Tuesday 29 March 2016

Cyanosis


This seems like a random curriculum item to me. A quick trawl through the Oxford Handbook of EM suggests I need to think about:
Anaphylaxis
Asthma
COPD
Aspiration
Pulmonary Embolism
Seizure
Toxicology - opioid poisoning, paraquat lung, petrol and paraffin poisoning, anthrax
Respiratory distress - chest wall injury, pneumothorax
Uncommon in cyanide poisoning

LITFL splits it further
Central Causes - low sats, metHb, altitude
Peripheral Causes - cold, reduced cardiac output including congenital heart disease.

References
http://www.rcemlearning.co.uk/exams/he-looks-a-bit-blue-doctor/ 
http://www.rcemlearning.co.uk/modules/papa-smurf-has-a-seizure/ 
http://lifeinthefastlane.com/resources/cyanosis-ddx/

Oxygen Therapy


Administering extra oxygen is easy, but there are some more things we could and should think about. Once 30% or more of the blood in the pulmonary circulation passes through an area of low V/Q, the hypoxia cannot be corrected by simply increasing the oxygen content of the inspired gas.

Hypoxic Drive
Oxygen induced hypercapnea is likely to include:
- Worsened ventilation-perfusion mismatch (due to pulmonary vasoconstriction)
- Decreased binding affinity of haemoglobin for carbon dioxide
- Reduced minute ventilation.
So giving extra oxygen is unlikely to be a problem but we need to be aware of it, and monitor it.

Alveolar Gas Equation 
PAO2 = 95 x FIO2(%) – 1.25 x PaCO2
Under normal circumstances the difference between this and the arterial O2 tension (PaO2) measured by the ABG machine is 2-4 kPa. This difference is known as the A-a gradient. Its calculation can help to distinguish between types of hypoxia.


References
http://learning.bmj.com/learning/module-intro/oxygen-therapy.html?moduleId=10053774&searchTerm=%E2%80%9Coxygen%E2%80%9D&page=1&locale=en_GB

http://www.rcemlearning.co.uk/modules/oxygen-in-human-physiology/

http://www.rcemfoamed.co.uk/portfolio/hypoxic-drive-fact-or-fiction/

http://emcrit.org/wp-content/uploads/2015/06/nejmoa1503326.pdf

http://www.annemergmed.com/article/S0196-0644(15)01500-0/abstract

Saturday 19 March 2016

Hyperkalaemia

Hyperkalaemia is a medical emergency that we should know how to manage. Following a guideline is easy - but sometimes we need to know more than just how to follow the guideline! So..if you have a high potassium consider:

1. Is it really hyperkalaemia?
- Prolonged TK time
- Haemolysis
- Acidosis causing transcellular shift
- The ABG analyser result does correlate well with a true result

2. Stop all likely causes
- Treat pre-renal (and renal) failure
- Stop drugs (amiloride, spironolactone, ACE inhibitors, NSAIDs)

3. Do an ECG
The changes don't appear at a set potassium level, but it does show the cardiac toxicity.
- Symmetrical T wave peaking - T wave looks uncomfortable to sit on
- PR interval prolongation
- Reduced P wave amplitude
- QRS complex widening
- sine wave formation
- Fine ventricular fibrillation and asystole
- Progressive bradycardia.

4. If ECG changes present, protect the heart - give some calcium.
Calcium Chloride - more toxic if extravasated
Calcium chloride contains about three times as much calcium as calcium gluconate (0.68 mmol/ml versus 0.22 mmol/ml) and  has a greater bioavailability than gluconate. If you use calcium gluconate, you are more likely to need to give repeated doses.

Give slowly over 20min + 10ml glucose 5% if on digoxin, as rapid calcium administration may precipitate myocardial digoxin toxicity.

5. Shift Potassium into the cells
- Insulin-Glucose IV infusion
- Nebulised sabutamol

6. Remove potasium from the body
- Consider calcium resonium which takes >2 hours to work.
- Sodium bicarbonate may precipitate pulmonary oedema due to its sodium load, or tetany, and is not very effective. You cannot give calcium salts and sodium bicarbonate via the same intravenous line because this causes precipitation of calcium carbonate. May be more useful in acidotic patients.
- Furosemide can help if you have good urine output.

7. Monitor

8. Look for signs and symptoms
Muscle weakness and paraesthesia may occur in patients with severe hyperkalaemia and may progress to flaccid paralysis. The respiratory muscles are usually spared. Muscle weakness normally starts in the lower limbs and progresses to the trunk and upper limbs, and is more common when serum potassium is more than 8.0 mmol/l

Generalised twitching
Confusion
Pericardial friction rub
Urinary retention

9. Understand normal
How does the body handle the overall balance of potassium?
A normal Western diet contains about 100 mmol of potassium per day. Most potassium is renally excreted.

10. Recheck and Review
Recheck potassium level after 4 hours and as indicated according to the levels obtained.



References
http://learning.bmj.com/learning/module-intro/hyperkalaemia-diagnosis-management.html?moduleId=6055258&searchTerm=%E2%80%9Chyperkalaemia%E2%80%9D&page=1&locale=en_GB
http://learning.bmj.com/learning/module-intro/hyperkalaemia.html?moduleId=10047565&searchTerm=%E2%80%9Chyperkalaemia%E2%80%9D&page=1&locale=en_GB
http://www.aliem.com/2013/mythbuster-calcium-gluconate-raises-serum-calcium-as-calcium-chloride/
http://first10em.com/2016/01/21/hyperkalemia/
http://www.rcemfoamed.co.uk/portfolio/hyperkalaemia/