Medical Image of the Week: Elemental Mercury Poisoning

Figure 1. Panel A: Abdominal x-ray showing radiopaque matter. Panel B: Repeat x-ray after colonoscopy.

A 34-year-old woman presented to the Emergency department with abdominal pain after ingestion of an unknown liquid that family felt might be poisonous. The patient had a past history of prior suicide attempts, as well as a history of polysubstance and alcohol abuse. The patient was confused, tangential and a difficult historian. The patient had a heart rate of 72, was normotensive, and had an oxygen saturation of 100% on room air.  She was confused and answered questions intermittently. The remainder of her physical examination including her neurological exam was normal. The initial serum chemistry, anion gap, lactate, liver function tests were normal. Urine drug screen was positive for benzodiazepines, for which the patient was prescribed. An abdominal x-ray was performed showing a radiopaque substance in the abdomen (Figure 1A). It was eventually determined she ingested elemental mercury. Blood levels were elevated, and she did eventually have hematochezia. Colonoscopy was performed which removed some of the metallic liquid mercury (Figure 1B).

Mercury in any form is poisonous, with mercury toxicity most commonly affecting the neurologic, gastrointestinal (GI) and renal organ systems (1). Poisoning can result from mercury vapor inhalation, mercury ingestion, mercury injection, and absorption of mercury through the skin.

Elemental mercury is poorly absorbed after ingestion but easily vaporizes at room temperature and is well absorbed (80%) through inhalation. Once absorbed elemental mercury is mostly converted to an inorganic divalent or mercuric form by catalase in the erythrocytes. This inorganic form has similar properties to inorganic mercury (e.g., poor lipid solubility, limited permeability to the blood-brain barrier, and excretion in feces).

Treatment of mercury toxicity consists of removal of the patient from the source of exposure, supportive care, and chelation therapy. Our patient had limited symptoms, and for this reason, chelation therapy was not performed. She made an uneventful recovery after discharge to psychiatry. Her blood levels eventually returned to normal in a few months.

Michel A. Boivin, MD

Pulmonary/Critical Care/Sleep Medicine

Department of Internal Medicine

University of New Mexico

Albuquerque, NM USA

Reference

1. Olson DA. Mercury poisoning. Medscape. August 14, 2017. Available at: https://emedicine.medscape.com/article/1175560-overview (accessed 5/22/18).

Cite as: Boivin M. Medical image of the week: Elemental mercury poisoning. Southwest J Pulm Crit Care. 2018;16(5):287-8. doi: https://doi.org/10.13175/swjpcc067-18 PDF 

Medical Image of the Week: Arachnoid Cyst

Figure 1. Axial T1 MRI of mass.

Figure 2. Coronal T2 weighted MRI demonstrating compressions onto mesial temporal lobes and stretching of the optic chiasm and tracts; upward displacement of the hypothalamus, third ventricle small in caliber and mild posterior displacement of the midbrain.

A 40 year-old woman with adult attention deficit hyperactive and bipolar 1 disorder presents with an altered mental status.  Per her family, she had been non-verbal, with reduced oral intake, confusion and sedated for the past three days. Per her husband, she had episodes of diarrhea and abdominal discomfort. She was on multiple medications including ramelteon 8mg nightly, atomoxetine 40mg daily, hydroxyzine 25mg twice daily, bupropion 75mg twice daily and risperidone 2mg daily with recent addition of lithium ER 1200mg/daily started one month prior to presentation with unknown adherence.

Upon arrival, vital signs were within normal limits. Physical exam revealed an overweight Caucasian woman with a significant coarse tremor visible at rest, restlessness and diaphoresis. Neurological examination was limited by patient hesitancy, however, it did not demonstrate focal deficits except for altered consciousness with Glasgow Coma Scale of 10. Notable laboratory findings were Na⁺ 134 mEq/L, K⁺ 3.2 mEq/L, and lithium level of 3.9 mmol/L, urine toxicology positive for cocaine, and EKG showed QT prolongation. Toxicology and psychiatry were consulted.

CT of her head without contrast showed a large midline lesion in the sellar/suprasellar estimated to be 5.2x 2.1x 3.2cm. On hospital day number 2 the patient was more somnolent with down trending lithium level of 2.6 mmol/L. Later that day the patient had an observed generalized tonic clonic seizure which required abortive therapy with lorazepam and levetiracetam. A MRI revealed large arachnoid cyst measuring 3.6x3.1x3.5cm causing mass effect on adjacent tissue. (Figures 1 and 2). Neurology was consulted and recommended neurosurgery evaluation who deferred intervention to an outpatient basis given her lithium overdose as a more likely etiology of her seizure and not the arachnoid cyst.

Arachnoid cysts are cerebral spinal fluid filled sacs located between the brain or spinal cord and the arachnoid membrane. They can be either primary, which are present at birth due to developmental abnormalities of the brain and spinal cord, or they may be secondary, which are the result of head injury, meningitis, tumors, or a complication of brain surgery. Symptoms are based on the size and location of the cyst and include headache, nausea and vomiting, seizures, hearing and visual disturbances, vertigo, and difficulties with balance and walking. If the cyst compresses the spinal cord or nerve roots, then individual may experience progressive back and leg pain and tingling or numbness in the legs or arms.

Diagnosis is usually via MRI which distinguishes between fluid-filled arachnoid cysts from other types of cysts. The treatment depends on the location and the size of the cyst. If the cyst is small and does not compress any of the surrounding structures, with an absence of symptoms, no treatment is necessary. The two main ways of treating symptomatic cysts include surgery or placing a permanent shunt to drain the fluid. Surgical approaches include microscopic open surgical fenestration procedure in which the neurosurgeon opens the skull to gain access to the cyst, then opens the cyst to release pressure, allowing contents to be absorbed by the brain. Another surgical approach involves endoscopic cyst fenestration in which an endoscope is used to drain the cyst internally without having to perform an open surgery. In some instances, formal craniotomy with excision/marsupialization of the cyst into the subarachnoid space is performed. The procedure performed depends on the surgeon’s comfort with the technique and the size/location of the cyst.

Matthew Erisman MD, Rozina Parbtani MS IV, and Faraz Jaffer MD.

Department of Internal Medicine

University of Arizona at South Campus

Tucson, Arizona USA

References

1. Al-Holou WN, Terman S, Kilburg C, Garton HJ, Muraszko KM, Maher CO. Prevalence and natural history of arachnoid cysts in adults. J Neurosurg. 2013 Feb;118(2):222-31. [CrossRef] [PubMed]
2. Eidlitz-Markus T, Zeharia A, Cohen YH, Konen O. Characteristics and management of arachnoid cyst in the pediatric headache clinic setting. Headache. 2014 Nov-Dec;54(10):1583-90. [CrossRef] [PubMed]

Cite as: Erisman M, Parbtani R, Jaffer F. Medical image of the week: arachnoid cyst. Southwest J Pulm Crit Care. 2016;13(4):181-3. doi: http://dx.doi.org/10.13175/swjpcc074-16 PDF