It’s an eerily quiet morning in the ED when in comes a vomiting patient…
The (Made-Up) Case 48 year old M, pmhx DM, chronic/heavy drinker, presents with 4 days of NBNB vomiting. He hasn’t taken his diabetes medication during this time either. Denies abdominal surgeries, fevers, diarrhea, constipation, blood in the stool. ROS o/w neg.
VS 120, 130/70, 99.1 F orally, 20, 100% on RA. FS is 384
PE Dry MM, ill appearing.
Abdomen is soft, nondistended with mild epigastric tenderness. Exam is o/w benign.
You order him some IVF a GI cocktail and some basic labs.
His labs are as follows
VBG: pH 7.3, PO2 102, PCO2 30, HCO3 14, lactate 3
BMP: Na 145, K 5.2, Cl 103, HCO3 15, BUN 10, Cr 0.5, gluc 301
Serum Osm: 298
Ketone: “unavailable due to manufacturer shortage”
Ua: mild ketones
Please describe:
(1) The acid-base derangement including the steps needed to determine it
(2) The diagnosis
(3) Treatment and dispo
By Dr. Andrew Grock
andygrock
- Resident Editor In Chief of blog.clinicalmonster.com.
- Co-Founder and Co-Director of the ALiEM AIR Executive Board - Check it out here: http://www.aliem.com/aliem-approved-instructional-resources-air-series/
- Resident at Kings County Hospital
Latest posts by andygrock (see all)
- A Tox Mystery…. - May 26, 2015
- Of Course, US Only for Kidney Stones… - May 18, 2015
- Case of the Month 11: Answer - May 12, 2015
- Too Classic a Question to Be Bored Review - May 5, 2015
- Case of the Month 11: Presentation - May 1, 2015
1. This is partially compensated metabolic acidosis. The pH is less than 7.4 putting us in acidosis territory. Since the bicarb is below 24 we have metabolic contribution towards acidosis. A pCO2 below 40 is a respiratory contribution towards alkalosis. Since the acidosis is ‘winning,’ the metabolic acidosis is primary and the respiratory alkalinity is compensatory. Interesting that the respiratory rate is only 20, this must be at county.
The anion gap (Na – Cl – HCO3) = (145 – 103 – 15) = 27, which is elevated.
2. The differential diagnosis for this patient with abdominal pain, vomiting, anion gap metabolic acidosis, lactate of 3, hyperglycemia, and mild ketonuria is DKA, alcoholic ketoacidosis, starvation ketoacidosis, toxic alcohol ingestion. Additionally, MUDPILES.
Although AKA often has normal blood sugar, a FS of >300 would be unusual. Quantitative ketone levels would be helpful here because AKA has higher ratios of beta hydroxyl butyrate to acetoacetate than in DKA (on the order of 5:1 vs 3:1). This is because these two ketones exist in dynamic equilibrium with NAD+ / NADH as back and forth oxidizers/reducers. Since EtOH requires NAD+ to be processed into acetaldehyde and finally vinegar, there is less NAD+ in AKA hence the difference in ratios.
Serum Osmolality (US) = (2 * (Na) + (BUN / 2.8) + (glucose / 18) + (ethanol/4.6)
We do not have the patient’s ethanol level. If it is zero, he has a serum osmolality of 316 which give an osmolality gap of 31. Could that gap be filled by ingestion of a toxic alcohol? We need an ethanol level to better evaluate this question.
3. Treatment and Dispo
EtOH level +/- assay for methanol/ethelyne glycol. If high suspicion for toxic alcohol give vodka to saturate alcohol dehydrogenase and slow production of toxic metabolites.
Mainstay treatment: treat as DKA with a little AKA tossed in (provide carbohydrates)
IV fluids fluids fluids, IV dextrose, odansetron, insulin drip, monitor K and replete as needed
Dispo: MICU for insulin drip and further management
Back of the mind issues
– EtOH dependence + tachycardia could be concomitant EtOH withdrawal
– Abdominal pain, vomiting, EtOH dependence could be pancreatitis. Patient needs fluids regardless.
– EKG should be performed
– Mg and phos should be drawn. Both of these may be abnormal in chronic EtOH users. Additionally, phosphate levels drop with insulin since the phosphate will follow glucose into cells to make glucose-6-phosphate, the first step in glycolysis.
Meh,it’s prolly just gastro….
I mean…what ablumenberg said.
1)DKA vs AKA vs starvation ketosis
A Blumenberg knows what’s wrong, but that’s only half the battle. So whaddya wanna do?
1) fluids- lots, LR is a good option, we don’t want to worsen the acidosis with too much chloride
2) antiemetics- it’s our job to make people FEEL BETTER
3) correct electrolyte abnormalities- fluids will help correct the acidosis, hyperosmolar problem but 2g of magnesium, phosphate are prolly in order.
4) Look for more sinister causes of his problem- pancreatitis, sepsis, HHS, MI
5) Give insulin
6) Admit.
Meh,it’s prolly just gastro….I mean…what ablumenberg said.
This is DKA vs AKA vs starvation ketosis.
ablumenberg knows what’s wrong, but that’s only half the battle. So whaddya wanna do?
1) fluids- lots, LR is a good option, we don’t want to worsen the acidosis with too much chloride
2) antiemetics- it’s our job to make people FEEL BETTER
3) correct electrolyte abnormalities- fluids will help correct the acidosis, hyperosmolar problem but 2g of magnesium, phosphate are prolly in order.
4) Look for more sinister causes of his problem- pancreatitis, sepsis, HHS, MI, toxic alcohols.
5) Give insulin.
6) Admit.
Oh…and for SURE thiamine and folate. You can’t fix glucose metabolism until thiamine is repleted. word.
1- Acid-base disorder is metabolic acidosis because pH 7.3 with low PCO2 and low HCO3. This metabolic acidosis appropriately compensated by resp alkalosis by applying the formula PCO2 = (1/5x[HCO3]) +8
Δ/Δ = 1.6 likely pure AG acidosis
patient has -ve osmolar gap which does not fit the picture. high Osm gap likely ethanol or other toxic alcohol
2- Dx DKA (Glucose >250, HCO3 <18 , pH acidosis, ketonuria, )
3- Insulin, folic acid, thiamine, IV hydration initially with NS then add D5 NS when glucose drop down.
admit to medicine floor