Toluene Poisoning / Intoxication

 Substance

 Toluene

 

Common name or Trade name 

 C₆H₅CH₃

 C₇H₈

 甲苯: 汽車排放的廢氣， 油漆、油漆稀釋劑、指甲油、噴漆及黏著劑 possibly contains甲苯

 Route: inhalation of fumes, ingestion, or transdermal absorption [1, 2]

 Exposure: 77% were male and mean age was 23.5 years [3]

 

Involving system

 CNS: marked atrophy of the lower cervical spinal cord, thoracic spinal cord, and conus medullaris. [4]

     Reversible symmetrical white matter changes [ 5]

 Lung: aspiration pneumonitis. [2]

 CV system: potential arrhythmogenic effect of endogenous catecholamines, occasionally resulting in fatality.[6]

 Kidney: Renal glomerular injury (proteinuria)戊 renal tubular acidosis[2]

 Muscle: Rhabdomyolysis occurred in 80% of patients, probably due to hypokalemia and hypophosphatemia [3, 7]

 Cardiopulmonary failure [1]

 The cause of death was in all cases due to cardiac rhythm abnormalities. [7]

 

Presentation

   Chronic: mild cognitive impairment, hearing impairment, dysarthria, marked hyperreflexia of the limbs, spastic paraplegia, slight impairment of deep sensation, and urinary disturbance. 4 stimulus-sensitive spinal myoclonus [8]

   Acute: Severe hypokalemia and acidosis.

  . Biliary tract injury (alkaline phosphatase and gamma-glutamyl transpeptidase elevations) disproportional to hepatocellular injury is common.

Altered mental status, severe acidosis, hypokalemia and acute oliguric renal failure. [3, 7]

Symptomatic hypokalemia [2]

Adrenal insufficiency secondary to bilateral adrenal hemorrhage [9]

 

Antidote and Treatment

  No antidote

  Standardly supportive treatment

 

Disposition

    If asymptomatic, observe 6 hours, and discharge when the CXR is unremarkable.[2]

Poor in patients who have altered mental status, renal failure, severe acidemia and female gender, and patients with these characteristics should be considered to be treated in an intensive care unit. [7]

 

References

 

 [1]https://pubmed.ncbi.nlm.nih.gov/24164003/

[2]. Goldfrank’s toxicologic emergencies. 11^th ed. P. 1415~1417

[3].https://pubmed.ncbi.nlm.nih.gov/22642292/

 [4]https://pubmed.ncbi.nlm.nih.gov/32238742/

[5].https://pubmed.ncbi.nlm.nih.gov/25117062/

[6]. https://pubmed.ncbi.nlm.nih.gov/9140324/

[7].https://pubmed.ncbi.nlm.nih.gov/26282250/

   [8]https://pubmed.ncbi.nlm.nih.gov/10845207/

[9]https://pubmed.ncbi.nlm.nih.gov/9711204/

 

Edited by Yu-Jang Su   Nov 8, 2023

Urinary alkalization and urinary acidification in poisoning

 

尿液鹼化原理是毒物從經由腎臟排除, 毒物為弱酸性的情況, 分佈於細胞外液並且protein binding不強. (像NSAID與protein binding強就無用)

 尿液鹼化適應症:

l  中重度salicylate毒性未達hemodialysis程度

(水楊酸中毒血液透析適應症: https://twmmhedpc.blogspot.com/2019/12/poison-hemodialysis-is-helpful.html

l  Phenobarbital (多劑量activated charcoal較優)[1].

 

l  Chlorophenoxy herbicides (2-4-dichlorophenoxyacetic acid and mecoprop): 須高尿流量 600 mL/h 較有效 [2, 3], forced diuresis 也是有幫忙的[4]

 

l  Chlorpropamide: supportive care/IV dextrose normally sufficient.

 

l  Toxicities of High-Dose Methotrexate [5]

 

尿液鹼化禁忌症

l  本來患者狀況fluid就overload

l  Renal impairment: CKD, uremia.

l  本來血鉀就很低(Uncorrected hypokalemia), 避免低血鉀引發VT [6] 最好keep 血鉀在4—4.5 mEq/L [7] 
 

尿液鹼化併發症:

l  Hypokalemia.

l  Volume overload.

l  鹼血症(Alkalemia);

l  輕度Hypocalcemia
 

尿液鹼化做法:

NaHCO₃^- 1 amp in N/S 1 BT run 125 ml, 有uremia, CHF, CKD 需調整滴速 [8]

1–2 mEq/kg IV bolus followed by 2 mEq/kg per h IV infusion

Sodium bicarbonate 4 amps in D5W 500ml run 250 mL/hr. (可以加20 mEq of potassium chloride避免低血鉀)

Keep urine output of 1 to 2 mL/kg per hour

 

尿液鹼化監測

urine pH 每 15 to 30分測尿的pH 保持7.5 to 8.5.

尿液鹼化曾用於Brazil 與 Iran的organophosphate poisoning 但並無有效實證。[9], 另抗發炎製劑Diflunisal和NSAID 也是無效 [10].

 

尿液酸化

urinary acidification 可以增加弱鹼的移除(包括 amphetamines和phencyclidine), 但產生的相關危險性(例如 rhabdomyolysis) 往往超過尿液酸化原本的好處.  

尿液酸化對MAOI的移除是無效的[4]

REFERENCES

 

[1]: Lindberg MC, Cunningham A, Lindberg NH. Acute phenobarbital intoxication. South Med J. 1992;85(8):803–807. doi:10.1097/00007611-199208000-00004

 

[2]: Bradberry SM, Proudfoot AT, Vale JA. Poisoning due to chlorophenoxy herbicides. Toxicol Rev. 2004;23(2):65–73. doi:10.2165/00139709-200423020-00001

 

[3]: Roberts DM, Buckley NA. Urinary alkalinisation for acute chlorophenoxy herbicide poisoning. Cochrane Database Syst Rev. 2007;(1):CD005488. Published 2007 Jan 24. doi: 10.1002/14651858.CD005488.pub2

 

[4]: Tintinalli’s Emergency Medicine, 8th ed. P.1227

 

[5]: Howard SC, McCormick J, Pui CH, Buddington RK, Harvey RD. Preventing and Managing Toxicities of High-Dose Methotrexate. Oncologist. 2016;21(12):1471–1482. doi:10.1634/theoncologist.2015-0164

 

[6] Tsai IH, Su YJ. Thyrotoxic periodic paralysis with ventricular tachycardia. J Electrocardiol. 2019; 54:93–95. doi: 10.1016/j.jelectrocard.2019.04.001

 

[7] Tintinalli’s Emergency Medicine, 8th ed. P.1268.

 

[8]. Table 176-2. Tintinalli’s Emergency Medicine, 8^th ed. P.1208 -1212.

 

[9]. Tintinalli’s Emergency Medicine, 8th ed. P.1320.

 

[10]: Balali-Mood M, Prescott LF. Failure of alkaline diuresis to enhance diflunisal elimination. Br J Clin Pharmacol. 1980;10(2):163–165. doi:10.1111/j.1365-2125. 1980.tb01734.x

 

 

-- edited 11th Jan, 2020 Yu-Jang Su.