adhesions (from prior operations)
strangulated hernia
malignancy (usually caecum)
volvulus
What are some risk factors for large intestinal obstruction?
colorectal malignancy (worse the lower down the bowel) older age
risk of perforation
What are some risk factors for sigmoid and caecal volvulus? (rotation of gut)
elderly
psychiatric illness
African/Asian (higher incidence)
What are some risk factors for paralytic ileus? (condition in which bowel ceases to function - no peristalsis)
Intestinal pseudo-obstruction = ogilvie’s syndrome
Chest infection Acute MI Stroke AKI Puerperium Trauma Severe hypothyroidism Electrolyte disturbance Diabetic ketoacidosis
Post-operative
What are different types of bowel obstruction?
mechanical obstruction eg. adhesions, malignancies etc.
volvulus (rotation of gut)
paralytic ileus/ogilvie’s syndrome (lack of peristalsis)
What are symptoms of bowel obstruction?
nausea/vomiting:
early in presentation =high-level obstruction
faeculant vomiting = low obstruction
dysphagia
abdo pain - diffuse, colicky, central (may be less/absent in paralytic ileus)
Severe pain and tension: suggest ischaemia or perforation
failure to pass bowel movements = earlier in lower obstruction
No flatus and no bowel movement: paralytic illeus
abdo distention:
Lower the level of obstruction = more
tympani
high-pitched bowel sounds
pseudo-obstruction presents like large bowel obstruction, but other medical history may indicate true nature.
What might you find on examination in ?bowel obstruction?
Dehydration: poor peripheral perfusion, tachycardia, hypotension
pyrexia - perforation or infarction of bowel
Abdo distension
Peristalsis may be visible
Distended bowel: resonant on percussion
Abdo mass may be palpable
Peritonism (tenderness and guarding) = strangulation or perforation
Hernial orifices
Tinkling bowel sounds = obstruction
Silence = reduced OR SILENT bowel sounds
How might you investigate someone for ?bowel obstruction?
Fluid charts - monitor fluid input and output
NG tube
Bloods: FBC U&Es Creatinine Group and cross-match Glucose Amylase (rule out pancreatitis)
Abdo X-ray (supine and erect)
US (to exclude small bowel obstruction)
ct scanning
What differentials might you consider for someone presenting with symptoms of ?bowel obstruction?
Gastroenteritis (wouldn’t necessarily get bloating and reduced bowel movement)
ischaemia of gut - usually bloody diarrhoea
Acute pancreatitis (can get associated paralytic ileus)
peptic ulcer, perforated diverticular disease, perforated carcinoma
TB
MI (small bowel) Ovarian cancer (large bowel)
How would you manage bowel obstruction?
All:
ABCDE management
Uncomplicated: conservative - fluid resuscitation, electrolyte replacement, intestinal decompression (via NG tube) and bowel rest, analgesia, anti-emetic
Antibiotics (prophylactic against bacteria)
Steroids (if inflammatory cause)
Illeus: stop medications that slow colonic motility
Endoscopy: decompression, dilation of strictures, stents
^ final treatment OR to allow for delay until elective surgical therapy
Emergency surgery (eg. complete small-bowel obstruction, closed loop obstructions, TOXIC MEGACOLON, bowel ischaemia and volvulus = surgical emergencies). Consider surgery if any signs of ischaemia, perforation, peritonitis
What are symptoms/features of toxic megacolon?
Symptoms may come on suddenly
Background of IBD
Abdo pain distended abdo abdo tenderness fever tachycardia shock bloody or profuse diarrhoea painful bowel movements
What is diverticulitis?
diverticular inflammation with or without localised symptoms and signs
What are the symptoms/features of diverticulitis?
LLQ pain (asians: RLQ) intermittent or constant change in bowel habit fever tachycardia (hypotension and shock are unusual) Anorexia, nausea and vomiting may occur Localised tenderness, palpable mass
Bowel sounds may be normal or increased
Rectal examination may show tenderness or a mass
may present with complications of diverticulitis
What are the complications of diverticulitis? (pts may present with these)
perforation: peritonitis
abscess: tender mass or persistent fever despite ABX
fistula
stricture/obstruction
Colovesical fistulas: pneumaturia (bubbles and dysuria) or faecaluria
colovaginal fistulas: frequent vaginal infections or copious vaginal discharge
bleeding - GI haemorrhage. abrupt painless bleeding, cramps, bloody stool
What examinations would you do for someone with ?diverticulitis?
Bloods: FBC (WBC raised in diverticulitis, raised platelets, anaemia) CRP LFTs U&Es
CXR - detect pneumoperitoneum
Abdo xray - demonstrate small or large bowel dilation/obstruction, ileum, pneumoperitoneum, soft-tissue density (abscesses)
pelvic ultrasound (in women - investigate gynae problems)
?colonoscopy (or risk of perforation)
CT
How would you manage a patient with diverticulitis?
Mostly managed at home: ABX, paracetamol, fluid-only diet for 2/3 days, followed by low-fibre diet (reduce faeces produced)
admit if: pain cannot be controlled by paracetamol
unable to drink enough fluids to keep hydrated
unable to take ABX PO
general health is poor
weakened immune system
suspected complications
symptoms failing to improve at home
ABCDE
Rehydration, symptomatic relief (pain killlers), IV ABX (metronidazole)
drainage of abscesses
elective surgery for removal of diverticula (4-6 weeks after diverticulitis attack)
emergency surgery: peritonitis, visceral perforation, sepsis, undrainable abscess, bowel obstruction or lack of improvement/deterioration with initial medical management
What is pancreatitis?
acute inflammation of pancreas
release of exocrine enzymes which cause auto digestion of the organ.
Other local tissues and distant organs can also be involved
What are the most common causes of pancreatitis?
I GET SMASHED idiopathic/iatrogenic gall bladder disease excess alcohol consumption trauma (post ERCP, blunt)
Steroids Mumps autoimmune scorpion stings Hyperlipidaemia, hyperparathyroidism (hypercalcaemia)) ERCP drugs
Ischaemia
IBD
How does acute pancreatitis present?
Symptoms: upper abdo pain (LUQ), penetrates to back (could also be general abdo) sudden onset vomiting pain increases over 72 hours
Signs: temperature (generally raised) tachycardia, pt. unwell and dehydrated jaundice may be present abdo rigidity (epigastric or general) bowel sounds usually present in early phase. Can get paralytic ileum (causing absent bowel sounds)
Severe cases: hypotension, pyrexia, tachypnoea, ascites, pleural effusion, Cullen’s sign, Grey Turner’s sign (due to retroperitoneal haemorrhage… pancreas is the retroperitoneum)
hypoxaemia
What investigations would you want to do on a patient with ?acute pancreatitis?
Bloods: FBC U&Es glucose CRP ABG (PaO2 and calcium - for GLASGOW score and may also get hypocalcaemia) LFTs (raised bilirubin and/or serum aminotransferase suggest gallstones) May see hypocalcaemia Amylase (3x normal or more) Lipase (more sensitive and specific)
Abdo xray - exclude other causes, may see calcification, elevated hemidiaphragm, pleural effusion
CT scan
US - see presence of gall stones (but otherwise not that helpful)
Endoscopic ultrasound
How would you manage a patient with mild acute pancreatitis?
Manage on general ward
Pain relief: pethidine or buprenorphine with/without benzos
NOT MORPHINE.
IV fluids, nil by mouth
NG tube for severe vomiting
ABX for specific infections
No other treatment, No CT necessary
pain, Sx and bloods under control: oral fluids, then solids resumed. Gallstones are the cause = consider common bile duct clearance
How would you manage a patient with severe acute pancreatitis?
Treat in ITU or HDU
Fluids (maintain urine output >0.5 ml/kg)
Oxygen if necessary
IV ABX for 7-14 days (cef and met or AMG) if there is necrosis
Evidence of pancreatic necrosis, IV antibiotics
NG tube feeding
ERCP for patients with co-existing cholangitis or biliary obstruction
Surgery (if there is infection and necrosis)
Percutaneous catheter drainage
What are the complications of pancreatitis?
pancreatic necrosis infected necrosis acute fluid collections pancreatic abscess acute pseudo-cyst pancreatic ascities acute cholecystitis
How does paracetamol overdose cause toxicity?
Paracetamol metabolised by P450 system: 95% metabolised into harmless metabolites
5% becomes NAPQI
glutathione makes NAPQI harmless
Overdose increases NAPQI levels, run out of glutathione
NAPQI builds up
Hepatocytes damaged
What should you do for patients presenting with paracetamol overdose?
ABCDE
Hx from patient
Look on toxbase (might need to make phonemail to NPIS - national poisons information services)
management of overdose depends on time after ingestion
Consider sectioning under 5(2) MHA (if on acutes, cannot do in ED)
What are the important parts of the history?
HPC: How much has been taken Time of first tablet (to last tablet) Any other substances taken what happened - fell, unconscious etc. Precipitating factors
Current symptoms: N+V, LOC, RUG pain
DH: Any regular meds, O/C
illicit drugs or alcohol alongside or regularly
ANYTHING INTERACTING WITH P450
PMH: anorexia, alcoholism (reduced glutathione stores)
PSYCH and social Hx
How would you treat paracetamol overdose?
< 1 hour since start of overdose: CHARCOAL
have to wait until 4 hours to take PCM level
4-8 hours: take level
higher than line on graph, treat with parvolex
8 hours or more: start on parvolex treatment
take PCM measurement
If above line, continue treatment
If below line, stop treatment
15+ hours: treat with parvolex
no need to do PCM level
What investigations would you want to do on a patient presenting with paracetamol overdose?
FBC
U&E
LFTs
PCM level - whether need to give parvolex
CLOTTING FACTORS (INR) - tells you about synthetic function of liver
Under what circumstances can you use the PCM level graph?
UNstaggered overdose (taken within less than an hour)
Know time of first tablet
After 4 hours
What is the treatment regimen for Parvolex in paracetamol overdose?
first bag: over 15mins
second bag: over 4 hours
third bag: over 16 hours (may need to give several of the third bags, until clotting returns to normal)
What adverse reactions might you see in a patient who has been given parvolex? How would you manage this?
mock allergic reaction (red and itchy)
Piriton
Start parvolex at half dose
What signs might you see in a patient with paracetamol overdose?
N+V within 24 hours
24-72 hours: jaundice
72 + hours: jaundice, bleeding and encephalopathy
What are some red flags of lower back pain?
TUNAFISH
T: TRAUMA, TB
U: UNEXPLAINED WEIGHT LOSS, NIGHT SWEATS
N: NEUROLOGICAL DEFICIT, INCONTINENCE or retention, saddle anaesthesia, hip/leg weakness, NIGHT PAIN
A: AGE (<20 or >55)
F: FEVER
I: IVDU, infection
S: STEROID USE OR IMMUNOSUPPRESSED
H: Hx OF CANCER, EARLY MORNING STIFFNESS (pain at rest)
What symptoms would make you think a patient might have a spinal cord compression? how would you treat this?
back pain leg weakness limb numbness ataxia (+ve Romberg's) urinary retention (with overflow) hyper-reflexia extensor plantars clonus
Where possible: decompression of the spinal cord
What symptoms would make you think a patient had caudal equina?
bilateral leg pain back pain urinary retention perianal sensory loss erectile dysfunction reduced anal tone
How would you investigate a patient that you thought might have a serious back problem (presented with red flags)?
Myeloma screen
Bloods: FBC U+E Calcium CRP ESR
plain Xray (esp. if suspect osteoporosis/infection - not routine)
MRI
(CT if MRI not available)
What are some causes of acute low back pain?
compression fractures to spine from osteoporosis Cancer involving spine fracture of spinal cord muscle spasm rupture or herniated disk sciatica spinal stenosis spine curvatures strain or tears to muscles or ligaments supporting back
AAA leaking Arthritis conditions Infection of spine Kidney infection or kidney stones pregnancy Conditions affecting female reproductive organs
What would you recommend for someone who has lower back pain, but does not appear to be due to sinister causes?
Stay as active as possible
exercises and stretches for back pain
NSAIDS (if safe)
Hot or cold compression packs for short term relied
Physiotherapists
How would you treat caudal equina?
URGENT surgery - relieve pressure on nerves
Other treatment depends on cause eg. infections = ABX, cancer = radiotherapy
What are the Ottawa ankle rules?
Guidelines for clinicians to help decide whether patient needs X-ray for foot or ankle:
Ankle - pain in the malleolar zone and any one of the following:
- Bone tenderness along the distal 6 cm of the posterior edge of the tibia or tip of the medial malleolus
OR
- Bone tenderness along the distal 6 cm of the posterior edge of the fibula or tip of the lateral malleolus
OR
- An inability to bear weight both immediately and in the emergency department for four steps.
Foot - any pain in the midfoot zone and any one of the following:
- Bone tenderness at the base of the fifth metatarsal (for foot injuries)
OR - Bone tenderness at the navicular bone (for foot injuries)
OR - An inability to bear weight both immediately and in the emergency department for four steps.
What does the surviving sepsis campaign bundle say should be completed within three hours of presentation?
Measure lactate level
Blood cultures (X2)
Administer broad-spectrum antibiotics - one hour in septic shock/severe sepsis
Administer crystalloid for hypotension or lactate >=4.
Essentially, buffalo
What are red flag features for herniated nucleus pulpous?
Major muscle weakness
foot drop
What can cause peptic ulcer disease?
H. pylori NSAIDS pepsin smoking alcohol bile acids steroids stress
How might peptic ulcer disease present?
epigastric pain and tenderness (usually 1-3 hours postprandial) Pain may wake patient at night Pain may radiate to back relieved by food Nausea Oral flatulence bloating distention intolerance of fatty food (like in gall stones) Heartburn (may be GORD) Pain may be relieved by antacids succussion splash on auscultation of abode
What are the differential diagnoses for someone with ?peptic ulcer disease?
AAA GORD Gastric cancer Gall stones Chronic pancreatitis Crohn's disease Diverticular disease IBS Drub-induced dyspepsia Hepatitis Acute ulcers Zollinger-Ellison syndrome Coronary heart disease
What investigations might you do for someone with suspected peptic ulcer disease?
Bloods: FBC (may show iron-deficiency anaemia) U+Es LFTs CRP
Carbon-13 urea breath test or stool antigen (to test for H. pylori)
Endoscopy - only necessary if patient presenting for the first time is 55yrs< or warning signs: iron-deficiency anaemia chronic blood loss weight loss progressive dysphagia persistent vomiting epigastric mass
In pts. aged over 55 (not presenting for first time), also do endoscopy if: previous gastric ulcer previous gastric surgery pernicious anaemia NSAID use family history of gastric carcinoma
How would you manage a patient with peptic ulcer disease?
Stop or replace causative drugs/ ask patient to take with food or alendrotnic acid
Cardiac risk pts: continue low-dose aspirin and full-dose naproxen
encourage cessation of smoking
H.pylori positive: eradication therapy
NSAID-induced: first line - PPI for two months
Second line - 8/52 of standard dose H2-receptor antagonist (ranitidine 150mg BD)
not H. pylori or drug-induced: may need sample of ulcer
Bleeding ulcer: endoscopic intervention with ablative/mechanical treatment
follow up endoscopy 6-8 weeks later
What are the first-line drugs recommended for eradication therapy (for H. pylori)?
7 day PPI plus amoxicillin 1g and either clarithromycin 500mg or metronidazole 400mg (all BD). Clarithro + metro if pt. penicillin allergic
what are some risk factors for urinary tract stones?
abnormal kidneys/ureters FHx HTN gout Hyperparathyroidism Immobilisation Relative dehydration increased excretion of solutes cystinuria drugs: diuretics and vit D supplements
How might renal colic present (if symptoms are present)?
sudden onset severe pain (may begin as dull ache)
loin pain, moves to groin
tenderness of login or renal angle
haematuria
stone high (in renal capsule): flank pain
pain may radiate down to testis, scrotum, labia and anterior thigh
rigors and fever (if infection is present) dysuria haematuria urinary retention nausea and vomiting hypotension may be present
What investigations might you want to do for someone with ?renal colic?
Bloods: FBC, CRP, renal function, electrolytes, calcium, phosphate, rate and creatinine
Prothrombin time and INR (if intervention planned)
Urine:
urine dip for blood, white cells, nitrites, ph<7 (urea-splitting organisms) ,<5 (uric acid stones)
microscopy, culture and sensitivities
US
CT
KUB
How would you manage a patient with renal colic (at hospital)?
NSAIDS: diclofenac IM or PR = first line
opiates only if severe pain NOT PETHIDINE
Anti-emetics
Conservative management for up to 3 weeks (unless infection of obstruction is present)
Medical expulsive therapy to help passage of stone: nifedipine or tamsulosin + steroid
May need surgical removal:
stent (if obstruction present)
extracorporeal shock wave lithotripsy (ESWL - shock waves break up stones)
other types of surgery available too.
For what reasons would you admit someone with renal colic?
fever
solitary kidney
inadequate pain relief or persistent pain
inability to take fluids due to nausea and vomiting
anuria
pregnancy
poor social support
inability to arrange outpatient follow-up
over 60 yrs if concerned about clinical condition
When might you consider managing a patient with renal colic as an outpatient?
patient has been relieved
patient able to drink large amounts of volume
good social circumstances
no complications evident
what complications can be associated with renal colic?
reduced eGFR
sepsis
ureteric stricture
pyelonephritis
What is a lower UTI?
Infection of bladder (cystitis)
What is an upper UTI?
pyelitis and pyelonephritis
What’s an uncomplicated UTI?
infection by usual pathogen in a person with usual urinary tract with normal kidney function
What’s a complicated UTI?
anatomical, functional or pharmacological factors predispose patient to persistent infection, recurrent infection OR treatment failure
What pathogens most commonly cause UTI?
E. coli
Staphylococcus saprophticus
proteus mirabilis
enterococci
What are less common causes of UTI? (eg. in patient with predisposition)
Klebsiella
Proteus vulgaris
Candida albicans
Pseudomonas
What are some risk factors for UTI?
Increasing age female instrumentation in renal tract abnormality of renal tract incomplete bladder emptying sexual activity use of spermicide diabetes catheter institutionalisation pregnancy immunosupression genetic
What are some common symptoms of UTI?
frequency painful frequent passing of small amounts of urine dysuria haematuria foul-smelling +/- cloudy urine urgency incontinence suprapubic or loin pain riggers pyrexia N+V acute confusional state (esp. in elderly patients)
How would you investigate someone for UTI?
Dipstick analysis of urine
(not for catheters). Treat fas bacteria if positive for nitrites and/or leukocytes
Urine microscopy
Urine culture (to exclude diagnosis, or high-risk, or failing to respond to empirical treatment)
ultrasound of upper UT (rule out obstruction and renal stone disease in acute pyelonephritis)
Febrile 72 hours post treatment: further imaging (?CT)
Which patients with UTI should be refered for imaging or cystoscopy?
Persistently not responded to treatment
Hx of renal tract disease or anomaly
Haematuria
WOMEN with recurrent infections, not responding to preventative measures
MEN with 2=< episodes in 3 mths
When might you investigate a patient for cancer if they present with UTI-like symptoms? How would you investigate this?
MALE nocturne, urinary frequency, hesitancy, urgency or retention OR visible haematuria: DRE and PSA
Refer under 2-week wait if: person under 45 has had unexplained visible haematuria without UTI OR visible haematuria which persists after successful treatment of UTI OR
60 or over unexplained non-visible haematuria and either dysuria or raised WCC on blood test OR
over 60 with recurrent/unexplained UTI
How would you treat a UTI?
lower UTI: Trimethoprim or nitrofurantoin
3 days in uncomplicated women
7 days for men
Pyelonephritis: ciprofloxacin 7-10 days. Co-amoxiclav is an alternative.
Asymptomatic bacteria should not be treated in adults with catheters or non-pregnant women
What can cause an acute ischaemic leg?
Embolism - gas, solid or liquid (most commonly of cardiac origin)
Thrombosis - peripheral vascular disease
Rarely: dissection or trauma
What are symptoms and signs of acute limb ischaemia?
Pain Pallor (but could also be red) Paresthesias Perishingly cold Pulelesness Paralysis
Skin changes: mottling (signifies irreversible changes)
Development of gangrene (late sign)
How long may a patient have had limb ischaemia for it to be called ‘acute’?
Less than 2 weeks
What investigations would you do for someone who you suspected had an acute ischaemic leg?
Bloods: FBC (ischaemia is aggravated by anaemia)
U+E (dehydration, K+ usually raised if tissue necrosis is occurring)
ESR (inflammatory disease causing ischaemia)
CK (raised if ischaemia has occurred)
Glucose
Lipids
Thrombophilia screen (clotting)
Group and save
ABG/VBG (acidosis secondary to ischaemia)
HAND-HELD DOPPLER US scan
Diagnosis in doubt: angiography (CT)
ECG (source of emboli)
Echo
Aortic ultrasound
Popliteal and femoral artery ultrasound
How would initially manage an acute ischaemic leg in the emergency department?
Analgesia: IV morphine
Oxygen
IV Heparin
IV fluids
tPA (tissue plasminogen activator) - given for 8-24 hours via Fogarty Catheter (arterial catheter) <2 weeks.
Refer to vascular specialist urgently. Delay risks the limb (if sensorimotor impairment). Thrombolysis or surgery!
What are the different stages of the Rutherford classification for acute limb ischaemia?
Stage 0: asymptomatic
Stage 1: mild claudication (salvageable)
Stage 2: moderate claudication (salvageable with immediate reconstruction)
Stage 3: severe claudication (major tissue loss or permanent nerve damage)
Stage 4: rest pain
Stage 5: ischaemic ulceration (not exceeding ulcer of digits of foot)
Stage 6: sever ischaemic ulcers or frank gangrene
How can you tell the difference between thrombosis end embolism in lower limb ischaemia (generally)?
Thrombosis onset: hours to days
Embolism onset: minutes
Upper limb effected: thrombosis = rarely, embolus = commonly
Multiple sites affected: not usually in thrombus
can occur in embolus
Previous claudication usually present with thrombus
Obstruction usually complete in embolus (no collaterals), but collaterals in thrombosis
What are some symptoms and symptoms might you see in someone with cellulitis?
Swollen area Red Well-defined border Warm Tender to touch/pressure Usually unilateral Pain onset: gradual
Malaise Chills Fever Tachycardia Tachypnoea Hypotension Skin sloughing Skin anaesthesia or high levels of pain Violaceaous bullae Lymphangitis spread
What elements of previous medical history might be in-keeping with a diagnosis of cellulitis?
General debility Immunocompromised Hx of infection DM (esp. if ulcerated or cut foot) Cancer Venous stasis Chronic liver disease Peripheral arterial disease CKD
What investigations would you do for someone you suspected have cellulitis?
Bloods: blood culture FBC, U+E and LFTs (baseline level) Creatinine (high) creatinine phosphokinase (high) CRP (high) VBG - bicarb (low)
Purulent lesion: debride and culture
Imaging: US
X-ray
CT (if concerned about necrotising fasciitis)
How would you manage a patient with cellulitis?
MARK AREA WITH SKIN-MARKING PEN
Analgesia (NSAIDS)
ABX: flucloxacillin 500mg QDS = first line
Erythromycin 500mg QDS if patient is penicillin allergic
Clindamycin is second-line treatment
Steroids (for anti-inflammatory)
Emollient
hydration
What is the difference between gout and pseudo gout? How can you tell this difference?
Gout: urate crystals
Psuedogout: calcium phosphate crystals
Differentiate by aspirating the joint
What is gout?
Crystal arthritis
High concentration of uric acid in blood stream
Not all patients with high blood urate level get gout
Low blood urate level doesn’t rule out diagnosis
What causes gout?
genetic susceptibility diet: meat and alcohol, food with high conc. of purine SE status Larger BMI Drugs: diuretic (esp. thiazide)
How might gout present?
mono arthritis - v. hot, red, swollen joint.
MTP is join affected in most patients (also PIP and DIP)
wakes patient at night
Tophi (urate crystal deposits in skin) - if long term
Synovitis
Pyrexia
Stone formation in kidney and bladder (may cause other symptoms)
What investigations might you do for someone you suspected had gout?
Bloods: FBC (WCC raised), U+E Serum urate (raised in 60% of cases) ESR (often raised)
Synovial fluid aspiration
x-ray (if assessing long-term damage)
How would you manage a patient with gout?
NSAIDSs
Colchicine
(allopurinol once episode has passed)
remove triggers
How does pseduogout usually present? How would you investigate this? How would you manage it?
Presents like gout
BUT knee most commonly affected (and bigger joints)
Joint aspiration
Radiographs (may show chondrocalcinosis)
Treatment: NSAIDS less effective than in gout
INTRA-ARTICLUAR INJECTIONS OF STEROIS useful in treating acute presentation
What are the symptoms of amphetamine overdose?
Tachycardia and arrhythmias Mydriasis Euphoria Formication Agitation or pacing Tremor Dilated pupils (sluggish response to light) Convulsions Hypertension HYPERTHERMIA (can get dangerously high) clenched jaw/jaw rigidity rapid speech Flushed face Hyper vigilance and paranoia
How would you investigate someone with suspected amphetamine toxicity?
A: airway
B: RR etc.
C: Bloods: U+Es Renal function LFTs creatine phosphokinase ECG Urine dipstick
D: blood sugar
CT head if Hx of head injury or altered consciousness
Assess for serotonin toxicity
How would you manage a patient with amphetamine toxicity?
A-E assessment
sedation: benzodiazepines
Fluids
Airway management, Oxygen, rapid calling etc. if necessary. Seizure control with benzodiazepines
How would opioid overdose present?
Opioid overdose triad:
pinpoint pupils
unconsciousness
respiratory depression
How should you manage a patient with opioid overdose?
A-E assessment
Naloxone (IV, IM, SC or intranasal). Start low (0.04-2mg IV) can give up to 4mg at a tim (if pt. severely poisoned)
IM if patient threatening to self-discharge
Can also be given as an infusion
Toxbase
How would you investigate a patient with opioid toxicity?
Urine drugs test
Bloods (baseline): FBC, metabolic screen, SK and ABG
CXR if pulmonary oedema suspected
ECG
How might tricyclic antidepressant overdose present?
Sedation (+/- apnoea) Confusion/delerium Arrhythmia Seizure Hypotension Anticholinergic effects: hyperthermia, flushing, dilated pupils nausea and vomiting headache
How would you investigate someone with TCA overdose?
ECG: sinus tacky, prolonged QRS, unusual R wave, prolonged QTc
Bloods: FBC U+E LFTs (baseline) ABG/VBG
How would you manage a patient with TCA overdose?
Airway management: may require intubation (GCS>8)
B: hyperventilate pt. to blow off CO2
C: IV access - sodium bicarb rapid bolus. Repeat until ECG changes seen. May want to set up infusion.
May need to give magnesium.
Fluids to raise BP, may need vasopressors (noradrenaline)
IV bentos for seizures
D: NG tube
E: temp
What is testicular torsion?
Torsion of spermatic cord
Occlusion of testicular blood vessels
Rapidly lead to ischaemia and loss of testis
How might testicular torsion present?
Usual neonatal or post-pubertal (but can be any age)
L more common than R
Bilateral = rare
Acute swelling of scrotum Sudden onset, severe pain Lower abdo pain Pain onset during physical activity May be history of this happening before and resolving Nausea and vomiting
What might you see in testicular torsion, when examining the testicle?
Redenning scrotal skin
Swollen, tender testis, retracted upwards
Lifting testis over symphysis increases pain
epididymis may be in anterior position
‘bell-clapper position’
Absence of cremasteric reflex
What investigations would you do for someone with suspected testicular torsion?
COLOUR DOPPLER
MRI
Urinalysis (eliminate other differentials)
Clinical suspicion high, surgical intervention should not be delayed
How would you manage a patient with suspected testicular torsion?
surgical exploration for anyone with high suspicion of torsion
Pt should be NBM
may be able to reduce torsion manually
Bilateral orchiopexy to fix testis in place
How might an ankle sprain present?
Severity depends on severity of sprain
Tenderness and swelling
Bruising
Functional loss (eg. pain on weight-bearing)
Mechanical instability (if severe)
Marked bruising (may indicate ligament tear or fracture)
What are differentials of acute ankle pain?
Achilles tendon injury Joint pathology Tendon injury Stress fractures Fracture
How can you classify (lateral) ankle sprains? (lateral ankle sprains make up 85% of sprains)
Grade I-III
Grade 1: ligament stretched mild swelling
no/little functional loss
no joint instability.
Pt can partially weight bear.
Grade 2: ligament stretched,
partial tearing,
swelling mod-severe, moderate function loss, mild-mod joint instability. Difficulty weight-bearing.
Grade 3: ligament is completely ruptured
swelling is immediate and severe
ecchymosis
Patient cannot weight bear or not without SEVERE pain
Mod-severe instability of the joint
How would you manage someone with an ankle sprain?
Pain relief Functional support (rather than immobilisation, unless severe e.g.. grade 3)
For the first 72 hours: PRICE
P: protection from further injury (eg. bandage, ankle tape, brace, high-top lace shoes)
R: rest ankle joint for 48-72 hours after injury. Consider crutches in this period.
I: apply ICE for about 10-30 mins after injury (NOT directly next to skin). Limits pain, inflammation and bruising)
Try for 15 mins every 2 hours (NOT during sleep)
C: compression bandage, limit swelling
E: elevation to limit and reduce any swelling
Range of motion exercises once not too painful
grade 3 spain may recover better with period of immobilisation first
advise to go to GP if no improvement
What things should you advise a patient to avoid in ankle sprain?
HARM
Heat
Alcohol
Running
Massage
All increase bleeding and swelling risk
What is the common cause of a Colle’s fracture?
FOOSH
How would a Colle’s fracture present?
Dorsal displacement and deformity (dinner fork deformity)
Ulnar styloid tenderness
Other than the obvious dinner-fork deformity, what else should you check in a patient with ?Colle’s fracture?
Ulnar styloid for tenderness Examine elbow (for co-exisiting radial head fracture) Neuromuscular function
How would you investigate a Colle’s fracture?
Xray (at least lateral view)
How would you manage a Colle’s fracture?
Analgesia (but careful as pt. may need to be NBM)
Reduce in emergency department (under sedation): longitudinal traction (pulling wrist) and dorsal pressure
Sedation: midazolam +/- fentanyl (ketamine in children)
Apply back slab
RE-XRAY to check bone alignment (may need to repeat if it is not)
Severely displaced/open-fracture: open surgical repair
Healing time 6-8 weeks
What are the complications of Colle’s fracture?
Medial and ulnar nerve damage
acute carpal tunnel syndrome
compartment syndrome
malunion/non-union
long term: deformity/loss of function/osteoarthiritis
How would you investigate someone with suspected hip fracture?
Bloods: FBC U+Es LFTs Group and save INR (if on warfarin) Clotting
ECG
X-ray hip and pelvis
How might a hip fracture present?
Hip pain
Hx of fall/trauma
Leg: shortened and externally rotated
How would you manage someone with hip fracture?
Urgent X-ray of the pelvis
(within an hour)
Pain relief +++ (fascia iliac block - local nerve block)
Minimal movement
Pressure sore care
Fluids etc. if necessary
C-spine immobilisation (if trauma)
call to surgeons - hemiarthroplasty
VTE prophylaxis (stockings)
What is Gardener’s classification of hip fractures?
Categorises fractures into severity, guiding management
Also predicts development of AVN
Garden stage I : undisplaced incomplete, including valgus impacted fractures.
Garden stage II : undisplayed complete
^ stable fractures, treated with internal fixation
Garden stage III : complete fracture, incompletely displaced
Garden stage IV : complete fracture, completely displaced
^unstable fractures treated with arthroplasty (semi or total)
What is septic arthritis?
Infection producing inflammation in native or prosthetic joint
Can be acute or chronic
Which groups might be more likely to get septic arthritis?
Children (under 5) Immunosuppressed Diabetics IVDU Prosthetic joints/joint surgery (old)
How might septic arthritis present?
single swollen joint with pain on active or passive movement warm joint Fevers or rigors may be present vomiting hypotension may have an abscess bacteraemia chest wall pain (if infected joint around chest)
Triad of fever, pain and impaired range of motion
OFTEN PRESENTS IN THE KNEE
immunosuppressive disease
recent steroid injection
STD
IVDU
What are the differential diagnoses of septic arthritis?
rheumatological disorders gout/pseudogout vasculitis drug-induced arthritis reactive arthritis lyme disease infective endocarditis
How would you investigate a patient with ?septic arthritis?
Bloods: FBC (raised WCC)
ESR and CRP
Synovial fluid examination:
aspirate - crystals, white cells and culture
DON’T ASPIRATE PROSTHETIC
Blood culture Tissue culture PCR Test for lyme disease Immunology
?imaging (X-ray, then ?CT) (for prosthetic joint)
How would you manage a patient with septic arthritis?
Consult microbiologist
Prescribe broad spectrum ABX that covers S. aureus and strep. Flucloxacillin, clindamycin if penicillin allergic.
MRSA - vancomycin
IV 2-3 weeks, switched to oral for 2-4 weeks
How might otitis media present?
More common in children
Ear features: Acute onset ear pain (otalgia)
Middle ear inflammation
Eardrum features:
Effusion or Purulent discharge (can be bloody) - reduce pain once this occurs
Bulging or erythematous tympanic membrane
Fluid level behind tympanic membrane
Perforated tympanic membrane
Hearing features:
Conductive deafness
Tinnitus
Other general features:
previous URTI
Fever
Imbalance
How would you manage a patient with otitis media?
Analgesia (NSAIDS etc).
Early otitis media:
Symptomatic treatment
+/- ABX (if pt. is well, analgesia and symptomatic relief)
ABX: co-amoxiclav
Bulging otitis media:
ABX (co-amoxiclav)
If these fail (or recurrent) = myringectomy (incise tympanic membrane to release fluid build up)
Discharging otitis media:
Antibiotics based on swab and culture
(most resolve within 7-14 days)
Recurrent = gromit insertion
What are common causes of otitis media?
Strep
H. influenza
What are common causes of tonsillitis?
30% bacterial
70% viral
(99% will recover without antibiotics)
Group A streptococcus
What are the symptoms of tonsillitis?
Sore throat, red and inflamed
Enlarged tonsils
Fever
Malaise/lethargy
What investigations might you do for someone with tonsillitis?
Generally no investigations done
throat swab, but this takes time
What investigations might you do for someone with tonsillitis?
Generally no investigations done
throat swab, but this takes time
General obs (check for systemic illness)
How would you manage patient with tonsillitis?
Paracetamol and ibuprofen
Avoid giving ABX unless meet censor criteria OR systemically unwell
Penicillin V (phenoxymethylpenicillin) used if meet criteria Erythromycin if penicillin-allergic
Which ABX should you not give to a patient with tonsillitis? Why?
Amoxicillin
Can cause rash if patient has glandular fever
What are the red flags of tonsilitis/sore throat?
Persistent sore throat for > 6 weeks Excessive drooling Trismus Unilateral facial swelling Dysphagia Dyspnoea Immunosuppressant medication such as carbimazole Persistent unilateral tonsillar enlargement Neck stiffness Photophobia Non-blanching rash
cancer, agranulocytosis
What are the two main presentations of meningococcal disease?
Meningococcal meningitis
Meningococcal septicaemia
What are the features of a meningitis prodrome?
Fever
Nausea and vomiting
Malaise
Lethargy
What are the features of meningococcal meningitis?
Severe headache
Neck stiffness (not always present in young children)
Photophobia
Drowsiness/confusion/impaired consciousness
Seizures (late sign)
Focal neurological deficit, incl. cranial nerve involvement and dilated/unequal/poorly-reactive pupils (late sign)
What generally kills people with meningococcal meningitis?
Raised ICP
What are features of meningococcal septicaemia?
Limb/joint pain Cold hands and feet Prolonged cap refill Plae/blue/mottled skin Tachycardia Tachypnoea, labour breathing, hypoxia Riggers Oliguria/thirst Rash (non-blanching) Abdominal pain (+/- diarrhoea) Drowsiness/confusion/impaired consciousness Hypotension Rapid deterioration
What generally kills people with meningococcal septicaemia?
Cardiovascular failure
How would you manage a patient with meningococcal septicaemia or meningitis?
A: airway may be needed
B: 15L NRB O2 (acutely unwell) Breathing sounds RR Sats ABG
C: blood cultures Cannula IV ABX - ceftriaxone +/- vancomycin (travel abroad or long-term ABX use). Up to 7 days. Fluids (restrict if raised ICP) Anticoagulants if patient has DIC corticosteroids
D: Neurological assessment (incl. pupils)
Blood glucose
AVPU/GCS
E: expose to look at/for rash
feel abdo
May need HDU/ICU bed
On top of treating the patient with meningococcal disease, what else must you do as a clinician?
Contact consultant in communicable disease control or public health medicine
Prescribe ciprofloxacin to close contacts + vaccinations
(prevents further spread FROM contacts as opposed TO contacts)
What investigations might you do on someone who’s ?mengingococcal disease
Blood cultures FBC (WCC and platelets ) CRP U+Es Renal function tests LFTs Clotting (aPTT, fibrinogen) - investigating ?DIC
PCR for N. meningitidis (use earliest sample possible)
Pharyngeal swab
Lumbar puncture (once stable) - check for ICP. Microscopy, culture, glucose and PCR. DO THIS EARLY IF MENINGITIS SUSPECTED, LATER IF SEPTICAEMIA
Which signs in meningococcal disease require URGENT review by senior +/- critical care review?
Rapidly progressive rash
Capillary refill time > 4 secs,
oliguria or systolic BP
< 90mmHg
Respiratory rate < 8 or >30
Pulse rate < 40 or >140
Acidosis pH < 7.3 or Base excess worse than -5
White blood cell count <4x109/L
Lactate > 4 mmol/L
Glasgow coma scale <12 or a drop of 2 points
Poor response to initial fluid resuscitation
what are some causes of diarrhoea?
Short-term:
virus
Bacterial (eg. food poisoning)
parasites (eg. giardiasis)
Anxiety Alcohol excess Allergy Appendicitis Radiotherapy
Drugs: ABX Antacids (containing magnesium) Chemo NSAIDS SSRIs Statins Laxatives
Long term: IBS IBD Coeliac disease Bile acid malabsorption Chronic pancreatitis Diverticular disease Bowel cancer
What counts as diarrhoea?
Stools more than 3 times a day
Stools become loose or watery
How would you manage diarrhoea?
Fluids (if dehydrated)
Loperamide
What is giant cell arteritis?
systemic immune-mediated vasculitis affecting medium and large-sized arteries
How might giant cell arteritis present?
Temporal headache (recent onset). Severe. Sometimes worse at night.
myalgia
malaise
fever
Jaw or tongue claudication
Enlarged, beaded or pulseless temporal artery
Scalp tenderness
Raised ESR
Anaemia
Visual disturbance (inflammation of ophthalmic artery, ischaemic optic neuritis): blurred vision, amaurosis fugax, transient or permanent visual loss, diplopia. Ischaemic changes may be seen on fundoscopy)
Classic presentation: over age of 50 scalp tenderness transient visual symptoms unexplained facial pain
CAN RESULT IN LOSS OF VISION
Systemic symptoms: weight loss, fever, sweats, carotid bruits
What investigations might you do for someone with ?GCA?
Bloods: FBC (normocytic normochromic anaemia)
LFTs
ESR
CRP
Temporal artery biopsy
Colour duplex ultrasonography
What criteria must be present to diagnose someone with GCA? How many need to be met to make the diagnosis?
Age of disease onset: >=50 yrs
New onset headache
Temporal artery abnormality
ESR >= 50 mm/hr
Abnormal artery biopsy
3/5 must be present to make the diagnosis
How would you manage a patient with GCA?
High dose corticosteroids
40mg prednisilone daily unless patient has iscahemic symptoms
Claudication/ischaemic symptoms: 60 mg
Visual symptoms: IV methyprednisilone
Once symptoms reduce - reduce slowly.
Low dose aspirin 75mg + PPI
How does a subarachnoid haemorrhage present?
Sudden onset headache (usually occipital) INTENSE from start Neck stiffness Vomiting Extensor plantar responses Impaired consciousness (usually shortly after onset, but can be after several hours) Cranial nerve signs Hemiplegia Hypertension
(sentinel headache)
Symptoms of stroke (following vasospasm after SAH - causing ischaemia)
What investigation would you do for someone with ?SAH?
CT (able to detect >90% lesions within 48 hours of onset). NON-CONTRAST
bleed found: angiography
Lumbar puncture (if CT negative, but strong clinical suspicion) - looking for xanthochromia (yellow CSF)
ECG
Bloods: Billirubin
How should you manage a a patient with SAH?
Call:
Med reg
neurosurgeon on call
anaesthetist (depending on GCS)
Stabilise patient haemodynamically
A-E
Prevent re-bleeding: nimodipine 60mg 4-hrly
low dose nitroprusside (vasodilator) and labetalol - maintain cerebral perfusion (but not enough to encourage re-bleeding)
Analgesia
Anti-emetics
Surgery: clipping (craniotomy) and coiling (clips around aneurysm via femoral catheterisation)
What is a stroke?
Sudden onset of brain dysfunction
Caused by alteration in cerebrovascular blood supply
How might a stroke present? (generally speaking)
Rapid, acute onset neurological changes eg. hemiplegia
What are the two main types of stroke?
Brain ischaemia (80-90%) Haemorrhage (10-20%)
What are the main causes of stroke?
Arterial embolism
Haemorrhage (cerebrum itself or SAH)
What are some risk factors for stroke?
Afro-carribean/asian Male Age HTN Smoking AF Diabetes Alcohol hypercholesterolaemia/hyperlipideamie Obesity heart disease FHx
When do most strokes occur?
BP lowered during the night whilst asleep
On waking, BP rises, more likely to dislodge any embolism
Where is the most common location for cerebral infarct to occur? How would this present?
Middle cerebral artery
Hemiparesis hemiplegia floppy limbs, lack reflexes reduced/absent Facial weakness hemianopia aphasia
symptoms usually develop rapidly. Recovery will occur gradually, over days, weeks etc. Longer time = worse prognosis
not usually a headache (if present, implies swelling, implies haemorrhage)
not usually any LOC
seizure v. rare
Reflexes reappear, but exaggerated
Extensor plantar response
What symptoms might you see in patient with anterior cerebral artery infarct?
weak leg +/- shoulder
CONTRALATERAL side
What symptoms might you see in patient with posterior cerebral artery infarct?
eye problems
What symptoms might you see in patient with a brainstem infarct?
(depends on location, but selection of symptoms):
semi/tetraparesis sensory loss diplopia facial numbness facial weakness nystagmus and vertigo dysphagia and dysarthria hornet's syndrome altered consciousness
coma
locked-in syndrome (loss of all motor neurone function)
pseudo bulbar palsy (dysarthria and dysphagia)
What symptoms may present with lacunar infarct?
Often symptomless
Very localised symptoms eg. purely sensory or purely motor
aphasia
hemiparesis
hemisensory loss
unilateral ataxia
How would you investigate suspected stroke?
CT:
infarctions = wedge shape
haemorrhage = blood appears bright white initially, gets darker over time. 1-2 weeks later = indistinguishable from normal brain tissue
New stroke <2 hours old, may not show up at all. 6-12 hours, will be clearly visible.
BP (manage)
ECG (looking for AF)
CXR (heart size), echo
Blood (rule out differentials): ESR (raised - ?GCA) FBC/platelets/clotting glucose cholesterol/lipids
How might a cerebral haemorrhage present?
Similar to infarct picture BUT
more likely to lose consciousness, headache
progressive neurological defects
Hydrocephalus (blood leaks in to ventricular system)
How would you manage ischaemic stroke?
A-E
Thrombolysis (if possible)
If unable to thrombolyse: 300mg aspirin for 2 weeks then 75mg a day (if not aspirin, clopidogrel)
Dipyridamole
Warfarin or NOAC in long-term
How would you manage haemorrhage stroke?
A-E
Mostly supportive
If anticoagulants and antiplatelets have been given, reverse with fit K, fresh frozen plasma and platelet transfusions
haemorrhagic mass >3cm = surgery (drain or craniotomy)
Manage BP is SBP>185mmHg
What are the clinical features of a DVT?
(result of obstruction to venous drainage)
Limb pain
Tenderness along line of deep veins
Swelling of calf or thigh (usually unilateral)
Bilateral - thrombosis in iliac bifurcation, pelvis veins or vena cava
Pitting oedema
Distension of superficial veins
Warm limb
Skin discolouration (erythema or cyanosed)
Palpable cord (hard, thick palpable vein)
Severe DVT: cellulitis-like
can also have cellulitis (as secondary to DVT or primary, leading to DVT)
What differentials might present similar to DVT?
Trauma Superficial thrombophlebitiis peripheral oedema, heart failure, cirrhosis, nephrotic syndrome venous/lymphatic obstruction vasculitis cellulitis septic arthritis
How would you investigate a patient with suspected DVT?
Depends on level of risk (calculated by a two-level Well’s score)
General bloods: FBC PT INR/APTT Renal function LFTs
How would you investigate a patient who has suspected DVT and a LIKELY two-level DVT Well’s score? (>=3)
Doppler US leg
D-dimer (if doppler -ve)
How would you investigate a patient who is at low risk of DVT? (<3 on two-level Well’s score)
D-dimer test
If positive: doppler US leg
(wouldn’t be done if D-dimer was negative)
If doppler US is negative and Wells score 1-2, reassess using US scan in 5-7 days time.
How would you manage someone with DVT?
Analgesics (avoid aspirin and NSAIDS)
LMWH (deltaparin, enoxaparin, tinzaparin) - start this immediately if diagnosis of DVT is likely on clinical grounds before definitive investigation
OR
Fondaparinux
For at least 5 days (or until INR 2
What are some contra-indications to anticoagulation that you need to consider when prescribing LMWH?
Active peptic ulceration alcohol excess liver disease PT>2 secs beyond normal range Thrombocytopenia (platelets <80) Uncontrolled hypertension (>180/100) Ophthalmic/neurosurgical intervention recently Hx of haemorrhage stroke biopsies pregnancy
What is included in Two-level DVT Wells score?
Each score one point, except final point, which is -2
Active cancer (treatment on-going or within 6 months OR palliative)
Paralysis, paresis or recent plaster immobilisation
Recently bed-ridden for 3 days or more
Major surgery within 12 weeks, requiring general or regional anaesthesia
Localised tenderness long distribution of deep venous system
Entire leg swollen
Calf swelling at least 3x larger than asymptomatic leg
Collateral superficial veins (non-varicose)
Previously documented DVT
An alternative diagnosis is at least as likely as DVT (-2)
What can cause vasovagal syncope?
Emotional: feat, pain, phobia, sudden unexpected sight sound or smell
Orthostatic: prolonged standing, hot places
What might people described in a history of vasovagal syncope?
Brief LOC
Warning: light-headedness, nausea, sweating, weakness, visual disturbance
No chest pain or SOB, not during exercise
Almost immediate restoration of appropriate behaviour and orientation (pt. might be v. tired)
Might be Hx of new medications
Syncope may be more likely in morning
Differential diagnosis?
Other causes of syncope Epilepsy Narcolepsy Drop attacks TIA
How would you investigate a patient with ?vasovagal syncope?
Many investigations to rule-out serious causes of harm.
BP measurement (lying and standing)
Bloods: FBC, blood glucose
ECG
What would you want to know about a patient to determine risk of severe cardiac problems in syncope?
coronary heart disease ECG changes (broad QRS, prolonged QT interval, non-sustained VT) Syncope during exercise or supine palpitations FHx of sudden cardiac death HR<50
How would you manage a patient with Vasovagal syncope?
Reassure and educate:
Avoid prolonged standing in warm environments
Avoid hot baths
At first sign of collapse: Lie down, legs in air
Sit agains wall, head between knees
squat down on heels
get up very carefully, return to position if feeling unwell again
How would you manage someone with high-risk NSTEMI or STEMI?
A-E assessment and management
MONAT
Morphine Oxygen (if sats <94% or 90% (COPD)) Nitrates (usually IV in NSTEMI/unstable angina) Aspirin (300 mg) Ticagrelor
After acute event, when stable:
beta-blocker
ACEi
Statins
How would you manage a patient with unstable angina?
A-E assessment and management
MONA
Morphine
Oxygen (if sats <94% or 90% (COPD))
Nitrates
Aspirin
What should your first actions be in cardiac arrest?
Call for help (ask them to call 2222)
Begin CPR
Administer oxygen if available
Attach defib, establish rhythm
Which rhythms are shockable in cardiac arrest?
VF
VT
If after sticking on Defib, you are told your rhythm is shockable, what should you do?
administer defibrillation
Immediately resume CPR for 2 mins
Establish vascular access
Recheck shockable rhythm after 2 mins. Shockable: shock.
Give 1mg IV adrenaline every 3-5 mins
Consider ET tube
Continue CPR for 2 mins
Check shockable rhythm: shock
CPR 2 mins
Amiodarone 300mg (after 3rd shock)
Establish and treat reversible cause
Which rhythms aren’t shockable?
PEA
Asystole
Once you’ve found out a rhythm isn’t shockable in cardiac arrest, what would you do?
Resume CPR for 2 mins
Establish IV access
Give IV adrenaline 1mg every 3-5 mins
Consider ET tube
Check whether rhythm shockable: no = return to CPR for 2 mins
establish and treat reversible causes
Continue to give IV adrenaline 1mg every 3-5 mins
Repeat process until shockable rhythm, ROSC or calling
What should you do if your rhythm suddenly becomes shockable/un-shockable in cardiac arrest?
Switch to other half of algorithm
What are the key drugs and doses to remember in cardiac arrest?
Adrenaline 1 mg every 3-5 mins
(give immediately in non-shockable, give after 2 shocks in shockable)
Amiodarone 300 mg first dose
2nd dose 150 mg
Give after third shock
What are the reversible causes of cardiac arrest?
5 H’s and T’s
H Hypoxia Hypovolaemia Hydrogen ions (acidosis) Hypo/hyperkalaemia Hypothermia
T Tamponade Tension pneumothorax Toxins Thrombosis (cardiac or pulmonary) Trauma
How would you manage a patient with HR>=150 (with pulse) with adverse features? (shock, syncope, MI or heart failure)
Cardioversion - synchronised DC shock. Up to 3 attempts.
After this, seek expert help.
Give amiodarone 300 mg IV over 10-20 mins
Repeat shock
Give amiodarone 900mg IV over 24 hours
How would you manage a patient with a regular broad QRS complex HR>=150 (with pulse) with NO adverse features? (shock, syncope, MI or heart failure)
VT (or uncertain rhythm):
amiodarone 300mg IV over 20-60 mins
THEN
900mg over 24 hours
(If SVT+BBB, treat like narrow-complex tachy)
How would you manage a patient with a irregular broad QRS complex HR>=150 (with pulse) with NO adverse features? (shock, syncope, MI or heart failure)
CALL FOR HELP
How would you manage a patient with a regular narrow QRS complex HR>=150 (with pulse) with NO adverse features? (shock, syncope, MI or heart failure). What are the likely causes of this rhythm?
Vagal manoeuvre: head down or blow in to syringe Adenosine 6mg rapid IV bolus no effect: 12 mg No effect: 12 mg (monitor with ECG continuously)
Sinus rhythm achieved -
record ECG of sinus rhythm
consider anti-arrhythmic prophylaxis
Probably re-entry paroxysmal SVT
If sinus rhythm NOT achieved - seek expert help
Consider rate control (beta-blocker)
?consider cardioversion
Probable atrial flutter
How would you manage a patient with a irregular narrow QRS complex HR>=150 (with pulse) with NO adverse features? (shock, syncope, MI or heart failure). Which rhythm is likely to cause this?
AF
Control rate with beta blocker or diltiazem
In heart failure: digoxin or amiodarone
Assess VTE risk, consider anticoagulation
What are the different types of SVT?
Regular: sinus tachy atrial flutter Sinus node re-entrant tachy Atrioventricular re-entry tachycardia (AVRT eg. WPW syndrome) AV nodal re-entry tachycardia (AVNRT) Automatic junctional tachycardia
Irregular:
AF
atrial flutter with variable block
How would you initially treat someone with bradycardia with adverse features? (shock, syncope, myocardial ischaemia, heart failure)
A-E assessment Oxygen IV access ECG BP SpO2 Identify and treat reversible causes.
Atropine 500 mcg IV
How would you initially treat someone with bradycardia with NO adverse features? (shock, syncope, myocardial ischaemia, heart failure)
A-E assessment Oxygen IV access ECG BP SpO2 Identify and treat reversible causes.
Work out risk of asystole: recent asystole mobitxz II AV block Complete heart block with broad QRS Ventricular pause >3s
No risk: observe
Risk: Atropine 500 mcg IV repeat to max of 3mg OR Isoprenaline 5mcg/min IV Adrenaline 2-10mcg/min IV alternative drugs OR transcutaneous pacing
Seek expert help
What would you do if initial management of someone with symptomatic bradycardia (atropine 500mcg IV), didn’t work?
Atropine 500 mcg IV repeat to max of 3mg OR Isoprenaline 5mcg/min IV Adrenaline 2-10mcg/min IV alternative drugs OR transcutaneous pacing
Seek expert help
How might shoulder dislocation present?
Hx of trauma
Pain
Anterior: Externally rotated arm
loss of shoulder roundness
anterior bulge
humeral head palpable anteriorly
abduction and internal rotation are resisted
may have loss of sensation in regimental badge area
Posterior: arm adducted and internally rotated
Posterior bulge
humour head palpable below acromion process
abduction and external rotation are painful
inability to externally rotate to neutral position and supinate
What things should you check on examination of someone with ?anterior shoulder dislocation?
radial pulse (assess vascular injury)
regimental badge area (axillary nerve damage)
thumb, wrist and elbow weakness on extensions and sensation on dorm of hand (radial nerve function)
rotator cuff (once joint is reduced)
How would you investigate shoulder dislocation?
x ray (AP and axillary or transcapular view)
How would you manage someone with shoulder dislocation?
Analgesia and sedation:
opiate and benzo
reduction
fracture dislocation: surgery
List some causes of AF
Cardiac: HF MI hypertension mitral valve disease congenital
Pulmonary:
PE
pneumonia
bronchocarcinoma
Other: hyperthyroidism alcohol post-op sepsis caffeine anti-arrhythmias hypoK hyperMg
LONE
How might AF present?
palpitations chest pain SOB dizziness syncope
Irregularly irregular pulse
apical pulse rate > radial pulse rate
signs of LV dysfunction
What might you find on an ECG of someone with AF?
no P waves irregular QRS - regular shape HT 75-190 bpm normal T waves V1 looks like atrial flutter
What investigations should you do for someone with AF?
ECG
Bloods: FBC (rule out anaemia as cause of palpitations)
U+Es
TFTs
Cardiac enzyme
Echo
How might you manage someone with an acute presentation of AF?
<48 hours after onset of symptoms
A-E
treat underlying cause
Control rate
Initiate anticoagulation (heparin)
Consider DC or chemical cardioversion
Acutely unwell: cardioversion in ITU with sedation
what drug is given for chemical cardioversion in AF?
Amiodarone IV 5mg/Kg in 1 hr, then 900mg-1.2g in a 24 hour period
Amiodarone PO 200mg/8hr for 1 week then 200mg/12hr for one week then 200mg/day maintenance
Can also use flecainide
What can cause atrial flutter?
atrial dilation open heart surgery HTN obesity alcohol abuse COPD cardiomyopathy atrial myxoma pericarditis thyrotoxicosis electrolyte imbalance sleep apnoea
How might atrial flutter present?
palpitations fatigue dyspnoea chest pain dizziness syncope heart failure TIA/stroke Pulse may be regular or irregular or regular pulse tachycardia signs of underlying cause HF hypotension
How would you investigate someone for ?atrial flutter?
Bloods: FBC U+E TFTs ESR LFTs coagulation screen
ECG: saw-tooth flutter waves II, III and aVF
Echo
How would you manage a patient with atrial flutter?
rate control - medications or cardioversion
treat underlying conditions
anticoagulation (like in AF)
What is cerebral venous sinus thrombosis?
acute thrombosis in dural venous sinuses (which drain blood from brain)
List some symptoms of cerebral venous sinus thrombosis
Headache (sudden to gradual onset)
ophthalmoplegia (papilloedema) and/or diplopia (usually unilateral to start with)
seizures (can be unilateral)
stroke-like symptoms: hemiparesis, lower limb weakness, aphasia and ataxia
Facial pain
pulsatile proptosis
hornet’s syndrome
Raised ICP: reduced consciousness, HTN, reduced HR
List some causes of venous sinus thrombosis
thrombophilia nephrotic syndrome chronic inflammatory diseases pregnancy and puerperium oestrogen-containing contraception meningitis and ENT infections
How would you investigate someone with ?cerebral venous sinus thrombosis?
Bloods: FBC (Hb may be elevated, WCC and platelets may be elevated)
U+E
LFTs
D-dimer
Urine dip
CT venogram (normal CT often appears normal)
ECG
How would you manage a patient with venous sinus thrombosis?
Elevate hear 30-40 degrees to help reduce intracranial pressure
anti-convulsants if seizures present
LMWH initially IV or SC
warfarin once patient stable
Severe: thrombectomy, endovascular therapy
What are signs of raised ICP?
headache: nocturnal, starting on waking, worse on coughing or moving head, altered mental state
Changes to mental state: lethargy, irritability, slow decision making, abnormal social behaviour
Vomiting
Pupillary changes
Fundoycopic changes eg. blurred disc margins, haemorrhages
unilateral ptosis
hemiparesis
raised BP, widened pulse pressure
bradycardia
How can raised ICP present acutely?
Head injury syncope headache meningism focal neuro deficit seizures
talk and deteriorate - talk and then go in to coma
How would you investigate a patient with suspected raised ICP?
GCS
CT scan
How would you manage a patient with raised ICP?
avoid pyrexia (hypothermia) manage seizures CSF drainage (intraventricular catheter) elevation of head analgesia and sedation neuromuscular blockade (reduce muscle activity, which can cause raised ICP)
Mannitol: intravascular osmotic agent
Hypertonic saline (3-30%)
Hyperventilation
decompressive craniotomy
How might a space-occupying lesion in the cerebellum present?
cerebellar ataxia intention tremor past-pointing dysdiadochokinesis nystagmus staccato speech
How might a space-occupying lesion in the temporal lobe present?
depersonalisation epilepsy deja vu dysphasia visual field defects forgetfulness fugue
How might a space-occupying lesion in the frontal lobe present?
anosmia
change in personality
dysphasia
hemiparesis or fits on contralateral side
How might a space-occupying lesion in the parietal lobe present?
hemisensory loss two-point discrimination stereognosis extinction neglect dysphasia
How might a space-occupying lesion in the occipital lobe present?
visual defeat - specific one depends on whereabouts lesion is
How might a pituitary tumour present?
homonymous hemianopia
endocrine changes
How would you investigate someone for a space-occupying lesion?
Bloods: FBC U&E LFTs CT head Biopsy of lesion
If unsure of primary tumour: CXR
mammography/ultrasound
Causes of space-occupying lesions:
malignancy haematoma hydrocephalus cerebral abscesses (RF: COPD) Cysts
How would manage a space-occupying lesion?
treat underlying cause
manage raised ICP
treat complications and symptoms of raised ICP
What is AKI?
Rise in serum creatinine >26 within 48 hours
OR
rise in serum creatinine 1.5 x baseline value within 1 week
OR
urine output <0.5ml/Kg/hr for 6 consecutive hours
What are the criteria for stage 1 AKI?
Rise in serum creatinine greater than 26 µmol/L within 48 hours
or
Rise in serum creatinine greater than 1.5-1.9 × baseline value
or
Urine output less than 0.5 ml/kg/hr for 6 hours
What are the criteria for stage 2 AKI?
Rise in serum creatinine greater than 2-2.9 × baseline value
or
Urine output less than 0.5 ml/kg/hr for 12 hours
What are the criteria for stage 3 AKI?
Rise in serum creatinine greater than 3 × baseline value
or
Rise of serum creatinine greater than 354 µmol/L
or
Commenced on renal replacement therapy
or
Urine output less than 0.3 ml/kg/hr for 24 hours or anuric for 12 hours
What are some risk factors for AKI?
Age greater than 75 years
Chronic kidney disease (estimated glomerular filtration rate < 30)
Hypertension (one or more anti-hypertensive drugs)
Cardiac failure
Liver disease
Diabetes Mellitus
Nephrotoxins (e.g. NSAIDs, gentamicin, iodinated contrast)
Hypovolaemia
Sepsis
List some pre-renal causes of AKI:
Hypovolaemia (vomiting, diarrhoea, burns, haemorrhage)
Hypotension
Sepsis
Cardiac failure
List some intrinsic caused of AKI:
Prolonged hypo-perfusion Nephrotoxins Glomerulonephritis Vasculitis Interstitial nephritis
List some post-renal causes of AKI:
Obstruction (renal stones, retro-peritoneal fibrosis, bladder cancer, pelvic mass, enlarged prostate)
How might AKI present?
Reduce urine output
Other signs of hypovolaemia: Hypovolaemia - assess volume status (capillary refill time, pulse, blood pressure, jugular venous pressure, skin turgor, pulmonary oedema, peripheral oedema, urine output, weight)
Palpable bladder?
Signs of vasculitis (weight loss, fever, rash, uveitis, haemoptysis, joint swelling)
Bruits (renal artery stenosis)
How would you investigate someone you suspect has AKI?
FBC U&Es Bicarbonate LFTs Calcium Phosphate Consider blood cultures if sepsis suspected
Urine dipstick (presence of blood and protein suggests infection or vasculitis)
Chest X-Ray (pulmonary infiltrates could indicate fluid, infection or haemorrhage)
Renal tract ultrasound (assess renal anatomy and exclude renal tract obstruction)
How would you manage someone with AKI?
STOP V:
Sepsis - complete BUFALO if suspected
Toxins - stop/avoid nephrotoxins eg. gentamicin, NSAIDS, iodinated contrast
Optimise blood pressure
Prevent harm - treat complications eg. hyperkalaemia, pulmonary oedema, acidosis, pericarditis
identify cause and treat
review all medications and doses
refer if renal replacement therapy necessary
monitor: daily volume assessment, fluid balance, U+Es and bicarbonate
What are common indications for renal replacement therapy?
intractable hyperkalaemis pH <7.15 intractable pulmonary oedema uraemia pericarditis encephalopathy
What is acute urinary retention? How might it present
inability to urinate in presence of painful bladder
Bladder might be distended, dull to percussion
well above symphysis pubis, almost at level of umbilicus
infected or malformed genitals
faecal impaction
reduced lower limb power and perineal sensation (cord compression or prolapsed disc)
What are common causes of acute urinary retention?
children: abdo pain, drugs
young people/adults: drugs, surgery, UTI, trauma, haematuria, constipation, kidney injury
elderly: surgery, tumour, BPH, kidney injury
How would you investigate someone for acute urinary retention?
Bloods: FBC
U+Es
creatinine
Urine: MSU
Bladder scan (quantify urine retained)
cystography
urodynamics
How would you manage someone in acute urinary retention?
catheterisation
treat underlying cause