Tasty Morsels of EM 125 – #FRCEM Diving & Altitude

23 Aug

I’m entering a few months prep for the UK and Ireland exit exam in Emergency Medicine: the FRCEM. I’ll be adding lots of little notes on pearls I’ve learned along the way. A lot of my revision is based around the Handbook of EM as a curriculum guide and review of contemporary, mainly UK guidelines. I also focus on the areas that I’m a bit sketchy on. With that in mind I hope they’re useful.

You can find more things on the FRCEM on this site here.

What is the physiology involved in diving illness?

  • atmospheric pressure changes in diving affect air filled cavities (barotrauma) and the solubility of gases in liquid (the dysbarism)
  • baseline atmospheric pressure is 760 mmHg
  • at 10 m it is double that.
  • Boyle’s law tells us that as pressure increases volume of a gas will decrease and vice versa
  • bartotrauma occurs when an air filled cavity (like the middle ear) can’t equalise with the surrounding pressure
  • Henry’s law states that the amount of any gas that dissolves in a liquid at a given temperature is directly proportional to the partial pressure of that gas. So as pressure decreases with ascent gases like nitrogen can no longer be dissolved and come out as gas bubbles causing decompression illness

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What type of barotrauma occurs with diving?

  • these normally occur on descent
    • middle ear
      • as atmospheric pressure increases the TM is pressed into the middle ear unless it can be equalised with the ambient pressure through the eustachion tube
    • inner ear
      • quite rare
      • round window rupture often during attempts to equalise
      • hearing loss
      • most concerningly severe vertigo (not good underwater)
  • pulmonary barotrauma normally occurs on ascent esp at shallow depths
    • a breath taken at depth will expand as the diver ascends and they need to exhale during ascent to avoid barotrauma
    • air will either be forced into the circulation or into the mediastinal or pleural space

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What is decompression illness and how do we manage it?

  • this normally occurs on ascent
  • usually when people are at limit of their dive tolerances (a combination of depth and length of dive)
  • covers a variety of manifestations
  • during ascent as per Henry’s law, small gas bubbles can form in the circulation. With increasing prevalence of bubbles in the vasculature come the symptoms
    • mechanical venous obstruction
    • inflammatory reaction (cutis marmorata)
    • thrombosis
  • nitrogen is very fat soluble and the myelinated CNS is a common cause of morbidity esp the spinal cord (classically T12/L1 with lower limb, bladder and priapism)
  • joints are also a common manifestations
  • occurs within hours of ascent (98% within 24 hrs as per Rosens)
  • Aterial gas embolism
    • when gas is forced across alveolar membrane into pulmonary venous circulation it is then free to enter the arterial circulation
    • can be after shallow and brief dives
    • cerebral and coronary embolism is the most serious
    • usually sudden dramatic and life threatening
  • Management is easy (he says…) as they all need recompression
  • give 100% oxygen in the mean time for the same reason we give it in pneumothorax – to replace the nitrogen with a metabolisable (?!?) gas.
  • Give fluid as well to most

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Any other diving problems worth knowing about?

  • nitrogen narcosis occurs while at depth. If you’re too deep with the wrong gas mix the increased amount of dissolved nitrogen can make you effectively intoxicated

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What is the physiology of altitude sickness?

  • the fraction of oxygen in air remains constant at 21% but the partial pressure decreases
  • when we hit altitude the chemoreceptors note a low oxygen and stimulate respiration and lower the CO2. Over time the kidneys compensate for the respiratory alkalosis and pH is normal and the higher ventilation rate and lower CO2 is the new normal. This is one part of the acclmitisation process. Acetazolamide helps with this process
  • there is a vasodilatory response to hypoxaemia in the systemic circulation (not in the pulmonary where pulmonary hypertension results) that leads to increased cerebral blood flow and impaired vascular autoregulation

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What is acute mountain sickness?

  • recent altitude gain
  • headache plus at least one
    • GI: nausea, vomiting
    • weakness, fatigue
    • dizzy, light head
    • not sleeping (due to the periodic breathing and apnoeas)
  • Managment
    • stop ascending and possibly descend
    • oxygen can improve symptoms
    • NSAIDs for headache (and possible prophylaxis)
    • acetazolamide (carbonic anhydrase inhibitor, increases bicarb loss causing a mild metabolic acidosis that stimulates respiration, also lowers CSF pressure and volume)
    • dexamethasone
  • Note that HACE (below) is probably the severe end of the spectrum of AMS

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What is HACE and HAPE?

  • both are wrongly spelt acronyms…
  • HACE = High Altitude Cerebral Oedema (basically really severe AMS)
    • altered consciousness
    • ataxia
    • management
      • descent/compression
      • oxygen
      • steroids
      • usual supportive care
  • HAPE = High Altitude Pulmonary Oedema
    • usually on 2nd or 3rd day of altitude
    • dyspnoea at rest is a red flag
    • mainly right heart driven with normal wedge pressures
    • Management
      • descent
      • the Gamow bags are portable hyperbaric chambers
      • oxygen and CPAP as expected (remember the importance of oxygen in controlling pulmonary circulation dilation)
      • avoid diuretics
      • nifedipine is recommended if oxygen and desecent not an option
      • PDE 5 inhibitors (the sildenafils etc…) are more suggested for prophylaxis

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