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Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

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Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011
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Page 1: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Acute Medical Cases

Dr Jack Bond

Clinical Teaching FellowNov 2011

Page 2: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Aims

To introduce you to the presentation and initial management of:

• Obstructive airways disease• Acute kidney injury• GI bleed

Page 3: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Group work

• Divide into groups of 4-6

• Each group given a case

• Spend 10 minutes working through the case

• Select a member of your group to present the case and management back to the whole group

Page 4: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

COPD - Objectives

• Be able to diagnose COPD • Describe the initial management of COPD exacerbation• List the indications/contraindications for NIV• Understand set up and monitoring of NIV• List complications associated with NIV

Page 5: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Case 1

A 75 year old man attends his GP with breathlessness over the last 6 months. He has been coughing up phlegm most days for the last few months, but worse over the last few days. He has smoked 20 cigarettes a day for the past 30 years.

On examination, sats are 93% on air, RR 24, temp 38.3, BP 124/75, HR 85. The chest shows widespread wheeze throughout.

Page 6: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Case 1

1. List your differential diagnosis

2. what diagnostic tests would confirm a diagnosis of chronic obstructive pulmonary disease?

3. How would you assess severity of COPD?

4. in A+E, what would be your initial management of this patient?

Page 7: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

COPD - Background

• COPD is predominantly caused by smoking and is characterised by airflow obstruction that:

- is not fully reversible

- does not change markedly over several months

- is usually progressive in the long term

Page 8: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Diagnose COPD

• over 35, and

• smokers or ex-smokers, and

• have any of these symptoms: - exertional breathlessness - chronic cough - regular sputum production,o frequent winter ‘bronchitis’ o Wheeze

• And no clinical features of asthma

[2004]

Page 9: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Differentiating COPD from asthma

Clinical features COPD Asthma

Smoker or ex-smoker Nearly all Possibly

Symptoms under age 35 Rare Often

Chronic productive cough Common Uncommon

Breathlessness Persistent and progressive

Variable

Night time waking with breathlessness and or wheeze

Uncommon Common

Significant diurnal or day to day variability of symptoms

uncommon Common

[2004]

Page 10: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Differentiating COPD from asthma: 2

• If diagnostic uncertainty remains:-

- FEV1 and FEV1/FVC ratio return to normal with drug therapy

- a very large (>400ml) FEV1 response to bronchodilators or to 30mg prednisolone daily for 2 weeks

- serial peak flow measuremenst showing significant (20% or greater) diurnal or day-to-day variability

[2004]

Page 11: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Diagnose COPD: assessment of severity

• Assess severity of airflow obstruction using reduction in FEV1

NICE clinical guideline 12

(2004)

ATS/ERS 2004 GOLD 2008 NICE clinical guideline 101

(2010)

Post-bronchodilator

FEV1/FVC

FEV1 % predicted

Post-bronchodilator

Post-bronchodilator

Post-bronchodilator

< 0.7 80% Mild Stage 1 (mild) Stage 1 (mild)*

< 0.7 50–79% Mild Moderate Stage 2 (moderate)

Stage 2 (moderate)

< 0.7 30–49% Moderate Severe Stage 3 (severe) Stage 3 (severe)

< 0.7 < 30% Severe Very severe Stage 4 (very severe)**

Stage 4 (very severe)**

* Symptoms should be present to diagnose COPD in people with mild airflow obstruction** Or FEV1 < 50% with respiratory failure

[new 2010]

Page 12: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

• 4 year survival o 0-2 Points: 80%o 3-4 Points: 67%o 5-6 Points: 57%o 7-10 Points: 18%

Page 13: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

COPD: acute exacerbations

• Increasing dyspnoea• Increasing sputum volume• Increasing sputum purulence

• (change in character)

→ treat as infective exacerbation

Page 14: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Initial management

• A-E - Sepsis!• Oxygen –

o high flow initally, consider controlled to aim sats 88-92% when stable

• Nebulised bronchodilators

• Steroids

• Antibiotics (sepsis six pathway)

Page 15: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

If not responding

Recheck A-E – your patient is probably septic and you haven't noticed

ABG

CXR

Consider NIV

Consider aminophylline

Page 16: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Case 2

An 76 year old man attends A+E with breathlessness. He has known COPD, with an FEV1/FVC 0.3, predicted FEV1 35% a few months ago. He uses oxygen at home, 2L for 16 hours a day. Over the last week he has had a productive cough with phlegm and fever.

His obs are RR 16, sats 85% on 2L oxygen, HR 110, BP 134/68, temp 33.5. The examination shows crackles in his right lung base, but widespread wheeze throughout both lung fields.

The paramedics have given him a few salbutamol nebs and some IV hydrocortisone in the ambulance an hour ago but he is not improving as yet.

What's your initial management plan?

Page 17: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Case 2 continued

The nurse calls you as he has become drowsy. You take an ABG which shows pH 7.23, pO2 8.3kPa, pCO2 8.4kPa, HCO3- 24 mmol/l. His obs are repeated and show RR 12, sats 90% on 4L oxygen, HR 115, BP 115/68.

What is your management plan?

How would you start someone on NIV?

How would you monitor their progress on the ward?

What are the indications for NIV?

What are the contraindications?

List complications of NIV

Page 18: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

NIV – non-invasive ventilation

Ventilation (V) = Tidal volume x Resp rate

Increase V, increase CO2 clearance

Page 19: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

NIV – BiPAP diagram

Page 20: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

NIV – indications in COPD

• Respiratory acidosis (pH <7.35, PaCO2 >6kPa) – Hypercapnic respiratory failure

• Persistent despite maximal medical therapy for no more than one hour

Page 21: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Other indications for NIV

Might be considered in:- controversial

Hypercapnic resp failure due to other causes Cardiogenic pulmonary oedema Weaning from tracheal intubation

Page 22: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

NIV contraindications

- respiratory arrest- uncooperative patients – confused- unable to protect airway- reduced conscious- facial, oesophageal, gastric surgery- face trauma

Page 23: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Starting NIV

• Dedicated area that allows high dependency nursingo HDU/ITUo Respiratory wardo A+E resuso Medical admissions

• Not usually on a general ward – the nursing staff will not know how to deal with it

Page 24: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Starting NIV

• Physio or nursing help• Select settings for IPAP, EPAP and resp rate

• IPAP start at 10cm H20• EPAP start at 5 cm H20• Backup rate of 8 breaths per minute

• Most patients tolerate these settings, but may vary, especially those on long term NIV

Page 25: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

NIV Management

• IPAP increased by 2-5 cm H20 every 10 mins until either therapeutic response or IPAP of 20 cm H20 reached

• Oxygen through circuit, aim sats 88-92%

• Bronchodilators can continually be given though it affects the pressures

Page 26: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Monitoring NIV

• Baseline ABG, RR, HR• Repeat ABG after one hour of starting• After every setting change, repeat ABG at 1 hour• Otherwise, every 4 hours, or if not well

• Aim minimum 6 hours treatment• Most people better by 24 hours on NIV• Weaning thereafter

Page 27: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Complications of NIV

• Increased IPAP – pneumothorax

• Decreased pre-load – may drop BP • Increased risk of aspiration

• Face mask discomfort

• Anxiety + confusion

Page 28: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Escalation of care

• Plan for the failure of NIVo Are they appropriate for invasive ventilation and

why?

• Factors limiting survivalo Pre-morbid stateo Severity of physiological disturbanceo Reversibility of acute illnesso Relative contraindicationso Patients wisheso Long term oxygen therapy

Page 29: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Decision making

• Consultant led, but involves MDT inputo You as the FY1 can influence thiso Nursing staff have valuable input

• Involve the patient where possible

• Family involvement is best practiceo However we are not asking them to make a

decisiono Decisions are the responsibility of doctors

Page 30: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Palliation

• Symptoms of breathlessness are distressing

• NIV can be continued if it provides symptom relief, but would normally be withdrawn

• Opiates and benzodiazepines for breathless are optimal therapy

• Palliative care team involvement

• Liverpool care pathways

Page 31: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

COPD Key Messages

Hypercapnic respiratory failure is indication for non-invasive ventilation in COPD

Call for early support (within 1 hour) of maximum medical therapy

Limits of care should be clearly planned when starting NIV

Page 32: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

AKI Questions

“Everything you wanted to know about kidneys but were afraid to ask”

• Write down your question• Pass it forward• Answers later

Page 33: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Acute Kidney Injury - Objectives

• To recognise AKI• To differentiate between pre-renal, renal and post

renal causes of AKI• To recognise and manage hypovolemia• To manage hyperkalemia and pulmonary odema

• To know indications for emergency dialysis

• How to call a nephrologist without getting shouted at

Page 34: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011June 2009

Page 35: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Definition of AKI

Rise in serum creatinine >50% from baseline

Or

Urine output <0.5ml/kg/hr for 6 hours

Page 36: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Creatinine criteria Urine output criteria

≥ 50-100% rise in Cr

Urine output <0.5 ml/kg/hrfor 6 hours(=240 ml at 80 kg)

SIMPLIFIED RIFLE OR AKIN DEFINITIONUsually based on Creatinine rise Loss and End stage components of RIFLE now dropped

101-200% rise in Cr

Urine output <0.5 ml/kg/hrfor 12 hours(= 480 ml at 80 kg)

>200% rise in Cr

Urine output <0.3 ml/kg/hr for 24 hours or anuria 12 hours

Risk orAKIN 1

Injuryor AKIN 2

Failureor AKIN 3

Highsensitivity

HighspecificityOliguria

Page 37: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Which scenario is AKI? T/F/Can't tell?1. 85 male, D+V, creat 120, usually 80

2. 82 female, D+V, Urea 15.2, Creat 150

3. 60 male, diabetic, creat 250, usual 200

4. 74 male, legionella pneumonia, Na 118, Creat 130, usual creat 70

5. 63 female, diabetic, myocardial infarct, eGFR 25, usual eGFR 35

Page 38: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Slow rise in Cr untileventually a new steady state is reached

Large acute drop in GFR with oligoanuria

Only a small early rise in Cr: not easy to recognise as AKI

Suspect AKI in a sick patient with a modest rise in their creatinine

GFR falls rapidly to near zero- only shown by oliguria

Page 39: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Effect of AKI on odds of deathChertow GM et al J Am Soc Nephrol 2005

Page 40: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Mehta et al. Critical Care 2007 11:R31

Rise in serum creat > 50% baseline

• baseline creatinine of 80 mmol/L

• Rises to 120 mmol/L

• Significant kidney injury

• This is the moment to act – it is too late when the creatinine reaches 400

Page 41: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Case 3

66 year old man is admitted to A+E with breathlessness. He has been unwell for a week, coughing up phlegm and having fevers. His past medical history includes diabetes and hypertension. His medication is metformin, aspirin, ramipril, atenolol and simvastatin.

On examination he is unwell. His obs are BP 85/50, HR 115, Sats 92% on air, RR 25, Temp 38.3. You hear coarse crackles on the right side of his chest. A CXR confirms pneumonia.

His blood results come back which show Na 130, K 4.5, Urea 14.3, Creat 189. The nurse asks you to assess him as he hasn't passed urine since admisssion.

Page 42: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Case 3

Outline the management you would undertake in A+E.

What is the likely cause for his renal failure?

Is this acute or chronic renal failure? How severe is his renal failure?

What investigations would you order and why?

What risk factors are evident in this man's case that make him more likely to have renal failure?

What information can be gained from a urine dipstick?

Page 43: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

AKI risk factors

• Most people have > 1 risk factor

• Age• Drugs (ACEi, diuretics, NSAIDS)• Chronic kidney disease• Hypovolemia/Sepsis• Diabetes

Page 44: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

AKI: causes

• Important to attempt to categorise broadly into one of 3 groups

• sepsis/hypovolemia 70%• drug related, acute GN 20%• obstruction 10%

PRE-RENAL

RENAL

POST-RENAL

Page 45: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Cause of AKI – 3 tests

3 assessments result in a 45% 36 months survival, compared with 15% for 0 assessments

o Fluid/volume assessment PREo Urinalysis RENALo Ultrasound POST

Page 46: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Question

Which of these is the most useful indicator of hypovolaemia?:1.capillary refill time > 5 seconds2. jugular venous pulse not visible at 30º3.postural pulse rise > 30 bpm4.systolic blood pressure < 95 mm Hg5.systolic BP rise with

250 ml saline bolus > 20 mm

Page 47: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Volume assessment - key

MEWS score Cap refillBP, HR, Postural BPJVPAuscultate lungsPeripheral odemaUrine output

Page 48: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Volume assessment

You are the FY1 covering orthopedics. You have been asked to see 74 female post #NOF as she has low urine outputPMH - diabetes, hypertension

Creat 150, baseline 100, urine output 20mls in last hourCRT 2 secs, BP 110/50, HR 98, JVP ??, chest couple of creps, no edema

Is patient fluid depleted, euvolemic or overloaded?

How much fluid would you prescribe?

Page 49: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Volume management

Most patients are hypovolemic (70%)

If not grossly overloaded – fluid challenge - 500ml + recheck

“Normal” BP for 75 year old – 150/70 - a post op BP of 110 is relatively hypotensive

Page 50: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Volume assessment

Most patients are likely 2-3 liters or more fluid deficient

Sepsis – doubly important

Page 51: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Urinalysis

- this points towards intrinsic renal disease Ie glomerulonephritis

- blood and proteinuria on dipstick = nephrology referral

Page 52: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

AKI investigations

u/s urinary tract

- suspect obstruction in men with prostatic symptoms

- palpable mass

- intra-abdominal malignancy compress ureters with no bladder palpable females

- where cause not obvious

Page 53: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

AKI investigations

By doing all 3 investigations survival significantly improved

- fluid assessment - urinalysis - u/s urinary tract

Page 54: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

AKI QUESTION TIME

Page 55: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Hyperkalaemia - True/False

1. Calcium gluconate acts by reducing the serum potassium T/F2. Insulin/dextrose infusion requires 30mins to shift potassium into cells T/F3. Insulin/dextrose infusion effects last for 24 hours T/F4. Salbutamol nebulisers have the same effect as insulin/dextrose infusion T/F5. IV sodium bicarbonate can reduce potassium T/F6. to treat hyperkalemia you would prescribe 50 units of actrapid in 50ml 50% dextrose T/F7. 10ml of 10% Calcium gluconate is the correct prescription for the treatment of hyperkalemia T/F 8. Calcium resonium acts within minutes to reduce serum K T/F

Page 56: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Hyperkalemia

K+ >6.5

- 1st – repeat measure on VBG/ABG (takes 5 mins) - if true – ECG - if life threatening changes

o Calcium gluconate 10ml 10% stat (through big vein – tissue burns)

- thereafter 10 units actrapid in 50mls 50% glucose over 30 mins.

Page 57: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Hyperkalemia

Insulin/dextrose – lasts 4 hours only

- in meantime correct cause of high K - Repeat ABG at 4 hours to see if better

If K+ still high – DIALYSIS MAY BE INDICATED

Page 58: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Hyperkalemia

Salbutamol nebs (10-15mg) have same action as insulin/dextrose and may be an option - caution in cardiac disease

IV sodium bicarbonate 1.26% - useful in dehydrated patient who is ACIDOTIC - discuss with senior, but consider if HCO3 <18 and

needs ongoing fluid replacement - worsens pulmonary oedema ++

Page 59: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Hyperkalemia

Key is to recheck after treatment

Correct underlying cause

Consider dialysis

Page 60: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Pulmonary oedema in AKI

ABCDE approachOxygenGTN infusionDiamorphineConsider large dose furosemide 250mg IVCPAPITU/ventilationCorrect cause of renal failure (days)

Page 61: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

Dialysis indications

• Consider haemodialysis/haemofiltration if:

• Resistant hyperkalaemia >6.0• Fluid overload and no urine output• Persistent acidosis pH<7.2

• Call for senior support in all cases• Nephrology referral for dialysis patients admitted

under any other specialty

Page 62: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

When to call nephrology

Any known dialysis patient admittedAny known renal transplant patient admitted

Any case of AKI where cause not clearWorsening AKIEmergency dialysis indicationsSuspect glomerulonephritis

Page 63: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

What info to have when calling nephrologist

Your (boss') reason for referral The history and background in your head – dont read the notes to me – check with patient if not clear historyThe notes by the phoneThe obs chart by the phone (MEWS, Urine output)A urine dipstick resultYour assessment of the patients fluid statusAn up to date venous blood gas (that day)

Page 64: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

AKI: Summary

• Small changes in creatinine can have grave clinical consequences

• ABCDE assessment and careful management of fluid status is mainstay of treatment

• Get help early

Page 65: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

What abnormalities can be seen?

Page 66: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

ECG features of hyperkalaemia

Any of: • Small or absent p waves• Arrhythmia-commonly AF• Wide QRS complexes• Increased P-R interval• Peaked, tented T waves• Sine wave pattern• Asystole!

Page 67: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Pulmonary Oedema T/F

1. Pulmonary oedema in a patient with pre-renal failure will respond to a fluid challenge T/F2. Furosemide 40mg IV will likely produce symptom relief T/F3. GTN infusion works in renal failure to relieve breathlessness T/F4. Venesection can be used to treat pulmonary oedema if the BP is <100mmHG T/F5. Patients in pulmonary oedema who are oligo/anuric will likely require dialysis T/F

Page 68: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Page 69: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Question 1

For most patients with AKI what is the most useful means of classifying the presence and severity of AKI:1.% creatinine rise 2.% estimated GFR fall 3.creatinine rise in micromoles/litre4.estimated GFR in ml/min/1.73m2

5.urine volume in ml/kg/hour

Page 70: Acute Medical Cases Dr Jack Bond Clinical Teaching Fellow Nov 2011.

11/21/2011

Question 2

What is the main diagnosis you are looking for when you do a dipstick in a new case of AKI?1.acute interstitial nephritis2.acute tubular necrosis3.obstructive uropathy4.glomerulonephritis5.renovascular disease


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