Case Study 7

History

A 45 year-old man presented to the hospital complaining of hand and foot pain so severe that he was unable to drive his car. The man had been well until several weeks earlier, when he began having gastrointestinal distress that he thought was “heartburn” and mild weight loss, which he attributed to his dyspepsia. He denied fever, chills, nausea, vomiting, or diarrhea. He also related that on the day prior to admission he was unable to eat a meal because he thought it was spoiled after taking a few bites. The next morning, while driving, he pulled off the road and phoned emergency medical services. He was taking no medications and had no allergies.

In the emergency department, the patient appeared well developed and well nourished, but was complaining of severe pain in his hands and feet. Vital signs were: blood pressure, 124/68 mm Hg; pulse, 92 beats/min; respiratory rate, 14 breaths/min; oral temperature, 98.6°F (37.0°C); oxygen saturation, 99% on room air; and a rapid reagent glucose of 128 mg/dL. Physical examination was notable for pupils that were equal, round (4 mm), and reactive to light; normal extraocular movements; and the absence of nuchal rigidity. His chest was clear to auscultation, and his heart sounds were normal. His abdomen was soft and nontender, with normal bowel sounds and no organomegaly. He was awake, alert, and oriented with normal symmetrical strength and brisk reflexes. Although he complained of pain in his hands and feet, his two-point discrimination, proprioception, and vibration sensation appeared normal. His gait was slightly wide based and slow, but this was thought to be secondary to pain. Cranial nerves II through XII appeared intact, and cerebellar testing was normal.

Although the patient appeared uncomfortable, there was no perception of an immediate life threat. An intravenous line was inserted, and blood was obtained for a complete blood count, electrolytes, and liver function testing. A urinalysis was requested as was an electrocardiogram and a chest radiograph. Acetaminophen was given for analgesia, without relief. The patient required parenteral opioids to diminish his pain, although he noted that the distribution had spread to include most of his legs and arms. He also became somnolent, and it was unclear if the ensuing somnolence was opioid related.

The major presenting symptom in this case is a painful sensory peripheral neuropathy (an uncommon clinical manifestation) associated with gastrointestinal symptoms (a common manifestation). Considerations include a variety of metabolic and endocrine disorders, infections, medications, and toxins. Severely painful symmetrical paresthesias are fairly uncommon and the differential diagnosis is limited. Considerations include freezing injury such as frostbite (Chap. 30), proximity to radioactive materials (Chap. 134), and topical exposure to hydrofluoric acid (Chap. 107). A list of xenobiotics that can cause such findings following ingestion is found in (Table CS7–1).

In addition to the above evaluation, a diagnosis of encephalitis was considered when the patient became somnolent, and a computed tomography (CT) scan of the head was obtained without intravenous contrast. A lumbar puncture was performed after the CT scan was interpreted as normal. The lumbar puncture showed: 2 red blood cells/mm3; 0 white blood cells/mm3; glucose, 85 mg/dL; and protein, 45 mg/dL.

Unfortunately, over the next 48 hours, the patient’s condition deteriorated and was characterized by encephalopathy with cranial nerve dysfunction and weakness with loss of deep tendon reflexes. A repeat lumbar puncture demonstrated elevated protein without abnormal cells or findings on the Gram stain.

A diagnosis of poisoning was considered, and a toxicology consult was obtained. The combination of gastrointestinal symptoms without significant diarrhea, severely painful ascending peripheral neuropathy and progression to encephalopathy with motor and cranial nerve findings strongly suggested metal poisoning, specifically thallium (Chap. 102). Treatment with Prussian Blue (Antidotes in Depth: A28) was recommended, and the original blood urine and cerebrospinal fluid were sent for thallium concentrations. Unfortunately, the patient’s illness progressed rapidly, and he suffered a cardiac arrest shortly after the diagnosis was considered. Ultimately, a spot urine thallium concentration was reported as 50,000 μg/L (normal <5 μg/L), and his serum was 8700 μg/L (normal <2 μg/L).

Postmortem findings and cerebrospinal fluid results of this case were reported in the following article: Sharma AN, Nelson LS, Hoffman RS: Cerebrospinal fluid analysis in fatal thallium poisoning: evidence for delayed distribution into the central nervous system. Am J Forensic Med Pathol. 2004;25:156–158.