Monatshefte für Chemie - Chemical Monthly

, Volume 149, Issue 9, pp 1647–1651 | Cite as

Severe suicidal self-poisoning with massive dose of potassium ferricyanide(III): hyperkalemia but not free cyanide may cause death

  • Lucie Lischková
  • Daniela Pelclová
  • Jiří Hlušička
  • Vaclav Kadlec
  • Sergey Zakharov
  • Tomáš Navrátil
Original Paper


Potassium ferricyanide(III), K3[Fe(CN)6], has a widespread use in blueprint drawing, photography, chemical industry, and metallurgy. In mice, the oral lethal dose 50 (LD50) is 1600 mg kg−1. We report the case of a suicide attempt in a 37-year-old male by intentional ingestion of 80 g of potassium ferricyanide(III) dissolved in water. The estimated ingested dose was 770 mg kg−1. The patient reported vertigo as the first sign of poisoning and six episodes of diarrhea with dark-colored stool 2 h after ingestion. The patient was transported by ambulance to the intensive care unit 8 h after ingestion. He was conscious and spontaneously ventilating, with a Glasgow Coma Scale (GCS) score of 15. On ECG performed at admission, tall “tented” T waves in V3–V6 and progressive flattering of P waves were registered. Serum concentrations of potassium of 7.2 mmol dm−3, urea of 7.1 mmol dm−3, and creatinine of 162 µmol dm−3 indicated development of acute renal failure. Despite the administration of intravenous insulin and 10% glucose infusion during the first hours after admission, there was a further elevation of serum potassium to 7.4 mmol dm−3 suggesting acute renal failure. For this reason, intermittent hemodialysis was performed [duration 200 min, blood flow rate 147 cm3 min−1, online clearance monitoring (OCM) clearance rate 100 cm3 min−1, and substitution fluid volume 5.8 dm3]. The condition of the patient stabilized and he was discharged from hospital on the fourth day after admission. This case report demonstrates the risks of life-threatening hyperkalemia and acute renal failure as complications of massive ingestion of potassium ferricyanide(III).

Graphical abstract


Potassium ferricyanide(III) Intoxication Hyperkalemia Acute renal failure 


Potassium ferricyanide(III), also known as potassium hexacyanoferrate, is a compound with chemical formula K3[Fe(CN)6]. The polymer consists of octahedral [Fe(CN)6]3− centers cross-linked with K+ ions that are bound to the CN ligands [1]. Potassium ferricyanide(III) is used in tempering steel, etching liquids, production of pigments, electroplating, sensitive coatings on blueprint paper, fertilizer compositions, and as a laboratory reagent [2].

Potassium ferricyanide(III) is considered to be the only of minor toxicity following ingestion in humans. In mice, the oral lethal dose (LD50) is 1600 mg kg−1. After ingestion of significant amounts, the typical signs and symptoms reported in humans are irritation of gastrointestinal tract, nausea, vomiting, diarrhea, abdominal pain, and hematemesis [3].

The compound is rapidly converted into ferrocyanide(II), which is further hydrolyzed to form hexacyanoferrate ion. It is assumed that free cyanide is not produced from this reaction because of the tight binding between the metal ion and the cyanide group preventing cyanide from release [3, 4]. Therefore, specific antidotal therapy of cyanide poisoning is not required.

We present a case report of severe poisoning with massive dose of potassium ferricyanide(III) demonstrating that a life-threatening condition can develop due to high hyperkalemia and acute renal failure, but not due to free cyanide release from the compound.

Case description


A 37-year-old male, 104 kg body weight, with a history of chronic alcohol abuse and social adaptation failure, ingested in a suicide attempt 80 g of pure potassium ferricyanide(III) (Fig. 1) dissolved in water. The estimated ingested dose was approximately 770 mg kg−1.
Fig. 1

The sample of the pure potassium ferricyanide(III) ingested by the patient

The patient had several co-morbidities: diabetes mellitus type 2, dyslipidemia, metabolic syndrome, obesity (BMI 36), arterial hypertension, hepatic steatosis, and left kidney cyst. His chronic medication included insulin Lantus 20 international units (IU) administered subcutaneously in the evening, metformin 1000 mg tablet twice daily, and Lipanthyl 267 M (fenofibrate) once a day.

Clinical and laboratory data

The patient reported vertigo as the first sign after ingestion and six episodes of diarrhea with dark-colored stool 2 h after ingestion, but no episodes of vomiting. He was found conscious with Glasgow Coma Scale (GCS) 15 by the ambulance staff about 8 h after ingestion, with blood pressure 160/80 mmHg (21.3/10.7 kPa), heart rate 105 min−1, respiratory rate 15 min−1, saturation 99%, and body temperature 36.9 °C.

The patient was transported to the intensive care unit. On admission, the patient was conscious, spontaneously ventilating, with normal skin coloration, blood pressure 160/90 mmHg (21.3/12 kPa), saturation 99%, and heart rate 99 min−1. On ECG, regular sinus tachycardia with heart rate 102 min−1, progressive flattering of P waves, and tall “tented” T waves in V3–V6 were registered (Fig. 2) as typical signs of hyperkalemia.
Fig. 2

ECG of the patient performed on admission with typical peaked T waves in V3–V6

The laboratory parameters on admission, serum potassium 7.2 mmol dm−3, urea 7.1 mmol dm−3, and creatinine 162.0 µmol dm−3 indicated development of acute renal failure. Other laboratory parameters included glucose 8.6 mmol dm−3, sodium 136.0 mmol dm−3, chloride 107.0 mmol dm−3, calcium 2.5 mmol dm−3, white blood count 15.7 × 109 dm−3, hemoglobin 168.0 g dm−3, liver enzymes ALT 1.45 µkat dm−3, AST 1.28 µkat dm−3, GMT 2.60 µkat dm−3, and INR 1.2. The chest X-ray examination showed no pathologies. The results of arterial blood gases’ measurements were: pH 7.37, pCO2 2.80 kPa, pO2 19.30 kPa, base excess − 10.80 mmol dm−3, saturation O2 98.8%, bicarbonate 16.30 mmol dm−3, COHb 0.7%, and MetHb 1.5%.

Due to elevation of serum potassium concentration, the treatment was initiated upon admission with infusion of 16 IU of insulin in 500 cm3 of 10% glucose with the rate of 250 cm cm3 h−1 and chronic medication with metformin was discontinued. The control laboratory tests 1.5 h after admission demonstrated further elevation of serum potassium to 7.4 mmol dm−3. Despite the intravenous administration of insulin and glucose, hyperkalemia progressed and acute renal failure developed, and intermittent hemodialysis was performed with the following parameters: duration 200 min, blood flow rate 147 cm3 min−1, OCM clearance rate 100 cm3 min−1, and substitution fluid volume 5.8 dm3.

At the end of hemodialysis session, the laboratory parameters were: potassium 4.4 mmol dm−3, sodium 139.0 mmol dm−3, chloride 107.0 mmol dm−3, urea 5.2 mmol dm−3, creatinine 115.0 µmol dm−3, glomerular filtration by Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula 1.16, hemoglobin 160.0 g dm−3, arterial blood pH 7.35, pCO2 5.08 kPa, pO2 5.40 kPa, base excess − 4.1 mmol dm−3, bicarbonate 20.5 mmol dm−3, COHb 1.0%, and MetHb 1.5%. Further treatment continued with intravenous fluid replacement, correction of electrolytes balance, and intravenous proton pump inhibitor (PPI) pantoprazole 40 mg twice a day. Microbiological cultivations of the upper airways (for Staphylococcus plasmacoagulasis, Streptococcus viridans, and Neisseria pharynges) and serology of hepatitis proved to be negative.

On day 2 of hospitalization, the laboratory parameters of the patient were: sodium 136.0 mmol dm−3, potassium 3.9 mmol dm−3, chloride 100.0 mmol dm−3, osmolarity 288.0 mmol dm−3, creatinine 141.0 µmol dm−3, urea 5.3 mmol dm−3, CKD-EPI 0.91, ALT 1.71 µkat dm−3, AST 2.27 µkat dm−3, GMT 2.64 µkat dm−3, ALP 0.57 µkat dm−3, hemoglobin 161.0 g dm−3, white blood count 17.3 × 109 dm−3, INR 1.2, arterial blood pH 7.43, pCO2 4.31, pO2 11.00 kPa, base excess − 1.9 mmol dm−3, COHb 1.4%, and MetHb 1.4%. The patient was conscious, oriented, and afebrile with blood pressure 150/80 mmHg (21.3/10.7 kPa), heart rate 103 min−1, and saturation 97%. The daily fluid intake was 2400 cm3.

On day 3 of hospitalization, all measured laboratory parameters were normal, and the patient was transferred to a standard care unit.

On day 4, the patient was discharged from hospital. The patient refused psychiatric hospitalization suggested by the psychiatric consultant; consequently, ambulatory follow-up psychiatric care was recommended.


Ferro- and ferricyanides are generally low-toxic compounds because they do not tend to release free cyanide. For example, the compound hexacyanoferrate(II) [5] is considered to be practically nontoxic because of the tight binding between the cyanide ions and the metal that prevents release of free cyanide ions (LD for humans is approximately 50–100 g [6]). Ingestion of potassium ferrocyanide(II) in humans leads to minor symptoms of gastrointestinal irritation. At present, only one case of acute ingestion of approximately one coffee spoon of potassium ferrocyanide(II) has been published [4].

The release of cyanide ions from the compound is minimal at physiologic blood pH. However, experimental in vitro and in vivo studies suggest that after ingestion, cyanide release may be facilitated in acidic gastric pH [4].

The acidity of gastric secretion can be modified by administration of proton pump inhibitors as the most effective drugs for inhibition of hydrochloric acid secretion [7]. Intravenous administration of PPI provides more rapid increase of gastric pH [8].

Hence, intravenous administration of pantoprazole to decrease the acidity and to treat the irritation of gastrointestinal tract might have an effect on the stability of ingested chemical compound.

On the other hand, ingestion of massive dose of potassium ferricyanide(III) could present severe condition with possible life-threatening complications. In the presented case, the ingestion of pure potassium ferricyanide(III) led to significant elevation of serum potassium due to rapid absorption of dissociated potassium ions from the stomach and duodenum. Severe hyperkalemia (serum potassium > 6.0–6.5 mmol dm−3) is considered as a potentially life-threatening condition requiring cardiac monitoring and immediate medical intervention. Serum potassium concentration and the balance between intra- and extra-cellular potassium concentrations play an important role in the cell membrane electrophysiology. Hyperkalemia leads to the decrease in myocardial resting membrane potential, increased cardiac depolarization, myocardial excitability, cardiac instability, and abnormalities of conductivity with arrhythmias progressing to ventricular fibrillation and asystole [9].

Typical ECG findings in hyperkalemia are tall, “peaked” T waves, shortened QT interval, lengthening of PR interval with loss of P waves, and widening of QRS complex culminating in the “sine wave” morphology [10]. In the case of our patient, serum potassium concentration continued to elevate to 7.4 mmol dm−3 despite the treatment with insulin and glucose infusion, which “shifts” potassium to the intracellular space. Short-term hemodialysis session led to efficient elimination of serum potassium.

The patient was admitted to hospital 8 h after ingestion; therefore, gastrointestinal decontamination was not performed. Gastric lavage generally is not recommended because the risks of decontamination are considered to outweigh any potential benefit [3]. Nevertheless, decontamination should be performed in the cases of ingestion of massive doses of ferricyanide(III) and presentation within 1 h after ingestion. Active charcoal does not bind effectively to potassium ferricyanide(III), but administration of laxatives or whole-bowel irrigation with polyethylene glycol may be considered.

Solubility of K3[Fe(CN)6] is up to 558 g dm−3 [11] under human body temperature (i.e., 37 °C). Therefore, it is supposed that the ingested amount of 80 g was completely dissolved and dissociated. The stability constant β [12] of this complex is 1042. The volume of blood presents approximately 60 cm3 kg−1 of body mass that is about 6 dm3. Accordingly, it could be calculated that the concentration of K3[Fe(CN)6] in blood was in the described case about 0.04 mol dm−3. Therefore, the concentration of cyanide anions released in blood [13] could be about 0.6 μmol dm−3. If the ingested amount was dissolved in minimum amount of blood necessary for its dissolution, i.e., in 0.14 dm−3, in such case, the concentration of CN ions would be about 1.1 μmol dm−3, i.e., in total about 3.8 mg of cyanide in blood.

The LD50 of cyanide for rats is about 10 mg kg−1 and LD in humans is approximately 2–3 mg kg−1, but generally it depends on many factors such as individual sensitivity and content of stomach [14, 15, 16, 17], i.e., in the presented case LD would be approximately 200 mg. Therefore, we conclude that the cyanide blood concentration was at least two to three orders lower than the lethal concentration.

It is known that the hydrolysis of [Fe(CN)6]3− is accelerated by light, but inside human body this process obviously does not take place. Furthermore, ferricyanide(III) in aqueous solution is reduced by hydrochloric acid into ferrocyanide(II), which is even less toxic.

Payen et al. [4] discussed the importance of administration of an antidote for cyanide poisoning, hydroxocobalamin in the case report on potassium ferrocyanide(II) poisoning. In the discussed case, the patient ingested two glasses of potassium ferrocyanide(II), developed vomiting, and collapsed within less than 1 h, requiring cardiopulmonary resuscitation. Elevated serum lactate (more than 15 mmol dm−3) and hyperkalemia were present on admission, but serum cyanide concentration (0.70 mg dm−3) was below lethal values (typically 2.5–3.0 mg dm−3). Despite treatment with antidote, the patient died after 3 days of resuscitation therapy because of cerebral death [4]. The cause of lactic acidosis is questionable in this case: in cyanide poisonings, high level of serum lactate is a hallmark, but in this case cardiac arrests due to hyperkalemia and anoxia were the most probable causes of high lactacidemia. Therefore, the effect of antidotal therapy of cyanide poisoning in the cases of potassium ferrocyanide(II) and potassium ferricyanide(III) massive ingestion remains disputable.


Massive ingestion of potassium ferricyanide(III) can be a life-threatening condition due to severe hyperkalemia refractory to treatment, but not due to significant release of free cyanide anions. A combination of insulin and glucose therapy with intermittent hemodialysis is indicated in these cases. The rationale for intravenous administration of proton pump inhibitors is to increase the gastric pH and to treat gastric irritation. Finally, gastrointestinal decontamination should be considered in massive doses shortly after ingestion. The administration of antidotal therapy for cyanide poisoning is not required.



The research was supported by the Ministry of Health of the Czech Republic (AZV) by the Grants nos. 16-27075A and 44/18D, by the Projects PROGRES Q25 and Q29 of the First Faculty of Medicine, Charles University in Prague, and research of T.N. was supported by the Czech Science Foundation (Project GA ČR no. 17-03868S).


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Copyright information

© Springer-Verlag GmbH Austria, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Department of Occupational Medicine, First Faculty of MedicineCharles UniversityPragueCzech Republic
  2. 2.Toxicological Information CentreGeneral University HospitalPrague 2Czech Republic
  3. 3.Department of Internal MedicinePardubice HospitalPardubiceCzech Republic
  4. 4.J. Heyrovsky Institute of Physical Chemistry of the Academy of Sciences of the Czech RepublicPrague 8Czech Republic
  5. 5.Institute of Medical Biochemistry and Laboratory Diagnostics, First Faculty of MedicineCharles University and General University Hospital in PraguePrague 2Czech Republic

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