opsi terapi keracunan sianida dan mekanismenya

Sebuah rangkuman terkait dengan opsi terapi keracunan sianida dan mekanismenya.

1 Hydroxo-cobalamine

Digunakan pada kondisi akut. Khususnya pada px dgn Co-existing CO-poisoning.

Alternatif lain:

2 Cyanide Antidote kit:

- Sodium nitrite 300 mg ampule

- Sodium thiosulfate 12.5 g ampule

Dosing:

Sodium nitrite:

DWS: 10 mg/kg given IV for 3 to 5 minutes

PED: 0.2 mL/kg, not to exceed 10 mL

Sodium thiosulfate:

DWS: 12.5 grams in 50 mL, given intravenously for 30 minutes

PED: 7 g/m2 and not to exceed 12.5 grams

Source:

https://www.ncbi.nlm.nih.gov/books/NBK507796/?report=reader#!po=18.0556

https://www.inchem.org/documents/antidote/antidote/ant02.htm#PartNumber:6 

https://en.m.wikipedia.org/wiki/Cyanide_poisoning

Mekanisme:

Sodium thiosulfate:

The major route of detoxification of cyanide in the body is conversion to thiocyanate.  This reaction requires a source of sulfane sulfur (divalent sulfur bonded to another sulfur) and is catalysed by sulfur transferases (e.g. Rhodanese)

Na2S2O3 + CN-   -->   SCN- + Na2SO3.

Sodium Nitrite:

The oxidation of haemoglobin to methaemoglobin by sodium nitrite is favoured when the oxygen partial pressure is high and haemoglobin is in the oxyhaemoglobin state (Tomoda & Yoneyama, 1979).  If methaemoglobin induction accounts for all, or part, of the antidotal action of sodium nitrite.

Amyl Nitrite:

The principal pharmacological action of amyl nitrite is to cause the relaxation of vascular smooth muscle. Peripheral venous resistance is decreased as a result of a selective action on venous capacitance vessels with resultant venous pooling of blood and decreased venous return to the heart.  The vasodilating effect of amyl nitrite on arteriolar resistance is less than that on the venous side.  As a result of this combined action, both venous filling pressure (preload) and, to a lesser extent, arterial impedance (afterload) are reduced (AHFS, 1988).