Grand Rounds Recap 1.26.22

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JOURNAL CLUB WITH DRS. HAMZA IJAZ AND SIMI MULLEN

Please stay tuned here and on our social media accounts (Twitter, Facebook) for summaries and breakdowns of the excellent journal club articles this week, which focused on interventions to assist ED patients in access to and follow up with primary care.

R2 CPC: DR. JOSH FERRERI VS. SPECIAL GUEST DR. TREVOR SKROBUT, CLASS OF 2021

The Case:

Middle aged patient w/ no PMHx, brought into ED for psychiatric evaluation by police after her husband called for erratic behavior over the past 3 weeks. On arrival she is calm and has no complaints. Per husband and PD, she believes her child is possessed and that a group of women have been spreading lies around her. Recent stressors in her life include a miscarriage 3 months ago with precipitous delivery of non-viable infant, the death of her mother in Africa and marital disputes with her husband. No drug or EtOH use. She denies any SI/HI/AVH. Review of systems is unremarkable. She does not take any medications. Vitals are within normal limits. Physical examination is unremarkable. 

Workup:

EKG: Normal sinus rhythm with nonspecific T wave inversions in AVL.

Labs: CBC is normal. BMP with an anion gap  of 20 and bicarb of 16 but otherwise unremarkable. VBG with pH 7.24, pCO2 39, C02 32, BE -9.8. Lactate 0.6. UA without pyuria, hematuria, nitrites or bacteriuria but demonstrates significant ketonuria. Serum beta-hydroxybutyrate elevated to 6.95. UDS negative. CK 399.  LFTs and TSH/T4  are normal. Acetaminophen, salicylate and ethanol levels are negative. Pregnancy test negative. 

…and then a test was ordered… 

Altered Mental Status/Bizarre Behavior Differential Diagnosis:

First things first–don’t forget to consider human trafficking as a possible contributory factor to her presentation. 

The differential for altered mental status is exceedingly broad. It includes both primary neurologic processes as well as pathology of the rest of the body:

  • Shock state

  • Electrolyte or glucose derangements

  • Sequelae of organ failure including hepatic encephalopathy or uremia

  • Ingestion/toxicologic syndromes

  • Respiratory failure leading to hypoxia or hypercarbia

  • Hypertensive encephalopathy

  • Infectious processes include meningitis, encephalitis or sepsis/delirium from a non-CNS source. 

    • This patient could also be at risk for more uncommon infections given recent travel history to Africa

  • Hypo/hyperthermia

  • Hematologic problems with systemic changes including TTP or porphyria

  • Trauma

  • Stroke or intracranial hemorrhage

  • Cancer/mass with intracranial extension

  • Paraneoplastic syndromes

  • Seizures

  • Dementia or primary decompens​ating neurologic disease

  • Primary psychiatric disease

Dr. Skrobut was told to ignore the acidosis in this case. While working through the differential, some specific considerations to keep in mind included:

  • Is this a “postpartum” complication? Including but not limited to Sheehan syndrome, eclampsia, infection, depression or psychosis, cardiomyopathy, thyroiditis → all can be ruled out by history, physical examination and labs except for depression/psychosis for which there is no test. 

  • Etiologies of Ketosis: EtOH/Acetone, starvation, DKA, salicylates, Inborn errors of metabolism, pregnancy, hyperthyroidism, low cortisol → all can be excluded by history, physical examination and other laboratory studies except for starvation.

Based on the information given by Dr. Ferreri, a narrowed differential diagnosis can be produced:

  1. Cushing’s 

  2. Vitamin Deficiency (Wernicke’s, B12, etc.)

  3. Porphyria

  4. Cancer/Mass

  5. Paraneoplastic Syndrome

  6. Encephalitis (autoimmune most likely)

Final guess? Autoimmune encephalitis with a confirmatory test of a lumbar puncture with anti-NMDA antibody testing. 

The Answer: Isopropyl Alcohol Toxidrome

Epidemiology:

  • Incidence of volatile acid toxidromes in the US: Isopropanol > ethylene glycol > methanol 

  • Rising rates due to increased access to hand sanitizer

  • Overall low fatality rate

  • 85% of cases are thought to be unintentional

  • These substances are often nontoxic at the time of ingestion then become a toxic, active metabolite

  • Most active metabolites of toxic alcohols lead to significant anion gap metabolic acidosis

    • Isopropranol is an exception to the rule and does not lead to significant metabolic acidosis

Isopropanol (Isopropyl Alcohol)

  • The second most commonly consumed alcohol only to ethanol

  • Can be found in common household items including rubbing alcohol, disinfectants and detergents, paint thinners, jewelry cleaners and, cosmetics as well as in industrial solvents

  • Nearly twice as potent a CNS depressant than ethanol

  • Duration of action is 2-4x that of ethanol

  • Toxic dose is 0.5-1mL/kg; lethal dose is 2-4mL/kg

  • Pathophysiology

    • Is rapidly absorbed in GI tract, symptom onset within 60 minutes of ingestion

    • Reaches peak serum levels in 30-120mins

    • Metabolized by the liver via alcohol dehydrogenase to its toxic metabolite, acetone

Acetone is converted into multiple additional toxic metabolites including ethylene glycol and lactate

  • Half life is 6-7hrs for isopropanol, 17-27 hours for acetone

  • Toxic Effects

    • Isopropanol

GI irritation with nausea, vomiting, abdominal pain. Can cause pancreatitis or hemorrhagic gastritis

If aspirated, can lead to pulmonary edema and hemorrhagic tracheobronchitis

Vasodilation and hypotension

Decreased cardiac inotropy

  • Acetone

CNS symptoms including headache, dizziness, ataxia, hypotonia, seizure, miosis, dysarthria, coma

Respiratory from CNS depression

Peripheral vasodilation exacerbating hypotension

May cause rhabdomyolysis and renal failure

Hypoglycemia

  • Physical Examination Findings

    • Altered mental status

    • Fruity odor

    • Hypotension

    • Evidence of GI bleed

  • Laboratory Findings:

    • Ketosis WITHOUT ACIDOSIS

    • Increased osmolar gap 

    • Elevated isopropanol or acetone level (although does not accurately correlate with clinical outcomes

    • Elevated creatinine (falsely so, acetone interferes w/ assay–BUN is normal)

  • Management:

    • Ingestions are rarely lethal

    • Primary management is supportive care

    • Monitor until asymptomatic for at least 6 hours

    • No role for GI decontamination.

    • GI protection with 80mg pantoprazole

    • Fomepizole and Ethanol not recommended as they can prolong half life

    • IVF for hypotension (usually 1-2L is sufficient)

      • Vasopressors if not fluid responsive

      • Hemodialysis if refractory to pressors

R4 CASE FOLLOW UP WITH DR. CHRISTA PULVINO

 The Case:

Patient presents from infusion clinic for evaluation of hypotension to 76/60. The patient notes that his blood pressure usually runs low. He has a rash over his entire body as well as edema to the face. States he recently stopped taking IV vancomycin.

Differential Diagnosis: Red Man syndrome:

  • Infusion reaction to vancomycin

  • Results in pruritic, erythematous rash over face, neck and torso

  • Can have associated hypotension and angioedema

  • Onset usually within 4-10 minutes of infusion

  • Treatment is with antihistamines and stopping vs slowing the infusion

The Case, continued…

Further chart review revealed the patient has actually had a rash over his body for 1 week. It has not been getting better with benadryl or topical steroids and continues to spread.  Denies systemic symptoms. Vancomycin was  stopped 1 week ago due to this rash and his therapy was  converted to ceftaroline–did not actually receive his infusion on this day. Physical examination notes facial edema without involvement of tongue or mucous membranes, crackles in the LLL, PICC line in LUE without erythema or discharge as site and an extensive, non-blanching erythematous papular rash with areas of coalescence and desquamation on the bilateral upper extremities including the palms as well as torso. 

Differential Diagnosis of a morbilliform rash:

  • Drug eruption

  • Viral exanthem

  • Secondary syphilis

  • Erythema multiforme

  • Scarlet fever

  • Toxic shock syndrome

  • Acute HIV infection 

  • Acute Graft-versus-host disease

Labs return notable for CBC with leukocytosis to 38 with significant eosinophilia (57.9%). The diagnosis is made–DRESS Syndrome. 

DRESS Syndrome

  • Drug reaction with eosinophilia and systemic symptoms

  • Usually occurs 2-8 weeks after introduction of drug

  • Most common presenting findings are fever, rash, and lymphedema

  • Rash is usually urticarial or maculopapular but can honestly be anything

  • Labs show eosinophilia and leukocytosis, abnormal LFTS

  • Typically have visceral organ involvement which causes it to potentially mimic any inflammatory syndrome (hepatitis, pericarditis, pneumonitis, colitis, etc)

  • Classic inciting medications include AEDS (especially carbemazepine), allopurinol

  • Diagnosed by the RegiSCAR Diagnostic Criteria

  • Overall carries an approximately 10% mortality rate

  • Treatment:

    • Early drug withdrawal

    • Steroids (systemic and topical)

    • IVIG or cyclosporin

Lessons From an R4:

  1. Ask yourself, “could I be wrong?” “What else could this be?” Be aware of the potential for anchoring. 

  2. Read the chart!

  3. It’s ok to use google or other resources when you don’t know something or something isn’t quite fitting. Consider using an application or resource to check your thinking. Dr. Pulvino recommends Diagnosaurus.

  4. When in doubt, try to help the patient out.

R1 CLINICAL DIAGNOSTICS: GASTROPARESIS AND CYCLIC VOMITING WITH OLIVIA GOBBLE

Please see Dr. Gobble’s comprehensive post on presentation, diagnosis and management of these conditions HERE!    

AIRWAY GRAND ROUNDS: NASAL ENDOSCOPY AND CRICOTHRYOTOMY WITH DR. STEVEN CARLETON

Starting Pearl of Wisdom: Only paralyze in the difficult airway if the practitioner has absolute certainty in their ability to rescue

Optimizing Nasal Endoscopy

  • Prepare

    • Pharmacologic and mechanical drying (get that suction set up!)

    • Decongest/vasoconstrict using oxymetazoline

    • Topical anesthesia, 4% lidocaine (atomized vs nebulizer vs cricothyroid membrane puncture vs spray as you go) then sedate to effect

      • If you spray as you go, you cannot use suction on the endoscope because it will just suck up the anesthesia. 

      • Be mindful of how much “dead space” your endoscope wand has in their injection channel (i.e. draw up dead space + desired amount to spray in a syringe)

        • Large scope = 5cc

        • Small scope = 1cc

    • Lubricated NPA to distend nostril, 2% lidocaine

      • Can split NP airway longitudinally to be able to pull apart as you pass an ET tube

    • Sedate as needed–the better you topicalize, the less sedation you need

  • Subtotal intubation vs preloading ET tube on scope

    • If highly confident you are heading towards a fiberoptic intubation via nose, probably best to subtotally intubate

      • Clean channel

      • Guarantee that tube fits in nose

      • Less movement of the scope wand during passage since the curved ETT tube descending on the wand automatically can cause  significant distortion of the wand

    • Regardless of method, pass tip of endoscope through cords all the way to the level of the carina before moving ET tube towards the glottis to minimize chance of malplacement

  • Augmenting endoscopy

    • Jaw thrust

    • Dual laryngoscopy with video laryngoscope in addition to endoscope via picture within a picture setting 

Cricothyrotomy

  • Indications

    • Rescue of failed airway

    • Aerodigestive tract bleeding

    • Facial trauma

    • Foreign Body Obstruction

    • Oropharyngeal edema

    • Massive emesis

    • Persistent masseter spasm despite paralytics

  • Predictors of difficulty (SMART)

    • S - Surgically altered airway

    • M - Mass

    • A - Access to neck/Anatomy

    • R - Radiation

    • T - Trauma

  • Complications

    • Most common is malposition, usually high (thyrohyotomy), maybe as frequently as in a third of cases

    • Hemorrhage

    • Pneumomediastinum

    • Cartilage laceration or fracture

    • Barotrauma

    • Infection

    • Dysphonia

    • Subglottic stenosis

  • FInding the CTM

    • Overall EM physicians are terrible regardless of what method they are using

    • Top Down Method - bracing nondominant hand over patients chin, use index finger to trace down the ridge of the thyroid cartilage until it dips at the cricothyroid membrane

    • Launcelott skin fold (inferior) crosses cricothyroid membrane in majority of people

      • Not everyone has one

    • Can use ultrasound as well

  • Equipment

    • Keep it simple!

    • Use an ETT! Don’t use shiley or other trach tubes

      • 6.0 in Males based on average height of CTM

      • 4.0-4.5 in Females based on average height of CTM

    • #10 blade is best 

      • Keep in mind diameter of trachea at the CTM is relatively small (0.5-1.0cm)–stab incision through CTM needs to be controlled

  • Bougie-assisted

    • Adult bougie will go through 6.0 ETT or larger

    • Pediatric bougie will go through 4.0 ETT or larger

    • Consider trach hook in high BMI patients as it can make passing the tube easier by creating a straighter tract

  • Open surgical technique is faster and more successful than percutaneous methods

    • 3-6cm vertical skin incision

  • Laryngeal handshake

    • Blocks the thyrohyoid membrane w/ hand

    • Allows for stabilization of the highly mobile larynx

    • Make sure to replace index finger on thyroid cartilage after moving it to complete vertical skin incision

  • Troubleshooting

    • Hang up while passing ET tube? Rotate bevel posteriorly prior to hitting skin

  • Practice! As a low rep, high stakes procedure, training and repetition is the only way to prepare adequately

    • 10 manikin repetitions reduced time to completion from 41 to 24 sections and increased success rate from 62% to 99%