Life in the Fast Lane Medical Blog » lecture notes

Mediterranean Emergency Medicine Congress – VI – Podcasts

Mike Cadogan — Sat, 31 Dec 2011 04:58:35 +0000

Life in the Fast Lane Medical Blog Mediterranean Emergency Medicine Congress – VI – Podcasts

Kos Greece – 12 – 14 September 2011

Joe Lex has just uploaded more than 170 free MP3 podcasts of talks from MEMC-VI on Kos Greece, from September 12-14 2011. You can either search directly for talks on Free Emergency Talks, visit the YouTube channel, use the catalogue of links below to access them or wait for them to be entered into the LITFL podcast database…enjoy

Day 1, Plenary

Patrick Croskerry (Canada): Diagnostic Error – A Case of Neglect
Ziad Kazzi (Georgia): The Public Health Impacts of a Nuclear Plant Crisis in Your Backyard

Day 1: Resuscitation

Day 1: Shock & Sepsis

Day 1: Toxicology & Pharmacology

Day 1: Medical Imaging

Day 1: History of Emergency Medicine

Day 1: Administration

Day 1: Research in Emergency Medicine

Day 2: Plenary

Day 2: Cardiovascular Emergencies

Day 2: Paediatric Emergencies

Day 2: Disaster and Mass Casualty

Day 2: Prehospital Medicine

Day 2: Abdominal Emergencies

Day 2: Pulmonary Emergencies

Day 2: Administration

Day 2: Medical Education

Day 3: Plenary

Day 3: Trauma

Day 3: Neurologic Emergencies

Day 3: Psychobehavioral Emergencies

Day 3: Environmental and Wilderness Emergencies

Day 3: HEENT Emergencies

Day 3: Ultrasound in Emergency Medicine

Day 3: Administration

Day 3: Research

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

Emergency Medicine in the Developing World 2011 (Part 2)

Chris Nickson — Fri, 18 Nov 2011 14:33:36 +0000

Life in the Fast Lane Medical Blog Emergency Medicine in the Developing World 2011 (Part 2)

You’ll remember from Part 1 that the 3rd biennial ‘Emergency Medicine in the Developing World‘ conference is being hosted in Cape Town, by the Emergency Medicine Society of South Africa (EMSSA). LITFL friend Sa’ad Lahri (from GF Jooste Hospital) is on the conference committee and feeding us a series of key points and pearls typed on the fly by Ross Hofmeyer. These notes are from Day 2 of the conference. The audio of these talks are to be made available on Free Emergency Medicine Talks in the near future.

Let’s rip into it…

Increase in demand for blood transfusion products but decreasing supply
African HIV epidemic straining supplies
Acute resus – Hb > 10g/dL probably required
ICU/longer term – Hb >7 g/dL should be sufficient unless background illness
Tissue oxygenation is what counts, not Hb (DO2 is the most important)
DO2 requires absolute minimum Hb 3 g/dL
Extraction reserve from Hb 25-75% (1-3 molecules ‘extra’ under normal conditions)
Increase a-v O2 gradient implies patient is nearing limit of reserve
ScvO2 use paired with ABG can thus be used as a guide (ala Rivers EGDT)
Lactate increase follows after decrease in ScvO2
ScvO2 >70% and/or lactate >8 may be a good triage criterion
Patient’s blood is best – keep it in!
Maintain normothermia – one litre of room-air fluid can drop core temperature by 0.5-1 degree C
Blood conservation in trauma – permissive hypotension where it is not contra-indicated. In SA with long delays (>90 minutes) need some more resus – aim for SBP>100/MAP>60. Vasopressin being researched.
Hemopure:

3 year shelf life
Bovine haemoglobin
Functions as a colloid – no clotting factors
Hypertension with rapid administration (due to NO binding)
Bridge to transfusion/neosynthesis of blood (Iron available in the Hemopure; increased EPO due to decreased red cell mass)

HBBS given a bad name by a very flawed meta-analysis
Potential uses of blood substitutes are legion
Blood conservation – intraoperative cell salvage (Takagi Arch Surg 2007). Can be used with a fresh bowel perforation
Anticoagulation:

Platelets effective in 4hrs after aspirin and 12 hrs after clopidogrel
Warfarin can be reversed in minutes with PCC(Haemosolvex), hours with FFP and days with Vitamin K
Best assessed with TEG if available.

Aim for

Platelets >50 (if bleeding)
PTT < 2x control
Fibrinogen <1 -> cryoprecipitate
Fibrinogen 1-2 -> 1-2u plasma
Fibrinogen >2 -> possible error; consider tranexamic acid

Conflicts of interest declared.

UMD Shock Trauma – about 70% of trauma patients need no more than 2-3 units of packed red blood cells
HBOC vs RBC – Bovine Hb vs human, higher O2 carrying capacity, much less viscosity, much shorter half-life; long shelf life. (Similar oncotic pressure etc).
Hemopure:

No cross-match/typing needed
Ready-to-use
No know disease transmission
Can be stored at 4-30 degrees for 3 years
Carries O2 and treats hypovolaemia
No known immune effects
Rheological advantage

Fewer resources and less infrastructure required to maintain a supply of HBOC rather than blood.
Transfusion errors are not an issue due to lack of cross-match requirement.
Testing blood for transmitted diseases now accounts for 50% of the cost of a unit.
Is Hemopure safe and efficacious?

HEM-115 study (n=688) – no mortality difference
Moderate needs (<3u) side effects and mortality identical
No MI’s in patients receiving <10u in Hemopure arm and one in RBC arm

Several case studies presented
Best use = when blood is not available or accessible.
JAMA meta-analysis (May 2008) – 5 different HBOC’s analysed as one group, 2 of which had already been withdrawn more than a decade before the meta-analysis was done. Removing 1 of these would change the result to positive!

Talk focus: primary intraparencymal/intracerebral haemorrhage
Constitutes 10-15% of strokes with mortality between 35 and 52%
Locations: brainstem, cerebellum, thalamus, basal ganglia, lobar.
Initial diagnosis: abrupt headache, vomiting, seizure, altered mental state, any focal or generalised neurological symptoms, and otherwise the same for acute stroke.
EMS evaluation: ABCs, cardiac monitoring, IV access, O2 if hypoxic, NPO, alert and transfer
Initial care: as per ‘suspected stroke’. Balance risk of loss of airway against loss of neuro exam. CT head ASAP whenever available.
Major predictors of outcome: Initial GCS and ICH volume
Factors associated with poor outcome that we can treat:

Hematoma expansion
Hyperglycemia
Hematoma evacuation
Seizures

Hematoma expansion – 38% of patients presenting within 3 hours of onset have significant haematoma growth .

Blood pressure control is controversial – minimal literature available (most of it intra-operative from neurosurgery). ‘Resetting’ of CBF autoregulation to a higher-than-normal level is a concern. INTERACT study (SBP<180 vs SBP<140): 36% decreased risk of haematoma expansion, but no effect on outcome. INTERACT2 (specifically powered to measure outcome effect) is currently underway. AHA guidelines exist (all class C) advising a moderate decrease in BP
Anticoagulation reversal – FFP use to reverse warfarin (contains factors II, VII, IX and X required) can require 10u (2000ml) to reverse INR. This can be a problem in patients with background of cardiac disease (for which they get the warfarin…). Time to reversal varies in studies: 7-32 hours due to practical considerations. PCC (prothrombin complex concentrate) has rapid action (about 20 minutes) with minimum volume required, but they are expensive and carry a risk of thrombotic complications and DIC. IV Vitamin K has an effect as early as 4 hours, and can reverse the INR as early as 8 hours. Risks include anaphylaxis (rare). Factor VIIa also reverses the INR within minutes, but once again there is a risk of increased thrombotic complication.

Hyperglycaemia

Associated with poor outcome, even in the absence of diabetes. Hyperglycaemia is neurotoxic.
GIST trial – n=933 (12% ICH), intensive insulin vs. sliding scale: No difference in outcome
QASC trial – n=1696 (5% ICH), glucose control vs. none (intervention group also had swallow screen and paracetamol for fever): Poor outcome 42 vs 58%

Large haematoma: surgical evacuation

STICH trial – n=477+505: OR 0.89 (CI 0.66-1.19) therefore no benefit to urgent evacuation
EVD placement for intraventricular blood – never been studied and probably never will be, as most people presume drainage of obstructive hydrocephalus is obvious.

Clinical seizures should be treated with anti-epileptics; routine prophylaxis is not indicated.

Most discuss the anatomically difficult airway – what about the physiologically difficult airway?
Pre-oxygenation vs. denitrogenation
Patients who are not breathing adequately cannot pre-oxygenate adequately!
Most patients needing intubation have some degree of physiological shunt
Overcoming shunt relies on increasing the mean airway pressure
BVM pre-oxygenation relies on assisted ventilation and a good mask seal… and you NEED A PEEP VALVE
NIV (CPAP) can be used for pre-oxygenation in the ED
Concept – using nasal oxygen while performing intubation to allow continued insufflation
Patient position for intubation (ear to sternal notch) assists ‘apnoeic oxygenation’
“Delayed Sequence Intuabtion” for the delirious patient using ketamine (or dexmedetomidine or fentanyl & midaz titrated).
Bicarb to buy time in severe acidosis?
‘Push dose’ pressors for pre-emptive control of drop in BP on induction – phenylephrine
Induction agents – ketamine or etomidate, but beware patients with maximum sympathetic stimulation – decrease dose.
Beware hypoventilation post intubation – measure ABG and watch pCO2

ABCDE approach as a basis
E = ECG – get a rhythm strip as a minimum, 12 lead ECG by preference
The Feeble – Bradycardia:
Signs of instability: hypotension, altered mental state, signs of shock, ischaemic pain/discomfort, acute heart failure.

Before giving atropine, exclude: hypoxia, hypothermia and head injury. Be cautious in head injury, hyperkalaemia and heart transplant.
If atropine is unsuccessful, consider adrenaline, dopamine, glucagon (beta- or Ca-channel blockage OD) or pacing

The Fast – Narrow Complex Tachycardia

HR>150 with QRS<0.12sec
If unstable: Cardiovert!
If stable: vagal manoeuvres – Valsalva, facial application of ice water, carotid sinus massage
or: drugs — Amiodarone, Beta-blockers, Ca-channel blockers, Digoxin

The Furious – Wide Complex Tachycardia

Usually unstable, but if stable, consider adenosine but amiodarone is the drug of choice
Cardiovert if unstable

Diagnosis is difficult based on common variables – limited sensitivity of physical examination, ECG and CXR (normal in 20%)
BNP >100pg/ml is more accurate than clinical criteria for diagnosis, but cannot be used alone. Greatest value is for the ‘intermediate’ patients. May be lower than expected in flash pulmonary oedema. Mild elevation can be found in cor pulmonale, PE and COPD. Inverse relationship with BMI and higher with renal failure.
Ultrasound for “lung comets” has proven to have good sensitivity in initial studies
ASCEND-HF clinical decision pathway useful in hypertensives
Morphine has gone out of favour – not good evidence. Perhaps good if intubation is inevitable
Nitrates very effective in controlling BP and reducing afterload
ACE-I may work – small studies showed decreased intubation rates
Furosemide helpful in the acute setting but nitrates better
NIV excellent
Hypotensive patients – fluid bolus if intravascularly depleted, then inotropes
Don’t forget to consider palliative care in the correct cases.
Ultrafiltration can be useful if it is available (although it is expensive and time intensive)

See Free Emergency Medicine Talks for talks – everything from this conference will also be there soon!
Be a skeptic, not a cynic
There are now more than 10 000 medical journals (a logarithmic increase!)
Remember that journals need to make money to survive. They have no fiduciary relationship with patients!
Peer review is the best we have – but it is a “flawed process at the heart of science” (in the words of the editor of the BMJ). It is prone to bias and abuse, and hopeless at spotting fraud and error. “Like poetry, love or justice”. “If peer review was a drug, it would never get onto the market.”
Publishing negative results, despite the quality of the study, is unpopular with readers and journal editors alike. However, consistent bias in reporting positive findings only skews the statistics when meta-analysis is done.
Peer review misses things – demonstrated in studies (see Baxt WB et al 1998)
Looking at articles, watch out for independent predictors, strong associations, citation bias, amplification, invention, work-up bias, spectrum bias, referral bias and so on
Least favourite statistic – Negative Predictive Value. If disease prevalence is low, the NPV will OF COURSE be low.
Citation bias – citing only articles that support our hypothesis
Beware multiple hypotheses!
Absolute vs relative risk reductions (eg. statins – JUPITER trial). Absolute risk from 0.7% to 0.4% is a 43% relative risk reduction…
Beware surrogate and composite endpoints!
Full slideset available from Prof Lex via email (as are the references)

119 million patients seen in ED’s in USA in 2009
Who drives patient care in emergency settings? Doctors, nurses, hospitalists, patients?
Ethnographic study of acuity assignation (2010)

Sample of emergency nurses, ethnographic approach, 12 participants, 150 initial patient encounters over 3 months
Patients reported acuity to be a function of patient presentation, complaint, duration of symptoms and body habitus. Acuity was also influenced by environmental and contextual challenges: language barriers, patient volume, unit leadership, communication with patients and providers, and length of time in waiting room prior to triage.
“Who’s in the back?” phenomenon – some nurses made decisions about acuity, further assessment and initial diagnostic tests based solely on the physician was.
Physiologic data was not rigorously collected nor considered as a primary determinant of acuity.
Moral reasoning and drive surfaced as an important factor.

Investigation of triage competency (2011)

Lack of understanding around critical cues – the signs, symptoms and history that send the provider down one path and away from another.
Intuitive vs hypothetico-deductive thinking – the former is efficient but inaccurate, where the latter is accurate but time-consuming

Core, intermediate and influential elements need to be considered in an integrative model for clinical decision making
Unit leadership is the best surrogate for (the almost impossible to teach concept of) moral reasoning
Proclivity for high moral reasoning is the factor that closes the loop in critical thinking; it inspires us to ask the questions “Am I right?” and “Is there a way I can be wrong?”
Important elements to consider:

Knowledge base
Moral reasoning
Drive to act
Environmental structure:

Standards
Communication
Teamwork
Autonomy of practice
“The end result of critical thinking is not thought: it is action”

Preparation and practice are key to being ready to manage difficult airways
Four important questions:

Is the airway difficult – Anatomic concerns?
Is the patient compromised – Physiologic concerns?
What is your primary approach?
What is your rescue approach?

Difficult airway situations to anticipate:

Difficult DL – LEMON – Look externally, Evaluate 3-3-2, Mallampati, Obstruction & Obesity, Neck movements
Difficult facemask – MOANS – Mask seal (anatomical abnormality, wounds, beards, etc), Obstruction & Obesity, Age (extremes), No teeth, Stiff (difficult ventilation)
Difficult EGD (Extraglottic device) – RODS – Restricted mouth opening, Obstruction & Obesity, Distortion, Stiff lungs or c-Spine
Difficult cric – SHORT – Surgery or disrupted airway, Haematoma (or other mass), Obstruction & Obesity, Radiation therapy, Tumour

Difficult airway principles:

Patients need oxygen… not necessarily and ETT
Patients with multiple difficult airway attributes may be unsafe for paralytics
“One-shot” airways may need paralysis if you’re forced to act
Always have a backup plan

Primary Airway Management Plan?

RSI?
Sedated, awake intubation?
Primary surgical airway?
One always needs an airway rescue plan: Double set-up, extraglottic, or something else?
Airway rescue plan?
RSI?
Rescue surgical airway?
Alternative airway devices

Alternative airway devices

Blind insertion device?
Optical stylet?
Video laryngoscopy?
Flexible fiberoptic?

Case 1: Angio-oedema (68yr female, just started on ACE-I)

Good plan – Awake intubation, flexible fiberoptic if possible, surgical airway as ultimate backup.
Dry and anaesthetise the airway – atomised and nebulised lignocaine. Nasal approach with flexible fiberscope. Judicious sedation or none at all. Surgical airway if precipitous failure.

Case 2: Aspirated foreign body (62yr male, “choking”, collapses in ED)

Good plan – “crash airway” -> immediate DL, remove foreign body if seen, intubate and ventilate if possible.
If obstruction is infraglottic, use ETT to push it all the way down into a bronchus, retract ETT and try again to ventilate.

Case 3: Severe Asthmatic (25yr female, tachycardic & tachypnoeic, beginning to desaturate)

Rapid RSI; EGD as backup; cric if complete failure
Lignocaine nebusised if time to reduce reactive airways
Ketamine good

Summary: All in the evaluation
Know your mnemonics
Always have a plan B
Remember some nuacnces of specific cases
Practice practice practice

1:2:4 principle

most casualties on the battlefield still bleed to death
Emergency care/ ALS within 1 hour
Surgical resuscitation within 2 hours
Definitive care within 4 hours

Level 1 resuscitation post as close to the battlefield as possible
Forward surgical capabilities near the battlefield
Rapid evacuation to definitive care at field hospital care on land/rail/sea and even in the air.
Caring for patients under the special circumstances such as chem/bio/nuke threats
Military fatality rates – major death in <5min and 11-30min time brackets. <5 usually fatally wounded; focus on the 11-30min bracket
78% of injuries now are blast injuries rather than gunshots in modern warfare
Potentially survivable deaths – 85% due to haemorrhage! Of this, 31% is compressible haemorrhage…
Algorithm starts with a C – Catastrophic Haemorrhage Control
Tourniquets save lives and red blood cells
Combat ready clamp for femoral artery and abdominal aorta tourniquet (inflatable wedge)
Internal Compression tourniquet especially useful in “junctional trauma” (shoulder and groin)
Extensive use of topical hemostatic agents (haemostatic bandages and combat guaze)
Tranexamic acid extensively supported in military literature
10-15% of preventable deaths due to airway obstruction
NPA useful and well tolerated in semi-conscious patients and is extensively used
Endotracheal intubation in the battlefield is not the answer (1 survival out of 492 cases)
Surgical airway is the first and last resort
Tension pneumothorax is a common cause of preventable death – bilateral needle decompression performed before calling death
Hemopure for blood substitute
Hypotensive resuscitation used
Intra-osseous lines in sternum and tibia very useful
Focus on resuscitation with blood products early
“In combat settings, casualties without head injury who are of normal mental status with a palpable radial pulse should not receive fluid resuscitation”
1:1:1 resus (or even higher ratios – 2:3)
Body warming bags and fluid warmers in vehicles
Damage control surgery very well adopted
Low threshold for early damage control
Ethical challenges:

Law of war (especially peace missions)
Civilian casualties
Own vs. enemy forces
Iraq – 93% of casualties are non-combatants, 34% under 14 years of age
Patients full of explosives… children with explosive belts… incubators with babies booby-trapped with explosives…
Prisoners of war

Paradigm challenges

Triage is fighting force orientated – get the healthiest fighting again fast
Quality compassionate care is possible under austere conditions
Unique approaches are required.

HPCSA EMS Protocols – Martin Botha

Consensus – mutually acceptable agreement that integrates interests of all parties, but does not require unanimous consent. All parties should be committed to its implementation.
Consensus on science is the most important.
Consensus on treatment recommendations is desirable, but only if there is good agreement
We need professionals with good research skills to develop evidence-based guidelines for SA EMS
(ILCOR process for analysing evidence and presenting it to consensus meeting demonstrated)
GRADE approach is becoming the standard assessment tool
HPCSA has begun the processes to review and develop protocols along these lines.
Questions and debates:

What is the role of protocols for independent practitioners in SA?
What is the role of protocols for EMS Professionals?
Varying levels of experience, training, scope of practice, clinical governance, models and self-regulation.
How to integrate changes quickly into guidelines to reflect current best evidence?

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

EBM Community Acquired Pneumonia

Mike Cadogan — Mon, 22 Nov 2010 02:00:00 +0000

Life in the Fast Lane Medical Blog EBM Community Acquired Pneumonia

Pedagogical disambiguation: Emergency Medicine Lecture Notes and Evidence Based emergency medicine principles from Professor A.F.T Brown and the Life in the Fast Lane team.

Community Acquired Pneumonia in Adults

Risk factors for CAP include:
- Age over 50 years, asthma, smoking, pre-existing COPD, DM, CRF, CCF, alcoholism, liver disease, neoplasia, stroke, seizures, aspiration, immunosuppression, institutionalisation, indigenous.

Johnson P, Irving L et al. Community-acquired pneumonia. MJA 2002; 176:341-347 [Reference]

Note that a normal CXR in a bed-ridden patient with suspected pneumonia does not rule it out (NPV 65%) and so CT may be indicated to confirm.

Esayag Y, Nikitin I, Bar-Ziv J et al. Diagnostic value of chest radiographs in bedridden patients suspected of having pneumonia. Am J Med 2010;123:88.e1-88.e6. [Reference]

Most common organism is Strep pneumoniae + causes most severe illness and deaths, especially in the elderly. Also Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella and H.influenzae (usually in COPD)
- Note rapid urinary antigen tests available for Strep pneumonia and Legionella, recommended in moderate to severe CAP.
‘Red flags’ for severe illness mandating admission include RR > 30/min, SBP < 90 mmHg, SaO₂ < 92%, acute confusion, pH < 7.35, PaO₂ < 60 mmHg and multilobar involvement on CXR.
Australian-derived severity scoring system for use when CAP is confirmed on CXR, dichotomoised for patients more than 50 years or ≤ 50 yr, is known as SMART-COP, and is scored out of 11.
- A score of 3-4 gives a 1:8 risk of needing intensive respiratory or vasopressor support (IRVS).
- SMART-COP score ≥ 5 gives a 1:3 risk needing IRVS = severe CAP.
- Better predicts need for IRVS / ICU than the Pneumonia Severity Index (PSI) or CURB-65 score, which are more heavily dependent of age and co-morbid illness in predicting 30-day mortality.

Charles P, Wolfe R, Whitby M et al. SMART-COP: A tool for predicting the need for intensive respiratory or vasopressor support in community acquired pneumonia. Clin Infect Dis 2008;47:375-84. [Reference]

Alternative scoring system is the 5-point CURB-65 score, with one point for each of Confusion, Urea > 7 mmol/l, Resp rate ≥ 30/min, Blood pressure low (SBP < 90 mmHg or DBP ≤ 60 mmHg), age ≥ 65 yr.
- Score 4 = 41.5%, and score 5 = 57% mortality or need for ICU.
- Score 0 or 1 = 0.7% and 3.2% mortality respectively.
- Thus score 0 or 1 patients could be treated at home, score 2 patients need hospital assessment and ≥ 3 are considered severe. Score ≥ 4 need referral to ICU.

Lim WS et al. Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study. Thorax 2003;58:377-82. [Reference]

Give empiric antibiotic treatment after 2 sets of blood cultures from separate venepuncture sites if severe (5-10% yield), and sputum if rapidly available (do not delay treatment to collect sputum, as yield ≤ 40% only).
Mild CAP:
- Give amoxicillin 1 g PO 8-hourly for 5-7 days. Or if Mycoplasma pneumoniae, Chlamydophila pneumoniae or Legionella is suspected, use doxycycline 200 mg PO for first dose then 100 mg PO daily for 5 days instead, or clarithromycin 250 mg PO bd f or 5-7 days.
- Patients who fail to improve by 48 hours of amoxicillin PO should have doxycycline or clarithromycin added to their regime.
- If history of immediate hypersensitivity to penicillin, give doxycycline or moxifloxacin 400 mg PO daily, depending on local practice.
Moderate severity CAP:
- Patients requiring hospital admission, give benzyl penicillin 1.2 g IV 6-hourly until significant improvement then change to amoxicillin 1 g PO 8-hourly for 7 days, plus either doxycycline 100 mg PO 12-hourly for 7 days or clarithromycin 500 mg PO 12-hourly for 7 days.
- Add gentamicin 5 mg/kg IV daily (assuming normal renal function) if Gram-negative bacilli are identified in blood or sputum. Alternatively, change the benzyl penicillin to ceftriaxone 1 g daily IV.
- If patient has immediate hypersensitivity to penicillin, substitute ceftriaxone 1 g daily IV for the penicillin, or use moxifloxacin 400 mg PO daily monotherapy as a single drug.
- Tropical areas, if the patient has risk factors for meliodosis (diabetes / alcohol / CRF / lung disease), give ceftriaxone 2 g daily IV plus gentamicin 5 mg/kg IV as a single dose.
- For both moderate and severe CAP admitted to hospital, consider use of oseltamivir 75 mg BD PO, particularly in ‘flu season.
Severe CAP (SMART-COP score ≥ 5):
- Refer to HDU / ICU.
- Give ceftriaxone 1 g IV daily; or benzyl penicillin 1.2 g IV 4-hourly with gentamicin 5 mg/kg IV daily, plus with either azithromycin 500 mg IV daily.
- If significant renal impairment or penicillin allergy, use moxifloxacin 400 mg IV daily with azithromycin.
Severe tropical pneumonia:
- Where Burkholderia pseudomallei (melioidosis) or Acinetobacter baumannii are prevalent, give meropenem 1 g IV 8-hourly plus azithromycin 500 mg IV daily.

Therapeutic Guidelines Ltd. Therapeutic Guidelines. Antibiotic; Version 14, 2010:221-258. [Reference]

In HIV patients, pneumocystis jiroveci (carinii) pneumonia is the commonest AIDS-defining illness and cause of death. Also TB has 100-fold increased relative risk, and can not be excluded on CXR findings alone.

Lim W, Baudouin S, George R et al. British Thoracic Society guidelines for the management of community acquired pneumonia in adults. Update 2009. Thorax 2009;64 (suppl II):iii1-iii55. [Reference]
Mandell L, Wunderink R, Anzueto A et al. Infectious Diseases Society of America/ American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007;44:Suppl 2: S27-72. [Reference] [Website]
Eddy O. Community-acquired pneumonia: from common pathogens to emerging resistance. Emergency Medicine Practice 2005;7 (12):1-24. [Website Reference]

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

EBM Spontaneous Pneumothorax

Mike Cadogan — Sun, 21 Nov 2010 02:00:42 +0000

Life in the Fast Lane Medical Blog EBM Spontaneous Pneumothorax

Pedagogical disambiguation: Emergency Medicine Lecture Notes and Evidence Based emergency medicine principles from Professor A.F.T Brown and the Life in the Fast Lane team.

Clinical Appraisal

Determine the following three criteria concerning the diagnosis of a spontaneous pneumothorax. Use an inspiratory CXR (PA, or lateral, if PA is normal and suspicion high). Expiratory CXRs are not recommended:

Chronic lung disease? (CLD): cystic, fibrotic, bullous or emphysematous lung disease. Patient will be admitted overnight irrespective of treatment.
Degree of breathlessness? (dyspnoea): ‘Significant means any deterioration in usual exercise tolerance.
Degree of collapse? (small or large):
- Small: visible rim < 2 cm at level of hilum.
- Large: visible rim ≥ 2 cm (equates to approximately 50% collapse).

Management

This is dictated by absence of CLD (primary pneumothorax) or presence of CLD (secondary pneumothorax); extent of pneumothorax on CXR (large or small); and degree of patient’s breathlessness (dyspnoea) ie. significant or not:

Non-interventional management:
- Patients without CLD, with no significant dyspnoea and with a small pneumothorax do NOT mandate any treatment at all.
- Aspiration may however be preferred by some to hasten resolution.
Simple aspiration under LA with 14-16 G cannula, until resistance is felt, patient coughs excessively or over 2.5 litres withdrawn:
- Perform this for a small pneumothorax with significant dyspnoea, in the absence of CLD, or for the majority of large pneumothoraces.
- May be attempted in CLD for a small pneumothorax if under age 50 and minimally dyspnoeic. However, must then admit for 24 hours observation and high-flow oxygen.
- Repeat CXR after aspiration and 6 hours later. If aspiration successful with resolution or only small residual air rim, no evidence continuing air leak and not dyspnoeic, discharge and arrange follow up.
- Aspiration may be repeated if patient is still breathless and less than 2.5 L was aspirated and catheter was blocked or kinked, but ICC insertion is more likely to be needed for this ‘aspiration failure’.
- Aspiration overall is safe and effective for the management of a primary spontaneous pneumothorax, with fewer hospital admissions and, if admitted, a shorter length of stay + appears less painful / less need for analgesia.
- However, small bore chest tube insertion (< 14 F) is now possible and popular using Seldinger technique – see ICC below.

Zehtabchi S, Rios C. Management of emergency department patients with primary spontaneous pneumothorax: needle aspiration or tube thoracostomy? Ann Emerg Med 2008;51:91-100. [Reference]

Intercostal catheter (ICC) 10 – 14F, using Seldinger technique; or blunt dissection having withdrawn / discarded trocar first. Note if need to replace a smaller ICC, can use a larger 20 -24 F. Small-bore ICC is indicated for:
- Following failed aspiration if patient remains breathless, or if pneumothorax relapses.
- CLD patients with small pneumothorax with dyspnoea or if over 50 yrs, and all large pneumothoraces with CLD.
- Bilateral pneumothorax.
Remove ICC if stopped bubbling and CXR re-expanded.
- If continues to bubble or pneumothorax fails to re-expand by 48 hrs, consider high-volume low pressure suction system (or look for a kinked tube), and consult respiratory physician.
- Never clamp a bubbling chest tube.
Indications for surgical advice include second ipsilateral pneumothorax, first contralateral pneumothorax, bilateral synchronous, persistent air leak / failure to expand, spontaneous haemothorax, pregnancy, at-risk profession (pilot / diver).
Follow up when discharged:
- All patients should be reviewed within 7-10 days by a respiratory physician. Risk of recurrence of spontaneous pneumothorax is up to 54% at 4 years, particularly in smokers, taller patients and age > 60 yr.
- Instruct patient to immediately re-attend Emergency if develops significant dyspnoea or increasing pain.
- Advise those allowed home to stop smoking, avoid extreme exertion, to return if become dyspnoeic, not to fly until at least 1 week after the CXR has returned to normal, and to never SCUBA dive (unless have had bilateral pleurectomies).

Treasure T. Minimal access surgery for pneumothorax. Lancet 2007;370:294-5. [Reference]
MacDuff A, Arnold A, Harvey J et al. Management of spontaneous pneumothorax: BTS pleural disease guideline 2010. Thorax 2010;65(Suppl 2):ii18-ii31. [Reference] [Website]

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

EBM Acute Asthma

Mike Cadogan — Thu, 18 Nov 2010 02:00:08 +0000

Life in the Fast Lane Medical Blog EBM Acute Asthma

Pedagogical disambiguation: Emergency Medicine Lecture Notes and Evidence Based emergency medicine principles from Professor A.F.T Brown and the Life in the Fast Lane team.

Clinical recognition of severe or critical asthma

Severe asthma indicated by any one of (admit every patient with severe):
- PEFR (or FEV_I) >33 50% predicted or best, or < 100 L/min (or I L for FEV_I).
- Unable to complete sentences in one breath.
- Resps 25 / min.
- Pulse 120 / min (110 / min British Guideline).

Global Initiative for Asthma (GINA). Global strategy for asthma management and prevention. 2009 (corrected Jan 2010). [Reference]
British Thoracic Society. Scottish Intercollegiate Guidelines Network. British guideline on the management of asthma. A national clinical guideline. Published May 2008, revised June 2009. (PDF full guideline) or (PDF quick reference guide).
National Heart Lung and Blood Institute. Expert Panel Report 3 (EPR 3). Guideline for the diagnosis and management of asthma. Section 5. Managing exacerbations of asthma. (PDF published Aug 2007).
National Asthma Council Australia. Asthma Management Handbook 2006. (6th edition of handbook 2006).

Life-threatening or critical asthma has any one of (admit to ICU):
- PEF 33% predicted or best
- Silent chest, feeble breaths, cyanosis.
- Bradycardia, hypotension.
- Exhaustion, confusion, coma.
Measure ABG if SaO₂ 92% on oxygen or any of the features above present, and look for PaO₂ 8 kPa (60 mmHg), low pH, raised PaCO₂6.0 kPa (45 mmHg), and low K⁺.
Note concern that long-acting beta-agonists salmeterol and formoterol with or without inhaled corticosteroids have increased risk intubation / death (OR 2.1)

Salpeter S, Wall A, Buckley N. Long-acting beta-agonists with and without inhaled corticosteroids and catastrophic asthma events. Am J Med 2010;123:322-8. [Reference] [Update Reference]
Holley A, Boots R. Review article: Management of acute severe and near-fatal asthma. Emerg Med Australas 2009;21:259-68. [Reference]

Management of Acute Asthma

[Note the American, Canadian, British, Australian and GINA guidelines all subtly differ in drug and dose recommendations].

Beta agonists
- Continuous oxygen-driven salbutamol nebulisers with 5-10 mg (1-2 ml) in 2 ml saline are appropriate in unresponsive severe, or critical asthma.
- Reduce to 5 mg 1-, 2-, or 3-times hourly nebs if improve. Note that there is a huge variation in respirable dose delivered by the different types of nebuliser.
- Intravenous salbutamol 3-10 g/kg then 5-20 g/min (dose unknown!) reserved for non-response to above, as side effects including hypokalaemia, arrhythmias and lactic acidosis are greater IV.
- IM or IV adrenaline reserved for precipitate anaphylactic asthma, or moribund asthmatic / respiratory arrest (see later).
Anticholinergic therapy
- Ipratropium 500 g added to first beta agonist nebuliser and repeated once after first hour, then 4 – 6-hourly. Has additive effects with salbutamol.
- Improves severe asthmatics, those not responding to salbutamol alone, and PEFR / FEV₁ in all, though not necessary in mild asthma.

Stoodley RG, Aaron SD, Dales RE. The role of ipratropium bromide in the emergency management of acute asthma exacerbation: a meta-analysis of randomised clinical trials. Ann Emerg Med 1999; 34:8-18. [Reference]

Corticosteroids
- Wide range of doses used, but little to support “more is better.”
- Give oral prednisone 0.5 – 1.0 mg/kg; or IV hydrocortisone 250 mg 6-hourly (British guideline considers hydrocortisone 100 mg 6-hourly as efficacious) only if vomiting / obtunded, as all IV steroid preparations can cause severe anaphylaxis.
- Parenteral methyl prednisolone shown to improve PEFR within 1-2 hours (likely class effect).

Krishnan J, Davis S, Naureckas E et al. An umbrella review. Corticosteroid therapy for adults with acute asthma. Am J Med 2009;122:977-91. [Reference]

Magnesium
- Magnesium 2g IV infusion over 20 mins once, if fail to improve after 1 hour of therapy. Improves PEFR and reduces admissions in severe cases in children. Adult data more limited. Note potential for NMJ blockade, hypotension and sedation in the non-ventilated patient.
- Nebulised isotonic solution of magnesium sulphate in addition to beta-2 agonist improves pulmonary function in severe asthma in adults. Paeds data limited effect.

Mohammed S, Goodacre S. Intravenous and nebulised magnesium sulphate for acute asthma: systematic review and meta-analysis. Emerg Med J 2007;24:823-30. [Reference]
Blitz M et al. Inhaled magnesium sulphate in the treatment of acute asthma. Cochrane Database Systemic Review 2005 Oct 19. [Reference]

Aminophylline
- Reduces need for intubation in severe asthma (children), but side effects of palpitations, nausea + vomiting and tremor common. Rare use in near fatal asthma in adults. Not recommended.

Parameswaran K, Belda J et al. Addition of intravenous aminophylline to beta-2 agonists in adults with acute asthma (Cochrane Review). The Cochrane Library 2001; Issue 3, Oxford. [Reference]

Miscellaneous
- CXR only for suspected consolidation, pneumothorax / pneumomediastinum, failure to respond to treatment. Not ‘routine’.
- Antibiotics – only indicated if definite bacterial illness.
- Fluid load – no published ‘evidence’, but necessary particularly prior to intubation when acute drop in preload is likely, or for K+ replacement in hypokalaemia from β2 agonists / steroids / (aminoph).
- Adrenaline – if in extremis, give up to 5 µg/kg slowly IV as 1:10 000 or 1:100 000 dilution. Or give 0.3 – 0.5 mg IM for asthma in anaphylaxis.
- Heliox – (helium/oxygen 80:20 or 70:30). High flow rate to increase respirable gas mass. Data mixed / not compelling + poor availability!

Discharge Planning

Must achieve 75% of predicted or best known PEFR for at least 1-2 hours off treatment AND not have any features of a severe attack to be allowed home.
Steroids
- Oral prednisone for 5-7 days, stopped abruptly.
- Oral prednisone for 10-14 days tapered off, if patient has a background of unstable or undertreated asthma; or has relapsed.
‘Asthma Action Plan’
- Action Plan for present attack, and future episodes should be drawn up, ideally in conjunction with LMO + see NAC Australia’s website.

Vanden Hoek T, Morrison L, Shuster M et al. Part 12: Cardiac arrest in special situations: 2010 AHA Guidelines for CPR and ECC. Circulation 2010;120(suppl 3):S829-S861. [Reference]
British Thoracic Society. Scottish Intercollegiate Guidelines Network. 6 Management of acute asthma. Thorax 2008;63(Supp IV):iv51-iv60. [PDF Reference]
Aldington S, Beasley R. Asthma exacerbations. 5: Assessment and management of severe asthma in adults in hospital. Thorax 2007;62:447-58. [Reference]
Currie G et al. Recent developments in asthma management. BMJ 2005;330:585-9. [Reference]

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

EBM Oesophagogastric Varices

Mike Cadogan — Wed, 17 Nov 2010 02:00:14 +0000

Life in the Fast Lane Medical Blog EBM Oesophagogastric Varices

Pedagogical disambiguation: Emergency Medicine Lecture Notes and Evidence Based emergency medicine principles from Professor A.F.T Brown and the Life in the Fast Lane team.

Epidemiology

5-12% upper G1 bleeds.
50% cirrhosis patients have varices, up to 85% in Child-Pugh C patients.
25-35% of patients with chronic liver disease will have a variceal bleed, which accounts for 50-90% of bleeding episodes in those patients.
Mortality of a first bleed 15-30%, with rebleeding in 30-60% after banding / sclerotherapy (highest risk in first 10 days), and a 32-80% 1-year mortality.

Management

Endoscopic:

Banding ligation. Lower rebleeding, mortality and complication rate than sclerotherapy.
Sclerotherapy. Rebleed in 20-50%; higher complication rate. May be followed by propranolol.
Tissue adhesive eg. cyanoacrylate or bucrylate especially for gastric varices; intravariceal thrombin.

Vasoactive drugs:

In absence of or awaiting (ie. during transfer); or as adjunct to (ie. octreotide) endoscopy.
- Octreotide 50 μg, then 25-50 μg/hr IV. Long-acting somatostatin analogue. 80% success with decrease in bleeding, borderline mortality benefit. Continue for 24-48 hours.
- Somatostatin. More expensive, shorter half-life.
- Terlipressin (Glypressin) 2 mg 6-hrly or vasopressin +/- GTN, to reduce portal pressure and deal with coronary ischaemia.
- [Beta blocker (propanolol /nadolol) +/- isosorbide. Used for primary and secondary prophylaxis of bleeding, but not in acute bleeding].

Antibiotics:

Norfloxacin 400 mg orally bd or ciprofloxacin IV at same dose, preferably before endoscopy, in any cirrhotic patient with an upper GI bleed. Ceftriaxone 1 g IV an alternative.

Fernandez J, Ruiz del Arbor L, Gomez C et al. Norfloxacin vs ceftriaxone in the prophylaxis of infections in patients with advanced cirrhosis and hemorrhage. Gastroenterology 2006;131:1049-56. [Reference]

Balloon tamponade (Sengstaken-Blakemore tube):

Temporising procedure only. Up to 25% complications including death from aspiration, migration and or perforation, 50% rebleed. Need airway protection by endotracheal intubation.

Variceal decompression:

Transjugular intrahepatic portosystemic shunt (TIPS). May be preferred to surgery in refractory or rebleed patients, possibly preceded by transjugular variceal embolisation. Also when liver transplantation being considered.
Surgery. Emergency direct portacaval shunt (EPCS) or oesophageal transection.
Either technique reduces re-bleed risk and mortality, with little increase in hepatic encephalopathy risk. However, 30-day mortality up to 80%.

Scottish Intercollegiate Guidelines Network (SIGN). Management of acute upper and lower gastrointestinal haemorrhage. Sept 2008. A national clinical guideline. [Reference]
Garcia-Tsao G, Sanyal A, Grace N et al. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology 2007;46:922-38. [Reference]
Gortzsche P, Hrobjartsson A. Somatostatin analogues for acute bleeding oesophageal varices. Cochrane Database Syst Rev 2005; CD000193. [Reference]
Sharara A, Rockey D. Gastroesophageal variceal haemorrhage. NEJM 2001; 345:669-681. [Reference]

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

EBM Upper GI Haemorrhage

Mike Cadogan — Mon, 15 Nov 2010 02:00:49 +0000

Life in the Fast Lane Medical Blog EBM Upper GI Haemorrhage

Pedagogical disambiguation: Emergency Medicine Lecture Notes and Evidence Based emergency medicine principles from Professor A.F.T Brown and the Life in the Fast Lane team.

Epidemiology

Commonest causes: peptic ulcer (35-50%); oesophagitis (20-30%); duodenitis/gastritis/erosions (10-20%); varices (5-12%); Mallory-Weiss tear (2-5%); tumour (2-5%); angiodysplasia (2-3%); aorto-enteric fistula (<1%).
Mortality 10 – 14%. Majority are over 65 years or variceal.
- Mortality / morbidity risk factors include: cause of the bleeding particularly varices; advanced age; shock; fresh red blood; low Hb; co-morbid disease; re-bleed; endoscopic findings.
- Endoscopic stigmata that predict re-bleeding, need for surgery and death include active arterial bleeding, adherent clot, non-bleeding but visible vessel, ulcer size and location. Scoring systems exists eg. Rockall (max post-endoscopy score 11); score 8 = mortality 41%.
Low-risk group who may be managed as outpatient without early endoscopy can be predicted by Glasgow Blatchford score (GBS), or the pre-endoscopic Rockall score.
- GBS of 0 safely allows discharge without endoscopy, although up to half may then not present for OP endoscopy! Note age is not scored.

Stanley A, Ashley D, Dalton H et al. Outpatient management of patients with low-risk upper GI haemorrhage: multicentre validation and prospective evaluation. Lancet 2009;373:42-7. [Reference]

Management

Medical therapy

Resuscitation, ABC including look for orthostatic hypotension etc. Consider transfusion for shock or acute fall in Hb below 7.0 g/dL (below 10.0 if IHD, PVD etc). Also FFP if INR >1.5 and or platelets if low < 50 x 10⁹/L.
Gastric lavage – of no proven benefit, but NGT may indicate ongoing bleeding.
Proton pump inhibitor by infusion ie. omeprazole / pantoprazole 80 mg stat and 8 mg/hr for 72 hours. Reduces high-risk stigmata and need for endoscopic therapy if given pre-endoscopy (OR 0.67). Reduces risk of rebleeding, surgery and death in high-risk patients if given after endoscopy (RR 0.4 / 0.43 / 0.41 respectively). Overall cost-effective and safe, and often now used routinely.

Lau J, Leung W, Wu J et al. Omeprazole before endoscopy in patients with gastrointestinal bleeding. NEJM 2007; 356:1631- 40. [Reference]
Leontiadis GI, Sharma VK, Howden CW. Proton pump inhibitor treatment for acute peptic ulcer bleeding. Cochrane Database Syst Rev 2006;1:CD002094. [2006 Reference] [2010 Reference]

H₂blocker IV. Cheap, safe but poor ability to consistently maintain a high intragastric pH >6. No evidence for effect in acute bleeding.
Somatostatin or octreotide reduce rebleeding, need for transfusion and surgery, but with no improvement in mortality. Also not routine.

Endoscopy within first 24 hrs of admission:

Early endoscopy provides diagnosis, prognosis and allows immediate therapy. Reduces overall LOS. Bleeding source found in over 90%, and most (>80%) will need no more than supportive therapy initially.
Otherwise may need injection therapy with adrenaline first line for active bleeding +/- other procedure such as second injectate, thermal contact, clips etc.
Other sclerosants, thrombin, tissue glue, heater probe, multipolar electrocoagulation, laser, mechanical endoclips (haemoclips) are alternatives, as adjuncts or as monotherapy.

Sung J, Tsoi K, Lai L et al. Endoscopic clipping versus injection and thermo-coagulation in the treatment of non-variceal upper gastrointestinal haemorrhage bleeding: a meta-analysis. Gut 2007;56:1364-73. [Reference]

Surgery / angiography

Surgery if endoscopy fails, and for high risk of re-bleed in the elderly.
Angiography for severe, persistent bleeding in high risk patient unsuitable for surgery. May then use intra-arterial gelatin, springs or tissue adhesive.

Barkun A, Bardou M, Kuipers E et al. International consensus recommendations on the management of patients with non-variceal upper gastrointestinal bleeding. Ann Intern Med 2010;152:101-13. [Reference]
Scottish Intercollegiate Guidelines Network (SIGN). Management of acute upper and lower gastrointestinal haemorrhage. Sept 2008. A national clinical guideline. [PDF Reference]

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

EBM Acute Liver Failure

Mike Cadogan — Sun, 14 Nov 2010 02:00:18 +0000

Life in the Fast Lane Medical Blog EBM Acute Liver Failure

Pedagogical disambiguation: Emergency Medicine Lecture Notes and Evidence Based emergency medicine principles from Professor A.F.T Brown and the Life in the Fast Lane team.

Definitions

Hyperacute liver failure
- Presents within 7 days of onset. 36% survival with medical management alone (single most common cause in UK and USA is paracetamol poisoning).
Acute liver failure
- Encephalopathy, coagulopathy and jaundice presenting within 8-28 days in patient with previously normal liver. More likely (with hyperacute group) to get cerebral oedema (80%).
Subacute liver failure
- Presents from 29-72 days, less likely to get cerebral oedema, but more likely to have ascites. Poorer 14% survival.

Aetiology

Commonest causes (note wide geographic variation):
- Viral: hepatitis A, E (faecal-oral), B +/- D, C, EBV, CMV, HSV, HZV, parvovirus B19. Hep G, TT, SEN very rarely implicated + unclear role.
- Drugs: paracetamol poisoning (single most common cause ALF in USA) – deliberate or inadvertent from multiple doses (including children), volatile anaesthetics, idiosyncratic reactions to isoniasid / rifampicin / nitrofurantoin / NSAIDs / valproate / phenytoin / statin, Ecstasy (methylmetamphetamine).

Jalan R, Williams R, Bernuau J. Paracetamol: are therapeutic doses entirely safe? Lancet 2006; 368: 2195-6. [Reference]

Rare (5% causes):
- Autoimmune CAH, Budd-Chiari, Wilson’s, fatty liver of pregnancy, pre-eclampsia (HELLP), mushrooms (Amanita spp), herbal remedies.
- Malignancy, ischaemia, heat stroke, Reye’s.

Management

General supportive:
- Hospitalise if INR >1.5; IPPV for Grade 3 or 4 coma or respiratory failure, invasive monitoring including ICP monitor (ICP < 25 mmHg) +/- jugular bulb O₂ (NB: clinical signs / imaging unreliable to detect the earliest signs cerebral oedema), infusion 5-10% dextrose (watch for hyponatraemia), fluids and vasopressor noradrenaline therapy. GI bleeding prophylaxis.
Specific to complications:
- Encephalopathy with cerebral oedema. Correct avoidable factors (hypoxia, sepsis, hyperthermia, haemorrhage, hypokalaemia, benzodiazepines), monitor ICP early. Give mannitol 0.5 g/kg if ICP ≥ 25 mmHg, or hypertonic saline 7.5% boluses 2.0 mL/kg. Moderate hypothermia 32-33^OC (e.g. awaiting transplantation) being trialed.
- Lactulose and neomycin appear not to work, and have complications such as aspiration and nephrotoxicity, respectively.
- Infection. Daily surveillance for bacterial (S.aureus, S.pneumoniae and E.coli) and fungal (Candida) infections, including primary peritonitis. Empiric and or prophylactic broad-spectrum antibiotics + antifungals given.
- Microcirculatory / haemodynamic failure including acute oliguric renal failure. Epoprostenol (PGI₂), angiotensin, vasopressors, NOS antagonists.
- Coagulopathy. Vit K 10 mg IV; FFP / platelets for active bleeding; recombinant Factor VIIa (rFVIIa) with FFP – use declining + many C/Is.
- N. acetylcysteine IV for paracetamol poisoning ideally within 24 hours, but even if ingested 48-72 hours before (given within 8-10 hours risk is nil to minimal).
- Orthotopic liver transplantation (OLT). Note there are different referral criteria for paracetamol poisoning from all other causes such as INR >3.0 / hypoglycaemia/ acidosis pH <7.30 / encephalopathy on Day 2.
  - liver unit referral shows 60->80% one year survival in selected patients. If in doubt – ring and discuss early…
- Liver support systems. ‘Bridging support’ to transplantation, but no conclusive evidence of benefit. Hepatocyte infusion experimental.

Shawcross D, Jalan R. Dispelling myths in the treatment of hepatic encephalopathy. Lancet 2005; 365:431-3. [Reference]
Bernal W, Auzinger G, Dhawan et al. Acute liver failure. Lancet 2010;376:190-201. [Reference]
Stravitz R, Kramer A, Davern T et al. Intensive care of patients with acute liver failure: Recommendations of the US Acute Liver Failure Study Group. Crit Care Med 2007;35:2498-2508. [Reference]

Acute on Chronic Liver Failure

Acute deterioration in liver function over days to weeks in patients with pre-existing chronic liver disease (CLD). Poor prognosis from underlying cirrhosis and end-stage liver disease (ESLD) with portal hypertension, ascites and multi-organ failure.
Much more common than ALF. Features include jaundice, coagulopathy, encephalopathy (precipitated by sepsis including spontaneous bacterial peritonitis, or GI bleed, alcohol, constipation, hypokalaemia, and drugs including NSAIDs and sedatives), hepatorenal syndrome and hepatopulmonary syndrome.

Macnaughtan J, Thomas H. Liver failure at the front door. Clinical Medicine 2010;10:73-8. [Reference]
Bailey C, Hern H. Hepatic failure: An evidence-based approach in the emergency department. Emergency Medicine Practice 2010;12(4):1-24. [Reference]

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

EBM Diabetic Ketoacidosis

Mike Cadogan — Thu, 11 Nov 2010 02:00:41 +0000

Life in the Fast Lane Medical Blog EBM Diabetic Ketoacidosis

Pedagogical disambiguation: Emergency Medicine Lecture Notes and Evidence Based emergency medicine principles from Professor A.F.T Brown and the Life in the Fast Lane team.

Epidemiology

New diagnosis of diabetes 10-27%.
Infection ~ 35%, inadequate insulin ~ 30%, surgery, trauma, alcohol, cocaine and drugs such as steroids, thiazides, sympathomimetics, pentamidine.
No cause in 19-38%, but poor compliance / economic reasons frequent.
Mortality 1% in adults, but 5% if over 65 years. Also high 15% in patients with hyperglycaemic, hyperosmolar non-ketotic syndrome (HHNS), when BSL usually > 50 mmol/L, more dehydrated with osmolality is > 320 mosm/L – can calculate latter by (2[NA + K] + glucose).

Diagnostic Criteria

Raised glucose >11.1 mmol/L
Acidosis with arterial / venous pH < 7.3, or venous bicarb < 15 mmol/L
Ketonaemia or ketonuria (urinalysis may miss 3-beta hydroxybutyrate early).

Management / Complications

Hypoperfusion
- Rapid initial crystalloid, especially for significant circulatory insufficiency, at 15-20 mL/kg in first hour ie. 1-1.5 L.
- Possible role for bicarbonate is in patients with impending cardiovascular collapse, if pH < 6.9. Dilute 100 mmol 8.4% bicarbonate in 250-1000 mL 0.45% NS, and give over 30-60 minutes with 20 mmol K via infusion pump. (Note there are no prospective data concerning bicarbonate use below pH 6.9, and from 6.9-7.1 morbidity and mortality outcomes are equivocal ie. not proven).
Fluid replacement
- Total body water deficit 100 mL/kg, and sodium deficit 7-10 mmol/kg.
- Restore normal hydration with 0.9% NS at 4-14 mL/kg/hr, to correct estimated fluid deficit over first 24 hours, without exceeding change in osmolality greater than 3 mOsm/kg per hour.
- One regime is NS 1000 mL in first hour, 500 mL/hr next 4 hours, then 250 mL/hr next 4 hours ie. around 4 L in first 9 hours.
- Aim to restore fluid deficits over 24 hours in adults, or up to 48 hours in children.

Dhatariya K. Diabetic ketoacidosis. BMJ 2007;334:1284-5. [Reference]

Insulin infusion
- Insulin infusion at 0.1 units/kg/hr (ie. 5-7 units/hr) short-acting insulin, until BSL < 15 mmol/L, then drop to 3 units/hr.
- Aim is to increase venous bicarb by 3 mmol/L/hr; or to drop blood ketone level by 0.5 mmol/L/hr.
- IV bolus of short-acting insulin 0.15 units/kg is unnecessary.
Hypokalaemia
- Total body deficit 3-5 mmol/kg. Give 10-30 mmol K⁺per L fluid, as soon as it is known serum K⁺level is below 5.0 mmol/L, and urine output is established.
- Give 40 mmol per L fluid if K⁺ < 3.5 mmol/L, but must use infusion pump for fluid.
Hypoglycaemia
- Insulin infusion will drop sugar roughly 3-5 mmol/L per hour, whilst ketones are cleared. Avoid BSL dropping below 15 mmol/L.
- Change to 5-10% dextrose if BSL 15 mmol/L, and continue insulin until ketonaemia is suppressed. Bedside ketone meters now available.
- If volume status is still not optimal, continue the NS together with the 10% dextrose at 125 mL/hr.
Hyperchloraemic acidosis
- Usually related to fluid therapy, but is mild and transient.
- Change to ¹/₂NS (0.45%) if Na 150 mmol/L. (Remember corrected serum Na level is higher than measured. Add 1 mmol/L to [Na] for each 3 mmol/L rise in BSL above normal).
Hypophosphataemia / hypomagnesaemia
- Despite significant depletion up to 1 mmol/kg phosphate, and 1-2 mEql/kg magnesium, which may not be reflected by serum levels, replacement of either does not appear to influence clinical course or outcome.
Cerebral oedema
- Suspect if sudden headache with neurological deterioration ie. altered level of consciousness and lethargy, usually within 4-12 hours treatment onset (but can occur before initiation of therapy).
- 0.7 – 1% incidence, usually child / adolescent. Mortality 25 -30% with significant neurological morbidity in 35-40%.
- Cerebral vasoconstriction with hypoxic ischaemia and disease severity implicated, plus possibly idiogenic osmoles (taurine, myoinositol) and defective Na/H ion exchange.
- Relates to a lower pH / (PaCO₂)and higher K+ and urea at presentation, and smaller increases in serum Na⁺.
- Also risk is increased with early (in 1^st hour) insulin administration (OR 12.7) and large volumes of fluid in first 4 hours (OR 6.55), but not use of bicarbonate (UK case control data).
- Rate of change of sugar level, and rates of fluid, sodium, or insulin delivery after first 4 hours do not correlate highly with cerebral oedema occurrence i.e. later therapy is not responsible.
- Give mannitol 0.5 – 2.0 g/kg (2.5 – 10 mL/kg 20% mannitol) IV and supplemental oxygen; or consider 3% hypertonic saline 5-10 ml/kg over 30 min instead. Hyperventilation and or dexamethasone appear unhelpful.

Edge J, Jakes R, Roy Y. The UK case-control study of cerebral oedema complicating diabetic ketoacidosis in children. Diabetologia 2006;49:2002-9. [Reference]
Glaser N, Barnett P et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. NEJM 2001; 344:264-269. [Reference] (Editorial Dunger D, Edge J. 302-303) [Reference].
Hom J, Sinert R. Is fluid therapy associated with cerebral edema in children with diabetic ketoacidosis? Ann Emerg Med 2008;52:69-75. [Reference]

Thromboembolism
- Prophylactic low-dose heparin, especially older patients (or if hyperglycaemic, hyperosmolar non-ketotic (HHNS) syndrome).

Joint British Diabetes Societies Inpatient Care Group. The management of diabetic ketoacidosis in adults. March 2010. [Reference]
Kitabchi A, Umpierrez G, Miles J, Fisher J. Hyperglycaemic crises in adult patients with diabetes. Diabetes Care 2009;32:1335-43. [Reference]
Savage M, Kilvert A (on behalf of Assoc British Clinical Diabetologists ABCD). ABCD Guidelines for the management of hyperglycaemic emergencies in adults. Practical Diabetes Int 2006;23:227-31. [Reference]
ESPE/LWPES consensus statement on diabetic ketoacidosis in children and adolescents. Arch Dis Child 2004;89:188-94 [Reference] [or Pediatrics 2004; 113:e133-e140].

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

EBM Subarachnoid Haemorrhage

Mike Cadogan — Wed, 10 Nov 2010 02:00:52 +0000

Life in the Fast Lane Medical Blog EBM Subarachnoid Haemorrhage

Pedagogical disambiguation: Emergency Medicine Lecture Notes and Evidence Based emergency medicine principles from Professor A.F.T Brown and the Life in the Fast Lane team.

Headache

Life threatening Causes
- Meningitis
- Subarachnoid haemorrhage
- Space occupying lesion
- Hypertensive encephalopathy
- Temporal arteritis (age over 50; ESR > 50)
- Pre-eclampsia

The majority of cases however are:

Migraine: common or classical
Tension-type headache
Post-traumatic headache
Disease in other cranial structures eg. glaucoma, iritis, sinusitis, otitis, TMJ dysfunction.

Subarachnoid Haemorrhage

5% of all acute strokes, but 25% of the fatalities, as case fatality rate around 50% overall (10-20% pre-hospital). 20-30% survivors have residual disability, epilepsy in 7-12% and 50% ‘good’ outcomes have neuropsychological and cognitive impairment.
Initially misdiagnosed in 20% as ‘migraine’ or ‘tension-headache’ on first encounter, as headache can abate or disappear. Up to 15% re-bleed early, and 40% in next 4 weeks, although risk is highest in those with large aneurysms / in poor condition.

Clinical Features

Typical Presentation
- Sudden, instantaneous onset, maximum within minutes “worst headache ever”; generalised and unrelenting. Associated vomiting, neck pain, meningismus, altered mental status (>60%), and localising neurological signs incl III N with PCA aneurysm. May collapse (syncopal episode) then recover.
- Overall one in 100 headache patients seen in ED will have SAH, and up to 10% of those with a severe, abrupt-onset headache
Atypical presentations:
- Low grade fever, neck or back pain, seizures (7%), coma (up to 30%), focal stroke, restlessness, confusion or delirium.

Kowalski R, Claassen J, Kreiter K et al. Initial misdiagnosis and outcome after subarachnoid haemorrhage. JAMA 2004; 291: 866 -9. [Reference]

Investigations

CT scan (thin < 3 mm cuts without contrast)
- First line investigation. Over 95% – 98% sensitivity in first 12 hrs, 93% by 24 hrs, but drops to 50% by day 7.
- May indicate site of bleed, early complications eg. hydrocephalus and cerebral oedema, or an alternative diagnosis.
Angiography
- CT angiography (CTA) sensitivity for aneurysm 97.9%.
- Negative CT followed by negative CTA will give post-test probability of excluding SAH of 99.43%. But note up to 2% population may have an ‘incidental’ small aneurysm.
- Digital subtraction angiography (DSA) traditional gold standard, but is invasive. Or possibly proceed to MRA particularly for suspected partial thrombosis or spinal cord / brain stem origin.

McCormack R, Hutson A. Can CTA of the brain replace LP in the evaluation of acute-onset headache after a negative noncontrast cranial CT? Acad Emerg Med 2010;17:444-51. [Reference]

Lumbar Puncture (LP)
- If CT is negative, though see CT/CTA combination NPV 99.43% above.
- Check for xanthochromia by spectrophotometry of spun CSF, shielded from light.
- Perform LP 12 hours post headache to most reliably differentiate from a traumatic tap (absence of xanthochromia and bilirubin). Minimum 6 hrs.
- Note complications of LP include failure, equivocal result (15-20%), post-LP headache (up to 40%), low back pain, local infection or traumatic neurology, and traumatic tap with difficulty in interpretation.

Boesiger B, Shiber J. Subarachnoid hemorrhage diagnosis by computed tomography and lumbar puncture: are fifth generation CT scanners better at identifying subarachnoid hemorrhage? J Emerg Med 2005; 29:23-7. [Reference]
Schwartz D. Feedback: Computed tomography and lumbar puncture for the diagnosis of subarachnoid haemorrhage: The importance of accurate interpretation. Ann Emerg Med 2002; 39: 190-2. [Reference]

Management

Airway, oxygen, analgesia, hydration, blood pressure control and ICU care including for possible hydrocephalus, pulmonary oedema, arrhythmias, hyponatraemia etc. Newer interest in statins, magnesium and neuroprotective agents.
Nimodipine 60 mg po 4-hrly upon confirmation of diagnosis if BP stable. Consider 1 mg/h IV increased to 2 mg/h after 2 hours if comatose.
- Reduces vasospasm by up to 50% and delayed ischaemic deficit by up to 60%, by vasodilating and protecting against reperfusion injury from calcium influx.
Endovascular platinum coils (GDCs) preferred first line management within first 72 hours, espec posterior circulation.
Alternative is early surgery clipping if patient presents within 2-3 days of onset, particularly if large neck to aneurysm. Or may be delayed up to 14 days if spasm and infarction occur.

Ferro J, Canhão P, Peralta R. Update on subarachnoid haemorrhage. J Neurol 2008;255:465-79. [Reference]
Edlow J, Malek A, Ogilvy C. Aneurysmal subarachnoid haemorrhage: update for emergency physicians. J Emerg Med 2008;34:237-51. [Reference]
van Gijn J, Kerr R, Rinkel G. Subarachnoid haemorrhage. Lancet 2007; 369: 306-318. [Reference]
Al-Shahi R, White P, Davenport R et al. Subarachnoid haemorrhage. BMJ 2006; 333:235-40. [Reference]
Suarez J, Tarr R, Selman W. Aneurysmal subarachnoid hemorrhage. N Eng J Med 2006; 354:387-96. [Reference]

Life in the Fast Lane Medical Blog - Emergency Medicine education blog