which revealed unilateral left vocal cord paralysis. The patient was then admitted for further management. On hospital day two, she developed new vesicular lesion at the level of the left C3 dermatome. Infectious disease was consulted for lesions consistent with herpes zoster. Empiric steroids were stopped and ganciclovir was prescribed as acyclovir was unavailable. By hospital day five, the patient’s hoarseness and dysphagia had significantly improved. She was treated with ganciclovir for a total of two weeks with complete resolution of symptoms. Discussion: Varicella zoster can become latent in the cranial nerve and dorsal root ganglia, reactivating later in life to produce shingles. Herpes zoster involving the seventh cranial nerve is well documented in the literature; however, isolated cranial nerve 10 involvement is rare. The diagnosis of vagus nerve palsy caused by herpes zoster is achieved by findings of uvula deviation and direct laryngoscopy of unilateral vocal cord paralysis, along with coinciding her- petic lesions of the head and neck. Early recognition and treatment with an antiviral agent is important for improved clinical outcomes. The Herbicidal Patient: Delayed Onset of Multi-Organ Failure and the Importance of the Material Safety Data Sheet Introduction: Ingestion of toxic chemicals, particularly organophosphates and the resultant physiologic effects are well known by physicians. However, not all herbicides contain organophosphates. The Material Safety Data Sheet (MSDS) provides the starting point to evaluate toxic pre- sentations of various herbicide components. Case: A 48-year-old Hispanic male with a past medical history of type 2 diabetes, hypertension, and depressionwas transferred to our hospital for psychiatric services after being evaluated 24 hours earlier at an outside hospital for a suicide attempt after consuming 32 oz of an extended control weed and grass killer. The patient had been evaluated within an hour of toxin consumption andwas given activated charcoal; vital signs were stable and serial labs drawnwere unremark- able. Medicine was consulted to evaluate hyperglycemia. At the time of evaluation, the patient complained of diarrhea, odynophagia, dysphagia, abdominal pain, and chest pain with food ingestion. Vital signs at the time were BP 126/62, HR 120, RR 14, T 98.9F. On physical exam, he was oriented, diaphoretic, had mild tachypnea, tachycardia, and Zargar Grade 2a caustic injury of his lips and oropharynx. Labs revealed WBC 18.5, 20% bands, glucose 623, CO2 18, BUN 57, Cr 6.42, AST 472, ALT 324, TBili 1.3, INR 0.8, AØ 70, with a AG = 18, Osm Gap = 15, and ABG 7.31/29/81/14.6. N-Acetylecysteine was started per poison control recom- mendations. The patient became anuric, with worsening metabolic acidosis, renal, and hepatic function. Following transfer to the ICU, he experienced respiratory decompen- sation requiring intubation. The patient had cardiac arrest and could not be resuscitated. R. Dhaliwal, S.M. Gupta, and S. Ahmed Leonard J. Chabert Medical Center, Houma
Discussion: Review of the MSDS revealed the presence of Dicamba and Diquat dibromide . The toxicology profile of Diquat dibromide seemed to fit our patient’s symptoms and labs. Diquat is corrosive substance, is renally excreted, and ingestion is usually fatal. Severe gastrointestinal irritation, tissue dehydration, nausea, vomiting, diarrhea, chest and abdominal pain, and respiratory distress are seen. Labs demonstrate toxic liver damage and kidney failure. Our patient appeared to have absorbed a significant amount of the toxin, despite early charcoal treatment. Confirmed herbicide ingestion and subsequent medical clearance does not rule out further delayed toxicity. Shock to the Heart ... ABlowFroma Surprising LiverMass M. Oncale and B. Lewis Tulane University Medical School, New Orleans Case: A 76-year-old man with hypertension, coronary disease, and diabetes presented for routine follow-up. Social historywas negative for alcohol, tattoos, travel, or illicit drug use. He denied blood transfusions or chemical exposures. Exam was benign. Labs revealed alkaline phosphatase 198 IU/L (38-126) and aspartate transaminase 49 IU/L (15-41). Bilirubin, creatinine, coagulation, and complete blood counts were normal; low-density-lipoprotein 86 mg/dl and hemoglobin A1c 6.8%. Alkaline phosphatase fractionated as hepatobiliary origin. HIV and hepatitis panels were nega- tive. Abdominal ultrasound revealed an 8 cm hepatic mass. Computed tomography (CT) revealed a 12 x 8 cm mass, inferior vena cava (IVC) compression, but no evidence of cirrhosis. He was referred to hematology-oncology, where repeat imaging one month later revealed an 11 x 13cmmass with IVC tumor infiltration and extension to the right atrium (RA), where a 4 x 4 cm mass was noted. Alpha-fetoprotein (AFP) was normal. Biopsy revealed moderately differenti- ated HCC; some hepatocytes had fatty changes, but no evidence of hemosiderosis or cirrhosis. Discussion: HCC is the third-leading cause of cancer- related mortality worldwide. Seventy-five percent of cases are attributable to viral hepatitis. Non-viral cases are due to non-alcoholic fatty liver disease. Most HCC cases are as- sociated with cirrhosis caused by viral hepatitis or alcohol. Cases of HCC in non-cirrhotics are typically symptomatic and occur in older adults. HCC commonly metastasizes to lymph nodes, bone, and lung. It also has a propensity for vascular invasion. Tumor extension to the portal system is common; invasion of the IVC and/or heart without inva- sion of the portal system is rare. Most patients with cardiac involvement also had cirrhosis and symptoms that included dyspnea, edema, shock, right heart failure, pulmonary em- boli, or sudden death. Mean survival in HCC patients with IVC or RA extension is four months regardless of treatment; therefore, aggressive therapy is often futile. To our knowl- edge, this is the first patient without hepatitis or cirrhosis to present asymptomaticallywith cardiac involvement of HCC. Our case is also unique in that the etiology of this patient’s HCC remains cryptogenic.
J La State Med Soc VOL 166 March/April 2014 87
Made with FlippingBook - Online catalogs