CONTINUOUS VENOVENOUS HEMOFILTRATION IN THE TREATMENT OF TOLUENE INTOXICATION: A CASE REPORT

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CONTINUOUS VENOVENOUS HEMOFILTRATION IN THE TREATMENT OF TOLUENE INTOXICATION: A CASE REPORT
Jose Fernando
Garcia Fuentes
Francisco Perez-Allende Perez franknefro1128@gmail.com Instituto Nacional de Cardiologia Ignacio Chavez Nefrologia Ciudad de Mexico
Elisa Mendoza Ramirez elimendozar21@gmail.com Instituto Nacional de Cardiologia Ignacio Chavez Nefrologia Ciudad de Mexico
Jose Daniel Juarez Villa daniel_00_5@hotmail.com Instituto Nacional de Cardiologia Ignacio Chavez Nefrologia Ciudad de Mexico
Magdalena Madero Rovalo madero.magdalena@gmail.com Instituto Nacional de Cardiologia Ignacio Chavez Nefrologia Ciudad de Mexico
 
 
 
 
 
 
 
 
 
 
 

Toluene is metabolized by cytochrome p-450 into benzoic and hippuric acid and , excreted by the   kidney. Its accumulation produces type 1 tubular acidosis and hypokalemia due to an increase in the gap between intracellular and extracellular potassium, altering membrane polarization. 

Objective: To describe the case of a patient with toluene poisoning treated with conventional hemodialysis and then continuous renal replacement therapy (CRRT).

Case presentation: A 53-year-old woman with a history of substance abuse presents to the emergency department with generalized weakness and stupor. Her vital signs at the time of admission were: heart rate 81 bpm, respiratory rate 35 bpm, blood pressure 92/60 mm Hg, temperature 35°C and oxygen saturation of 95%. On examination, she was drowsy, polypneic and anuric. Laboratory studies revealed a creatinine 4.3 mg/dl, Na 139 meq/L, K 2.4 meq/L, Cl 105 meq/L, phosphorus 6.16 mg/dL, magnesium 2.34 mg/dL, Alb 2.93 g/dL, AST 29.8 U/L, ALT 11.5, lactate dehydrogenase 250 U/L, total bilirubin 0.2 mg/dL, , direct bilirrubin 0.1 mg/dL, indirect bilirrubin 0.1 mg/dL, alkaline phosphatase 187 U/L, prothrombin time 13.4 seconds, partial thromboplastin time 36.5 seconds, INR 2.9, pH 6.89, pCO2 11 mmHg, HCO3 2.1 meq/l, lactate 1.1 mmol/L, Anion Gap was 28 mmol/L. Other causes of gap anion metabolic acidosis were ruled out and due to the history of drug abuse toluene intoxication was suspected, which was later confirmed by her relative. 

Management of toluene intoxication is usually supportive management, however due to anuria and stage 3 AKI we considered initiating conventional hemodialysis. During the session she became hypotensive requiring vasopressors and mechanical ventilation. Due to the risk of recurrence of metabolic acidosis the patient was transitioned to continuous venovenous hemodiafiltration (CVVHDF) with an additional potassium infusion in the replacement bags.

The evolution was favorable and the patient was extubated with adequate recovery of the neurological status, being discharged two days later without complications.


LABS PRIOR TO CONVENTIONAL HAEMODIALYSIS

DATE AND HOURS

pH

pCO2

HCO3

LActate

Ca++

na

K

Cl

anion gap

23.02.23 16:30

6.89

11

1.8

0.9

0.9

124

1.7

105

17.2

 

LABORATORIES AFTER CONVENTIONAL HAEMODIALYSIS WAS INITIATED

DATE AND HOURS

pH

pCO2

HCO3

LActate

Ca++

na

K

Cl

anion gap

23.02.23 22:31

7.08

29

8.8

0.7

1.15

132

2.9

106

17.2

 

LABORATORIES AFTER CRRT WAS INITIATED

DATE AND HOURS

pH

pCO2

HCO3

LActate

Ca++

na

K

Cl

anion gap

26.02.23 7:56 hrs

7.43

39

25.6

0.7

1.09

141

3.1

106

9.4

Toluene intoxication is characterized by paralysis or weakness, altered mental status, severe acidemia, and severe anion gap metabolic acidosis.  In severe cases, toluene toxicity can be treated with CRRT and additional potassium replacement. 

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