Lab Case 232 Interpretation

25 years old female is brought to ED by SJA with c/o nausea and vomiting and intermittent tachycardia of upto 180 . She admitted ingesting at least 30 tablets of slow K ( potassium chloride) 3 hours ago with intent to kill herself.

There was no other co ingestion. On arrival to ED her GCS was14.HR was 85, BP 130/70, afebrile, sats 98 RA. Her ECG showed sinus tachycardia, hyper acute T waves, prolonged PR interval. Her VBG results were as followed.

PH                          7.29

PCO2                     40

HCO3                     21

Na                          132

K                             8.0

Cl                            98

lactate                     3.9

BSL                          7

 

Answers:

  1.  PH 7.29 ( Acidemia) , Low bicarbonate > Metabolic acidosis.

Compensation =  1.5 x 21 + 8 = 39.5  ( appropriate compensation)

Anion Gap =132+ 8 –  98+ 21  =  21  > High anion gap metabolic acidosis probably secondary to raised lactate.

Delta ratio =   Change in AG/ change in HCO3 =  5/ 3=  1.66 > consistent with High anion gap metabolic acidosis.

2.   The 3 most important considerations are Risk assessment , Decontamination and Haemodialysis. 

Risk Assessment : Deliberate self poisoning with potassium chloride is rare, but it can lead to life threatening hyperkalemia and cardiac arrest. Slow K tablets are of concern especially in people with cardiac and pre existing renal disease.

Ingestion of more than 2.5 mmol /kg theoretically can lead to hyperkalemia. The lethal dose of KCL each containing 8 mmol in an adult is not well defined.

Massive ingestion of KCL tablets ( > 40 X 600 mg ) needs early planning of dialysis as hyperkalemia can not be treated by other means.

Slow release KCL tablets are radio opaque and AXR can help in risk assessment.

Above patient had disclosed taking atleast 30 tablets , but on AXR there were more than 30 in stomach, and 4-6 were seen in lower part of bowel.

Decontamination :  Remember charcoal is contraindicated in acid, alkalis, metals ( ions) and alcohols. Slow K tablets can be decontaminated by whole bowel irrigation but it can not be achieved rapidly enough to prevent life threatening rise of potassium. The main role of WBI lies in completing decontamination once hyperkalemia has been controlled with dialysis.

Haemodialysis: Dialysis is the definite treatment for hyperkalemia after massive ingestion and early planning after risk assessment is the key. It is indicated if:

ingested > 40 X 600 mg tablets confirmed on AXR.

renal impairment.

cardiovascular instability.

serum potassium > 8

rapidly rising K .

dialysis continues untill WBI confirms decontamination on AXR, and thereafter potassium levels are closely monitored. A rising level indicates incomplete decontamination.

 

3.   Initial Mx needs address to Airway , breathing, circulation. Then 12 lead ECG for signs of hyperkalemia. and urgent VBG for K levels, paracetamol level. AXR for risk assessment.

Treat hyperkalemia aggressively with :

Calcium chloride 10 ml of 10 percent calcium cholride slow IV.

10 units of actrapid in 50 ml of 50 percent dextrose IV over 15 minutes.

Salbutamol nebulizer 5 -20 mg

Sod Bicarbonate 50-100 mmol slow Iv.

 

Added: Above patient was treated initially which brought K down to 6.6 in ED, but then jumped back up to 7.7 in ICU. AXR showed more than 30 tablets in stomach so she received haemodialysis for 12-16 hours. Her potassium got normalized and remained stable afters.Patient did not require WBI as she passed 15-20 tablets in stools next morning and her levels post dialysis remained stable. Patient was then discharged from ICU and seen by psych team.