Patrick L. West

Iatrogenic lipid emulsion overdose in a case of amlodipine poisoning.

Introduction. Intralipid therapy has been used successfully as “rescue therapy” in several cases of overdose. We present a case of iatrogenic lipid emulsion overdose because of a dosing error. Case Report. A 71-year-old female overdosed on 27 tablets of 5 mg amlodipine. Although initially stable in the Emergency Department, she became hypotensive, oliguric, and respiratory failure developed despite medical therapy. The primary treating team felt that meaningful recovery was unlikely to occur without rapid improvement in clinical status, and 12.5 h after presentation, intralipid rescue therapy was initiated. A protocol for intralipid specifying a maximum infusion of 400 mL of 20% lipid emulsion was faxed, but the infusion was continued until 2 L of lipid emulsion was infused. There were no detectable adverse hemodynamic effects of the intralipid infusion. After this time, laboratory values were difficult to obtain. Three hours after the infusion, a metabolic panel was obtained from ultracentrifuged blood showing hyponatremia. A white blood cell (WBC) was obtained from a complete blood count (CBC) performed 22 h after the infusion, hemoglobin and hematocrit could not be obtained from this blood. A platelet count was obtained by smear estimate. Hematocrits were obtained from centrifuged blood and appeared elevated. No oxygenation could be obtained on blood gas. The patients family chose to withdraw care on hospital day 2 and no further laboratory draws were obtained. Amlodipine was 1,500 ng/mL (ref. 3–11 ng/mL). Discussion. Lipid emulsion overdose caused no detectable acute adverse hemodynamic effects. The following laboratory values were unobtainable immediately after infusion: white blood cell count, hemoglobin, hematocrit, platelet count, and a metabolic panel of serum electrolytes. Ultracentrifugation of blood allowed for detection of a metabolic panel 3 h after the infusion. Centrifuged hematocrits appeared to be higher than expected.

Amanita smithiana mushroom ingestion: A case of delayed renal failure and literature review

IntroductionIn the Pacific Northwest a new pattern of mushroom ingestion has emerged, attributed toAmanita smithiana, in which renal failure has been the predominant manifestation.Case ReportA 55-year-old male ate 3 raw wild mushrooms in a salad and had onset of severe nausea and vomiting within 6 hours. His vital signs were unremarkable. His labs were significant for a BUN of 14mg/dL (5.0 mmol/L), and a creatinine of 1.0 mg/dL (88umol/L), transaminases were elevated with an AST of 56 U/L (nl 9–40) and an ALT of 131 U/L (nl 14–72). Treatment was initiated with N-acetyl cysteine, penicillin, and milk thistle extract on the presumption that this was an amanitin-toxin containing mushroom. He developed acute renal failure that was not responsive to our treatment. Dialysis started on day 4 with a creatinine of 6.5 mg/dL, which peaked on day 7 at 10.2 mg/dL. We were able to obtain a positive mushroom identification by a mycologist asAmanita smithiana. The patient was discharged from the hospital for outpatient dialysis on day 10 and dialysis catheter was removed 39 days after ingestion with a creatinine of 1.4 mg/dL (123.8 umol/L).DiscussionAmanita smithiana mushroom poisoning presents within 6 hours of ingestion with GI toxicity, and develops delayed onset of renal insufficiency over the first 1 to 4 days. The early hospitalization of this case allowed a profile of the onset of liver and renal injury. Mild elevation of hepatic transaminases occurred on presentation and peaked 24 hours after the ingestion. Renal injury was detected 1 day after presentation, and progressed to require hemodialysis by 4 days postingestion. This pattern of delayed-onset renal toxic mushroom ingestion is emerging among mushroom ingestions in Western North America.

Poison Hemlock-Induced Respiratory Failure in a Toddler

The ingestion of poison hemlock, or Conium maculatum, is described in a 2-year-old boy. He had the onset of abdominal pain and weakness after being fed C. maculatum picked by his sister from the roadside 2 hours earlier. He had a rapidly progressive muscular weakness and was intubated for respiratory failure. His symptoms completely resolved within 24 hours of the ingestion. Conium maculatum is a common weed that causes toxicity by its primary toxin, coniine, which stimulates nicotinic receptors and causes a syndrome of rapidly progressive muscle weakness and paralysis. We describe the course of a benign-appearing plant ingestion resulting in respiratory failure.

Zigadenus poisoning treated with atropine and dopamine

IntroductionZigadenus (commonly known as “death camas” or “mountain camas”) is a common plant in the lilly family found throughout the United States. Its onion-like roots can be mistaken for an edible plant. Ingestion may cause hemodynamic instability which has successfully been treated with atropine. It has been suggested that vasopressors may be an effective therapy for this ingestion. We report the successful use of dopamine as therapy inZigadenus ingestion.Case ReportA 45 year-old, previously healthy male presented to the ED with complaints of severe nausea and vomiting after ingesting two “wild onion” bulbs. He was noted to have marked hypotension and bradycardia in the ED, which initially responded to treatment with IV fluids and atropine. The plant was identified as a species ofZigadenus. After a second drop in heart rate and blood pressure in the ICU, hypotension and bradycardia were treated successfully with a dopamine infusion.DiscussionZigadenus ingestion presents with vomiting, hypotension and bradycardia. The hemodynamic instability responded well to atropine for 1–2 hours. Dopamine infusion was used to stabilize both heart rate and blood pressure. With supportive care, poisoned individuals become relatively asymptomatic within 24 hours of their ingestion. Patients may be discharged once asymptomatic, typically the day after ingestion, and do not have any known long term sequelae.ConclusionZigadenus poisoning causes vomiting, hypotension and bradycardia. The hemodynamic instability may be treated with atropine administration and dopamine infusion.

Muscle spasm associated with therapeutic use of Cang Er Zi Wan

Introduction. Cang Er Zi Wan (CEZW) is a herbal medication derived from Xanthium sibiricum that is used to treat allergies and upper respiratory problems. Its toxicity has been described in grazing animals, in experimental studies, and in human overdoses. We describe a case of muscular spasm that was associated with the therapeutic use of CEZW. Case report. A 17-year-old female was prescribed CEZW for chronic allergies. Shortly after her second dose of 10 pills BID, she developed intermittent muscular spasms. She was seen in an Emergency Department and had normal vital signs and no significant laboratory abnormalities. Her physical exam was significant only for intermittent spasm of the muscles of the face, neck, and upper extremities. No tremor, fasciculation, dystonia, akisthisia, chorea, bradykinesia, or clonus was noted. She discontinued the CEZW and the symptoms slowly decreased over 4 days. Testing of the product did not detect any other medications or drugs. Discussion. CEZW is a herbal medication that contains X. sibiricum. X. sibiricum is a widespread weed that has caused muscular spasm, seizures, and death in animals that graze on it as well as animals experimentally exposed to it. Eleven cases of accidental human ingestion of Xanthium leading to spasm, somnolence, hypoglycemia, renal, and liver toxicity have been described. We describe a unique case of isolated muscular spasms because of the therapeutic use of a CEZW product.

After the fall: A teenager with unusual intermittent muscle spasms

A 14-year-old boy is transported to the emergency department by emergency medical services after an injury. His mother states that he fell down the stairs and has a chin laceration. The teenager adds to the history by telling that he slipped and fell down about 6 stairs, hitting his chin on a doorknob on the way down. Emergency medical services personnel arriving to the scene protected him with a cervical collar and backboard for transport to the emergency department. The boy denies any loss of consciousness, vomiting, or headache. His mother, a registered nurse, says he looked like he was having a seizure at the bottom of the stairs, except that he was awake and yelling for help the entire time. He has had no similar episodes previously. There has been no loss of bowel or bladder function. The boy’s medical history includes attention-deficit disorder, which is treated with methylphenidate. His immunizations are up to date, and he reports no recent injuries (other than today). On physical examination, the boy appears to be a previously healthy boy lying on a bed; although alert, he appears anxious and uncomfortable, and his face is covered in blood. All 4 of his limbs are relaxed and extended at rest, but he is noted to have 3 episodes of sudden tonicclonic movements, each lasting several seconds and resolving. He is able to respond in full sentences during these episodes, but reports that his arms and legs hurt. The spasms seem to worsen when he tries to move his extremities or when he is examined physically. He has hyperthermia (temperature, 38.4-C measured rectally), tachycardia (heart rate, 137 beats/min), borderline systolic hypertension (blood pressure, 133/66 mm Hg), tachypnea (respiratory rate, 22 breaths/min), and normal blood hemoglobin oxygen saturation (98% measured transcutaneously breathing room air). He has a 2-cm laceration on his anterior chin. There is no other evidence of trauma on his head, face, or neck. His neck is nontender with full range of motion. He is tachycardic without murmur, his lungs are clear, and his abdomen is benign. He has no extremity bruising or swelling. Intermittent muscle spasms are noted bilaterally in all extremities (flexor in the upper extremities, extensor in the lower extremities), and spasms of the back muscles occur that cause the back to arch. These wax and wane over the course of 30 seconds and then resolve to allow full motion. In between the spasms, the teenager is able to follow commands and has a full range of motion of his arms and legs. His is awake, alert, and oriented at all times during the examination. His cranial nerves and sensation are intact. He has full strength in his extremities between episodes of spasm. He has no ataxia or nystagmus. His pupils are midposition and reactive. He is treated with intravenous (IV) lorazepam, and the frequency of his episodes decreases. He is additionally treated with IV normal saline and with IV morphine for pain in his extremities. His laboratory and radiographic evaluation is noted in Table 1.