Its the end of the week and those brain cells are slowing down a little, so here is a little diagnostic quiz for you. The feared blood gas! Now I know some of you say that I don’t do arterial gases any more, just venous, so I don’t need to worry about it………..common have a try at it, you know you want to!
This was a recent Fellowship question that I worked through with my Kamikaze Fellowship group and thought it would be a good one to try. You have about 7 minutes to do it, but take more…enjoy.
Now you might say that the findings won’t change my management, so I don’t care. What if I told you that, the patient will not give a history and the findings will affect your management!
Please enter your answer in the ‘comments’ section (please don’t email them to me, as they won’t be judged) and we can all see what people’s thoughts are.
The best answer gets an ipod nano!’
Remember to answer in the ‘comments’ section.
I will put the correct answer in a few days.
Respiratory and metabolic alkalosis and ARF secondary to dehydration from vomiting and hyperventilation ; needs urgent rehydration with NS and K and most things should settle down
It’s an Alkalosis,
and easy to see,
it’s combined resp and metabolic,
and the Rules agree.
The kidneys are off,
the chloride way low,
I bet they look dry,
and are vomiting up a show.
Put up some saline,
with potassium as well,
work out why they’re vomiting,
I’m sure they’ll be swell.
Metabolic & respiratory alkalosis , hypothalamic & hypochloraemia due to vomiting , dehydration & hyperventilation . Could be underlying sepsis there.
1. Respiratory Alkalosis
2. Superimposed Hypocholeremic Metabolic Alkalosis( Bicarb decrease for given pco2 is not sufficient, should have been some were around 17.5).
3. Hyponatremia
4. AKI
Plan:
Rehydrate by 0.9% Saline, should settle by 12 to 24 hrs.
And for Hypokalemia aprpt. correction.
This patient has tripple acid base disorder ie resp alkalosis (PH 7.8, Pco2 15), calculated HCO3(19) is lower than hco3;23, so another acid base disturbace is present ie Metabolic acidosis, A Gap 33.5 (HAGMA), High Aa gradient 74.5, possible Metabolic alkalosis ( hco3;23), low osmolarity; 238, pre renal failure, severe hypo kalemia, hyponatremia and hypochloremia requiring uregent fluid hydration and potassium replacement
D/d, salicylate poisoning, sepsis with aspiration, lactic acidosis, PE, pnemonia
Great answer. Correct it is a triple disorder! Now you are one of my Fellowship guys, but I didn’t say you couldn’t put in an answer.
Can anyone make it better? Let’s really focus on the diagnosis.
Common, I’m looking at this ipod nano on the desk and its ready to go!!!
I’ll put the answer up in a couple of days.
So, unable to sleep after my night to day transition thought I’d have a go….
Alkalosis (pH 7.80)
Factors contributing to alkalosis:
Respiratory component (pCO2 15)
Metabolic (Base excess 10.1)
However, large discrepancy between base excess of 10.1 and HCO3 of 23.
Given that HCO3 dominant base contributing to, or buffering acid/base disturbance, there must be an addition contributor to the alkalosis (it’s worth noting that the overall alkalosis is pretty significant at 7.80 for a BE of 10.1).
HCO3 and base excess are not directly measured, they are calculated figures based on pH and pCO2. The calculation assumes normal electrolytes, albumin and Hb (not the case here).
Other potential alkalising factors include chloride and albumin (and maybe phosphate a tiny bit).
1. Chloride:
In this example, hypochloraemia (Cl 65), in context of global electrolyte derangement, particularly hyponatraemia (Na 119). Here, we have lost more Cl than Na. Normal Cl:Na ratio is around 75%. Here, the ratio of Cl:Na is 55% (65/119×100). We can estimate the contribution of chloride to the base excess using the equation Na-Cl-32. In our example, 119-65-32=22 (i.e 22 on the BE). The significant hypochloraemia relative to sodium contributes significantly to the alkalosis.
2. Albumin:
Not supplied here. It’s a weak acid. We could estimate its contribution to the base excess (in mEq/l) as about 25% of it’s concentration (in g/l).
So, we have a metabolic alkalosis (pH 7.80), with a respiratory component, (pCO2 15) and a metabolic component (BE 10.1). There is also significant hypochloraemia relative to sodium(Cl:Na 55%) which alone should give us a BE contribution of 22….. We’re missing another disturbance.
We don’t seem to have a high enough BE given all three components contributing to the alkalosis. There must be hidden acid. Probably a metabolic acidosis given the high anion gap ((Na119 K2.5)-(HCO3 23 Cl65)=33).
Other clues, renal failure (Ur 10.3, Cr 0.187). Glucose normal, no lactate or ketones given.
Acute problems:
– severe hypokalaemia
– hyoonatraemia
– severe hypochloraemia
– ARF
– In context of respiratory alkalosis metabolic alkalosis (hidden) metabolic acidosis
Differential
– Addison’s
Global electrolyte disturbance, low Na, dehydration, vomiting leading to H/K/Cl ion loss (giving the metabolic alkalosis), hypoperfusion and lactic acidosis.
– Toxin
Ingestion, vomiting, metabolic alkalosis, aspiration, dehydration, ARF, hypoperfusion, lactic acidosis/primary toxin mediated renal acidosis – ? methanol/aspirin……
– Sepsis
hypoperfusion, lactic acidosis, ? primay GI pathology leading to GI losses….
Bit rambling, apologies. Off to sleep.
I prefer the rhyming verse answer…..
Wow, very nice!
I suppose CCF might give this picture too:
1. Respiratory distress – resp alk
2. Hypoperfusion/ARF – met acid (? lactic)
3. Vomitting – GI losses (met alk hypochloraemia)
way over my seven minutes now….
Metabolic alkalosis and acidosis, together with respiratory alkalosis.
Primarily the vomiting has induced most changes…ie loss acids leading to alkalosis, and further vomiting of deeper intestinal contents ie loss of alkali lead to the metab component of acidosis.
Hyperventilation/anxiety lead to the respiratory alkalosis.
All this vomiting leading to the ARF.
I wonder if this could be alcohol intoxication .. Large anion gap.
Treatment would be fluid replacement, KCL and some thiamine!