Grand Rounds Recap 5.4.22

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Taming the sru: polypharmacy overdose WITH dr. Carl Goff

  • Case: College aged male presented with a polypharmacy intentional overdose of ibuprofen and multiple SSRIs. Approximately 1 hour prior to presentation. For EMS, the patient was hemodynamically stable with a normal FSBS initially, however just prior to arrival to the ED he had a generalized tonic-clonic seizure which resolved without intervention. Upon arrival at the ED the patient was confused and unable to provide reliable history. Family arrived shortly thereafter and suggested he may have also ingested alcohol and that the ingestion was actually 5-6 hours prior to arrival.  They also reported that the patient likely ingested additional substances including bupropion, vitamin D, methylphenidate, Lurasidone, and fluoxetine. 

  • Physical Exam: The patient was alert and conversant but confused and mildly agitated. He was noted to have foamy around the mouth and bleeding from a small tongue laceration. He was pale, diaphoretic, PERRL, he was tachycardic and normotensive with a regular rate, had clear lungs and was in no respiratory distress. He was noted to be tremulous in his bilateral upper and lower extremities and was hyper-reflexic with clonus. 

  • Diagnostics: VBG demonstrated a severe mixed respiratory and metabolic acidosis with a ph< 7.0 and an extremely elevated lactate > 18. EKG demonstrated tachycardia, a widened QRS and QTC, and terminal R waves in aVR

  • Discussion

    • Bupropion

      • MOA: D2 and NE agonist

      • Toxic dose: > 10mg/kg

      • Toxidrome: Agitation, seizure, tremor, hallucination, tachycardia, conduction disturbances, HTN, nausea, and vomiting

      • Treatment: Benzodiazepines, whole bowel irrigation, intralipid, vasopressors, ECMO.

    • Methylphenidate

      • MOA: CNS stimulant via dopamine agonism

      • Toxic dose: > 60mg/daily

      • Toxidrome: Agitation, psychosis, aggressive behavior, tachycardia, ectopy and arrhythmias, nausea and vomiting, acute kidney injury, and rhabdomyolysis.

      • Treatment: Benzodiazepines and IVF.

    • Vitamin D

      • MOA: Involved in calcium homeostasis

      • Toxic Dose: > 4000 IU/daily

      • Toxidrome: may cause hypercalcemia presenting with irritability, confusion, stupor, abdominal pain, nausea and vomiting, pancreatitis, peptic ulcer disease, nephrolithiasis, and polyuria. 

      • Treatment: IVF, calcitonin, bisphosphonates.

    • Fluoxetine

      • MOA: SSRI

      • Toxic dose: >1500mg

      • Toxidrome: Sedation, respiratory depression, serotonin syndrome

      • Treatment: Supportive care, cyproheptadine (5-HT receptor antagonist)

    • Lurasidone

      • MOA: 2nd generation atypical antipsychotic with D@ antagonism and mixed 5-HT agonism/antagonism

      • Toxic dose:  unclear

      • Toxidrome: QTc prolongation, sedation, akathisia, parkinsonism

      • Treatment: Supportive

R1 Clinical Knowledge: Pituitary Disorders  WITH Dr. Cole Davis

  • The pituitary gland has anterior and posterior lobes with the anterior lobe comprising about 80% of the pituitary

Pituitary problems

  • Pituitary adenomas 

    • Incidence of about 1/1000. About 40% are nonfunctional, the remaining 60% present with indolent space occupying symptoms of headaches and visual changes. Additional symptoms depend on which hormone is being secreted from the adenoma but can result in things like menstrual irregularities, testicular enlargement, acromegaly, Cushing's disease, and so on. 

  • Pituitary Apoplexy

    • An acute bleed or infarction of the pituitary. All-comer incidence is around 0.17/100,000 per year but they are more common in patients with pituitary tumors (14.4%), as expansion causes infarction and vessel breakdown. 

    • One study found that 97% of patients present with a thunderclap headache, 71% present with visual field cuts (bitemporal superior quadrantanopia being the most common as the inferior fibers of the optic chiasm are impinged first), and 66% present with decreased visual acuity

    • Can also present with life threatening bradycardia and hypotension due to the acute loss of ACTH which leads to acute adrenal failure.

    • Significant neurologic signs such as altered mental status or fluctuation in level of consciousness may indicate compression of the internal carotid artery which necessitates rapid action

    • In the emergency department, CT is probably our first line imaging modality, however it has a fairly low sensitivity (21-46%) if there is delay in presentation and urgent MRI (sensitivity 88-90%)  is preferred in these cases if possible.

    • Obtain PRL, TSH, FT4, Testosterone, GH, Estradiol, IGF1, LH, FSH to assess levels of endocrine function. 

    • Treatment is centered around hemodynamic support. Give a bolus of hydrocortisone to assist with the acute adrenal failure (ideally after endocrine labs are drawn), and consult neurosurgery and endocrine. Patients with severe visual field cuts or altered mental status almost always require surgical management.

  • Central Diabetes insipidus

    • Occurs when the posterior pituitary fails to produce vasopressin or when there is destruction of the neurophysis due to anatomic lesions, trauma, autoimmune destruction,  or surgery.

    • Patients present with excessive thirst (3-30L of day) with a preference for ice cold water (assuages physiological thirst more efficiently). These patients become rapidly dehydrated when they lose access to water. 

    • Obtain POC glucose, renal panel, UA with urine electrolytes and osmols, measured serum osmols, CBC, ADH, and a CT/MRI if altered. 

    • Labs will show hyperosmolar serum (>295) and hypo-osmolar urine (typically < 100)

    • Place a foley to help with exact I/Os. Calculate their free water deficit and volume resuscitate these patients, admit them for further workup and volume replacement.

R4 Capstone: Sharing Information with your Patients WITH Dr. MEaghan Frederick

  •  Informed consent is the process by which physicians share information regarding their concerns and proposed evaluation and treatment with patients, and the patients provide consent to proceed with that plan in accordance with exercising their right to autonomy. 

    • Informed consent is the minimum bar that we are required to meet with regards to information sharing in the clinical setting. 

  • In the busy emergency department, it can be easy to skip explicit discussion of some of the finer details of the proposed evaluation plan. The idea that somebody presenting with chest pain will certainly get an EKG, bloodwork, and maybe a chest x-ray is obvious and routine for us, but likely novel to our patients. We are in the ED every day, hopefully our patients are not. As such it is our duty and responsibility to guide them through the encounter.

  • Patients who have higher levels of information sharing and involvement in shared decision making have higher satisfaction scores, decreased resource utilization, are more likely to be adherent with treatment plans, and ultimately better outcomes. 

  • Dr. Frederick's suggestions for improving communication

    • Discuss the initial plan for evaluation → this helps with expectation management of what is to come

    • Discuss your proposed treatment plan → this helps ensure you don’t double up on medications they may have taken at home and ensures your medication choices align with their values and wishes (especially when it comes to opiates).

    • Provide updates throughout the evaluation and any anticipated delays or absences (for instance if you have multiple traumas coming in and may not be able to come talk with them for a bit)

    • Ask “what questions do you have” instead of “do you have any questions” to create more space for patient questions and physician-patient discussion.

R2 CPC WITH Drs. MArtina Diaz and Sim Mand

  • Case: An elderly female with a history of multiple myeloma, CHF, and seizures presents with AMS. The patient herself is unable to provide useful history due to her AMS but her nursing facility reports that the patient was in her usual state of health when she went to bed last night, woke up this morning and was altered, had a seizure, and has remained altered. The patient had been recently admitted to the hospital for confusion and at that time was found to have a subdural hematoma. 

  • Physical Exam: She was normotensive but bradycardic to the 40s with normal respirations and saturations on room air. She was well appearing and in no acute distress but was speaking nonsensical words, had horizontal nystagmus with left beat nystagmus being more severe than the rightward nystagmus, otherwise her physical exam was largely unremarkable. 

  • Evaluation: Bloodwork demonstrated a normal VBG, mild hyponatremia between 130-135, a normal CBC, normal LFTs, a mildly elevated HsTn, and a UA with mild proteinuria, <5 WBCs and RBCs, and many squamous epithelial cells. She gets a CXR which has a subtle consolidation in the left base read as atelectasis vs pneumonia, a CTH which shows an improving SDH, and an EKG which demonstrates bradycardia with a newly widened QRS and concern for complete heart block. And then a test was ordered…

  • Lamotrigine toxicity

    • Overdose is frequently asymptomatic but can present with drowsiness, dizziness, ataxia, nystagmus, and myoclonus.  Severe overdoses can result in altered mental status, seizures, QRS and QT prolongation leading to arrhythmias (via sodium channel blockade), hypertension, tachypnea, and coma. Cases of rhabdomyolysis have also been reported. 

    • There is some correlation with serum levels and severity of symptoms with a serum level >25 mg/L suggesting increased likelihood of severe toxicity in adults.

    • Treatment is supportive care including symptom control, airway protection, and cardiovascular support.  

  • Adverse Drug Reactions

    • Lamotrigine can result in the development of SJS. This is not necessarily related to toxicity, but is rather an adverse drug reaction. This is more common in the early phase of starting this medication (typically within the first 60 days).