Grand Rounds Recap 9.8.21

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R1 clinical diagnostics: OUD and MAT WITH Dr. Jackson

  • The mortality of opiate use disorder has drastically increased since 2015 and continues to rise every year. Unfortunately, Ohio has one of the highest age-adjusted rates of opioid overdose related deaths. 

    • A retrospective observational study in Massachusetts by Weiner et al evaluated the 1-year mortality in patients treated for non-fatal opioid overdoses in the ED. Out of 11,557 patients included in the study, 1.1 % died within 1 month and 5.5% died within 1 year. 

  • Patients who have ‘revealed’ opiate use disorder are more amenable to intervention and medication assisted therapy. Ideally, we would like to convert patients from ‘unrevealed’ to ‘revealed’, in order to target efforts and offer assistance to those who need it.

  • Opiates are highly addictive and the desire to avoid withdrawal symptoms is severe. Remember this and try to adequately treat withdrawal in the ED and throughout their hospital stay when caring for patients with opiate use disorder. Depending on the opiate they used, withdrawal symptoms can last for weeks. 

  • Signs of opiate withdrawal

    • Restlessness

    • Nausea and vomiting

    • Diarrhea

    • Piloerection

    • Diaphoresis

    • Yawning

    • Midriasis

    • Autonomic hyperactivity

  • COWS (Clinical Opiate Withdrawal Score) can be used to help quantify the severity of withdrawal 

  • Treatment of opiate use disorder:

    • Buprenorphine is a partial agonist which results in a ceiling effect which prevents significant euphoria or respiratory depression. Because buprenorphine has a very strong affinity for the mu receptor, it can ‘kick off’ other mu agonists and precipitate withdrawal in patients who have used recently (typically in the last 12-24 hours, methadone can last up to 48 hours)

    • Buprenorphine is frequently combined with naloxone as a combo medication to prevent parenteral use.

    • A Meta-Analysis by Gowing in 2017 demonstrated that patients in the buprenorphine group had less severe withdrawal symptoms than comfort treatment alone, and patients in the buprenorphine group stayed in treatment longer and were more likely to complete opiate use treatment. This meta-analysis demonstrated a NNT = 4 for buprenorphine, so for every 4 patients treated with buprenorphine, 1 additional person will complete withdrawal treatment over comfort treatment alone.

  • How to handle acute pain in patients on medication for opioid use disorder

    • Unfortunately, there isn’t a lot of literature to guide this.

    • Treat their pain as you would for any other patient, noting that they may need higher doses

    • Make sure to make the MOUD provider aware if you administer narcotics to avoid interruption in their medications.

Heme/Onc Consultant Corner: Immunosuppression WITH dr. chaudhary

New therapies are taking hold in oncology: chemotherapy, immunotherapy, targeted therapy, and anti-angiogenesis therapy

  • Chemotherapy

    • Neoadjuvant - Before surgery or radiation, is given for organ preservation but there is usually no survival therapy

    • Adjuvant - patient has no visible disease but has a high chance of recurrence. Adjuvant chemotherapy is given adjuvant to surgery or radiation therapy to decrease the risk of recurrence. Patients are clinically cured when receiving adjuvant therapy. 

  • When should we be most worried about fevers and expect low blood counts after receiving chemotherapy?

    • 7-14 days

    • Febrile neutropenia had a mortality as high as 90% before the institution of empiric antibiotics as standard of care. Make sure if patients are in this post-chemotherapy window that you get a CBC, start empiric antibiotics early, and always call the treating oncologist. Do not wait for the CBC to start antibiotics in the ED. 

  • Remember when calculating the ANC, make sure to include neutrophils and bands in your percentage calculation!

    • Example: A patient presents 7 days after CHOP therapy with a fever of 102 and chills. The patient has a total white count of 800 with 50% neutrophils, 10% bands, 30% lymphocytes, and 10% other.  What is his ANC?

      • 480

  • Targeted therapy

    • Example: bevacizumab - it blocks VEGF which stimulates blood supply to the tumor. Essentially bevacizumab starves out the tumor. Because this targets blood vessels, there can be complications like wound dehiscence, port extrusion, strokes, and myocardial infarction.

  • Immunotherapy

    • Immunotherapy boosts or changes the way your immune system works and stimulates your own immune system to attack cancer cells. Many of the immunotherapeutic agents are checkpoint inhibitors, which take intrinsic regulators off of your immune system. Think of it as letting guard dogs off the leash. 

    • Side effects of immunotherapy: Really any “-itis”

      • Pneumonitis

      • Colitis

      • Neuritis

      • Hepatitis

      • Pancreatitis

      • Nephritis

    • Most people don’t get any side effects until after their second dose of immunotherapy. Treatment for any immunotherapy induced “-itis” is 1 mg/kg of prednisone or an equivalent IV steroid dose. 

    • As ED providers, we reliably think about sepsis in these patients, but patients on immunotherapy are also at risk for adrenal insufficiency and panhypopituitarism, so don’t forget to think about these!!

    • If you are concerned for panhypopituitarism:

      • Labs

        • TSH and Free T4

        • ACTH

        • AM Cortisol (ideally) but a random cortisol level is also acceptable (before you give steroids!!!)

        • Electrolytes

        • Consider an MRI with pituitary cuts (this can be done later)

      • Start stress dose steroids!

    • Causes of death or serious toxicity from immunotherapy

      • Myocarditis (get a BNP and Troponin)

      • Guillain Barre

      • Type 1 DM/DKA

      • Secondary Adrenal Insufficiency

      • Colitis and perforation

      • Pneumonitis (Get a CT chest)

        • Pneumonitis is likely to become more common as immunotherapy becomes increasingly used for lung cancer

      • Nephritis

      • Hepatitis

r3 taming the sru WITH dr. chuko

  •  The Case:

    • The case started with a telephone call from EMS who was bringing in a patient found unresponsive by family at home after 4 days of worsening mental status. En route to the hospital the patient became unresponsive and went into SVT with a thready pulse. She was successfully cardioverted but then reverted back to SVT with a heart rate in the 200s. A second cardioversion was performed and was successful prior to arrival to the hospital. The EKG on arrival demonstrated NSR with a RBBB and a QTc of 518.

    • On arrival, the patient was a middle aged person with a history of hypertension, gout, and kidney stones which required stent placement previously. They were alert and oriented and endorsed lethargy with diffuse abdominal pain for the preceding 4-5 days, with nausea and decreased po intake. They denied any fevers or chills and denied melena or hematochezia. Home Medications included amlodipine, ibuprofen, naproxen, meloxicam, and oxycodone/APAP.

    • Bloodwork and imaging were ordered including a CTH, CTPA, and CT A/P. As the patient was preparing to go to the CT scanner, they became tachypneic and hypoxic to 86% on room air, they were hypotensive with a BP 81/36, and HR was 104. The patient was still alert and oriented and was started on an IVF of LR and  2L NC, and a RUSH exam was performed which was largely unremarkable.

    • A VBG resulted several minutes later at 6.98/49/12 with a lactic acid of 14.7 and a glucose of 35. The patient was given 1 amp of D50, the LR was switched to normosol. She was given calcium and broad-spectrum antibiotics including flagyl, and blood cultures were obtained.

    • The remainder of the bloodwork demonstrated an anion gap of 36, a BUN of 114, Cr of 2.48, and a WBC of 29.8 with platelets of 64. She also had a mild transaminitis (60s) and mild elevation in both direct and indirect bilirubin. Urinalysis was positive for leukocyte esterase and nitrites. Imaging demonstrated no significant abnormality in the head or chest however the CT of her abdomen demonstrated pneumoperitoneum from a suspected perforated peri-pyloric ulcer.

    • Acute care surgery was consulted, 2 amp of bicarb were administered, and the patient was given an additional bolus of normosol.  Aircare was called and the patient was transferred downtown for emergency surgery.

  • Perforated Peptic Ulcers

    • NSAIDs and H. Pylori infections are the most common causes of perforated peptic ulcers. 

    • Even in modern medicine patients with bleeding peptic ulcers still have a mortality of 10%. 

    • Treatment:

      • Patients with GI perforation are at high risk for volume losses and electrolyte abnormalities, so resuscitate them and monitor electrolytes carefully.

      • Keep them strict NPO

      • Start broad spectrum antibiotics with coverage for abdominal flora

      • Protonix: a study by Sath et al in 2016 demonstrated unclear benefit of protonix in perforated ulcers, but a clear benefit in bleeding ulcers

      • Fluconazole: A study by Li et al in 2017 demonstrated no improvement in all-cause 30-day mortality in patients with community-acquired perforated ulcers with candida species isolates. 

      • Perforated gastric ulcers require definitive operative management

r4 case follow-up WITH dr. berger

  • The Case:

  • Tracheostomy vs laryngectomy, what’s the difference? 

    • We as ED providers frequently see front-of-neck airways and assume they are tracheostomies. 

    • A tracheostomy is a window into the trachea through the anterior wall of the trachea. Importantly the larynx is still intact and so their airway still has continuity between the mouth and the lower airway.

    • A laryngectomy patient has had their larynx removed, and so they no longer have continuity between their mouth and their lower airway. This is critical as these patients cannot be intubated and cannot be ventilated via their mouth.

  • Troubleshooting a front-of-neck airway

    • Step 1 (both): Remove any caps or inner cannulas

    • Step 2 (both): Attempt to pass a flexible suction catheter

    • Step 3 (both): if there is a cuff/balloon, deflate it

      • Some balloons may accidentally displace the tube anteriorly against the airway and result in obstruction

    • Step 4 (both): Remove the entire cannula

      • Apply oxygen to the face and stoma

    • Step 5: If a trach, assess breathing and airflow at the mouth and stoma - oxygenate and attempt to ventilate at the same locations. If a laryngectomy tube, evaluate only at the stoma -above the stoma will not help you!

    • Check out the National Tracheostomy Safety Project’s Emergency Algorithms found here!

R1 Clinical knowledge: cerebral venous sinus thrombosis WITH Dr. Moulds

  • The cerebral veins include both a deep system and a superficial system

    • Superficial: Includes the superior sagittal sinus, the inferior sagittal sinus, and the cavernous sinus. These drain the cerebral cortex, the superficial white matter, and the face.

    • Deep: Includes the straight sinus, the transverse sinus, the great cerebral Vein, and the sigmoid sinus. These drain the deep white matter, basal ganglia, brain stem, and thalamus. 

  • Cerebral Venous Sinus Thrombosis

    •  A complete or partial occlusion of one of the major cerebral venous sinuses or smaller feeding cortical veins. 

    • Makes up 0.5-1.0% of all strokes. 

    • There is a 3:1 female predominance

    • The median age is 37 years old

  • 85% of patients who suffer a CVST have at least one risk factor. Risk factors include:

    • Head and neck infections

    • Recent neurosurgical procedure including LPs

    • COVID-19 infection

    • Pregnancy/postpartum/OCPs and HRT

    • Malignancy

    • Inflammatory diseases

  • Pathophysiology

    • Initially when there is a clot in the cerebral veins, they dilate to compensate for the increased resistance and pressure. As the pressure overwhelms this compensatory measure, the blood brain barrier is disrupted which leads to fluid shifts and ultimately vasogenic edema.  As Na/K pumps fail, tissue edema and cellular swelling results in cytotoxic edema. Increased venous pressure can lead to vessel rupture and hemorrhage. 

  • Presentation - 3 types of presentations are common with CVST: Isolated intracranial hypertension, focal neuro deficits, or encephalopathy. 

    • Isolated intracranial Hypertension

      • Presents with headaches that are worse in the morning or bending forward, vomiting, vision changes, papilledema. 

      • Typically presents subacute to chronic. 

      • Usually indicates superior sagittal sinus involvement. 

    • Focal Neuro Deficits

      • Can be any type of focal neurological deficit

      • Typically indicative of involvement in the superficial venous system which affects the cerebral cortex. 

    • Encephalopathy

      • Presents as mental status changes, stupor, and coma

      • Most commonly indicates involvement of the deep venous system which affects the brain stem and basal ganglia. 

    • Symptoms

      • Headache (89%) can be subacute or thunderclap. 

      • Focal Deficits (40%), typically motor and visual symptoms, may be subacute in onset compared to arterial thrombosis

        • Motor > Visual > Aphasia > Sensory

      • Seizures (40%)

      • Visual symptoms (20-30%)

        • Involvement of visual symptoms may suggest cavernous sinus involvement. Look for fever, facial infection, eye pain, chemosis, diplopia, or CN 3, 4, or 6 palsies. 

  • Diagnosis

    • No single lab test can confirm or rule out CVST

    • If a patient is found to have a CVST, a thrombophilia workup is recommended

    • In 2020, there was a new multicenter prospective cohort study of ~350 patients that proposed a new clinical risk score to categorize patients

      • Using d-dimer alone, 10-25% of CVSTs were missed

      • They developed a clinical risk score that includes seizures at presentation, known thrombophilia, OCPs, sx > 6 days, worst HA of life, focal neuro deficit at presentation

        • Low risk = 2 points or less

          • Low-risk pts: Still missed some CVST, NPV 94.1%

          • However, when low-risk pts + d-dimer <500 ug/L: NPV 100%

      • However, this was overall a small study and has not yet been further validated; additionally, CVST may be the first presentation of thrombophilia

    • Imaging

      • ⅓ of patients will have direct signs of a CVST on a non-contrast head CT

        • Dense triangle sign

          • Triangular or round hyperdensity

          • Indicative of a thrombus of superior sagittal sinus

        • Empty delta sign

          • Similar to dense triangle sign, but triangular region of enhancement with central clearing

          • Seen with superior sagittal sinus thrombosis

        • Cord Sign

          • Curvilinear hyperdensity over the cerebral cortex, caused by thrombosis of cortical veins

    • Head CT may also show indirect signs of CVT, including:

      • Hemorrhage

      • Dilated veins

      • Edema

      • Hypoattenuation suggesting infarction that doesn’t correlate with arterial pattern

    • Definitive Neuroimaging

      • Includes either a CT venogram or an MR venogram

  • Management

    • Treat underlying dehydration/sepsis/stop prothrombotic medications, control seizures and manage elevated ICP

      • ICP: osmotic therapy, elevate head of bed, sedation, hyperventilation, ICP monitoring

    • TO-ACT Trial

      • A multinational RCT of 67 pts with severe CVST

      • Early endovascular thrombolysis (mechanical thrombectomy or local tPA) did not improve functional outcome measured by modified Rankin scale compared to medical therapy alone, no significant difference in mortality

      • Stopped early due to futility

    • Anticoagulation

      • Expert consensus says to treat with AC, but the evidence is actually not robust

        • One meta-analysis in the early 2000s only included two small trials which both had methodologic problems

        • Total of 79 patients

        • Anticoagulation trended towards reduction in death or dependency but was not statistically significant.

        • In one study, IV heparin vs placebo, was stopped early due to increased mortality in the placebo arm.

      • UFH or LMWH

        • Based on a RCT in 2012 with 66 pts, LMWH had decreased in-hospital mortality and higher complete recovery.

        • UFH can be used if pt is clinically unstable,  invasive interventions planned, renal failure, or other contraindication to LMWH.

      • Duration of anticoagulation

        • 3-6 months if provoked, 6-12 months if idiopathic, lifelong if recurrent or underlying severe thrombophilia.

        • Recent systematic review from 2020 indicates NOACs are as effective as warfarin with no significant difference in death, recurrence, or hemorrhage events.

      • Is AC safe in ICH from CVST?

        • A meta-analysis of studies on anticoagulation for CVST which included patients with ICH...

          • No pts on heparin developed new ICH, but 3 in the placebo group did. However, the studies are from the 1990s and had relatively low enrollment numbers. 

        • Expert guidelines in the past have said that ICH is not a contraindication. Ultimately risk/benefit discussion should be had with consultants and the patient/patient family. 

high value care WITH dr. lane

  • What are areas of EM clinical Decision-making with identified variation?

    • Utilization of testing and imaging. Varies with:

      • Training environment 

      • Provider experience level

        • A study by Hodgson et al evaluated whether ED providers who order more tests are more likely to also admit patients. They did find a positive correlation between testing and admitting.

        • Another study by Ulrich et al evaluated whether greater CT utilization by ED physicians also correlated with a higher admit rate, and they also found a positive correlation. 

      • Outpatient resources and follow up available

      • Hospital and Admitting service expectations

  • What are ways of talking about variation in healthcare

    • Level of analysis

      • Regional variation

      • Hospital differences

      • Physician variation

      • Shift variation

        • A retrospective cohort study by Patrick et al found that patients who encountered an ED provider later in their shift had a higher chance of admission

      • Disease process or chief complaint variation

    • Units of analysis

      • Utilization of resources

        • This is typically what is most focused on

      • Cost of healthcare

    • Explainability  - How much of the variation in the above measures is explainable vs random. 

      • Studies have shown that hospitals (vs providers or region) have the greatest degree of variation but also the greatest degree of explainability. This suggests that practice patterns within a health system are likely cultural and therefore might be difficult to change. 

  • How can we move towards models of value-based payment in emergency medicine 

    • Targeting decreased admission rates, then choosing what condition to go after

      • Find a clinical disease with variation in practice pattern

      • Is your institution culturally ready?

      • Is there a clinical guideline or pathway (clinical decision rule)?

      • Are there outpatient resources and follow up?

      • What effect will we have on resource utilization?

      • What effect was there on patient satisfaction and outcomes?