Grand Rounds Recap 3.27.19

M&M - Community tips - Transfusion rxn - Cpc: NCSE - Alt EKGs - Refractory shock

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Morbidity and Mortality Conference WITH DR. MURPHY

Cavitary Lung Lesions

• Definition- lucent area contained within a consolidation, mass, or nodule

  • Acute <12 weeks

  • Chronic >12 weeks

• Risk Factors

  • IVDU/Homelessness/Travel to Endemic Areas

  • Immunosuppression

  • Structural Lung Disease

• Basic Approach

  • Identify risk factors

  • Establish time course

  • If a new cavitary lesion in a patient with risk factors, treat for abscess and rule out TB

• Differential

  • Acute

    • Mycobacterial disease- TB more common in at risk populations, MAC more common in those with structural lung disease

    • Abscess- Typically unilateral and solitary, involves multiple organisms including anaerobes, so treat with anaerobic coverage (Clindamycin/Augmentin)

    • Septic Emboli- Imaging will show cavitations in various stages of development, treat the underlying source

    • Nocardia- Gram positive bacteria found in the soil, which will develop in those with a deficiency in cell mediated immunity (Stem-cell transplant, AIDS, leukemia/lymphoma)

    • Fungal pathogens- In immunodeficient hosts, can present with more invasive and severe pathogens such as mucormycosis, cryptococcus, invasive aspergillosis

  • Chronic

    • Fungal pathogens- In immunocompetent hosts, can present more indolent and be treated as an outpatient. Examples include histoplasmosis (the OH river valley), blastomycosis, chronic aspergillosis

    • Paragonamiasis- found commonly in ingestion of crab/crayfish, treated with praziquantel

    • Echinococcus- tapeworm found in dogs that forms liver cysts and elsewhere throughout the body

    • Malignancy

    • Autoimmune- including but not limited to rheumatoid arthritis and granulomatosis with polyangitis

Chronic Pain Management

• Background

  • Over 100 million in the USA affected, costing $550-650 billion per year

  • Nociceptors will sense pain, in which an ascending dorsal horn pathway will carry the signal to the brain, and then a descending pathway will send an inhibitory signal via endogenous opioids.

  • With chronic pain and injury, macrophages will release growth factors for repair. However, this is nonspecific, so sometimes nerves are regenerated to sense non-painful stimuli as painful, leading to allodynia and hyperalgesia.

  • With chronic pain and repeated stimulation of the dorsal horn, the neurofibers will be sensitized modulated by the NMDA receptor

• Opioids

  • Interferes with descending dampening pathway and the ability to self-regulate pain

  • Leads to tolerance and addiction

• Ketamine

  • NMDA receptor antagonist, which is a hypnotic, analgesic, amnestic

  • In a study of 60 patients, was shown to reduce the amount of rescue opioid needed when used as an adjunct

  • Ketamine was also shown to perform equivalently to morphine in subdissociative doses for pain, but had increased minor side-effects (dizziness, disorientation, mood changes)

  • In a study comparing IV push of ketamine vs. an infusion over 15 minutes, a slow infusion reduced minor side-effects with no difference in pain scores

• Haloperidol

  • Was created as an analogue of meperidine when scientists were searching for a more powerful opioid than morphine

  • Is a non-selective D2 blocker reducing nausea, but also modulates pain as an NMDA antagonist

  • In 52 patients with proven gastroparesis, administration of 5mg of IM haldol vs. standard of care lead to a decrease in hospital admission as well as a decrease in morphine equivalents administered

  • In 33 patients with gastroparesis, 5mg of IV haldol was shown to lower the intensity of pain and nausea at one hour

  • It has shown noninferiority compared to standard care for a variety of other indications, including migraine, and chronic pain management

  • Though there are multiple case reports, there is not a robust amount of literature to support its use in cannabis hyperemesis syndrome

Neuroleptic Malignant Syndrome

• Background

  • A syndrome characterized by hyperthermia, rigidity, and altered mental status in the setting of antipsychotic use

  • Most often is symptomatic within the first 2 weeks of starting or up-titration of a antidopaminergic medication

  • Affects all age groups

  • Pathogenesis is unknown, but thought to be due to dopamine regulation in the brain of heat dissipation in the hypothalamus and rigidity in the corpus striatum

• Diagnosis

  • Mental status change is typically early, where lead pipe rigidity is a later finding and not always present

  • Also characterized by autonomic instability and hyperthermia

  • Compared with first generation of antipsychotics, second generation antipsychotics tend to present with less rigidity

  • Differential diagnosis includes alcohol and baclofen withdrawal, sepsis, malignant hyperthermia, and serotonin syndrome

  • Diagnosis can be aided by calculating a point score developed by consensus recommendation at the International Consensus of Neuroleptic Malignant Syndrome

• Treatment

  • Stop the causative agent

  • Supportive care

  • Targeted therapy- no good evidence to support typical use of these

    • Dantrolene- skeletal muscle relaxant that inhibits calcium release, but can be associated with hepatotoxicity

    • Bromocriptine- dopamine agonist

    • Amantadine- has some dopaminergic and anticholinergic effects

  • Mean recovery time is 7-11 days with a 5-20% mortality

• Clozapine

  • Typically used in the case of treatment resistant schizophrenia

  • 1-3% of patients will have neutropenia

Graft Versus Host Disease

• Definitions

  • Allogenic Transplantation: transplant of cells to a recipient from a genetically non-identical donor

  • Graft Versus Host Disease: T-cells in the donated tissue recognize the recipient as foreign and therefore attack it

• Risk Factors

  • 30-50% of those with allogenic cell transplantation have GvHD

  • Higher degree of HLA mismatch leads to higher likelihood of disease

  • Receipt of transplant from an unrelated donor increases the likelihood

  • Donor/Recipient gender disparity leads to higher likelihood

  • GvHD risk can be minimized by limiting risk factors, and starting patients on immunosuppression

• Presentation

  • Maculopapular rash or bullae, skin sloughing

  • GI symptoms such as diarrhea with bleeding, mucositis, and nausea/vomiting

  • Liver disease and ascites, with lab testing showing early bilirubin and alkaline phosphatase elevations more typically than transaminitis

• Treatment

  • Grade 1: Skin Involvement <50% TBSA

    • Topical steroids

    • Ensuring adequate underlying immunosuppression with methotrexate or mycophenolate and tacrolimus or cyclosporine

  • Grade 2 and up: anything else

    • IV Methylprednisolone 2mg/kg/d in divided doses

    • PO Beclomethasone/budesonide for GI involvement

Sepsis Without a Source

• Background

  • This is fairly common, with 26% of patients admitted to the ICU for sepsis not having an identifiable source at 24 hours in one retrospective study of 10 hospitals

  • The majority of these patients had an abdominal or pulmonary source

  • In those without sepsis, the most common mimic was adverse reactions to drugs

  • In a similar retrospective study of those admitted for severe sepsis from the ED, 18% of those admitted had non-infectious mimics

• Differential Diagnosis

  • Medication-related

  • Mesenteric ischemia

  • Pancreatitis

  • Adrenal Insufficiency

  • PE

• Should we CT scan all patients with severe sepsis?

  • In a study of 50 patients meeting criteria for severe sepsis, in those without a source, 5/7 had their source identified only on CT scan

  • In the undifferentiated shock patient with concern for sepsis without a source, consider CT or further diagnostics as mobility is limited once the patient is in the ICU.

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discharge, transfer, or admit: ENT/Ophtho/Dental  WITH DR. Lafollette

Quincke’s Edema

• Swelling of the uvula, in the abensce of systemic infectious symptoms should be considered angioedema and treated as a Type 1 hypersensitivity reaction with (H1 and H2 blockers, steroids)

• Disposition: Warrants observation, so consider transfer to a facility with ENT capabilities

Complicated Facial Lacerations

• Exam- do a thorough neurologic exam to ensure no cranial nerve involvement

• Anesthesia- use long acting anesthetics (bupivacaine) as more complex repairs typically take longer than one hour when solo coverage

• Evaluate for need for muscle repair to ensure the subcutaneous layer approximates

• Ensure adequate outpatient follow-up

Dental Fractures

• Ellis System

  • Ellis 1- enamel involvement only, does not require coverage

  • Ellis 2- dentin involvement, requires coverage with calcium hydroxide paste

  • Ellis 3- pulp involvement, requires coverage with calcium hydroxide paste and may require root canal for pulp necrosis

  • All require rapid referral to dental

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Transfusion reactions WITH DR. hunt

Febrile Non-hemolytic Transfusion Reaction

• 0.1-1% of all transfusions, more commonly in children

• Present with a fever of at least 1 degree celsius, thought to be due to cytokines

• Products stored for more than 48 hours are more susceptible to this

• Starts within 1 to 8 hours of transfusion

• Management includes acetaminophen and supportive care

• No role for acetaminophen or diphenhydramine premedication, as this can mask fever and more insidious transfusion reactions

Hemolytic Transfusion Reactions

• 1 in 70k transfused units lead to these

• Typically due to ABO compatibility, where the host’s immune system attacks the donor red blood cells

• Presents with fever, renal failure, hypotension, tachycardia, and signs of DIC

• Management involves halting the transfusion and supportive care

• If oliguric, consider using furosemide to maintain UOP 1cc/kg/hr

Anaphylactic Transfusion Reactions

• 1.7-4.3 per 100k blood transfusions

• Due to some allergen in the transfused product, commonly in IgA deficient patients reacting to IgA, though has been seen in those who have peanut allergy post transfusion

• Presents with rapid onset of shock, hypotension, lip swelling, respiratory distress, and GI symptoms

• Stop the transfusion and treat with typical anaphylaxis medications (epinephrine, steroids, histamine blockers)

Urticarial Transfusion Reactions

• 1-3% of transfusions

• Present with isolated hives, but no fever or other system involvement

• This is well tolerated, and the only transfusion reaction that does not require you to stop the transfusion

Transfusion Associated Lung Injury

• Occurs in 1 in 5000 transfused units, and the leading cause of transfusion related mortality in the US

• Occurs due neutrophil accumulation within the lungs that are activated during transfusion

• Usually occurs in 1 to 2 hours, but up to 6 hours after transfusion

• Presents with pulmonary infiltrates and hypotension

• Manage with supportive care including airway management and halting the transfusion, paying attention to low tidal volume ventilation, similar to ARDS management

• Daily breathing trials has been shown to decrease the time on the ventilator

Transfusion Associated Circulatory Overload

• 0.06% of transfusion reactions, but up to 6% of those in the MICU who were transfused develop TACO

• Higher volumes are associated with higher likelihood of TACO, with OR of 113 for those with Hemorrhagic Shock

• On physical exam, patients may have evidence of fluid overload such as hypoxia, HTN, tachycardia, pulmonary edema, and JVD

• Patients will be managed as circulatory overload, with nitrates and diuretics, as well as respiratory management

Transfusion Associated Sepsis

• 1 in 30k RBC and 1 in 2k platelets have some level of bacterial contamination

• Bacterial contamination is more common in platelets as they are stored at room temperature

• Present rapidly with fever, rigors, tachycardia, and hypotension

• Treat as you typically would treat sepsis (fluid challenge, pressors as needed, broad spectrum antibiotics, blood cultures)

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Clinical pathologic conference WITH DRs. HALL And plash

Non-Convulsive Status Epilepticus

• Presentation

  • On-going alteration and EEG confirmed seizure activity for at least 30 minutes

  • No major motor signs or symptoms (there can be some subtle motor signs of twtiching, eye deviation)

  • Changes in behavior or cognition (mild confusion to coma)

  • This is very difficult to diagnose. Of the 23 patients who were diagnosed with status epilepticus, only 13 were diagnosed within 23 hours in a retrospective review

• Etiology

  • Acute events such as metabolic abnormalities, infections, structural lesions, medications and intoxication can cause this

  • Chronic insults such as remote history of stroke, head trauma, or anoxia can be susceptible to this

• Diagnosis

  • Requires a high index of suspicion

  • EEG is the gold standard of diagnosis

  • Can do a trial of benzodiazepines if EEG is not immediately available, but not alway definitive

• Treatment

  • No randomized controlled trials to guide our treatment

  • Should follow general seizure treatment protocols for status epilepticus

  • Identify and treat any underlying causes (medications, infection, intoxication)

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Alternative ekg lead placement WITH Dr. Connelly

See Dr. Connelly’s Introduction post Here

• 12-lead EKG in ACS

  • This is used to identify patients who need emergent catheterization, not determine if they need catheterization

  • 20-27% of NSTEMIs have acute coronary occlusion

  • Posterior circulation is overrepresented in these missed occlusions

  • In left circumflex disease, only 50% will have ST elevation on their EKG

  • 6 month mortality is worst in patients with RCA/LCx in those with NSTEMI

• Posterior Leads

  • Place V7-V9 in the below configuration

  • STE> 1mm if age <40, but 0.5 in all other populations

  • This technique helped diagnose an additional 18 of 57 patients with nondiagnostic EKG in one study

  • Isolated ST depression in the anterior leads should be managed as a STEMI according to the 2014 AHA/ACC guidelines

• Double-Speed EKG

  • In 45 EKGs with Aflutter, Afib, pSVT, sensitivity of EM physicians for the diagnosis was increased to 71% from 63% when using double speed EKGs

  • If p-waves are buried within the t-wave, you must look carefully at the t-wave morphology, as double speed will not “pull these” out of the t-wave

• Lewis Lead

  • Enhances the appearance of atrial activity

  • To set this up, put the RA lead to the manubrium, LA lead to the R sternal border, LL lead to the R lower costal margin, and the RL lead stays on the R leg. Monitor Lead 1.

  • This can help differentiate wide complex tachycardia, as is there is AV dissociation, this is Ventricular Tachycardia

  • In 47 patients in the EP lab, VA dissociation was detected in 71% with Lewis Leads and only 43% in those without

• Right Ventricular Leads

  • Isolated Right Ventricular Infarction is rare(<3%) , and nonfatal

  • Typically involves concomitant inferior wall MI, which is more serious

  • However, if there is RVI, patients should not be given nitro

  • Set up leads as a mirror image of typical V1-V6, which if elevated, should deter you from giving nitrates

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 taming the sru: Refractory Septic Shock WITH DR. klaszky

• Steroids

  • The physiologic theory behind this is that the endogenous upregulated steroids are inhibiting the steroid feedback loop, leading to a relative adrenal insufficiency, which we can supplement with exogenous steroids

  • In patients given steroids for septic shock on mechanical ventilation, there was no mortality difference found in patients given 200mg of hydrocortisone per day. However, they had a relatively low mortality rate of 21% in this study group, not in refractory septic shock.

  • In a later study with a sicker patient population (49 v 43% mortality), there was a 6% decreased rate of mortality in patients treated with fludrocortisone plus hydrocortisone

• Albumin

  • In patients with severe sepsis, albumin replacement+crystalloid versus crystalloid alone was not found to affect mortality of those with severe sepsis. However, in those with septic shock, there was found to be a mortality difference.

• Bicarbonate

  • In those with severe acidosis of pH < 7.2 and AKI, there was a 12% mortality difference when giving 250cc of 4.2% bicarb for their acidosis versus standard care

• Hypocalcemia

  • 80-90% of critically ill patients have hypocalcemia

  • Often occurs with hypomagnesemia

  • Hypocalcemia also causes decreased cardiac function and increased smooth muscle vasodiliation, leading to worsening shock

• Metabolic Resuscitation

  • In a paper by Marik et al., Hydrocortisone 50mg, Vitamin C 1.5 G, Thiamine 200 mg were shown to reduce mortality by 32% in a pre-post trial that was retrospective

  • This data was all retrospective and not randomized so further data is needed before broad acceptance of this.

• Methylene Blue

  • Works as a nitric oxide inhibitor to inhibit vasodilitation

  • Other nitric oxide inhibitors have shown higher MAPs with use in refractory sepsis, but this worsened or did not change mortality

  • There is no literature to support the use of this