Just Plain Ruff Posted November 6, 2007 Share Posted November 6, 2007 It's Marburg. Link to comment Share on other sites More sharing options...
Just Plain Ruff Posted November 6, 2007 Share Posted November 6, 2007 aside from my jokiing post Did they harvest any fresh mushrooms over the past day or so? Link to comment Share on other sites More sharing options...
hammerpcp Posted November 6, 2007 Share Posted November 6, 2007 Looking at Hammers recap, I have a few questions: 1. Does this kid has some unknown metabolic disorder? A 60 pound 12 year old, things that make you go hmmmmmm. 2. What meds was he taking and who was giving them to him? 3. Is anyone else at home or at school sick? Hammer, why can't this be meningitis? A kid with fever, possible sepsis and mental status changes could definitely have meningitis. Agreed, I initially was also thinking that as part of the differential. The Pt has no nuchal rigidity, and a negative LP. In scenario world that's a rule out I think. Also there was no complaints of headache, and a hx of three days of GI symptoms followed by neuro probs is a little slow onset.....at least for bacterial meningitis. Link to comment Share on other sites More sharing options...
Just Plain Ruff Posted November 6, 2007 Share Posted November 6, 2007 symptoms of amanita poisoning Vital signs Tachycardia Hypotension Skin Poor turgor Jaundice, bruising (with hepatic failure) Abdomen Mild tenderness Diarrhea, may have a positive result on a Hemoccult test (guaiac positive) Neurologic (if hepatic failure or hypoglycemia) Confusion Lethargy Coma Link to comment Share on other sites More sharing options...
ERDoc Posted November 6, 2007 Share Posted November 6, 2007 Agreed, I initially was also thinking that as part of the differential. The Pt has no nuchal rigidity, and a negative LP. In scenario world that's a rule out I think. Also there was no complaints of headache, and a hx of three days of GI symptoms followed by neuro probs is a little slow onset.....at least for bacterial meningitis. I missed the negative LP, so I would have to agree, that pretty much rules out meningitis. Without that, this kid still buys an LP. I would say that in his current state it is hard to assess for Brudzinski or Kernig signs. Even if he was reliable, they are still not that sensitive or specific. He may have hematogenous spreading of his infection to his mininges (assuming this is an infection and we are not going down the wrong path). Link to comment Share on other sites More sharing options...
Chief1C Posted November 6, 2007 Share Posted November 6, 2007 Well? Link to comment Share on other sites More sharing options...
brock8024 Posted November 7, 2007 Author Share Posted November 7, 2007 sorry everyone been working alot. Ok so as you are about to leave in the ambulance the mother comes running out to the truck and and says "I do not know if this is important but this bottle of pepto bismo is almost empty. He must have taken it today for his tummy. We have been giving it to him for his tummy." Link to comment Share on other sites More sharing options...
Just Plain Ruff Posted November 7, 2007 Share Posted November 7, 2007 ok now we need to assess for Aspriin and it's derivatives overdose. The following is taken directly from the website listed. It sure sounds like this kid has most of the signs and symptoms from this website for overdose of salycilates(sic) http://www.emedicine.com/ped/topic2031.htm Salicylates stimulate the respiratory center, leading to hyperventilation and respiratory alkalosis Salicylates cause both direct and indirect stimulation of respiration. A salicylate level of 35 mg/dL or higher causes increases in both rate (tachypnea) and depth (hyperpnea). Salicylate poisoning may cause noncardiogenic pulmonary edema (NCPE) in a few patients. Although the exact etiology is not known, hypoxia is considered a major factor. Increased cellular metabolic activity due to uncoupling of oxidative phosphorylation may produce clinical hypoglycemia, even though the serum glucose levels are within reference range. As intracellular glucose is depleted, the salicylate may produce discordance between levels of plasma and cerebrospinal fluid (CSF) glucose Salicylate poisoning may result in dehydration because of increased gastrointestinal tract losses (vomiting) and insensible fluid losses (hyperpnea and hyperthermia). All patients with serious poisoning are more than 5-10% dehydrated. Renal clearance of salicylate is decreased by dehydration. Hypokalemia and hypocalcemia can occur as a result of primary respiratory alkalosis. Central nervous system effects Salicylates are neurotoxic, which is manifested as tinnitus, and ingestion can lead to hearing loss at doses of 20-45 mg/dL or higher. CNS toxicity is related to the amount of drug bound to CNS tissue. Other signs and symptoms include nausea, vomiting, hyperpnea, and lethargy, which can progress to disorientation, seizures, cerebral edema, hyperthermia, coma, and, eventually, death. Gastrointestinal tract effects Nausea and vomiting are the most common effects. Pylorospasm and decreased GI tract motility can occur with large doses. Hepatic effects Hepatitis can occur in children ingesting doses at or above 30.9 mg/dL. Reye syndrome is another form of pediatric salicylate-induced hepatic disease characterized by nausea, vomiting, hypoglycemia, elevated levels of liver enzymes and ammonia, fatty infiltration of the liver, increased intracranial pressure, and coma. Hematologic effects Hypoprothrombinemia and platelet dysfunction are the most common effects. Bleeding may also be promoted either by inhibition of vitamin K–dependent enzymes or by the formation of thromboxane A2. Musculoskeletal effects Rhabdomyolysis can occur because of dissipation of heat and energy resulting from oxidative phosphorylation uncoupling. Clinical and laboratory manifestations Phase 1 of the toxicity is characterized by hyperventilation resulting from direct respiratory center stimulation, leading to respiratory alkalosis and compensatory alkaluria. Both potassium and sodium bicarbonate are excreted in the urine. This phase may last as long as 12 hours. In phase 2, paradoxic aciduria in the presence of continued respiratory alkalosis occurs when sufficient potassium has been lost from the kidneys. This phase may begin within hours and may last 12-24 hours. Phase 3 includes dehydration, hypokalemia, and progressive metabolic acidosis. This phase may begin 4-6 hours after ingestion in a young infant or 24 hours or more after ingestion in an adolescent. Nausea, vomiting, diaphoresis, and tinnitus are the earliest signs and symptoms of salicylate toxicity. Other early effects include vertigo, hyperventilation, hyperactivity, agitation, delirium, hallucination, convulsion, lethargy, and stupor. Hyperthermia is an indication of severe toxicity. Most telling --- from the website According to the Toxic Exposures Survey from the American Association of Poison Control Center, 24% of analgesic-related deaths are due to aspirin alone or aspirin in combination with other drugs. Early identification of salicylate poisoning can be lifesaving. Link to comment Share on other sites More sharing options...
CC64 Posted November 7, 2007 Share Posted November 7, 2007 Next question for mom is how much was left in the bottle last time she saw it. size of bottle? GI upset, probably viral. On top of that, accidental OD of salacylates. Link to comment Share on other sites More sharing options...
ERDoc Posted November 7, 2007 Share Posted November 7, 2007 Is there anything we need to think about besides salicylate OD? Link to comment Share on other sites More sharing options...
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