Lab Case 238 Interpretation

78 years old female is brought to ED by her daughter with complaint of increasing lethargy, confusion for last few days. She has been vomiting intermittently for last 3 days . No diarrhoea, no fever. Her oral intake is reduced but she has been compliant with her medications. she has background of atrial fibrillation, T2 DM, HTN, and increased cholesterol.

OE : GCS 13-14. Pupils equal reactive, CT Head normal.  HR 35 – 38, BP 109/70, afebrile, RR 22, sats 95 RA. Her Venous blood as is as followed.

PH             7.30

HCO3         22

PCO2         40

Na             141

K               5.7

Lactate      2.7

BSL          6.7

Cl              95

Questions:

  1. What are the main abnormalities on this VBG? what is the underlying metabolic disorder?

2.  On further collateral she is known to be on digoxin for Atrial fibrillation, and ECG  shows atrial fibrillation with slow ventricular response. what further investigations  you  would like to do ??

3.  How will you treat above patient?

Answers:

  1. PH 7.30 (mild  acidemia), HCO3 22  ( metabolic), expexted CO2= 1.5 x HCO3 + 8= 41 ( appropriate compensation). AG = 141 + 5.7 – 22 + 95 = 30 ( HAGMA)

Moderate hyperkalemia, raised lactate.

  1. Given above clinical picture Chronic Digoxin toxicity is most probable diagnosis and further investigations should be a) Digoxin level, b) urea and electrolytes.

Diagosis is based on steady state level 6 more hours after last dose. Levels near therapeutic range correalte poorly with severity of intoxication. Patients digoxin lwvwl comes back at 2.5

Chronic digoxin Toxicity is an underdiagnosed condition with mortality within one week of about 15 – 30 %.

Usually occurs in elderly patients with multiple comorbidities with recent intercurrent illness leading to renal impairment.

Onset is insidous over days to weeks. Clinical features include CVS any bradyarrytmias, ventricular arrythmias, hypotension, syncopy. GIT= nausea, vomit, abd pain, CNS= confusion, lethargy, delerium. VISUAL= decreased visual activity, xanthopsia and chromatopsia.

  1. Treatment of ch digoxin toxicity involves identifying and treating life threats i.e cardiac arrest, dysrrythmias, hypotension . THEN correcting hypovolemia, treating hyperkalemia, and treating intercurrent illness.

Immediate Life threats= Dig Fab is antidote.

Cardiac arrest = upto 20 ampules if available , if haemodynamically unstable 5 amuples to start with.

In Ch dig toxicity = clinical features with elevated dig levels , 1-2 ampules is usually sufficient to reverse all features of toxicity. If clinically there is strong suspicion of chronic digoxin toxicity dig fab can be given without waiting for dig levels which can take upto an hour.

Treat Hyperkalemia with : insulin dextrose, salbutamol, sod bicarbonate. Calcium administration is avoided.

Iv fluids, monitoring of fluid balance.

In case of dysarrythmias if dig fab is not availabe immediately other options are atropine 600 mic upto 1.8 mg, lignocaine 1mg/ kg for ventricualr arrythmias.

And off course discontinue digoxin.

Early treatment with dig fab decreases mortality, is cost effective and reduces hospital stay time.