Raspberry urine?

Hydroxocobalamin has been administered.

A red discolouration to the skin and mucous membranes may also be noted in addition to the urine^1,2.

This patient had suspected cyanide toxicity.

The indications^1,4 for hydroxocobalamin in suspected cyanide toxicity include:

• Altered mental status
• Seizures
• Hypotension
• Lactic acidosis

Cyanide toxicity^1,3 results from cyanide binding to the ferric ion (Fe3+) of cytochrome oxidase, inhibiting oxidative phosphorylation in mitochondria.

Early clinical features include

• Nausea and vomiting
• Headache
• Tachycardia and tachypnoea
• Agitation
• Seizures

Late clinical features include

• Hypotension and bradycardia
• Confusion
• Tetany
• Respiratory depression
• Coma

Investigations usually reveal

• hyperlactataemia and high anion gap acidosis.
• high venous O2 saturation, with a low arterial-venous oxygen difference (i.e. a low O2 extraction ratio as mitochrondria are unable to utilise oxygen).

Hydroxocobalamin is a vitamin B₁₂ precursor^1,4,5.

In high doses it chelates cyanide, forming cyanocobalamin which is non-toxic and excreted in urine

Aerobic metabolism can then resume normally.

Hydroxocobalamin is available as a “Cyanokit®” containing 2 vials of 2.5g hydroxocobalamin as a powder, and 2 vials of 100ml 0.9% NaCl for reconstitution.

To administer:

• Reconstitute one vial (2.5g) in 100ml of 0.9% NaCl, and give over 15 mins
• Repeat with the second vial
• This should be sufficient to bind 100mg of cyanide (but often quantity is unclear with inhalational injury)
• If patient is in cardiac arrest, give 5g as an IV push.

Note that this dose is huge in comparison to the dose given for Vitamin B12 deficiency (250 – 1000mcg per IM injection).

Hydroxocobalamin has a low side effect profile, in that if it is given to a patient without cyanide poisoning, there is low risk of an adverse outcome.

Sodium nitroprusside.

SNP contains 5 cyanide groups and one nitric oxide group attached to a central iron molecule covalently bonded to Na.

When SNP reacts with oxyhaemoglobin in red blood cells, it releases nitric oxide (causing arterial and venous vasodilation and reducing MAP), and also 5 cyanide ions.

At high dose this can cause cyanide toxicity.

1. Murray L, Little M, Pascu O, Hoggett K. Toxicology Handbook, 3^rd Edition. Australia: Elsevier Australia; 2016
2. Cescon D, Juurlink D. Discoloration of skin and urine after treatment with hydroxocobalamin for cyanide poisoning. CMAJ 2009; 180(2): 251
3. Nickson CP. Cyanide Poisoning. LITFL CCC.
4. Nickson CP. Hydroxocobalamin. LITFL.
5. Therapeutic Goods Administration: Product and Consumer Information. Hydroxocobalamin. Accessed 23 Feb 2022.
6. Chee-How E. What drug was given?! Twitter 2022
7. Borron SW, Baud FJ, Barriot P, Imbert M, Bismuth C. Prospective study of hydroxocobalamin for acute cyanide poisoning in smoke inhalation. Ann Emerg Med. 2007 Jun;49(6):794-801
8. Shepherd G, Velez LI. Role of hydroxocobalamin in acute cyanide poisoning. Ann Pharmacother. 2008 May;42(5):661-9
9. Rogers J. Cherry red or Raspberry Urine. LITFL 2022