Acute

Question 1

Primary survey

Answer 1

Airway: Protect cervical spine

Assess patency + manage

Breathing: Check resp rate, chest expansion, auscultation, percussion

If no resp effort-> tx as arrest, intubate and ventilate

If compromised-> high concentration O2 (15L)

Circulation: Check pulse, BP, capillary refill, evidence of haemorrhage

Tx shock. IF no CO-> treat as arrest

Disability: AVPU score and pupils (size, reactivity)

GCS if time

Exposure: Undress but cover (prevents hypothermia)

Get hx from relatives, surrounding events, PMH (diabetes, asthma, COPD, alcohol, opiate or st drugs, recent head injury, epilepsy, travel), PDH, allergies. After resuscitation get full hx. (AMPLE)

Question 2

Pneumonia: General Management

Answer 2

Pneumonia:

1. ABCDE
2. Oxygen to maintain PaO2>8
3. Tx hypotension and shock
4. Invx- CXR, O2 sats, ABGs, FBC, U&E, LFTs, CRP, atypical serology, Blood cultures, pleural fluid aspirate, brochonscopy and bronchiolar lavage if immunocompromise
5. Calculate CURB-65
6. Abx co-amoxiclav 1.2g/8h IV AND clarithromycin 500mg/12h IVI. For legionella add levofloxain + rifampicin. For Chlamydia add tetracycline. For PCP add co-trimoxazole. If hospital acquired consider IV gentamicin + antipseudomonal penicillin
7. IV fluids may be required
8. Analgesia for pleuritic chest pain e.g. paracetamol 1g/6h or NSAID
9. Some patients may need intubation and a period of ventilator support.

Question 3

Meningitis: General Management

Answer 3

Meningitis: (/meningococcal sepsis=sepsis 6)

• ABC
• High flow O2 and fluid resus
• Ask nurse to draw up cefotaxime 2g; if immunocompromised/age 55+ then add ampicillin 2g/6h
• Invx- U&E, LFT, glucose, coagulation screen, blood culture, throat swabs, rectal swab for viral serology. If aseptic meningitis you would do viral serology.
• If mainly septicaemic signs (reduced capillary refill, cold hands and feet):
• DO NOT attempt LP
• Cefotaxime 2g IV
• Help from critical care team
• If there are signs of shock take to ITU for fluid resuscitation, pre-emptive intubation, inotropes/vasopressors and activated protein C. Aim for a BP of >80 and urine flow of >30mL/h.
• If meningitic signs predominate:

Dexamethasome 4-10mg/6h IV

If signs of raised ICP take to ITU (NO LP)

If no shock or ICP do LP

2g cefotaxime

Nurse at 30 degrees; have a low threshold for intubation; don’t rely on CT to rule out raised ICP

• Careful monitoring and repeat review
• Cefotaxime 2-4g/8h IVI e.g. for 10d, with less dose in renal failure
• Maintenance fluids
• If poor response consider intubation/ventilation and inotropic/vasopressor support.
• For people who have kissed the patient’s mouth and household contacts give rifampicin 600mg/12h for 2d or ciprofloxacin 500mg PO 1 dose

Question 4

Status Epilepticus: General MAnagement

Answer 4

Status epilepticus:

1. Open an maintain the airway, lie in the recovery position
2. Remove false teeth if poorly fitting, insert oral/nasal airway, intubate if necessary
3. Oxygen, 100% + suction
4. IV access and take blood- U&E, LFT, FBC, glucose (e.g. BM test), Ca2+, toxicology screen if indicated, anticonvulsant levels
5. Thiamine 250mg IV over 10 mins if alcoholism or malnourishment expected. Glucose 50mL 50% IV, unless you know the glucose is normal
6. Correct hypotension with fluids
7. Slow IV bolus phase- to stop seizures e.g. lorazepam 2-4mg. Second dose of lorazepam if no response within 2min
8. IV infusion phase- if seizures continue start phenytoin 18mg/kg at a rate of <50mg/min. Monitor ECG and BP.
9. If fits continue, diazepam 100mg in 500mL of 5% dextrose
10. Dexamethasone 10mg IV if vasculitis/cerebral oedema possible
11. Continuing seizures require expert help with paralysis and ventilation with continous EEG monitoring in ITU
12. After the seizures are controlled switch to oral therapy

Question 5

Pulmonary embolism: General Management

Answer 5

Pulmonary embolism:

1. 100% O2
2. Obtain IV access, monitor closely, start baseline invx- U&E, FBC, clotting, ECG, CXR, ABG, serum D-dimer, CTPA/VQ scan
3. Morphine 10mg IV with antiemetic if pain or distress
4. Suspect massive PE if systolic BP<90 or fall of 40mmHg for 15min
5. If critically ill with massive PE consider immediate thrombolysis (e.g. 50mg bolus of alteplase) or surgery
6. IV access and heparin e.g. LMWH tinzaparin 175u/kg/24h
7. Get senior help
8. If BP>90 start warfarin 10mg/24h
9. If BP<90 start rapid colloid infusion. If BP still low after 500mL colloid give dobutamine 2.5-10microgram/kg/minn IV. If STILL low consider noradrenaline. If STILL low and you’re pretty sure its a PE consider starting thrombolysis.
10. Future prevention with compression stockings
11. Use heparin+ warfarin at least 5 days. Stop herapin when INR>2. If clear cause, warfarin is given for 6 weeks; otherwise at least 3-6m. Is there an underlying cause?
12. LMWH prophylaxis postop. Avoid COCP is at risk undergoing surgery. Recurrent PEs are prevented by anticoagulation.

Question 6

DKA: General Management

Answer 6

Diabetic ketoacidosis:

1. ABC
2. Check plasma glucose- if >20 give 4-8u soluble insulin IV
3. Tests- lab glucose, U&E, HCO3, osmolality, amylase, blood gases, FBC, blood culture. Check urine ketones, MSU, CXR
4. Set up IVI- 1L stat, then 1L over the next hour, 1L over 2 hours, 1 L over 6h- adjusted according to urine output. Use 5% dextrose when blood glucose is <10.
5. NG tube if nauseated/vomiting/unconscious
6. Insulin pump dilute to 1unit/mL start at around 6units/h for an average adult. Expect blood glucose to drop by around 5 mmol/hour. When blood glucose<10, reduce rate to 3units/h and continue until food by mouth is possible. Don’t stop the pump before routine sc insulin has been started. If there is no pump load with 20u IM, then give 4-6u/h IM while glucose is >10.
7. Check GCS, glucose, U&E and HCO3 regularly, urine output
8. Continue fluid replacement and K+ replacement (remember don’t add K+ to the first bag)
9. Give LMWH until mobile
10. Change to SC insulin when ketones <1 and eating

Question 7

Acute Upper GI bleed: General management

Answer 7

Acute upper GI bleeding:

1. ABC
2. Is patient shocked (cool and clammy, pulse >100, JVP<1cm, BP<100, postural drop>20, urine <30ml/h)? If NOà 2 large bore cannulae with slow saline IVI to keep them patent, check bloods and monitor vital signs and urine output. Otherwise, proceed as below
3. Protect the airway and keep NBM
4. Insert 2 large bore cannulae 14-16G
5. Draw bloods, FBC, U&E, LFT, glucose, clotting screen. Xmatch 6units.
6. High flow O2
7. Rapid IV crystalloid infusion up to 1L
8. If remains shockedà give blood
9. Otherwise slow saline infusion
10. Transfuse as directed by haemodynamics
11. Correct clotting abnormalities- vitamin K, FFP, platelet concentrate
12. Risk assessment- Rockall score- age, comorbidity, liver disease, haemodynamic disturbance, continued bleeding, elevated blood urea
13. Set up CVP line to guide fluid replacement- aim for >5cm H20.
14. Catheterise and monitor urine output, aim for 30mL/h
15. Monitor vital signs every 15 mins until stable, then hourly
16. Notify surgeons of all major bleeds
17. Endoscopy- within 4h if you suspect variceal bleeding and within 12-24h if shocked on admission with significant comorbidity. During endoscopy you can give an injection of 1:10,000 adrenaline, thermocoagulation or endoscopic clipping
18. If variceal bleeding: urgent endoscopy for diagnosis and control of bleeding- banding/sclerotherapy. Give terlipressin 2mg before and after endoscopy. If there is a massive bleed or bleeding continues, pass a Sengstaken-Blakemore tube.
19. Post-endoscopy give high dose IV PPI e.g. omeprazole 80mg bolus followed by an 8h infusion for 72h in patients with major peptic ulcer bleeding
20. Discontinue NSAIDs if possible and start concomitant PPI therapy. Test patients with peptic ulcer bleeding for H. Pylori and give eradication therapy if appropriate.

Question 8

Coma: causes

Metabolic/neurological

Answer 8

Metabolic Causes: Drugs, poisoning (CO, alcohol, tricylics)

Hypo/hyperglycaemia

Hypoxia, CO2 narcosis

Septicaemia

Hypothermia

Myxoedema, Addisonian crisis

Hepatic/uraemic encephalopathy

Neurological causes: Trauma

Infection- meningitis, encephalitis (e.g. HSVà acyclovir), malaria, typhoid, typhus, rabies, trypanosomiasis

Tumour

Vascular-stroke, subdural/subarachnoid hypertensive encephalopathy

Epilepsy- non-convulsive status or post-ictal state

Question 9

Coma Management

Answer 9

1. ABC

Intubate if GCS<8, IV fluids if needed

Give O2

1. IV access
2. Stabilise cervical spine
3. Blood glucose
4. Control seizures
5. Tx reversible causes e.g. IV 50ml 50% glucose/ thiamine/ naloxone 0.4-2mg IV/ flumezanil (IF airway compromise)
6. Brief examination- signs of trauma, stigmata of other illness (e.g. alcoholic liver disease), skin (needle marks/cyanosis/pallor/rash/diabetes), breath (alcohol, hepatic fetor, ketosis, uraemia, opisthotonos, meningism, pupils, chest exam, abdo exam, foci of infection, meningitis, neuro exam
7. Brief hx- speed of onset? Suicide note? Seizure? Recent headache/fever/vertigo/ depression? Recent surgery for sinusitis/otitis/neurosurgery/ENT? PMH- diabetes/asthma/HTN/cancer/epilepsy/psychiatric illness, PDH, travel
8. Invx- ABG, FBC, LFT, ESR, CRP, ethanol, toxic screen, drug levels, blood/urine culture, consider malaria, CXR, CT
9. If unclear diagnosis, tx treatableà Pabrinex, Naloxone, Cefotaxime (sepsis), Artemether/quinine (malaria), acyclovir (HSV)
10. Reassess and arrange further invx

Question 10

Hypothermia: General Management

Answer 10

1. Check oral/axillary temp
2. Urgent U&E/plasma glucose/amylase/TFT/blood culture/ECG
3. Ventilate if comatose/resp insufficiency
4. Cardiac monitoring
5. ?abx to prevent pneumonia. Always in patients >65y with temp <32.
6. ?urinary catheter to monitor renal function
7. Slow rewarming- hot drinks etc
8. Twice hourly rectal temp/BP/pulse/resp rate
9. IF there is sudden hypothermia from immersion, there has been cardiac arrest and temp<30 so you may need mediastinal warm lavage, peritoneal or haemodialysis and cardiopulmonary bypass
10. Before discharge review meds, liaise with GP

Question 11

Raised Intercranial Pressure: General Management

Answer 11

Raised intracranial pressure:

1. ABC
2. Correct hypotension and tx seizures
3. Brief examination; hx if available
4. Elevate the head of the bed to 30-40 degrees
5. If intubated, hyperventilate to reduce PaCO2
6. Osmotic agents- mannitol 20% solution 102g.kg IV over 10-20min
7. IF the problem is oedema surrounding a tumour, give dexamethasome
8. Fluid restrict to <1.5l/d
9. Monitor patient closely
10. Aim to make a diagnosis
11. Treat cause of exacerbating factors e.g. hyperglycaemia, hyponatraemia
12. Definitive treatment if possible

Question 12

Head Injury:

General management

Question 13

Thyrotoxic storm: General Management

Answer 13

1. IVI 0.9% saline 500ml/4h. NG tube if vomiting
2. Take blood for t3/t4/TSH/cultures
3. Sedate if necessary
4. Propanolol 40mg/8h PO- if asthma OR poor COà esmolol beter
5. High dose digoxin e.g. 1mg over 2h IVI
6. Antithyroid drugs- carbimazole 15-25mg/6h PO; after 4h give Lugol’s solution
7. Hydrocortisone sodium succinate or dexamethasone
8. Tx suspected infection e.g. cefuroxime 1.5g/8h
9. Adjust IV fluids as necessary, cool with tepid sponging + paracetamol
10. After 5d reduce carbimazole to 15mg/8h PO

Question 14

Acute Renal Failure: General Management

Answer 14

1. Catheterise to assess hourly urine output, and establish fluid charts
2. Assess intravascular volume- BP/JVP/turgor/fluid balance/weight/CVP/attach to cardiac monitor
3. Invx- U&E, Ca2+, PO3, FBC, ESR, CRP, INR, LFT, CK, LDH, protein electrophoresis, hepatitis serology, auto-antibodies, blood cultures, urgent urine microscopy and cultures, USS of renal tract, ECG, CXR
4. Identify and tx precipitating cause
5. Tx life threatening hyperkalaemia- 10mL calcium gluconate IV over 2min, insulin + glucose, nebulised salbutamol, calcium resonium, dialysis
6. If dehydrated, give fluid challenge- aim for CVP 5-10cm. Once fluid replete continue fluids at 20mL. If volume overload, consider dialysis
7. For acidosis- sodium bicarbonate e.g. 50mL of 8.4% IV
8. Tx of sepsis
9. Avoid nephrotoxic drugs
10. If anuric despite fluid challenge, do USS to exclude obstruction, ? bilateral nephrostomies needed. If worsening renal function, consider renal biopsy. High calorie, high protein diet.

Question 15

Paracetamol Poisoning: General MAnagement

Answer 15

1. Gastric lavage if >12g within 1h
2. Activated charcoal if <1h since ingestion
3. Measure glucose/U&E/LFT/INR/ABG/FBC/HCO3 and paracetamol levels at 4h
4. If high levels at <8h start acetylcysteine 150mg/kg in 200ml of 50% glucose. Rash common SE. Alternative is methionine.
5. If ingestion time unknown or presentation >15h after ingestion, tx MAY help; get advice!
6. Hourly BMs and 12h INR
7. Next day do INR/U&E/LFT. If INR rising continue N-acetylcysteine until <1.4
8. Transfer to specialist unit if (1) Encephalopathy or raised ICP (2) INR <2 at <48h (3) Renal impairment (4) Blood pH<7.3 (5) Systolic BP <80

Question 16

Salicylate poisoning: General Management

Answer 16

1. 150mg/kg= mild, 250mg/kg=moderate, >500mg/kg=severe
2. Correct dehydration
3. Gastric lavage with charcoal if <1h
4. Measure- paracetamol and salicylate level, glucose, U&E, LFT, INR, ABG, HCO3, FBC
5. Monitor urine and glucose +/- salicylate/pH/U&E
6. Correct acidosis with HCO3
7. If >500 give HCO3 with KCl to alkalinise urine
8. If >700/renal failure/heart failureà dialyse
9. Discuss serious cases with toxicological service/national posions information service

Question 17

Burns: General Management

Answer 17

1. Assessment- site, depth (partial vs full thickness) and size
2. Resuscitate- (1) Airway- airway obstruction following hot air inhalation? Consider flexible laryngo/bronchoscopy with early intubation (2) Breathing- exclude life-threatening chest injuries and constricting burns. Give 100% O2. (3) Circulation- 2 large bore cannulae if partial thickness burns >10% in a child and >15% in an adult.
3. Use a ‘burns calculator’ formula

Parkland formula: 4 x weight x %burn = mL Hartmanns in 24h

Muir and Barclay formua: [weight x %burn]/2= mL colloid per unit time

Fluid replacement- aim for 0.5ml/kg/h

1. Gauze/clingfilm
2. Analgesia
3. Tetanus
4. Definitive dressing/ skin grafting

Question 18

Upper GI bleed

Presentation (O.E).Hx.

Answer 18

• PResentation
  
  • Haematemesis and or malaena
  • Epigastric discomfort
  • Sudden collapse
  • signs of CLD
  • PR: melaena
  • Shock:
    
    • Cool, clammy, CRT>2s
    • low BP (<100), postural hypoTN
    • reduced urine output
    • Tachycardia
    • low GCS
• Hx:
  
  • Previous bleeds
  • Dyspepsia, known ulcer
  • liver disease or oesophageal varices
  • dysphagia, wt loss
  • drug / ETOH use
  • comorbidities

Question 19

Causes of oesophageal bleeding: and presenting features

Answer 19

• PUD: 40% (DU)
• Acute erosion/gastitis
• Mallory-Weiss tear: 10£
• Varices: 5%
• oesophagitis: 5%
• Ca stomach/oesophagus <3%

Oesophageal

• oesophagitis: small volume of fresh blood, often streaking vomit, malaena=rare, ceases spontaneously, Hxof GORD Sx
• Cancer: small colume of blood unless preterminal event with erosion of major vellels. Often assoc Sx; dysphagia, constitutional Sx (weight loss), may be recurrent episodes
• Mallor Weiss Tear: brisk small to mod volume of bright red blood following bouts of refeated vomiting. malaena=rare, ceases spontaneously
• Varices: large volume of fresh blood, swallowed blood=malaena, assoc with haemodynamic compromise, may stop spontaneously but rebleeds common until Mx

Gastric

• Gastric Ca: may be frank haematemesis or altered blood mixed with vomit. Usually prodromal features of dyspepsia, may have constitutional symptoms. amount of bleeding variable but erosion of major vessel may produce considerable H’gge
• Dieulafoy lesion: no prodromal features prior to haematemesis and malaena, AV malformation->considerable H’gge, difficult to detect endoscopically
• Diffuse erosive gastritis: Usually haematemesis and epigastric discomfort. usually underlying causes e.g. recent NSAID use, large volume h’gge may occur with considerable haemodynamic compromise
• Gastric ulcer: low volume bleeds more common, presents as IDA, erosion into sig vessel may produce considerable h’gge and haematemesis

Duodenum:

• Ulcer: Most common causes = posteriorly sited ulcer erosion of gastroduodenal artery. Hx of pain occuring hrs after eating.
• fistula; rare complication of AAA surgery with aorto-enteric fistulation

Question 20

Management of UGiBleed

acutely

Answer 20

ABCDE: CIRCULATION!

• Resuscitate:
  
  • Head down
  • Airway: Early control of airway is vital (e.g. Drowsy patient with liver failure) -> protect the airway
  • Breathing: 100% O2
  • 2x 14G cannulae:
    
    • Bloods: cross match blood, check FBC, LFTs (ETOH abuse), U+E (protein meal) and Clotting and ABG (lactate + Hb) and glucose
    • IV crystalloid infusion up to 1L (avoid dilution)
  • D: blood glucose, GCS, Temperature, expose (PR; maleana)
• Major H’gge protocol: on-going bleeding and haemodynamic instability are likely to require O negative blood pending cross matched blood
  
  • _​_keep Hb >10
• Upper GI endoscopy (scoring systems)
  
  • all within 24 hours of admission.
  • If unstable = immediately after resuscitation or in tandem with it.

Specific

• Varices:
  
  • terlipressin prior to endoscopy​ (splanchnic vasopressor)
  • Prophylactic ABx e.g. ciprofloxacin 1g/24h
  • Varices should be banded or subjected to sclerotherapy, adrenaline coagulation
  • If this is not possible owing to active bleeding then a Sengaksten- Blakemore tube (or Minnesota tube) should be inserted. This should be done with care; gastric balloon should be inflated first and oesophageal balloon second. Remember the balloon with need deflating after 12 hours (ideally sooner) to prevent necrosis.
  • Portal pressure should be lowered by combination of medical therapy +/- TIPSS.
• Oesophagitis/gastritis:
  
  • Patients with erosive oesophagitis / gastritis should receive a proton pump inhibitor.
  • Patients with diffuse erosive gastritis who cannot be managed endoscopically and continue to bleed may require gastrectomy
• Haemostasis of vessel or ulcer
• • Identifiable bleeding points should receive combination therapy of injection of: adrenaline and either a thermal/laser coagulation, fibrin glu, endoclips.
    
    • All who have received intervention should receive a continuous infusion of a proton pump inhibitor (IV omeprazole for 72 hours) to reduce the re-bleeding rate.
    • Bleeding ulcers that cannot be controlled endoscopically may require:
      
      • Gastric ulcer
        
        • Under-running of the bleeding site
        • Partial gastrectomy-antral ulcer
        • Partial gastrectomy or under running the ulcer- lesser curve ulcer (involving left gastric artery)
        • Total gastrectomy if bleeding persists
      • Duodenal ulcer:
        
        • Laparotomy, duodenotomy and under running of the ulcer. If bleeding is brisk then the ulcer is almost always posteriorly sited and will have invaded the gastroduodenal artery. Large bites using 0 Vicryl are taken above and below the ulcer base to occlude the vessel. The duodenotomy should be longitudinal but closed transversely to avoid stenosis.
• Mallory Weiss: tears will typically resolve spontaneously

Post endoscopy:

• Omeprazole IV + continuation PO (↓s re-bleeding)
• Keep NBM for 24h → clear fluids → light diet @ 48h
• Daily bloods: FBC, U+E, LFT, clotting
• H. pylori testing and eradication
• Stop NSAIDs, steroids et.c

Other:

• Catheter and consider CVP (aim for >5cm H2o)
• Correct coagulopathy: vit K, FFP, Plts
• Thiamine if EtOH
• NB. Avoid 0.9% NS in uncompensated liver disease (worsens ascites). Use blood or albumin for resus and 5% dex for maintenance.
• Notify SURGEONS if severe bleed, Indications for surgery:
  
  • Patients > 60 years
  • Continued bleeding despite endoscopic intervention
  • Recurrent bleeding
  • Known cardiovascular disease with poor response to hypotension

Question 21

What scoring system can be use for upper GI bleeds?

TWO!

Answer 21

Rockall Score: (Prof T Rockall, St. Mary’s)= Prediction of re-bleeding and mortality

• 40% of re-bleeders die
• Initial score pre-endoscopy
  
  • Age
  • Shock BP, pulse
  • Comorbidities
• Final score post-endoscopy
  
  • Final Dx + evidence of recent haemorrhage
    
    • Active bleeding
    • Visible vessel
    • Adherent clot
• Initial score ≥3 or final >6 are indications for surgery

Blatchford score = The need for admission and timing of endoscopic intervention

• patients
  
  • Hb
  • serum urea
  • pulse rate
  • BP
• 0 = low risk, all others are considered high risk and require admission and endoscopy.

Question 22

PAthophysiology of oesophageal varices and causes of portal HTN

Answer 22

Oesophageal Varices

• Portal HTN → dilated veins @ sites of porto-systemic anastomosis: L. gastric and inferior oesophageal veins
• 30-50% c¯ portal HTN will bleed from varices
• Overall mortality 25%: ↑ c¯ severity of liver disease.

Causes of portal HTN

• Pre-hepatic: portal vein thrombosis
• Hepatic: cirrhosis (80% in UK), schisto (commonest worldwide), sarcoidosis.
• Post-hepatic: Budd-Chiari, RHF, constrict pericarditis

Question 23

What is Transjugular intrahepatic porto-systemic shunt

Answer 23

• IR creates artificial channel between hepatic vein and portal vein → ↓ portal pressure.
• Colapinto needle creates tract through liver parenchyma which is expand using a balloon and maintained by placement of a stent.
• Used prophylactically or acutely if endoscopic therapy fails to control variceal bleeding

Question 24

Asthma ‘attack’/exacerbation classification

mod/severe/LT

Answer 24

Question 25

Acute Severe Asthma

Presentation (and important History)

Answer 25

Acute breathlessness and wheee

Hx:

• Precipitant: infection, travel, exercise?
• Usual and recent Rx?
• Previous attacks and severity: ICU?

Question 26

Acute severe asthma

Investigations

3x

Answer 26

1. PEFR
2. ABG
   
   • PaO2 usually normal or slightly reduced
   • PaCO2 reduced
   • PaCO2 incresed-> !! Send to ITU for ventilation
3. Bloods
   
   • FBC
   • U&E
   • CRP
   • Blood cultures

Question 27

Acute severe asthma differential

Answer 27

acute exacerbation of COPD

Pneumothorax

Pulmonary oedema

Question 28

Admission criteria (3)

AND

discharge criteria (2)

Answer 28

Admission Criteria:

• life threatening attack
• feature of severe attack persisting despite initial Rx
• May discharge if PEFR >75 1 hr after initial Rx

Discharge when

• Been stable on discharge meds fo 24hrs:
  
  • PEFR >75
  • With diurnal variability <25%

Question 29

Asthma: acute severe

Management

Answer 29

Question 30

AMPLE History

Answer 30

Allergies

Medication

Past medical history

Last meal

Events leading to revent

Question 31

GCS Scale

Answer 31

Question 32

General Shock Management

Answer 32

1. If BP unrecordable call the cardiac arrest team
2. ABC (including high flow oxygen)
3. Raise foot of the bed (unless cardiogenic)
4. IV access and 2 x large bore cannulae; get help if this takes >2min
5. Assessment:
6. • rate/rhythm/ischaemia

General- cold/anaemic/dehydrated/features of anaphylaxis

1. • HR, difference in BP between arms
2. 3. • trauma/aneurysm?
3. Identify and tx underlying cause:

For septic shock- gentamycin + antipseudomonal penicillin. NB- if patient remains hypotensive despite fluids and vasopressors give low-dose steroids or recombinant human activated protein C.

For hypovolaemic shock- fluid replacement titrated against BP, CVP, urine. If >1L fluid needed then ?blood transfusion.

For heat exhaustion- tepid sponging and fanning, 0.9% saline + hydrocortisone. ? chlorpromazine to stop itching. Stop cooling when temp <39.

1. Give crystalloid fast to restore BP (unless cardiogenic shock)
2. Seek expert help early
3. Invx- FBC/U&E/glucose/CRP, X-match and clotting, blood/urine cultures, ECG, CXR, lactate, echo, abdominal CT, USS
4. Consider arterial line, CV line, bladder catheter
5. Tx underlying cause
6. Fluid replacement as dictated by BP/CVP/urine output
7. Don’t overload with fluids if cardiogenic shock
8. If persistently hypotensive consider inotropes

Question 33

Hypovolaemis Shock

Causes

Answer 33

Blood loss

• Trauma
• GI bleeding (haematemeisis, melaena)
• Ruptured AAA
• Ruptured ectopic pregnancy

Fluid loss / redistribution (‘third spacing’)

• Burns
• GI losses (vomiting, diarrhoea)
• Pancreatitis
• Sepsis

Question 34

Hypovolaemic shock

Management

Answer 34

• ABCDE
• Give high flow O2 by mask
• Venous access
  
  • FBC, U&E, glucose, LFT, lactate, coagulation screen
  • Blood cultures if appropriate
• Monitor vital signs
  
  • Pulse, BP, O2
• Check ABG
• ECG and CXR
• Insert urinary catheter and monitor urine output hourly
• For shock associated with decreased effective circulating volume:
  
  • IV crystalloid (0.9% saline) 20ml/kg bolus
  • Give further IV fluids including colloid +/- blood
    
    • Aim for haemocrit >30%
• Look for the cause(s) of shock:
  
  • Echo
  • USS
  • CT

Surgical intervention

• Treat the specific cause of shock:
  
  • Laparotomy: Ruptured AAA, splenic or liver trauma, ruptured ectopic pregnancy, intra-abdominal sepsis
  • Thrombolysis / angioplasty: MI
  • Thrombolysis: PE
  • Pericardiocentesis/cardiac surgery: Cardiac tamponade
  • Antibiotics: Sepsis
    
    • Depends on perceived cause and local policies
    • If there is no obvious source, empirical combination therapy is advised (e.g. co-amoxiclav + gentamycin + metronidazole)
    • Obtain specialist microbiological advise early especially in neutropenic / immunocompromised patients
• Inotropic and vasoactive therapy, assisted ventilation and invasive monitoring (including arterial and CVP lines) are often needed as part of goal directed therapy. Get specialist ITU help Early

Question 35

Management of haemorrhagic shock

Answer 35

1. Management:

• C ABCDE
• Haemorrhage control
  
  • Apply pressure to the wound

Question 36

Anaphylactic Shock

Definition

Common causes

Answer 36

1. Definition:
   * Severe, life-threatening, systemic hypersensitivity reaction
2. Common Causes:

• Food e.g. nuts
  
  • Most common cause in children
• Drugs
  
  • Penicillin’s
  • Anaesthetic drugs
  • Contrast media
  • Blood products
• Venom e.g. wasp stings

Question 37

Anaphylactic shock

Early signs

Worrying signs

Answer 37

1. Early Signs:

• Utricaria
• Bronchospasm / stridor
• Vomiting +/- diarrhoea
• Flushing
• Abdominal pain
• Sense of impending doom

1. Worrying signs:

• BP <90mmHg systolic
• Decreased O2 sats
• Chest tightness
• Stridor

Question 38

Anaphylactic shock management

Answer 38

1. Secure the airway- give 100% O2. Intubate if respiratory obstruction
2. Remove the cause, raise the feet of the bed
3. Adrenaline IM 0.5mg, every 5mins as guided by BP/pulse/resp function
4. Secure IV access
5. Chlorphenamine 10mg IV and hydrocortisone 200mg IV
6. IVI 0.9% saline over 15mins (up to 2L may be needed); titrate against BP
7. If wheeze, tx for asthma; may require ventilator support
8. If still hypotensive, admit to ITU and give IVI adrenaline +/- aminophylline and nebulized salbutamol; get expert help
9. Admit to ward. Monitor ECG
10. Continue chlorphenamine 4mg/6h PO if itching
11. Medic Alert bracelet
12. Teach about Epipen
13. Skin prick tests to identify cause

Question 39

ACS STEMI

Management

Answer 39

1. ABCDE
2. Attach ECG monitor and 12 lead ECG
3. O2 2-4L aim for SaO2>95% (mask or nasal prongs)
4. IV access- bloods for FBC, U&E, glucose, lipids, cardiac enzymes
5. Brief assessment:

Hx of CV disease; risk factors for IHD, contraindications to thrombolysis? Examine: pulse, JVP, cardiac murmurs, signs of heart disease, scars from previous surgery

1. Aspirin 300mg PO, +/- clopidogrel
2. Morphine 5-10mg IV + antiemetic e.g. metoclopramide 10mg IV
3. GTN sublingually or 2 puffs or 1 tablet PRN
4. Primary PCI (best if ongoing ischaemia and presentation within 12h) or thrombolysis (target time <30mins. DO NOT thrombolyse if ST depression alone, T wave inversion alone or normal ECG). Streptokinase 1^st line for non-anterior MI 1.5million units 100mL 0.9% saline IVI over 1 hour. Tenecteplase IF anterior MI/ previous use of SK/ systolic BP<100/ new LBBB. IF allergic reaction to SK give alteplase
5. B-blocker e.g. atenolol 5mg IV + ACEi
6. DVT prophylaxis until mobile
7. Continue medication except calcium channel antagonists
8. Admit for 48h of bedrest and continous ECG
9. Daily examination
10. Aspirin 75mg
11. B-blockers for 1 year to maintain HR<60
12. Continue ACEi
13. Start statin
14. Address risks

Question 40

ACS: NSTEMI

Management

Answer 40

1. ABCDE
2. Attach ECG monitor and 12 lead ECG
3. O2 2-4L aim for SaO2>95% (mask or nasal prongs)
4. IV access- bloods for FBC, U&E, glucose, lipids, cardiac enzymes
5. Brief assessment:

Hx of CV disease; risk factors for IHD, contraindications to thrombolysis? Examine: pulse, JVP, cardiac murmurs, signs of heart disease, peripheral pulses, scars from previous surgery

1. Morphine 5-10mg IV + antiemetic e.g. metoclopramide 10mg IV
2. GTN sublingually or 2 puffs or 1 tablet PRN
3. Aspirin 300mg PO, +/- clopidogrel 300mg (add clopidogrel IF increased troponin, ACS already on aspirin, ST depression on resting ECG, ACS after recent MI, patients being transferred for angioplasty, aspirin intolerant)
4. Oral B blocker e.g. metoprolol 50-100mg/8h (if CI give diltiazem 60-120u/kg/12h)
5. Heparin e.g. enoxaparin 1mg/kg/12h. If LMWH is unavailable give unfractionated heparin 5000IV bolus then IVI. Check APTT 6-hourly
6. IV nitrate if pain continues (e.g. GTN 50mg in 50mL 0.9% saline at 2-10mL/h) titrate to pain and maintain systolic BP>100mmHg
7. Record ECG in pain
8. If patient high-risk (persistent or recurrent ischaemia, ST depression, diabetes, increased troponin) infuse a GPIIb/IIIa antagonist (e.g. tirofiban) and, ideally, urgent angiography. Add clopidogrel. Then optimise drugs- B-blocker/Ca2+ channel antagonist/ACEi/nitrate. Intensive statin regimens, start at top doses e.g. atorvastatin 80mg. If symptoms fail to improve, refer to a cardiologist for urgent angiography +/- PTCI or CABG
9. If the patient is low-risk (no further pain, flat or inverted T waves, or normal ECH and negative troponin), the patient may be discharged if a repeat troponin (>12h) is negative. Treat medically and arrange further invx e.g. stress test, angiogram
10. Wean off GTN infusion when stabilised on oral drugs
11. Start heparin when pain-free for 24h but give at least 3-5 days of therapy
12. Check serial ECGs, and troponin >12h after pain
13. Address modifiable risk factors: smoking, HTN, hyperlipidaemia, diabetes
14. Gentle mobilisation

Question 41

Types of Tachycardia

1.

Answer 41

Narrow Complex Tachycardia:

• Regular:
  
  • Sinus tachy
• Irregular:
  
  • Possible AF

Broad Complex Tachycardia:

• Regular
  
  • Assume VT
• Irregular
  
  • AF with bundle branch block

Question 42

Management of VT

Answer 42

• ABCDE
• Haemodynamically unstable: Immediate cardioversion
  
  • Signs of heart failure (basal crepitations, raised JVP)
  • Signs of shock
• Not-haemodynamically unstable:
  
  • Amiodarone
    
    • Ideally through a central line
  • If drug therapy fails:
    
    • Electrophysiological study
    • Implantable cardioverted-defibrillator

Question 43

Management of Broad complex Tachycardia

Answer 43

1. If no pulseà cardiac arrest protocol
2. ABCDE
3. O2, ECG and IV access
4. Connect patient to cardiac monitor and have a defibrillator to hand
5. Assess if there are any adverse signs i.e. systolic BP<90/chest pain/ heart failure/ HR>150
6. If NO adverse signs:

Correct electrolyte problems

If regular rhythm Amiodarone 300mg IV over 20-60min, then 900mg over 24h. OR lidocaine

If irregular rhythm the diagnosis is usually AF or pre-excited AF (amiodarone) or polymorphic VT e.g. torsade de points (Mg IVI)

If this fails, get expert help

Sedation

Synchronised DC shockà 200J-300J-360J (monophasic)

1. If YES adverse signs

Get expert help

Sedation

Synchronised DC shock 200J-300J-360J (monophasic)

Amiodarone 300mg IV over 20-60min; then 900mg over 24h

K+ and Mg2+ correction (up to 60mmol KCl at 30mmol/L and 4ml 50% MgSO4)

Further cardioversion if needed

For refractory cases consider: lidocaine/procainamide/felcanide/overdrive pacing

1. Establish the cause
2. IF VT occurs after MI IV amiodarone/lidocaine for 12-24h or amiodarone (if poor LV function). Can prevent recurrent VT using surgical isolation of the arrhythmogenic area or an ICD

Question 44

AF

Types

Answer 44

Epidemiology:

• Most common sustained cardiac arrhythmia
• Present in about 5% of patients over aged 70-75 / 10% in patients aged 80-85

Types:

• First detected episode
• Recurrent:
  
  • 2>=
  • If the episodes of AF terminate spontaneously = paroxysmal AF – Last less than 7 days (typically < 24hr)
  • If not self-terminating then persistent AF is used (such episodes last >7 days)
• Permanent AF:
  
  • Can’t be cardioverted / or attempts are deemed inappropriate
  • Treatment goals are therefore rate control and anticoagulation if appropriate

Question 45

AF

Symptoms, signs, investigations

Answer 45

• Symptoms:
  
  • Palpitations
  • Dyspnoea
  • Chest pain
• Signs:
  
  • Irregularly irregular pulse
• Investigations:
  
  • An ECG is essential to make the diagnosis as other conditions can give an irregular pulse, such as ventricular ectopics or sinus arrhythmia

Question 46

AF: with haemodynamic compromise

Management

Answer 46

• Seek immediate senior help
• Treat shock
  
  • O2
  • IV access
  • DC cardioversion
  • If unsuccessful – Amiodarone

Question 47

Management of heamodynamically stable AF

Answer 47

Question 48

Severe Pulmonary oedema

CXR Features

Answer 48

• Interstitial oedema
• Bat’s wing appearance
• Upper lobe diversion (increased blood flow to the superior parts of the lung)
• Kerly B lines
• Pleural effusion
• Cardiomegaly may be seen if there is a cardiogenic cause

Question 49

Management of Pulmonary oedema: Dyspnoea, orthopnoea, pink, frothy sputum

Answer 49

1. ABCDE
2. 100% oxygen
3. IV access and monitor ECG; treat any arrythmias
4. Invx: CXR, ECG, U&E, ‘cardiac’ enzymes, ABG, consider ECHO
5. (during treatment monitor progress with BP/pulse/cyanosis/resp rate/JVP/urine output/ABG)
6. Diamorphine 2.5-5mg IV slowly- caution in liver failure and COPD
7. Furosemide 40-80mg IV slowly- larger doses in renal failure
8. GTN 2 puffs SL or 2 x 0.3mg tablets SL (NOT if BP<90)
9. Necessary invx, examination and hx
10. If systolic BP>100 give isosorbide dinitrate 2-10mg/h IVI; keep systolic BP>90
11. If patient is worsening: further dose of furosemide 40-80mg. Consider ventilation (invasive or non-invasive e.g. CPAP; get help) or nitrate infusion.
12. If systolic BP<100mmHg, tx as cardiogenic shock i.e. insert Swan Ganz catheter and inotropic support
13. Daily weights; BP and pulse/6h. Repeat CXR
14. Change to oral furosemide or budesonide
15. If on large doses of loop diuretic consider the addition of a thiazide e.g bendroflumethiazide 2.5-5mg daily PO
16. ACE-i if LV failure. If contraindicated/blackà hydralazine is better
17. Consider B-blocker and spironolactone
18. Is the patient suitable for biventricular pacing and cardiac transplantation?
19. Consider digoxin and warfarin esp if AF

Question 50

Management of Cardiogenic shock

Answer 50

1. ABCDE
2. Oxygen titrated to adequate arterial saturations
3. Diamorphine 2.5-5mg IV for pain and anxiety
4. Invx- ECG, U&E, cardiac enzymes, ABG, CXR, ECHO. IF indicated do CT thorax or V/Q scan
5. Monitor- CVP, BP, ABG, ECG, urine output. 12 lead ECG hourly until diagnosis. Consider Swanz-Ganz catheter for pulmonary wedge pressure and cardiac output, and an arterial line to monitor pressue. Catheterise for urine output.
6. Correct arrhythmias, U&E abnormalities or acid-base disturbance
7. Optimise filling pressure (if available measure pulmonary capillary wedge pressure)
8. IF PCWP<15 fluid load-> Give a plasma expander every 15min IV, aiming for PCWP 15-20. IF PCWP>15-> give inotropic support e.g. dobutamine 2.5-10microgram/kg/min IVI. Aim for systolic BP >80mmHg
9. Consider renal dose dopamine 2-5microgram/kg/min IV initially
10. Consider intra-aortic balloon pump if you expect the underlying condition to improve or you need time awaiting surgery
11. Look for and tx any reversible cause e.g. thrombolysis for MI/PE, surgery for valve problems

Question 51

Asthma classification

Answer 51

Note that a patient having any one of the life-threatening features should be treated as having a life-threatening attack

Question 52

Acute Asthma management

Answer 52

• Follow the BTS/SIGN guidelines
• ABCDE
• High flow O2
• Put the bed back and rails up so the patient is sitting up and holding onto the side rails
  
  • To use pectoral muscles as accessory muscles
• If patient cannot talk, start treatment but get senior ED and ICU help in case intubation and ventilation are required
• Check trachea and chest signs for pneumothorax
• Ask about previous admissions to ITU
• Administer high dose nebulised beta-2 agonists
  
  • E.g. Salbutamol 5mg
  • Or 10 puffs salbutamol into a spacer device and face mask
  • For severe asthma or asthma that responds poorly to the initial nebuliser, consider continuous nebulisation
• Give a corticosteroid
  
  • Prenisolone 40-50mg PO
  • Hydroxortisone 100mg IV
• Add nebulised ipratropium bromide (500mcg) to beta-2 agonist treatment for patients with acute severe or life-threatening asthma or those with a poor initial response to beta-2 therapy
• Magnesium sulphate recommended as next step for patients who are not responding
  
  • Consult with senior medical staff
  • E.g. 1.2-2g IV over 20 mins
• Little evidence to support use of IV aminophylline (still mentioned in management plans)
• If no response consider IV salbutamol
  
  • Consult with senior medical staff
• Avoid ‘routine’ ABx
• Repeat ABG within the hour
• Hypokalaemia may be caused or exacerbated by beta-2 agonists and / or steroid therapy

OR:

1. Hx- usual and recent tx, previous acute episodes, best PEFR, ITU admissions
2. Assess severity

Severe- unable to complete sentences, RR>25, HR>110, PEFR<50%

Life-threatening- PEFR<33%, silent chest, bradycardia/hypotension, exhaustion

For severe attack: 01912817256, 07904144006, 07886420

1. Sit patient up at give 100% O2 via non-breathable bag
2. Salbutamol 5mg plus ipratropium bromide 0.5mg nebulised with O2
3. Hydrocortisone 100mg IV or prednisolone 40-50mg PO
4. ABG, CXR, FBC, U&E
5. Monitor O2 sats, HR and resp rate
6. IF life-threatening featuresà inform seniors and give magnesium sulphate 1.2-2g IV over 2 min. Give salbutamol nebulisers every 15min (with monitoring for arrhythmias)
7. IF patient improvesà 40-60% O2, prednisolone 40-50mg/24h PO for 5 days, nebulised salbutamol 4hourly
8. IF patient doesn’t improve after 15-30mins, continue 100% O2 and steroids, give hydrocortisone 100mg IV or prednisolone 30mg PO if not already given, salbutamol nebulisers every 15 mins, continue ipratropium 0.5mg every 4-6h
9. IF patient still doesn’t improve, discuss with seniors and ITU, salbutamol nebulisers every 15 mins, magnesium sulphate 1.2-2g IV over 20mins. Consider aminophylline 5mg/kg IVI over 20mins. If no improvement, transfer to ITU with doctor prepared to intubate.
10. Record PEFR pre- and post- B agonist in hospital at least 4 times
11. Once the patient is improving, wean down and stop aminophylline over 12-24h. Reduce nebulised salbutamol and switch to inhaled B-agonist. Initiate inhaled steroids and stop oral steroids if possible. Continue to monitor PEF. Look for deterioration on reduced treatment and beware early morning dips in PEF. Look for the cause.
12. Before discharge they must have been stable on medication for 24h, had inhaler technique checked, PEFR>75%, steroid and bronchodilator therapy, own a PEFR and management plan, GP appointment within 1 wk, Resp clinic appointment within 4 weeks.

Question 53

Asthma criteria for admission

Answer 53

• Admit patients with any features of:
  
  • A life-threatening or near-fatal attack
  • Severe attack persisting after initial treatment

Question 54

Acute asthma Refer to ICU

Answer 54

Refer any patient requiring ventilator support or with acute severe or life threatening asthma failing to respond to therapy, evidenced by:

• Drowsiness, confusion
• Exhaustion, feeble respiration
• Coma or respiratory arrest
• Persisting or worsening hypoxia
• Hypercapnoea
• ABG showing acidosis
• Deteriorating peak flow

Question 55

Cardiac arrest in acute asthma

Answer 55

• Underlying rhythm is usually PEA
• This may reflect one or more of the following:
  
  • Prolonged severe hypoxia
  • Hypoxia related arrhythmias
  • Tension pneumothorax
• Give ATLS
• Treat tension pneumothorax if present

Question 56

Acute exacerbation of COPD

Organisms

Answer 56

• Most common bacterial organisms:
  
  • Haemophilus influenzae (most common cause)
  • Streptococcus pneumoniae
  • Moraxella catarrhalis
• Respiratory viruses account for around 30%
  
  • Most important is the human rhino virus

Question 57

Acute exacerbation of COPD

• Worrying signs*
• Symptoms*
• Signs*

Answer 57

• Worrying signs:
  
  • Low GCS
  • Rising CO₂
• Symptoms:
  
  • Breathlessness
  • Cough
  • Increased sputum
  • Tight chest
  • Confusion
  • Decreased exercise tolerance
• Signs:
  
  • Wheeze
  • Cyanosis
  • Barrel-chest
  • Poor expansion
  • Tachypnoea

Question 58

Acute exacerbation of COPD

Investigations

Answer 58

• ABG
  
  • Often deranged in COPD
  • Compare with previous sample
  • Pay close attention to FiO2
  • Repeat after 30 mins
• CXR:
  
  • Hyper-expanded chest
  • Flat diaphragm
• Spirometry:
  
  • Decreased FEV1
  • Decreased FEV1:FVC ratio (<70%)

Question 59

Acute Exacerbation of COPD

Answer 59

• ABCDE
• Sit the patient up
• Give oxygen to maintain sats >/ 88%
  
  • Aim for PaO2 ~8kPa
• Give salbutamol 5mg +/- ipratropium 500mg nebs
  
  • Drive by air
  • Leaving nasal O2 cannulae on under mask if necessary
• Steroids
  
  • Add prednisolone 30mg PO
  • Or hydrocortisone 200mg IV
• Sputum for M, C & S
• ABG
• CXR
  
  • Portable if unwell
• Use ABG results and clinical observation to guide further management:
  
  • Normal ABG (for them) continue current O2 and give regular nebs
  • Worsening hypoxaemia increased FiO2, repeat ABG <30 min, watch for confusion which should prompt for ABG sooner, consider NIV
  • Increasing CO2 retention or worsening GCS, request senior help urgently, consider:
    
    • ICU input/assessment
    • Aminophylline 5mg/kg bolus over 20 min unless the patient us on oral aminophylline or theophylline
    • NIV
• Consider prescribing ABx if the patient has increased SOB, fevers, worsening cough, purulent sputum or focal changes on CXR

OR

1. ABC
2. Hx- usual/recent tx, smoking status, exercise capacity
3. PEFR, ABG, CXR, FBC, U&E, CRP, ECG, Blood cultures, sputum culture
4. Controlled O2 therapy, starting at 24-28%. Aim for PaO2>8
5. Nebulised bronchodilators Salbutamol 5mg/4h and ipratropium 500 microgram/6h
6. Steroids IV hydrocortisone 200mg and oral prednisolone 30-40mg (continue for 7-14d)
7. Abx if evidence of infection e.g. amoxicillin 500mg/8h PO
8. Physiotherapy to aid sputum expectoration
9. If no responseà repeat nebulisers and consider IV aminophylline
10. If no responseà consider NIPPV if resp rate >30 or pH<7.35
11. Consider intubation and ventilation if pH<7.26 and PaCO2 is rising
12. Consider a respiratory stimulant drug e.g. doxapam 1.5-4mg/min IV
13. Prior to discharge liaise with GP regarding steroid reduction, domiciliary oxygen, smoking and vaccines
14. For stable COPD: advice stop smoking, exercise, tx poor nutrition/obesity, influenza, vaccines. For mild diseaseà short acting B-agonist or ipratropium bromide PRN. For moderateà regular short acting B2 agonist +/or ipratropium. Consider steroid trial. For severe diseaseà combination therapy with regular short-acting B agonist and ipratropium. Consider steroid trial and assess for home nebulisers.
15. For more advanced disease- consider pulmonary rehabilitation and long term oxygen therapy if O2<7.3. Surgery if recurrent pneumothoraces, isolated bullous disease, volume reduction surgery. Assess the social circumstances and support required. Air travel may be hazardous.

Question 60

Pneumothorax: spontaneous

• Definitions*
• RFs*

Answer 60

Definitions:

• Primary = No underlying lung disease
• Secondary = Underlying lung disease

Risk Factors:

• Primary = Tall, thin, male, Marfan’s, recent central line, pleural aspiration or chest drain
• Secondary = COPD, asthma, infection, trauma, mechanical ventilation

Question 61

Pneumothorax: Spontaneous

• Symptoms*
• Signs*
• Investigations*

Answer 61

• Symptoms:
  
  • Breathlessness
  • +/- Chest pain
• Signs:
  
  • Hyper-resonant
  • Reduced air entry on affected side
  • Tachypnoea
  • Tracheal deviation
• Investigations:
  
  • CXR

Question 62

Pneumothorax: Spontaneous

Management

Answer 62

• General Management:
  
  • ABCDE
  • Sit patient up
  • Give O2
• Primary Pneumothorax (BTS Recommendations):
  
  • If rim of air is <2cm and the patient is not short of breath then discharge should be considered
  • Otherwise aspiration should be attempted
  • If this fails (defined as >2cm or still SOB, then a chest drain should be inserted)
  • Patients should be advised to avoid smoking to reduce the risk of further episodes
• Secondary Pneumothorax:
  
  • If the patient is >50 years old and the rim of air is >2cm and/or the patient is SOB then a chest drain should be inserted
  • Otherwise aspiration should be attempted if the rim of air is between 1-2cm
    
    • If aspiration fails then a chest drain should be inserted
  • All patients should be admitted and observed for at least 24hrs
  • If <1cm then the BTS guidelines suggest giving O2 and observing for 24hrs

Question 63

Pneumothorax: Iatrogenic

Answer 63

• Less likelihood of recurrence than spontaneous pneumothorax
• Majority will resolve with observation, if treatment is required then aspiration should be used
• Ventilated patients need chest drains, as may some with COPD

Question 64

Tension Pneumothorax

• Mechanism*
• Sign*

Answer 64

• Mechanism:
  
  • Air trapped in the pleural space is under +ve pressure
  • Mediastinal shift may occur, compressing the contralateral lung and reducing venous return
• Signs:
  
  • Hypotensive
  • Circulatory shock is the single most reliable sign of tension pneumothorax
  • Tachycardia
  • Tachypnoea
  • Unilateral hyper-resonance
  • Reduced air entry
  • Raised JVP
  • Tracheal deviation

Question 65

Management of Tension Pneumothorax

Answer 65

• ​This is an emergency and will worsen if not treated
• ABCDE
• Sit the patient up and give 15L oxygen
• Treat prior to CXR
• Thoracocentesis - Insert large cannula (orange / grey) into the 2^nd intercostal space, midclavicular line
  
  • Listen for a hiss
  • Leave in situ
• Insert a chest drain on the same side (with an underwater seal)

Question 66

Pneumonia

Causes

Answer 66

• Bacterial (80-90%)
  
  • Streptococcus pneumoniae = Most common cause of community acquired pneumonia
  • Others include mycoplasma pneumoniae, haemophilus influenzae, legionella
  • Always consider TB, particularly in chronic alcoholism, poor social circumstances, immigrants and those travelling to developed countries
  • Immunosuppressed patients (e.g. HIV, steroid therapy) are at increased risk of TB and Pneumocystis jirovecii
• Viral (10-20%):

Question 67

Pneumonia

Assessment (admit or discharge?)

Answer 67

• Some patients with ‘mild’ illness, good social circumstances and no significant co-morbidity may be safely discharged with appropriate antibiotics (e.g. amoxicillin 0.5-1g PO tds), simple analgesia and GP follow up
• Patients with a CURB-65 score >= 3 have severe pneumonia with a high risk of death (->ITU)
• Patients who score 2 are at increased risk of death and should be considered for inpatient treatment or hospital supervised outpatient care
• Patients with a CURB-65 score of 0-1 are suitable for home treatment

Question 68

Pneumonia

Management

CURB <1

CURB 2

CURB 3+

Answer 68

• Patients deemed suitable for discharge:
  
  • Simple analgesia
  • Oral ABx
  • GP follow up
• Patients admitted but not severely unwell
  
  • Oral: Either amoxicillin 0.5-1g PO tds + erythromycin 500mg PO qds (or clalithromycin 500mg bd)
  • IV: Ampicillin 500mg IV qds + erythromycin 500mg IV qds (or clalithromycin 500mg bd)
  • Monitor SpO2 and provide O2 accordingly
  • Provide simple analgesia
• Patients with sepsis or severe sepsis:
  
  • IV crystalloid fluids
  • Take blood cultures
  • Administer IV ABx
    
    • E.g. co-amoxiclav + clalithromycin
  • Contact ITU and make preparations for arterial line, central line and urinary catheter insertion

Question 69

Pneumonia

Differential Diagnosis

Answer 69

• Pulmonary oedema
• Pulmonary infarction
• Pulmonary vasculitis
  
  • SLE PAN, Churg-Strauss and Wegner’s
• Aspergillosis
• Allergic alveolitis
• Bronchial or alveolar cell carcinoma

Question 70

Pleural effusion

Causes

Answer 70

Causes:

An exudate is diagnosed if the pleural fluid:serum protein >0.5, fluid:serum LDH >0.6 or the fluid LDH is >2/3 the upper limits of lab normal value

• Exudates:
  
  • Pneumonia (bacterial, viral, mycoplasma)
  • Malignancy (bronchial carcinoma, mesothelioma, lymphoma)
  • TB
  • PE, with pulmonary infarction
• Transudates:
  
  • Cardiac failure
  • Nephrotic syndrome
  • Hepatic failure
  • Ovarian hyperstimulation
  • Ovarian fibroma (Meig’s syndrome)

Question 71

Pleural Effusion

• Symptoms*
• Signs*
• Investigations*

Answer 71

• Symptoms:
  
  • Usually due to underlying disease process
  • A mild dull ache
  • Dyspnoea (initially at exercise and later at rest) may occur if large
  • A history of vomiting followed by chest pain points to a ruptured oesophagus – a surgical emergency
• Signs:
  
  • Not apparent until >500ml is present
  • Dyspnoea
  • Stony dull to percussion
  • Absent breath sounds over the effusion are characteristic
  • Bronchial breathing may be heard just above the effusion
  • Very large unilateral effusion may produce evidence of mediastinal shift
• Investigations:
  
  • CXR can demonstrate pleural effusions as small as 250ml
  • Blunting of the costrophrenic angle

Question 72

Pleural effusion

Treatment

Answer 72

• Provide O2 and resuscitate as necessary, according to the underlying pathology
• Emergency therapeutic pleural aspirations are rarely required in the ED except where haemothorax is suspected
• Refer to medical team for further investigation
  
  • US gluided diagnostic pleural aspiraton

Question 73

Pulmonary embolism

Presentation

Answer 73

• Pleuritic chest pain
• Dyspnoea
• Haemoptysis
  
  • Patients can present with virtually any cardio / respiratory symptom

Question 74

Pulmonary embolism

Wells score and respective management

Answer 74

• All patients with symptoms or signs suggestive of a PE should have a history taken, examination performed and a CXR to exclude other pathology
• If a PE is still suspected then a two-level Wells score should be performed
• > 4 = PE likely

PE likely:

• Arrange an immediate computed tomography pulmonary angiogram (CTPA)
• If there is a delay in getting the CTPA then give low-molecular weight heparin until the scan is performed

PE unlikely:

• Arrange a D-dimer test
• If positive arrange an immediate CTPA
• If there is a delay in getting the CTPA then give low-molecular weight heparin until the scan is performed

If patient has an allergy to contrast media, V/Q scan should be arranged instead

Question 75

PE: ECG

Answer 75

• S1Q3T3
  
  • Large S wave in lead I
  • A large Q wave in lead III
  • An inverted T wave in lead III
• Right bundle branch block and right axis deviation are also associated with PE
• Sinus tachycardia may also be seen

Question 76

PE: Management

Answer 76

• Low molecular weight heparin (LMWH) or fondaparinux should be given initially after a PE is diagnosed
  
  • An exception to this is for patients with a massive PE where thrombolysis is being considered
  • In such a situation, unfractionated heparin should be used
• A vitamin K antagonist e.g. warfarin should be started within 24 hours of diagnosis
• The LMWH or fondaparinux should be continued for at least 5 days or until the INR is 2.0 or above for at least 24 hours, whichever is longer
• Warfarin should be continued for at least 3 months
  
  • At 3 months, NICE recommend that clinicians should assess the risks and benefits of extending treatment
• NICE advise extending warfarin beyond 3 months for patients with an unprovoked PE
  
  • This essentially means that if there was no obvious cause or provoking factor (surgery, trauma, significant immobility) it may imply the patient has a tendency to thrombosis and should be given treatment longer than the norm of 3 months
• For patients with active cancer, NICE recommend LMWH for 6 months

Thrombosis:

• Thrombolysis is now recommended as first-line treatment for massive PE where there is circulatory failure e.g. hypotension

Question 77

DVT

Diagnosis

Answer 77

• If a patient is suspected of having a DVT, a two-level DVT Wells score should be performed:
• Clinical probability simplified score:
  
  • 2 points or more = DVT likely
  • 1 point or less = DVT unlikely
• DVT likely (2 points or more)
  
  • Proximal leg vein USS should be carried out within 4 hours and, if the result is negative, a D-dimer test
  • If a proximal leg vein USS cannot be carried out within 4-hours, a D-dimer test should be done and LMWH administered whilst waiting for a proximal leg vein USS (which should be performed within 24 hours)
• DVT unlikely (1 point or less)
  
  • Perform a D-dimer and if positive manage:
  • A proximal leg USS within 4 hours
  • If a proximal leg vein USS cannot be carried out within 4-hours, a D-dimer test should be done and LMWH administered whilst waiting for a proximal leg vein USS (which should be performed within 24 hours)

Question 78

Management of DVT

Answer 78

• LMWH or fondaparinux should be given initially after a DVT is diagnosed
• A vitamin K antagonist (e.g. warfarin) should be given within 24 hours of the diagnosis
• The LMWH or fondaparinux should be continued for at least 5 days or until the INR is 2.0 or above for at least 24 hours
  
  • I.e. LMWH or fondaparinux is given at the same time as warfarin until the INR is in the therapeutic range
• Warfarin should be continued for at least 3 months
• At 3 months NICE say you should review the risks and benefits of continuing treatment
• Consider extending warfarin over 3 months for patients with unprovoked proximal DVT if their risk of VTE is high and there is no additional risk of major bleeding
• For patients with active cancer, NICE recommend using LMWH for 6 months

Question 79

Further investigation post management of a DVT

Answer 79

Investigation for malignancy:

• Both malignancy and thrombophilia are obvious risk factors for DVT
• NICE make recommendations on how to investigate patients with unprovoked clots
• Offer all patients diagnosed with unprovoked DVT or PE who are not already known to have cancer the following investigations for cancer:
  
  • A physical examination (guided by the patient’s full history)
  • A CXR
  • Blood tests (FBC, serum calcium, LFTs) and urinalysis
  • Consider further investigations for cancer with an abdomino-pelvic CT scan (and mammogram for women) in all patients aged over 40 years with a first unprovoked DVT or PE

Thrombophilia screening:

• Not offered if patients are on lifelong warfarin (e.g. wont alter management)
• Consider testing for antiphospholipid antibodies if unprevoked DVT or PE
• Consider testing for hereditary thrombophilia in patients who have had an unprevoked DVT or PE and who have a first degree relative who has had a DVT or PE

Question 80

HEad Injury

Triage

Answer 80

Each ED requires a rapid initial assessment of head-injury patients

• Exact system will depend on local policy
• It must enable urgent treatment of those patients liable to complications
• Experienced nursing staff can quickly identify those patients in need of urgent attention based upon:
  
  • Mechanism of injury
  • History from ambulance crew
  • An assessment of vital signs
  • Consciousness according to GCS
  • Limb power
  • Pupil responses
  • BMG
• Patients who are heamodynamically stable, alert and orientated
  
  • Take full history

Question 81

Meningitis Causes

0-3mo

3mo-6yrs

6-60yrs

>60yrs

immunocomp

Answer 81

• 0-3 months
  
  • Group B Streptococcus
  • E.Coli
  • Listeria monocytogenes
• 3 months – 6 years
  
  • Neisseria meningitides
  • Streptococcus pneumoniae
  • Haemophilus influenzae
• 6 years – 60 years
  
  • Neisseria meningitides
  • Streptococcus pneumoniae
• > 60 years
  
  • Streptococcus pneumoniae
  • Neisseria meningitidis
  • Listeria monocytogenes
• Immunosuppressed
  
  • Listeria monocytogenes

Question 82

Meningitis Investigations

Answer 82

• Bloods:
  
  • FBC
  • CRP
  • Coagulation
  • Blood culture
  • Whole blood PCR
  • Blood glucose
  • Blood gas
• Lumbar puncture
  
  • No signs of raised ICP
  • CSF Analysis
    
    • The Ziehl-Neelsen stain is only 20% sensitive in the detection of tuberculous meningitis and therefore PCR is sometimes used (sensitivity = 75%)
    • *mumps is unusual in being associated with a low glucose level in a proportion of cases. A low glucose may also be seen in herpes encephalitis

Question 83

Meningitis Management

Answer 83

• All patients should be transferred to hospital urgently
• If patients are in a pre-hospital setting (e.g. GP) and meningococcal disease is suspected then IM benzylpenicillin may be given if it does not delay the transit to hospital
• Antibiotics: TABLE
• If the patient has a history of immediate hypersensitivity reaction to penicillin or to cephalosporins the BNF recommends using chloramphenicol
• n.b manage contacts

Question 84

Meningitis

Management of contacts

Answer 84

• Prophylaxis needs to be offered to household and close contacts of patients affected with meningococcal meningitis
• Oral ciprofloxacin or rifampicin may be used
• The risk is highest for the first 7 days but persists for at least 4 weeks
• Meningococcal vaccination should be offered to close contacts when serotype results are available, including booster doses to those who had the vaccine in infancy
• For pneumococcal meningitis no prophylaxis is generally needed
  
  • There are however exceptions to this

Question 85

Subarachnoid haemorrhage

Causes

Answer 85

• 85% are due to rupture of berry aneurysms
  
  • Conditions associated with berry aneurysms:
    
    • Adult polycystic kidney disease
    • Ehlers-Danlos syndrome
    • Coarctation of the aorta
• AV malformations
• Trauma
• Tumours

Question 86

Subarachnoid haemorrhage

• Symptoms*
• signs*

Answer 86

symptoms:

• Rapid onset (<2mins), severe, continuous (>2hr) headache
  
  • Occipital
• ‘Hit around the head’
• Vomiting
• Dizziness
• +/- seizures

Signs:

• LOC
  
  • Most concerning
• Neck stiffness
• Drowsy / Decreased GCS
• Photophobia
• Focal neurology

Question 87

SAH

Investigations

Answer 87

CT: Negative in 5%

LP: after 12hrs (allow time for xanthochromia to develop)

Question 88

SAH

Complications

Answer 88

• Cerebral ischaemia
• Rebleeding (in 30%)
• Obstructive hydrocephalus (due to blood in ventricles)
• Vasospasm leading to cerebral ischaemia
• Death

Question 89

SAH

Management

Answer 89

• ABCDE
• 15L/min O2
• Analgesia
  
  • Codeine 30mg PO
  • 5mg morphine IV
• Anti-emetic:
  
  • Metoclopramide 10mg IV/IM
• Reassess often and request neurological observations
• Lie patient flat and advise not to get up or eat
• Involve anaesthetist and neurosurgeon early and consider transfer to ICU if low GCS
• Neurosurgical option
  
  • No clear evidence over early surgical intervention against delayed intervention
• Post-operative nimodipine
  
  • Has been shown to reduce the severity of neurological deficits but doesn’t reduce rebleeding

Question 90

Stroke

• Definition*
• Epidemiology*

Answer 90

Definition

• Also known as cerebrovascular accident (CVA)
• Sudden interruption of the vascular supply to the brain
• Remember that neural tissue is completely dependent on aerobic metabolism so any problem with oxygen supply can quickly lead to irreversible damage

Epidemiology

• Significant cause of morbidity and mortality
• In the UK alone there are over 150000 strokes per year with over 1.2 million stroke survivors
• 4^th largest cause of death in the UK

Question 91

Stroke

Types

Answer 91

• Ischaemic
  
  • <24 hours = Transient ischaemic attack
  • >24 hours = Ischaemic stroke
• Haemorrhagic

Question 92

Stroke

symptoms and signs

Answer 92

• Rapidly developing clinical signs of focal (at times global) disturbance of cerebral function lasting more than 24hrs or leading to death with no apparent cause other than that of vascular origin
  
  • WHO
• Features include:
  
  • Motor weakness
  • Speech problems (dysphasia)
  • Swallowing problems
  • Visual field defects (homonymous hemianopia)
  • Balance problems
• Cerebral hemisphere infarcts may have the following symptoms:
  
  • Contralateral hemiplegia
    
    • Initially flaccid then spastic
  • Contralateral sensory loss
  • Homonymous hemianopia
  • Dysphagia
• Brainstem infarction:
  
  • May result in more severe symptoms including quadriplegia and locked in syndrome
• Lacunar infarcts:
  
  • Small infarcts around the basal ganglia, internal capsule, thalamus and pons
  • This may result in pure motor, pure sensory, mixed motor and sensory signs or ataxia

Question 93

Stroke

Oxford Stoke Classification

Answer 93

• The following criteria should be assessed:
  
  • Unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  • Homonymous hemianopia
  • Higher cognitive dysfunction e.g. dysphagia
• Whilst symptoms alone cannot be used to differentiate haemorrhagic from ischaemic strokes, patients who’ve suffered haemorrhages are more likely to have:
  
  • Decreased level of consciousness: seen in upto 50% of patients with haemorrhagic stroke
  • Headache is also more common in haemorrhagic stroke
  • Nausea and vomiting is also common
  • Seizures occur in upto 25% of patients

Question 94

Stroke

What is the FAST campaign

Answer 94

• Face – Has their face fallen on one side, can they smile?
• Arms = Can they raise both arms and keep them there
• Speech = Is their speech slurred
• Time = Time to call 999 if you see any single one of these signs

Question 95

Stroke: Investigations

Answer 95

• Patients with suspected stroke need to have emergency neuroimaging
• The main cause for urgency is to see whether a patient may be suitable for thrombolytic therapy to treat early ischaemic strokes
• The two types of neuroimaging used in this setting are CT and MRI

Question 96

Stroke (ischaemic) : Management

Answer 96

• If stroke is ischaemic and certain criteria are met, the patient should be offered thrombolysis
• Example criteria include:
  
  • Patients present within 4.5 hours of onset of stroke symptoms
  • The patient has not had a previous intracranial haemorrhage, uncontrolled HTN, pregnant
• Once haemorrhagic stroke has been excluded, patients should be given aspirin 300mg as soon as possible and antiplatelet therapy should be continued

nb: contraindications to thrombolyrsis

Question 97

Stroke (TIA!): Management

Answer 97

• The treatment of TIAs focus on reducing their risk of further attacks
• ABCD2 prognostic score TABLE
• This gives a total score ranging from 0-7
• >= 4 – Higher risk of stroke should be given:
  
  • Aspirin 300mg daily, started immediately
  • Specialist assessment and investigation within 24 hours of onset of symptoms
  • Measures for secondary prevention introduced as soon as the diagnosis is confirmed including discussion of individual risk factors
• <= 3
  
  • Specialist assessment within 1 week of symptom onset, including decision on brain imaging
  • If vascular territory or pathology is uncertain, refer for brain imaging
• >= 2 episodes in one week (crescendo TIA) should be treated as being at high risk of stroke, even though they may have a ABCD2 score of <=3

Question 98

Stroke (haemorrhagic) management

Answer 98

• Neurosurgical consultation to advise further management
• Vast majority of patients are not suitable for surgical intervention
• Management is therefore supportive for haemorrhagic stroke
• Anticoagulants e.g. warfarin and antithrombotic agents e.g. Clopidogrel should be stopped to minimise further bleeding
• If a patient is anticoagulated then this should be reveres as quickly as possible
• Trials have shown improved outcomes in patients who have their blood pressure lowered acutely and this is now part of protocols of haemorrhagic strokes

Question 99

Status Epilepticus

Definition

Answer 99

• Definition:
  
  • Convulsive status epilepticus is defined as a convulsive seizure which lasts for a prolonged period
    
    • > 5 mins
  • Or when convulsive seizures occur one after the other with no recover in between

Question 100

Status Epilepticus

RF

Answer 100

• < 5 years
• Elderly
• Genetic predisposition
• Intellectual disability
• Structural brain pathology

Question 101

Status Epilepticus:

Life threatening causes

Answer 101

• Hypoxia/cardiac arrest
• Hypoglycaemia
• Metabolic (low Ca, high/low Na)
• Trauma
• Meningitis, encephalitis, malaria
• Raised ICP and CVA
• Drug overdose
• Hypertension / eclampsia (pregnancy)

Question 102

Status Epilepticus

Management

Answer 102

• ABCDE
  
  • A = Check airway is patent, consider manoeuvers / adjuncts
  • B = If no respiratory effort, call arrest team
  • C = If no palpable pulse, call arrest team
  • D = If GCS 8, call anaesthetist
• Call for senior help
• Start timing
• 15l oxygen for all patients
• Keep patients safe and put into recovery position is possible
• Monitor:
  
  • HR, O2 sats, BP, cardiac trace, temp.
• Venous access (after 3-4 mins). Take bloods:
  
  • FBC, U&E, LFT, Ca2+, glucose, blood cultures, anticonvulsant levels
• Check glucose:
  
  • If <3.5mmol/l give 100ml 20% glucose STAT
• Priority is termination of the seizure:
  
  • 1^st line = Benzodiazapines such as diazepam or lorazepam
    
    • Lorazepam IV 4mg over 2 min, repeat every 10 min if no effect
    • Diazepam 10mg PR, repeat every 10 min if no effect upto 30mg total
    • Buccal midazolam if unable to secure immediate IV access

If ineffective within 10 mins…

• 2^nd line = Phenytoin, sodium valproate, phenobarbital
  
  • Phenytoin 20mg/kg IV at <50mg/min
  • If taking phenytoin: phenobarbital 10mg/kg IV over 10 min

If no response within 30 minutes:

• 3^rd line = Induction of GA

Question 103

Delirium

• Definition*
• and delirium vs dementia*

Answer 103

Definition:

• Clouding of consciousness leading to an acute confusional state
• Also known as:
  
  • Acute confusional state
  • Acute organic brain syndrome

Question 104

Causes of delirium

Answer 104

• Infection (UTI, chest, meningitis):
  
  • Fever
  • Dysuria
  • Cough +/- sputum
  • Headache, photophobia, neck stiffness
• Withdrawal:
  
  • Alcohol
  • Drugs
• Acute metabolic:
  
  • Hypoglycaemia
  • Failures (cardiac, respiratory, renal or liver)
• Trauma:
  
  • Falls
  • Accidents
• CNS lesion:
  
  • Fits, faints or funny turns
  • Vision
• Hypoxia:
  
  • Shock / haemorrhage
• Deficiency
  
  • B1
  • B6
• Diagnosed with dementia before
• Endocrine:
  
  • Thyroid
  • Adrenal
• Acute vascular insult:
  
  • Stroke in the past
  • Smoker
  • HTN or high cholesterol
• Toxins:
  
  • Prescribed drugs account for 40%
  • New medications
  • Changed doses of any medications recently
• Heavy metals:

Question 105

Delirium

RF

Epidemiology

Answer 105

• What is the most important risk factor for delirium?
  
  • Underlying cognitive impairment
• Epidemiology:
  
  • Affects upto 30% of elderly patients admitted to hospital

Question 106

Delirium

Features

Answer 106

• Memory disturbances (loss of short term > long term)
• May be agitated or withdrawn
• Disorientation
• Mood change
• Visual hallucinations
• Disturbed sleep cycle
• Poor attention

Question 107

Delirium

Management

Answer 107

• Treat the underlying cause
• Modification of environment
  
  • Clock for orientation
  • Photographs
  • Calendar
  • Side room
  • Good lighting
  • Low noise levels
• Sedative
  
  • Avoid if possible
  • Haloperidol 0.5mg

Question 108

Delirium

differential Dx

Answer 108

• Recent falls: Subdural haematoma
• Incontinence: Normal pressure hydrocephalus
• Rapid fluctuations: Lewy Body Dementia
• Hypertension: Ischaemic Heart Disease
• Sexual contact HIV & Syphilis
• Family History: Huntington’s

Question 109

Acute Upper GI Bleed

Causes

Answer 109

• Non-variceal
  
  • Oesophagitis/gastritis
  • Mallory-Weiss
  • Peptic ulcer disease
  • Malignancy
  • Drugs
• Variceal
  
  • Decompensated liver disease

Question 110

Upper GI Bleed:

RF

Answer 110

• Gastric irritant medications (NSAIDs)
• Lack of gastro-protective medication
• Ulcers
• Alcohol / ALD
• Reflux / GORD
• Persistent vomiting
• Endoscopy / stenting procedures
• Past abdo surgery

Question 111

Called re Upper GI Bleed

• Ask on the phone:
• Ask the nurse:

Answer 111

• What to ask on the phone?
  
  • Is the patient alert and talking?
  • Blood streaked in the vomit or vomiting blood
  • Urine output?
  • Has he been drinking recently
  • On any anticoagulants?
  • Is he cannulated?
• Ask the nurse:
  
  • Do repeat set of observations including lying and standing BP
  • Leave his notes and drug chart on the desk
  • If he is not cannulated, prepare kit
  • If he is not catheterised, get the catheter kit ready
  • If he gets worse put out the appropriate MET call (medical emergency team)

Question 112

UGIB: Initial assessment and investigations

Answer 112

Initial Assessment

• AVPU
• ABCDE
• IV access for fluid resus and bloods
• Call senior
• Major haemorrhage protocol/Bleed reg

Investigations:

• Bloods:
  
  • FBC, VBG (lactate), LFTs, clotting screen, X-match 4-6 units
• Consider:
  
  • ECG
  • Perforation?
    
    • Erect CXR, surgical input early
  • Urgent endoscopy if significant drop in Hb or significantly low Hb (<70)
    
    • Gastroenterology/Bleed reg

Question 113

Upper GI Bleed

Management

Answer 113

• 15L of high flow oxygen
• Continuous monitoring
• FBC, U&E, LFT, CRP, Clotting, X-match 4-6U
  
  • Give O- in an emergency (discuss with transfusion lab)
• In the meantime:
  
  • Careful fluid resus STAT – Care diluting Hb and clotting factors
  • Transfuse blood if haemodynamically unstable or Hb less than 70
• PPI:
  
  • Omeprazole 80mg IV STAT – Then 8mg/hr IVI for 72hrs
• Variceal bleeding:
  
  • Terlipressin 2mg IV QDS 24hr then 1mg IV QDS if bleeding settled
• Endoscopy:
  
  • GBS, Rockall score
  • Urgent if active bleeding, significant drop/low Hb
  • Within 24hrs for all else

Question 114

UGIB

Medication review

Answer 114

• Withhold:
  
  • All anticoagulants
  • NSAIDs
• Consider:
  
  • Antiemetic
  • PPI (lansoprazole is indicated for patients on aspirin and Clopidogrel, omeprazole if not)
  • Reverse anti-coagulation (10mg Vit K for warfarin, protamine (1mg/100units)

Question 115

Upper GI Bleed

Key history Qs

Answer 115

• Past GI bleeds
• Dyspepsia / known ulcers
• Known liver disease / oesophageal varices
• Dysphagia
• Vomiting
• Drugs
• Alcohol
• Serious comorbidity

Question 116

Upper GI Bleed scoring systems

Answer 116

• Risk- stratification
  
  • Mortality
  • Re-bleeding risk
• Pre-endoscopy
  
  • Glasgow-Blatchford
    
    • Predicts treatment needs
    • Most useful for discharge with score 0
  • Rockall (pre-endoscopy)
• During-endoscopy
  
  • Forrest score
    
    • Best for re-bleeding risk
• Post-endoscopy
  
  • Rockall
    
    • Good at looking at mortality from UGIB

Question 117

Renal Colic

Initial management (medication and imaging)

Answer 117

• Medication:
  
  • Analgesia – Diclofenac
    
    • IM / oral
  • ??Alpha-adrenergic blockers
    
    • Aid ureteric stone passage
• Imaging:
  
  • USS 1^st line
    
    • Sensitivity = 45%
    • Specificity = 90%
    • Complications such as hydronephrosis can be quickly identified
  • Con-contrast CT
    
    • Confirm diagnosis

Question 118

Renal Colic:

Prognosis

Answer 118

• Stones <5mm will usually pass spontaneously
• Lithotripsy and nephrolithotomy may be used for severe cases

Question 119

Acute Pancreatitis

Causes

Answer 119

• Main cause:
  
  • Alcohol
  • Gallstones
• Causes: GET SMASHED
  
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps (other viruses include Coxsackie B)
  • Autoimmune (e.g. polyarteritis nodosa)
  • Scorpion venom
  • Hypertriglyceridaemia, Hypercalcaemia, Hypercholomicronaemia, Hypothermia
  • ERCP
  • Drugs
    
    • Azathioprine
    • Mesalazine
    • Frusemide

Question 120

Acute Pancreatitis

• Features*
• Examination*

Answer 120

Features

• Severe epigastric pain
• Vomiting is common
• Rarely: Temporary or permanent blindness
  
  • Iscaemic (Purtscher) retinopathy

Examination

• Tenderness
• Ileus
• Low grade fever
• Periumbilical discolouration
  
  • Turners sign
  • Rare
• Flank discolouration
  
  • Grey-Turners
  • Rare

Question 121

Acute Pancreatitis

Diagnosis

Assessment of severity

Answer 121

• Diagnosis:
  
  • Serum lipase > serum amylase
    
    • More sensitive and specific
    • Longer t1/2
    • Does not correlate with disease severity
• Assessment of severity:
  
  • Glasgow, Ransorn scoring systems and APACHE II
  • Biochemical scoring e.g. using CRP

Question 122

Acute Pancreatitis

Management

Answer 122

• ABCDE
• Nutrition:
  
  • Rationale is it helps prevent bacterial translocation
• Use of ABx therapy
  
  • Some surgeons give
• Surgery
  
  • Patients with acute pancreatitis due to gallstones should undergo early cholecystectomy
  • Patients with an obstructed billary system due to stones should undergo early ERCP
  • Patients who fail to settle with necrosis and have worsening organ dysfunction may require debridement
  • Patients with infected necrosis would undergo either radiological drainage or surgical necrosectomy

Question 123

Acute Cholecystitis

• Definition*
• Cause*
• Features*

Answer 123

• Definition:
  
  • Inflammation of the gallbladder
• Cause:
  
  • Gallstone in cystic duct
    
    • ->Bile stasis
      
      • ->Bacteria overgrowth -> ascending cholangitis
• Features:
  
  • Mid-epigastric > RUQ pain
  • Nausea and vomiting
  • Fever
  • Murphy’s sign of examination
  • Occasionally mildly deranged LFTs
    
    • Especially if Mirizzi syndrome
    • Increased ALP
    • Increased conjugated bilirubin

Charcot’s cholangitis triad is the combination of jaundice; fever, usually with rigors; and right upper quadrant abdominal pain. It occurs as a result of ascending cholangitis (an infection of the bile duct in the liver).

Question 124

Acute Cholecystitis: Investigations

Answer 124

• Investigations:
  
  • USS
    
    • Sonographic Murphy’s sign
    • Gallbladder wall thickening
    • Sludge
    • Distension of GP and bile duct

Question 125

Acute Cholecystitis

Management

Answer 125

Management:

• ABCDE
• Supportive
  
  • Analgesia
  • Fluids
  • ABx
• Cholecystectomy
  
  • Usually within 48 hours of presentation

Complications: Rupture and peritonitis

Question 126

Alcohol Withdrawal

Mechanism

Answer 126

• Chronic alcohol consumption enhances GABA mediated inhibition in the CNS (like benzodiazepines) and inhibits the NMDA-type glutamate receptors
• Alcohol withdrawal is thought to lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)

Question 127

Alcohol withdrawal

Features

Answer 127

• Symptoms start at 6-12 hours
  
  • Tremor
  • Sweating
  • Tachycardia
  • Anxiety
• Peak incidence of seizures at 36 hours
• Peak incidence of delirium tremens is at 48-72 hours:
  
  • Coarse tremor
  • Confusion
  • Delusions
  • Auditory and visual hallucinations
  • Fever
  • Tachycardia

Question 128

Acohol Withdrawal: Management

Answer 128

• 1^st line = Benzodiazepines e.g. chlordiazepoxide
  
  • Usually part of a reducing dose protocol
  • Carbamazepine also effective in treatment of alcohol withdrawal

AND prevent Korsakoffs with pabrinex (B1 thiamine)

Question 129

DKA

• Pathophys*
• Precipitating factors*
• Presentation*

Answer 129

Pathophysiology:

• Absolute or relative decrease in insulin levels
• A high plasma glucose causes an osmotic diuresis with Na and water loss
  
  • Hypotension
  • Hypo-perfusion
  • Shock

Precipitating:

• Infection – Commonly UTI, RTI, skin
• Infarction – MI, stroke, GI tract
• Insufficient insulin - Missed insulin doses
• Intercurrent illness -

Presentation

• May be a complication of existing T1DM
• May be a first presentation
• Features:
  
  • Abdominal pain
  • Polyuria, polydipsia, dehydration
  • Kussmaul breathing (deep hyperventilation)
  • Acetone-smelling breath (‘pear drops smell’)

Question 130

DKA: Diagnostic criteria

Answer 130

Question 131

DKA: Investigations

Answer 131

• Check to confirm diagnosis and possible underlying cause(s)
  
  • Check BMG and test urine for glucose and ketones
  • Send bloods for U&E, blood glucose, creatinine, osmolality
  • ABG to check for metabolic acidosis +/- respiratory compensation
  • FBC and CXR to look for pneumonia
  • Blood cultures and if appropriate, throat or wound swabs
  • Urine/sputum microscopy and culture

Question 132

DKA: MAnagement

Answer 132

• ABCDE
• If altered consciousness/coma is present, provide and maintain a patent airway
• Give high FiO2
• Fluid replacement:
  
  • Most patients with DKA are deplete around 5-8 litres
  • Normal / isotonic saline is used initially (0.9% NaCl)
    
    • 1L over 0.50-1hr
    • 500ml/hr for next 2-3 hours
  • Persistent hypo-perfusion may require increased infusion rate or colloids
  • Avoid over-rapid infusion with the risk of pulmonary oedema and ARDS especially in the elderly
• Insulin:
  
  • Fixed rate IV infusion at 0.1 U/kg/hour
  • Check plasma glucose levels every hour
  • Once blood glucose is <15mmol/l an infusion of 5% dextrose should be started
• Correction of hypokalaemia
  
  • Monitor urine output (most accurate with urinary catheter)
  • Arrange admission to ICU, HDU or acute medical admissions unit

Question 133

DKA: other aspects of management

In addition to fluid, insulin, potassium

Answer 133

• Signs of infection:
  
  • Often masked
  • Temperature is rarely raised
  • If in doubt treat with broad spectrum ABx
• Over-rapid fluid replacement:
  
  • Can cause cardiac failure, cerebral oedema and ARDS
  • Especially in elderly or those with cardiac disease
  • CVP monitoring may be needed
• Clotting:
  
  • Hyperglycaemia causes a hypercoagulable state
  • DVT or PE may occur
  • Administer prophylactic anticoagulation with LMWH in DKA

Question 134

AKI

Definition

Incidence

Risk Factors

Answer 134

• Definition:
  
  • Reduction in renal function following an insult to the kidneys
• Incidence:
  
  • Around 15% of patients admitted to hospital develop AKI
• Risk factors:
  
  • Chronic kidney disease
  • Other organ failure / chronic disease e.g. heart failure, liver disease, DM
  • History of AKI
  • Use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, ARBs, diuretics) within the past week
  • >65 years

Question 135

AKI: causes

Answer 135

• Pre-renal
  
  • Hypovolaemia secondary to diarrhoea/vomiting
  • Renal artery stenosis
• Renal
  
  • Glomerulonephritis
  • Acute tubular necrosis
  • Acute interstitial nephritis
  • Rhabdomyolysis
  • Tumour lysis syndrome
• Post-renal
  
  • Kidney stone in ureter or bladder
  • Benign prostatic hyperplasia
  • External compression of the ureter

Question 136

AKI: What happens when the kidneys stop working?

Answer 136

• A reduced urine output.
  
  • The term oliguria is defined as a urine output less than 0.5ml/kg/hr
• Fluid Overload
• A raise in molecules that the kidney normally excretes / maintains a careful balance of:
  
  • Potassium, urea and creatinine

Question 137

AKI:

Symptoms & signs

Answer 137

Symptoms & signs:

• Many patients with early AKI experience no symptoms.
• However, as renal failure progresses the following may be seen:
  
  • Reduced urine output
  • Pulmonary and peripheral oedema
  • Arrhythmias (secondary to changes in potassium and acid-base balance)
  • Features of uraemia (e.g. pericarditis or encephalopathy)

Question 138

AKI:

• Detection*
• Investigation*

Answer 138

Detection

• Detect AKI in line with the (p)RIFLE, AKIN or KDIGO definitions by using any of the following criteria:
  
  • A raise in serum creatinine 20 micromoles/L or greater within 48 hours
  • A 50% or greater rise in serum creatinine known or presumed to of occurred within the past 7 days
  • A fall in urine output less than 0.5ml/kg/hr for more than 6 hours in adults

Investigations:

• All patients with suspected AKI should have urinalysis
• Imaging:
  
  • If patients have no identifiable cause for the deterioration or are at risk of urinary tract obstruction they should be offered a USS within 24 hours of assessment

Question 139

AKI: Management

Answer 139

• Largely supportive
  
  • Careful fluid balance to ensure that the kidneys are properly perfused but not excessively to avoid fluid overload
• Medication review: TABLE
• Manage hyperkalaemia:
• Renal replacement therapy e.g. haemodialysis
  
  • Used when the patient is not responding to medical treatment of complications e.g. hyperkalaemia, acidosis and uraemia

Question 140

Hyperkalaemia

• Define*
• Causes*

Answer 140

Normal range for [K+]: 3.5-5.5mM

Causes:

• Ineffective elimination:
  
  • AKI/CKD
  • Medications
    
    • K+ sparing diuretics
    • ACE-I
    • AT-2 blockers
    • Spirinolactone
  • Mineralocorticoid deficiency
• Excessive cellular release
  
  • Transcellular shift: acidosis (DKA), beta-blockers, suxamethonium
  • Rhabdomyolysis
  • Burns
  • Tumour lysis syndrome
• Excessive intake
  
  • Potassium supplements
  • Laxatives containing K+ (Movicol)
• Pseudohyperkalaemia:
  
  • Tourniquet time
  • Test tube haemolysis

Question 141

Hyperkalaemia patient:

• What to ask on the phone?*
• What to ask the nurse to do?*

Answer 141

• What to ask:
  
  • Are they alert and talking?
  • Any chest pain?
  • Urine output?
  • New or old problem?
• Ask nurse to:
  
  • Do an ECG
  • Gather notes and drug chart on the desk
  • If they are not cannulated, prepare kit
  • If they are not catheterised, prepare kit

Question 142

Hyperkalaemia:

• Initial Aprroach*
• and*
• History*

Answer 142

• Initial approach:
  
  • AVPU
  • ABCDE
  • ECG
  • Unwell or stable?
  • Fluid balance?
• History:
  
  • Acute? / Chronic accumulation?
  • Patient have CKD?
  • Cardiac history? Eplerenone, are they being diuresed?
  • Look at fluid charts?
  • Is patient diabetic?
  • Symptoms:
    
    • Palpitations / dizziness

Question 143

Hyperkalaemia

Investigations (and findings)

Answer 143

• Investigations:
  
  • Repeat sample if unsure of accuracy of hyperkalaemia e.g. haemolyis
  • ABG/VBG
    
    • Helpful if you suspect a spurious result
  • ECG signs:
    
    • >5.5
      
      • Tall, peaked T waves
    • >6.5
      
      • Flat P waves
      • Prolonged PR segment
    • >7.0
      
      • Bizarre QRS
      • Conduction block
      • Sinus bradycardia / AF
      • Sine wave
      • VF

Question 144

Hyperkalaemia:

Management

Answer 144

• Follow trusts hyperkalaemia protocol
  
  • Treat if K+ > 6.5 or if K+ >5.5 with K+ related ECG changes
• Stabilise the myocardium:
  
  • Calcium gluconate
  • 30mls 10% over 10 min
• Shift K+ into cells:
  
  • Insulin and glucose
    
    • Activates Na+/K+ ATPase
    • 10 units Actrapid in 100mls 20% dextrose
    • IV fluids if dehydrated
  • Salbutamol
    
    • Similar effect to insulin
    • 5mg NEB
    • 2-hourly
    • Effect reduced if on dialysis, beta-blocker or digoxin
• Lower total body potassium:
  
  • Stop drugs that increase K+
  • Advise on diet
    
    • No chocolate, fruit juice, bananas until dietician review
• Calcium resonium:
  
  • If K+ rebounds

Question 145

Potassium and hydrogen physiological interaction

Answer 145

• K+ and H+ can be thought of as competitors
• Hyperkalaemia tends to be associated with acidosis because as the potassium levels rise, fewer hydrogen ions enter cells
• Hypokalaemia with alkalosis:
  
  • Vomiting
  • Diuretics
  • Cushing’s syndrome
  • Conn’s syndrome
• Hypokalaemia with acidosis:
  
  • Diarrhoea
  • Renal tubular acidosis
  • Acetazolomide
  • Partially treated DKA

Question 146

Causes of Hypokalaemia

Answer 146

• Hypokalaemia with HTN
  
  • Cushing’s syndrome
  • Conn’s syndrome (primary hyperaldosteronism)
  • Liddle’s syndrome
  • 11-beta hydroxylase deficiency
    
    • 21-hydroxylase deficiency, which accounts for 90% of congenital adrenal hyperplasia, is not associated with HTN
• Hypokalaemia without HTN
  
  • Diuretics
  • GI loss (diarrhoea, vomiting)
  • Renal tubular acidosis (types 1 and 2)
  • Bartter’s syndrome
  • Gitelman syndrome

Question 147

Features of hypokalaemia

Answer 147

• Muscle weakness
  
  • Hypotonia
  • Hypokalaemia predisposes patients to digoxin toxicity
    
    • Care should be taken if patients are on diuretics
• ECG Features:
  
  • U waves (see below)
  • Small or absent T waves
  • Prolonged P-R
  • ST depression

Management: SLOWLY correct electrolyte imbalance

Question 148

Bowel Obstruction

Question 149

Neutropenic Sepsis:

Question 150

Acute Appendicitis:

Question 151

Hypoglycaemia Coma:

Question 152

Blood Transfusion & Blood Products Reactions:

Question 153

Acute Lower GI Bleed: