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Potassium Dichromate poisoning

                                                     Potassium dichromate poisoning-Case Report



Potassium dichromate, K2Cr2O7, is a common inorganic chemical reagent, most commonly used as an oxidizing agent in various laboratory and industrial applications . Potassium dichromate poisoning is a rare presentation and  intoxications by chromium (Cr) compounds are very life threatening and often lethal. After oral ingestion of 1 to 3 grams of hexavalent Chromium (Cr6+), gastrointestinal injury, hepatic and renal failure often occurs which  leads to a fatal outcome in most patients. Cellular toxicity is associated with mitochondrial and lysosomal injury by biologically reactive Cr6+  intermediates . After Cr6+ has been absorbed, there is not much that can be done except to control the main complications as the treatment is only symptomatic. The biotransformation of Cr6+ to Cr3+ reduces the toxicity because the trivalent form does not cross cellular membranes as rapidly

Keywords: Potassium dichromate poisoning , Hexavalent chromium , Ascorbic acid.

A Case report:

A 39 year old male working in a match industry presented to our emergency department  with alleged h/o consumption of Potassium dichromate mixed with water . Patient was immediately taken to a local hospital where he was treated symptomatically.

On receiving the patient was conscious ,oriented, afebrile. His vitals were BP 130/70 mm Hg , heart rate 96/min , SpO2  98% on 5 litres of O2 facemask , systemic examination was unremarkable .

In the ED , patient was managed with IV fluids , anti-ulcer , anti – emetic,  IV ascorbic acid. Blood investigations were sent for Hemoglobin , Electrolytes , Renal function test , Liver function test and viral markers which were found to be within normal limits. After emergency resuscitation patient was shifted IRCU & toxicology department for further management .There patient was managed with  facemask-O2  , IV fluids, broad spectrum antibiotics , anti-ulcer drugs ,N-acetyl cysteine infusion , D-pencillamine , MgSO4 , vitamin C and other supportive measures. Psychiatrist opinion was sought. Patient was discharged in a hemodynamically stable condition without any expected complications.



Most naturally occurring chromium exists as chromite in which chromium is in the Cr 3+ state which is relatively non toxic.In contrast ,many industrial applications like metal finishing , match industry and pigments use chromates in which chromium is in the Cr 6+ oxidation state which is both highly toxic and a confirmed carcinogen. Some commonly encountered chromate Cr6+ compounds include sodium chromate (Na2CrO4) , Potassium dichromate (K2Cr2O7) , and ammonium dichromate {(NH4)2Cr2)O7} .



Toxicokinetics :

Hexavalent chromium compouds are highly reactive , powerful oxidizing agents that are absorbed by all routes of exposure.Some reduction of ingested Cr 6 + occurs in the stomach. Absorbed chromates readily cross cell membranes through anion channels .Within cells reduction of Cr 6+ to Cr 3+ occurs. . In fact, more than 80% of Cr6+ is cleared in urine as Cr3+.

Mechanisms of toxicity :

Although hexavalent chromium salts are recognized to be far more toxic than trivalent chromium salts ,paradoxically trivalent chromium is the final perpetrator of chromium-induced carcinogenicity .This occurs both via Cr 3+ binding to cellular and nuclear proteins and as a result of oxidative damage to lipids ,proteins and DNA caused by reactive oxygen species produced during the intracellular reduction of Cr 6+ to Cr 3+.

Properties of Potassium dichromate :

  • Potassium dichromate (also called chromic acid , bichromic acid , potassium bichromate or chromic oxide ) is a common industrial and laboratory agent.
  • It is a bright orange-red crystals used in electroplating , aircraft building, ship building , dye casting, match industry , metal cleaning and tanning.
  • Medically it has been used externally as an astringent, antiseptic, and caustic. When taken internally, it is a corrosive poison.
  • Potassium dichromate is dangerous because of its oxidizing potency , not its acidity.
  • Lethal dose : 0.5 to 1 g

Clinical features of Acute Potassium dichromate poisoning:


On inhalation of potassium dichromate compounds , it  becomes highly irritant to mucous membranes causing inflammation of nasal mucosa , hoarseness , cough , bronchospasm and dysnoea. Headache , chest pain , pulmonary edema and cyanosis may ensue.

Ingestion :

On ingestion, potassium dichromate compounds are highly water soluble . It leads to nausea , vomiting , abdominal pain ,diarrhea and burning sensation in the mouth ,throat and stomach. Gastrointestinal hemorrhage is a frequent complication. Methemoglobinaemia , hemolysis , disseminated intravascular coagulation , renal failure and hepatic failure have also been reported.



Topical exposure :

Chromic acid splashes produce severe burns. Percutaneous absorption may lead to kidney and liver failure.


Clinical features of Chronic Potassium dichromate poisoning:


Inhalation of potassium dichromate compounds has led to atrophy ,ulceration and perforation of the nasal septum .Pharyngeal and laryngeal ulcers may also occur .Asthma may be precipitated by exposure to fumes .Lung fibrosis, bronchitis ,emphysema and proximal tubular damage have resulted from occupational exposure.

Topical exposure :

“Chrome ulcers” may develop after repeated topical exposure to hexavalent chromium compounds. They are also skin sensitizers and contribute to development of cement dermatitis and contact dermatitis from paint primer , tanned leather , tattoo pigments and matches.

Carcinogenicity :

Occupational inhalation of Cr6+ is associated with an increased incidence of Lung cancer . There is also evidence that excess chromium ingestion via contaminated drinking water is associated with increased mortality from lung and stomach cancer though the threshold for this effect remains unknown.


Occupational exposure to potassium dichromate can be prevented  primarily by avoiding exposure via instigation of appropriate health and safety measures .Systemic uptake of chromium can be assessed by measuring blood and urine chromium concentrations.

Basic treatment:

  • Airway:  Establish a patent airway. Suction if there are lots of oral secretions. Orotracheal or nasotracheal intubation is considered if there are respiratory insufficiency, respiratory arrest or in unconscious patient.
  • Breathing: Administer oxygen via non-rebreather facemask at 10 – 15 litre/min . Positive pressure ventilation with a bag valve mask device is beneficial .
  • Circulation:  Start an IV access. Use lactated ringer’s solution if signs of hypovolemia are present. Watch for signs of fluid overload. Consider drug therapy for pulmonary edema. In patients with normal fluid volume but hypotensive, consider the use of vasopressors.



  • Management of potassium dichromate inhalation is supportive with Oxygen , bronchodilators , and mechanical ventilation as required.
  • Chemical pneumonitis associated with pulmonary edema should be treated with Continuous positive airway pressure or in severe cases with intermittent positive pressure or positive end expiratory pressure ventilation.
  • Antibiotics will be required if pneumonia develops.

Ingestion :

  • Corrosive ingestion requires prompt vigourous resuscitation and early grading via endoscopy or CT scan with contrast. Early surgical excision of necrotic tissue may be life saving.
  • The amount of chromium removed by hemodialysis or hemodiafiltration is small and these measures the increase chromium clearance significantly in patients with established renal failure. Failure of renal dialysis might lead to rapid progression of methemoglobinemia.
  • Successful liver transplantation has been performed in case of fulminant hepatic failure complicating ingestion of potassium dichromate.
  • Plasmapharesis has been advocated in the treatment of severe systemic chromium poisoning.
  • The role of ascorbic acid is controversial . Animal studies have suggested that parenteral ascorbic acid administered up to 2 hours post ingestion may reduce nephrotoxicity but administration beyond 3 hours resulted in increased toxicity . Based on these data high dose parenteral ascorbic acid may be considered shortly after exposure but there is insufficient evidence in clinical practice to justify its routine use.The suggested dose is 5 to 10g IV within 2 hours of ingestion. Later administration may enhance toxicity by accelerating intracellular hexavalent to trivalent chromium reduction.In addition,high doses of ascorbic acid risk oxalate nephropathy.
  • The use of dimercaprol, acetylcysteine,D-pencillamine and DMPS as chelating agent has been suggested in the management of systemic  hexavalent chromium poisoning but their efficacy is unproven.

Topical exposure:

  • First rinse with plenty of water for at least 15 minutes, then remove contaminated clothes and rinse again.
  • Early aggressive excision of exposed skin is advocated in all chromic acid burns in order to minimize systemic hexavalent chromium uptake.
  • There are also clinical data to support the topical application of 10% ascorbic acid to increase the rate of healing of hexavalent chromium induced dermatitis and ulceration.But there are however insufficient data to advocate the routine use of ascorbic acid systemically or topically in the treatment of chromic acid burns.



Potassium dichromate ingestion should be suspected in any patient presenting with hepatorenal syndrome after alleged suicidal consumption.Occupational exposure have to reduced by instigating proper health and safety measures. If presenting early, treatment with ascorbic acid can be attempted and for persons presenting late, referral to a center equipped with facilities for dialysis and liver transplantation is the only option available.



Dr.Anand MD (Anaes),

Sr.Consultant & Intensivist,

Dept of Intensive Respiratory Care Unit.


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