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204
CASE LETTERS
Fatal unsuspected iron ingestion Dear Editor, Iron intoxication might result in severe toxicity or death. Intoxication might easily be missed because it is not detected with routine toxicological screening. In this letter we describe a diagnostic dilemma we faced in a patient with shock and metabolic acidosis. A 47-year-old man presented to the ED of a local hospital with signs of shock and coma. The patient had a history of schizophrenia and drug abuse. Physical examination showed no abnormalities besides black watery faeces. There were no signs of infection. Toxicologic screening was positive for cannabis and methadone and negative for previously prescribed paracetamol, valproate, haloperidol and biperiden hydrochloride. The patient was noted to have a mixed acid–base picture on presentation with respiratory alkalosis and metabolic acidaemia, which was attributed to possible septicaemia or intoxication with an unknown agent (Table 1). Because of hemodynamic instability and respiratory failure, the patient was admitted to the ICU. Treatment consisted of supportive care and antibiotics. The patient was transferred to our tertiary ICU on day 2 post-presentation because of developing renal failure, raised anion gap metabolic acidosis, acute respiratory distress syndrome (ARDS) and liver failure.
TABLE 1.
Intoxication with an unknown substance was suspected but could not be confirmed because of the patient’s comatose state. When we checked the medication history, it was discovered that our patient used ferrous fumarate. Blood samples from the first days of admission were analysed retrospectively. The serum iron concentration on admission was 41 μmol/L (10– 30), confirming the diagnosis of iron intoxication. Desferrioxamine was started. Within 3 days, the serum iron concentration dropped to 23, and the hemodynamic condition stabilised (Table 1). Four weeks after admission, massive gastrointestinal bleeding occurred that was not treatable with endoscopy or angiography. Despite mass transfusion, the bleeding continued and the patient died. Deliberate self-poisoning with iron is uncommon in adults. This might have a mortality rate of up to 10%.1 Intoxication is often a clinical diagnosis suspected on history of iron ingestion.2 However, as seen in this case, patients might present without a history of ingestion with initial gastrointestinal (GI) symptoms and gradually developing systemic toxicity and metabolic acidaemia over the first 12–24 h. It is in these patients with recent GI symptoms and unexplained raised anion gap metabolic acidosis that exclusion of iron poisoning should be considered in the
toxicologic differential diagnosis as a part of the MUDPILES raised anion gap acidaemia mnemonic (M-methanol; U-uremia; D-diabetic/alcoholic ketoacdosis, P-propylene glycol; I-iron/ isoniazid; L-lactate; E-ethylene glycol; S-salicylates). Initial treatment for iron intoxication is aggressive fluid resuscitation and other supportive measures. The current recommended antidotal treatment is desferrioxamine. It binds iron in a water-soluble ferrioxamine complex, which can be excreted by urine or removed through haemodialysis. Indications for desferrioxamine are: serum Fe concentration >90 μmol/L at any time, elevated serum Fe >60 μmol/L with metabolic acidaemia and systemic toxicity and/or shock.3 Desferrioxamine therapy given longer than 24– 48 h might lead to ARDS.4 Although all signs and symptoms in our patient fitted the clinical diagnosis of iron intoxication, serum iron concentration was only slightly elevated because of the delayed presentation. The fact that the iron concentration was still elevated in the presence of acidaemia suggests that desferrioxamine might still have been of benefit in reducing iron load and ongoing toxicity. Despite the presence of metabolic acidaemia on presentation, the treating clinicians might have been biased by previous experience with this
Metabolic parameters
Time (h/days) pH pCO2 (kPa/mmHg) pO2 (kPa/mmHg) Sat (%) Base excess (mmol/L) HCO3− (mmol/L) Iron (μmol/L) Glucose (mmol/L) Anion gap
0h
24 h
36 h
48 h
3 days
4 days
7 days
7.52 1.9/14.3 16.6/124.5 98.8 −8.7 12 41.0 7.5
7.33 4.3/32.3 6.7/50.3 82.9 −8.3 16
7.20 4.7/35.3 11.9/89.3 95.0 −13.7 13
7.26 5.9 8.4/63.0 92.0 −7.4 19
26.5
4.5 21.5
7.25 5.0/37.5 8.6/64.5 92.0 −10.0 16 33.0 6.8 20.9
7.32 5.3/39.8 11.5/86.3 96.0 −5.3 19 30.0 6.6 14.5
7.50 4.3/32.3 10.3/77.3 96.0 1.9 25 23.0 7.8 6.7
© 2014 Australasian College for Emergency Medicine and Australasian Society for Emergency Medicine
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205
CASE LETTERS
patient. The focus was on sepsis and psychotropic drug poisoning as potential diagnoses. Failure to consider other causes of high anion gap metabolic acidosis resulted in a delay to diagnosis of iron poisoning. Clinicians should be aware that when intoxication is suspected in the presence of metabolic acidaemia, a systematic rule out of MUDPILES toxicants should be undertaken.
Author contributions JMW: first draft of the manuscript and literature search. MS: supervision manuscript preparation. JGZ: final draft of the manuscript.
Competing interests None declared.
References 1. Kroeker S, Minuk GY. Intentional iron overdose – an institutional review. CMAJ 1994; 150: 45–8. 2. Reynolds LG. Diagnosis and management of acute iron poisoning. Baillieres Clin. Haematol. 1989; 2: 423–33. 3. Tenenbein M. Toxicokinetics and toxicodynamics of iron poisoning. Toxicol. Lett. 1998; 102–103: 653– 6. 4. Tenenbein M, Kowalski S, Sienko A, Bowden DH, Adamson IY. Pulmonary toxic effects of continuous
desferrioxamine administration in acute iron poisoning. Lancet 1992; 339: 699–701.
Johanna M WOLTERS,1 Marije SMIT2 and Jan G ZIJLSTRA2 1 Department of Emergency Medicine, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands, and 2Department of Critical Care, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands doi: 10.1111/1742-6723.12194
Pitfalls of triage by imaging in spinal epidural abscess Dear Editor, Spinal epidural abscess (SEA) is a relatively uncommon disorder, which can cause death or persistent neurological deficit if left untreated.1,2 Manifestations include back pain, fever and neurological symptoms.2 However, these symptoms are non-specific, and misdiagnosis is common.3 The current literature emphasises the need for emergency MRI with gadolinium contrast (Gd-MRI) in suspected SEA. We use a recent case to demonstrate that excessive reliance on this technically difficult study to rule out SEA may lead to inappropriate management, resulting in preventable morbidity. A 40-year-old man was transferred from a peripheral hospital with 4 days of increasing back pain and neurological symptoms. The patient had injected methamphetamines 2 weeks earlier. Specifically, the patient described waking up with severe interscapular pain, which spread over days to the lumbar spine and right arm. He was unable to weight bear and micturate.
On examination, the patient had marked lower limb and mild right arm weakness in a pyramidal tract distribution, increased deep tendon reflexes, bilateral positive Babinski reflexes and thoracic vertebral tenderness. No fevers were documented, but the patient reported night sweats. He had a white cell count of 14.6 × 109 and CRP of 307 mg/L, consistent with an infective process. A Gd-MRI was performed on the day of admission. However, the patient was severely claustrophobic and did not tolerate the scan, despite sedation. Therefore, post contrast views and Short T1 Inversion Recovery sequences were limited to the lumbar spine. The scan was reported as normal. In consequence, further neurosurgical input was not offered. Other diagnoses were then considered, including transverse myelitis and anterior spinal artery stroke. However, the patient was given IV flucloxacillin empirically. The GdMRI was repeated under general anaesthesia 5 days later demonstrating an epidural abscess from C7 to T12,
probably arising from infection at the right T1/2 facet and T2 transverse process (Fig. 1). The next day the patient underwent T1/2 laminectomy and evacuation of the phlegmon. Tissue specimens were positive for methicillin sensitive Staphylococcus aureus. The i.v. flucloxacillin was continued for 6 weeks. The patient was then commenced on oral dicloxacillin, aiming to continue for 3–6 months, depending on progress. On transfer to rehabilitation, although limb weakness remained, he was walking. His bowels were working normally, but he had failed multiple trials without a urinary catheter. Here we describe a patient who presented typically for SEA, where inadequate spinal MRI resulted in delayed diagnosis and treatment. In SEA, patients generally present with severe back pain, fevers and neurological symptoms.1 Neurological symptoms range from paraesthesias, radiculopathy, motor weakness and sphincter dysfunction to severe paraplegia.1–3
© 2014 Australasian College for Emergency Medicine and Australasian Society for Emergency Medicine
204
CASE LETTERS
Fatal unsuspected iron ingestion Dear Editor, Iron intoxication might result in severe toxicity or death. Intoxication might easily be missed because it is not detected with routine toxicological screening. In this letter we describe a diagnostic dilemma we faced in a patient with shock and metabolic acidosis. A 47-year-old man presented to the ED of a local hospital with signs of shock and coma. The patient had a history of schizophrenia and drug abuse. Physical examination showed no abnormalities besides black watery faeces. There were no signs of infection. Toxicologic screening was positive for cannabis and methadone and negative for previously prescribed paracetamol, valproate, haloperidol and biperiden hydrochloride. The patient was noted to have a mixed acid–base picture on presentation with respiratory alkalosis and metabolic acidaemia, which was attributed to possible septicaemia or intoxication with an unknown agent (Table 1). Because of hemodynamic instability and respiratory failure, the patient was admitted to the ICU. Treatment consisted of supportive care and antibiotics. The patient was transferred to our tertiary ICU on day 2 post-presentation because of developing renal failure, raised anion gap metabolic acidosis, acute respiratory distress syndrome (ARDS) and liver failure.
TABLE 1.
Intoxication with an unknown substance was suspected but could not be confirmed because of the patient’s comatose state. When we checked the medication history, it was discovered that our patient used ferrous fumarate. Blood samples from the first days of admission were analysed retrospectively. The serum iron concentration on admission was 41 μmol/L (10– 30), confirming the diagnosis of iron intoxication. Desferrioxamine was started. Within 3 days, the serum iron concentration dropped to 23, and the hemodynamic condition stabilised (Table 1). Four weeks after admission, massive gastrointestinal bleeding occurred that was not treatable with endoscopy or angiography. Despite mass transfusion, the bleeding continued and the patient died. Deliberate self-poisoning with iron is uncommon in adults. This might have a mortality rate of up to 10%.1 Intoxication is often a clinical diagnosis suspected on history of iron ingestion.2 However, as seen in this case, patients might present without a history of ingestion with initial gastrointestinal (GI) symptoms and gradually developing systemic toxicity and metabolic acidaemia over the first 12–24 h. It is in these patients with recent GI symptoms and unexplained raised anion gap metabolic acidosis that exclusion of iron poisoning should be considered in the
toxicologic differential diagnosis as a part of the MUDPILES raised anion gap acidaemia mnemonic (M-methanol; U-uremia; D-diabetic/alcoholic ketoacdosis, P-propylene glycol; I-iron/ isoniazid; L-lactate; E-ethylene glycol; S-salicylates). Initial treatment for iron intoxication is aggressive fluid resuscitation and other supportive measures. The current recommended antidotal treatment is desferrioxamine. It binds iron in a water-soluble ferrioxamine complex, which can be excreted by urine or removed through haemodialysis. Indications for desferrioxamine are: serum Fe concentration >90 μmol/L at any time, elevated serum Fe >60 μmol/L with metabolic acidaemia and systemic toxicity and/or shock.3 Desferrioxamine therapy given longer than 24– 48 h might lead to ARDS.4 Although all signs and symptoms in our patient fitted the clinical diagnosis of iron intoxication, serum iron concentration was only slightly elevated because of the delayed presentation. The fact that the iron concentration was still elevated in the presence of acidaemia suggests that desferrioxamine might still have been of benefit in reducing iron load and ongoing toxicity. Despite the presence of metabolic acidaemia on presentation, the treating clinicians might have been biased by previous experience with this
Metabolic parameters
Time (h/days) pH pCO2 (kPa/mmHg) pO2 (kPa/mmHg) Sat (%) Base excess (mmol/L) HCO3− (mmol/L) Iron (μmol/L) Glucose (mmol/L) Anion gap
0h
24 h
36 h
48 h
3 days
4 days
7 days
7.52 1.9/14.3 16.6/124.5 98.8 −8.7 12 41.0 7.5
7.33 4.3/32.3 6.7/50.3 82.9 −8.3 16
7.20 4.7/35.3 11.9/89.3 95.0 −13.7 13
7.26 5.9 8.4/63.0 92.0 −7.4 19
26.5
4.5 21.5
7.25 5.0/37.5 8.6/64.5 92.0 −10.0 16 33.0 6.8 20.9
7.32 5.3/39.8 11.5/86.3 96.0 −5.3 19 30.0 6.6 14.5
7.50 4.3/32.3 10.3/77.3 96.0 1.9 25 23.0 7.8 6.7
© 2014 Australasian College for Emergency Medicine and Australasian Society for Emergency Medicine
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205
CASE LETTERS
patient. The focus was on sepsis and psychotropic drug poisoning as potential diagnoses. Failure to consider other causes of high anion gap metabolic acidosis resulted in a delay to diagnosis of iron poisoning. Clinicians should be aware that when intoxication is suspected in the presence of metabolic acidaemia, a systematic rule out of MUDPILES toxicants should be undertaken.
Author contributions JMW: first draft of the manuscript and literature search. MS: supervision manuscript preparation. JGZ: final draft of the manuscript.
Competing interests None declared.
References 1. Kroeker S, Minuk GY. Intentional iron overdose – an institutional review. CMAJ 1994; 150: 45–8. 2. Reynolds LG. Diagnosis and management of acute iron poisoning. Baillieres Clin. Haematol. 1989; 2: 423–33. 3. Tenenbein M. Toxicokinetics and toxicodynamics of iron poisoning. Toxicol. Lett. 1998; 102–103: 653– 6. 4. Tenenbein M, Kowalski S, Sienko A, Bowden DH, Adamson IY. Pulmonary toxic effects of continuous
desferrioxamine administration in acute iron poisoning. Lancet 1992; 339: 699–701.
Johanna M WOLTERS,1 Marije SMIT2 and Jan G ZIJLSTRA2 1 Department of Emergency Medicine, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands, and 2Department of Critical Care, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands doi: 10.1111/1742-6723.12194
Pitfalls of triage by imaging in spinal epidural abscess Dear Editor, Spinal epidural abscess (SEA) is a relatively uncommon disorder, which can cause death or persistent neurological deficit if left untreated.1,2 Manifestations include back pain, fever and neurological symptoms.2 However, these symptoms are non-specific, and misdiagnosis is common.3 The current literature emphasises the need for emergency MRI with gadolinium contrast (Gd-MRI) in suspected SEA. We use a recent case to demonstrate that excessive reliance on this technically difficult study to rule out SEA may lead to inappropriate management, resulting in preventable morbidity. A 40-year-old man was transferred from a peripheral hospital with 4 days of increasing back pain and neurological symptoms. The patient had injected methamphetamines 2 weeks earlier. Specifically, the patient described waking up with severe interscapular pain, which spread over days to the lumbar spine and right arm. He was unable to weight bear and micturate.
On examination, the patient had marked lower limb and mild right arm weakness in a pyramidal tract distribution, increased deep tendon reflexes, bilateral positive Babinski reflexes and thoracic vertebral tenderness. No fevers were documented, but the patient reported night sweats. He had a white cell count of 14.6 × 109 and CRP of 307 mg/L, consistent with an infective process. A Gd-MRI was performed on the day of admission. However, the patient was severely claustrophobic and did not tolerate the scan, despite sedation. Therefore, post contrast views and Short T1 Inversion Recovery sequences were limited to the lumbar spine. The scan was reported as normal. In consequence, further neurosurgical input was not offered. Other diagnoses were then considered, including transverse myelitis and anterior spinal artery stroke. However, the patient was given IV flucloxacillin empirically. The GdMRI was repeated under general anaesthesia 5 days later demonstrating an epidural abscess from C7 to T12,
probably arising from infection at the right T1/2 facet and T2 transverse process (Fig. 1). The next day the patient underwent T1/2 laminectomy and evacuation of the phlegmon. Tissue specimens were positive for methicillin sensitive Staphylococcus aureus. The i.v. flucloxacillin was continued for 6 weeks. The patient was then commenced on oral dicloxacillin, aiming to continue for 3–6 months, depending on progress. On transfer to rehabilitation, although limb weakness remained, he was walking. His bowels were working normally, but he had failed multiple trials without a urinary catheter. Here we describe a patient who presented typically for SEA, where inadequate spinal MRI resulted in delayed diagnosis and treatment. In SEA, patients generally present with severe back pain, fevers and neurological symptoms.1 Neurological symptoms range from paraesthesias, radiculopathy, motor weakness and sphincter dysfunction to severe paraplegia.1–3
© 2014 Australasian College for Emergency Medicine and Australasian Society for Emergency Medicine
