Methemoglobinemia & Hemolytic Anemia Secondary to Hematite (Geru Powder) Ingestion in a G6PD Deficient Patient

Case Report

Austin J Environ Toxicol. 2016; 2(1): 1010.

Methemoglobinemia & Hemolytic Anemia Secondary to Hematite (Geru Powder) Ingestion in a G6PD Deficient Patient

Naidu S*, Datta K, Das I, Patel M, Verma S and Kole T

Department of Emergency Medicine, Max Hospital, India

*Corresponding author: Sarat Naidu, Department of Emergency Medicine, Max Hospital, Shalimar Bagh, India

Received: March 15, 2016; Accepted: May 02, 2016; Published: May 03, 2016


A 3 years old previously healthy boy presented with h/o fever, gross hematuria and vomiting after ingesting a locally popular ayurvedic drug formulation called GERU which contains Ferric oxide.

On investigations he was found to be G6PD deficient which lead to Intravascular hemolysis and Methemoglobinemia due to oxidative stress.

He was aggressively managed and was discharged in a stable condition after 5 days.

Keywords: G6PD Deficiency; Glucose-6-phosphatase dehydrogenase; Hemolysis; Hemoglobinuria; Methemoglobinemia; Geru; Hematite; Toxicity; Ayurvedic medication; Ferric oxide; India


Hematite is a chemical compound containing silicate of alumina and iron oxide (ferric oxide, Fe3+).

It is a mineral, coloured black, brown, grey or red. In India it is popularly called as GERU and is widely used for multiple purposes. In some areas of India it is used for jewelry making, painting earthenware pots, medicinal use topically in allergic rash, headache, bleeding, constipation etc.

G6PD (Glucose-6-Phosphatase Dehydrogenase) is an intracellular enzyme which plays an important role in protection of RBCs against oxidative stress like oxidant drugs, infections, fava beans etc [1-8].

G6PD deficient patients can develop acute hemolysis during oxidative stress [1].

The presence of methemoglobinemia has significant diagnostic and therapeutic consequences in G6PD deficient patients who are exposed to oxidative stress [1].

We report a previously healthy 3 yrs old boy who presented with severe acute hemolytic anemia and methemoglobinemia after ingesting a locally popular ayurvedic drug formulation called GERU (Hematite). He was subsequently diagnosed to have G6PD deficiency and was managed with conservative treatment successfully.

Case Study

A previously healthy 3 years old boy of Indian origin was brought to the emergency department at around 10 pm by his parents with h/o passing grossly dark coloured urine (hematuria), multiple episodes of vomiting and mild fever since 1 day.

They also mentioned that the child had some allergic skin rash 2 days back for which he was given orally some ayurvedic drug formulation locally known as Geru powder, following which he developed the above symptoms.

He otherwise had no known medical or surgical conditions and was not known to be allergic to any medications.

There was no h/o jaundice and was not on any medications.

There was no family h/o jaundice and blood disorder.

Physical examination revealed the child was conscious and oriented but was in mild to moderate respiratory distress with respiratory rate of 30/min.

He was pale, mildly jaundiced and febrile (101.5 deg F) but was not cyanosed.

His pulse rate was 100/min, BP was 100/50 mmHg, RBS was 120 mg%, SpO2 was only 75% at RA.

He had no hypothermia or rash.

Neurological, Cardiovascular, Respiratory and per abdominal examinations were insignificant.

Patient was immediately taken to the resuscitation bay and O2 supplementation was started @15LPM through non-rebreathing face mask but the SpO2 did not increase beyond 80%.

Arterial blood gas analysis showed pH = 7.442, PO2 = 32 mmHg, PCO2 = 27.9 mmHg, Lactate = 1.23 mmol/L, Methemoglobin levels = 21.3%, Hb = 6.4 gm%, O2 sat = 90%.

Chest x ray did not show anything significant.

In view of above findings, IV fluids were started with Dextrose 10% 100ml + Sodabicarb 8.4% 35ml @ 75ml/hr.

Nephrology and Hematology consultations were requested and the patient was shifted to Paediatric ICU after 2 hrs of aggressive management in the ER.

Course in the hospital and outcome

The diagnosis of acute severe hemolysis with methemoglobinemia was made.

Investigations revealed hemoglobin 6.8 gm/dl, TLC 24,000/cmm, raised unconjugated bilirubin, total lron levels 497 mcg/dl [Normal adult = 50-170, Children = 50-120].

G6PD activity showed 1.36 IU/gm Hb [Normal range 3.8 - 5.9 IU/ gm Hb in a child > 3 months age].

Blood Peripheral Smear exam showed Normocytic normochromic anemia with e/o hemolysis and no e/o basophilic stippling.

Kidney function test and Direct Coomb’s test were within normal limits.

Forced alkaline dieresis was started and Inj Frusemide was 20mg + 10mg given IV. Blood transfusion was started with packed red blood cells after which Hb increased to 12gm/dl.

He was started on Furosemide infusion @ 0.2mg/kg/hr and Vitamin C 500mg/day orally.

In view of fever, raised TLC and raised CRP, Piperacillin + Tazobactum antibiotic was started @ 1gm IV TDS.

After 12 hrs of presentation, patient’s respiratory distress decreased and MethHb levels reduced to 7.1%. Patient started maintaining SpO2 with minimal O2 requirement.

On day 3, MethhZb levels reduced to 2.6%.

On day 4, urine colour started improving (became lighter coloured) and finally became normal coloured and Bilirubin levels also became normalized.

Total iron levels reduced to 120mcg/dl.

Subsequently he was shifted to ward after 4 days of ICU stay and was discharged in stable condition after 5 days of hospitalization.

During the entire hospital stay, the child had normal higher mental functions and was on the improving trend since the start of the treatment.

Discussion and Therapeutic Considerations

This case report illustrates that severe intravascular hemolysis [9,1,4,10,7] and methemoglobinemia [9,1,2,11,12,10,13,5,6,8] can occur in a G6PD deficient patient following ingestion of ironcontaining (Fe3+) substances like hematite (geru powder) (Figures 1 & 2).