2.14.19 Conference Summary

Sepsis 2019: Best Practices versus CMS Mandate: Dr. Michael Filbin

Why is sepsis a problem?

  • Deadlier than other emergencies that we prioritize care for (ie trauma, stroke, MI)

  • In the US, 4.3% of patients had an ICD diagnosis of sepsis at discharge

    • Accounts for 35% of all inpatient deaths

Sepsis pathophysiology

  • Inflammatory/metabolic effects

  • Metabolic activation similar to exercise

  • Hemodynamic effects (Macro- what we usually see)

    • Volume depletion/redistrict

    • Pathologic vasodilation

    • Myocardial depression

Definitions:

  • Sepsis = SIRS criteria + source of infection

  • Sepsis = life threatening organ dysfunction caused by a dysregulated host response to infection

  • Shock = subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities (vasopressor dependent, persistent lactate >2)

ProCESS Trial 2014

  • EGDT vs process sepsis care vs usual care demonstrated no difference in outcomes

Early identification is key, yet challenging

  • Symptoms are often vague

  • Many true septic patients have normal BP at triage

  • Previous culture of “wait and see” for sepsis treatment

  • When do you make the call? Are they infected? Is there organ dysfunction due to sepsis?

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qSOFA score

  • Criteria that predict bad outcomes in patients with a suspected infection'

  • Presence of 2 of 3 criteria predicted death/prolonged ICU stay

    • SBP < 100, RR >22, GCS <15

Sepsis 3 Criteria

New Definitions: Issues

qSOFA as a screening tool

  • Identifies patients already very sick/meets sepsis criteria

  • What is the PPV in undifferentiated patients?

  • We are more interested in who has sepsis and does not address the issue of “suspected infection”

  • Lack of operation common sense

SPoT (Shock Precautions in Triage) Filbin et al 2018

  • 141 patients admitted to ICU with septic shock

  • 100% of patients had SBP <100 or shock index (HR/SBP) >1

  • 96% had a sepsis risk factor (age >65, immunocompromised, active cancer, institutionalized, permanent neurologic disability, dialysis, CHF limiting function, COPD on O2, cirrhosis, percutaneous drains/tubes, prior sepsis, recent major surgery

  • Other 4% (ie young and healthy) were in extremis

  • Based on initial note, 33% probable infection/67% possible infection

SPoT validation

  • 19,670 patients over 2 months

  • 11% met SPoT vitals

  • Sensitivity: 90% sensitive, 56% at triage (more than qSOFA)

Does presenting with vague symptoms matter?

  • Patients that we delay antibiotics with: vague presenting symptoms, triaged to lower acuity area

  • Presenting with vague symptoms = antibiotic delay = increased mortality

  • Different phenotypes of sepsis (ie UTI, pneumonia, intra-abdominal

Linking Quality to Payment

  • 3 hour bundle

    • initial lactate, blood cultures, antibiotics, 30 cc/kg bolus

  • 6 hours bundle

    • Repeat lactate, document response to fluid bolus, start vasopressors

  • Does this lead to better outcomes? At face value yes, unadjusted mortality 11% vs 18% but differences insignificant when adjusting for other factors

    • Failing time to antibiotic still have a significant difference in mortality

Lactate

  • Lactate = metabolic stress

  • Increasing lactate = worst prognosis, patients who clear their lactate do better

  • Repeat your lactate

Hemodynamic Resuscitation: Dr. Michael Filbin

Cornerstones of septic therapy: identification, early antibiotic administration, hemodynamic support, source control

Where did 30 cc/kg come from?

  • EGDT trials x3- most got around this

  • Safety of 30 cc/kg in CHF patients (abstract)- 333 patients with sepsis and CHF

    • CHF history + hypotension gad a low mortality when receiving a bolus

  • Positive fluid balance over time is bad

    • Badness starts at around 30 cc/kg

Bolus therapy in the ED

  • Restore depleted intravascular volume in those with signs of volume depetion, differentiate from isolated hypovolemia and distributive shock, increase preload/cardiac output

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Cystralloid resuscitation: potential harm

  • Crystalloid is a medicine

  • Not all hypotension will benefit from volume

    • Is sepsis really a condition of volume depletion

  • Hemodynamic response short lived in true sepsis

    • Must assess responsiveness to fluids

Venous fluid dynamics

Distributive shock: Do not always have a decreased overall volume, just have a redistribution of fluids

Use of POCUS

  • IVC diameter as indices of fluid responsiveness

    • collapsible with preserved/hyperdynamic cardiac function will tolerate/respond better to fluids than a distended IVC with little variation with respirations and poor cardiac function

    • repeat assessment to monitor response

  • Utility of POCUS for undifferentiated shock?

    • SHoC-ED trial showed that use of a POCUS protocol in select ED patients with undifferentiated shock did not confer a 30-day or in-hospital mortality benefit compared to usual care

    • however, this was a limited study, didn’t include certain dx that POCUS might

Type of fluid - normal saline vs LR (too much chloride can be harmful to kidneys)

Physiologic vasopressors

  • Norepinephrine is physiologic hormone

  • Epinephrine has more beta effect

  • Vasopressin is an endogenous substance deficient in septic shock

Crystalloid liberal or vasopressors early resuscitation in sepsis (CLOVERS)

  • Multicenter randomized prospective study looking at restrictive vs liberal (2L) fluid strategy in the first 24 hours of septic shock in 90-day mortality

CPC: Dr. Summers vs Dr. Abraham

Case: Young male w/ history of recent diagnosis of endocarditis on IV abx with PICC complicated by DVT 1 week prior on Lovenox transitioned to eliquis, presented with headache and vomiting. His had R sided headaches that he has a neuro appointment for but this is different. No improvement with ibuprofen at home. Had a worsening of headache leading to vomiting. It is worse when he lies flat.

  • Exam: Sitting up, vomiting into bucket. Exam otherwise benign, including intact neuro exam

  • Labs: WBC 16.9, RFP/coags otherwise unremarkable

  • CT head: No acute intracranial abnormality

  • Treatment: toradol, reglan, 2L NS, 1g depakote, 2g magnesium

Approach to the Case: Dr. Abraham

  • Pertinent history: worse lying flat, nausea, vomiting, no fever/neck stiffness, orchiectomy (cancer?), no IVDU

  • Differential diagnosis:

    • Less likely: Carbon monoxide, giant cell arteritis, meningitis/encephalitis, opportunistic infection, zoster, fungal sinusitis, influenza, malaria, arachnoid cyst, dissection, primary headache, traumatic (negative noncon head CT)

    • More likely: Intracranial abscess, possible SAH (gradual in onset), venous sinus thrombosis, malignancy

  • Next tests: CT angiogram, CT venogram, CT with IV contrast, MR angiogram, MR venogram, optic nerve sheath diameter

    • Test of choice: MRI with contrast

Answer: Diagnostic test of choice: CT venogram

Diagnosis: Cerebral venous sinus thrombosis

Cerebral venous sinus thrombosis:

  • Common presenting symptoms: headache, AMS, nausea, vomiting, seizures, coma

  • Most commonly thrombosis are transverse sinus and superior sagittal sinus

  • More common in younger patients and women

  • Mortality: Mortality 7-12%, untreated up to 50%

Imaging: Gold standard is MRA/MRV, can use a CTV. Do not always see anything on CT head

  • MT delta sign, dense clot sign, venous infarction

Treatment:

  • Heparin: bolus and drip, even if the patients have a small amount of hemorrhage

  • LMWH had a decreased risk of death but less easily reverse

  • Seizure prophylaxis: only if they seizure

  • 3-12 months of anticoaguiation

Disposition: Neurosurgery consult, consider ICU for craniotomy watch especially with focal deficits

Lung Ultrasound: Dr. Vicki Noble

Pneumothorax:

  • Look for a lung sliding

    • If you are in the left chest near the midclavicular line, if you can see the heart, there cannot be a huge pneumothorax

    • Lung pulse: Intermittent barcode vs sandy beach when looking at the right side

  • Look for little “blips” on the pleural line = means that visceral and parietal pleura have to be touching

  • Find the lung point- where lung sliding stops

    • Start where there is not sliding and ultrasound until you find sliding.

    • Most useful to track


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Interstitial Syndrome

  • A lines: No fluid

    • Sound waves bouncing between the pleura and the skin

B lines: Fluid

  • The more B lines, the denser the fluid

  • Technique: Use a low frequency probe, by convention, set to 18 cm

  • More than three B lines per scan field- pathologic

  • Multiple etiologies for interstitial fluid- ie CHF, ARDS, pneumonia, TB, etc

  • B line have to match the patient: for example, if there are only a few scattered B lines and patient is in distress, the fluid might not be the cause

  • B lines will respond to treatment in real time Cardiology:

  • People with more B lines do worse long term

Pleural Effusions

  • Anechoic fluid: above the diaphrahm

  • Hepatization in the lung: likely pneumonia

  • Spine signs: If you can see the spine above the diaphragm, it is always pathologic

 Subpleural Consolidations:

  • If the pleural line is deformed/bumpy with fluid behind it, start worrying about infectious or inflammatory process

Vent management:

  • Are you using enough PEEP?

  • More B lines, consolidation with less or inadequate PEEP

Seizures- Dr. Ashley Rogers

Epilepsy: At least two unprovoked seizures occurring greater than 24 hours apart or one unprovoked seizure and a probability of further seizures similar to the general recurrent risk after two unprovoked seizures, occurring over the next 10 years.

  • Epilepsy- Prevalence 0.5-1%

  • Seizures- 9% lifetime occurrence (1/3rd are febrile seizures)

What are the symptoms?

  • Nonepileptic event vs epileptic seizure, where is the seizure from?

Etiology: Usually try MRI w/wo contrast epilepsy protocol

Most common cause in adults is a seizure from a stroke

Semiology:

  • Sensory sphere = auras

  • Autonomic sphere = autonomic seizure

  • Cognition sphere = dyscognitive seizure

  • Motor sphere = motor seizure

Dialeptic seizure: characterized by relative unresponsiveness and amnesia for the seizure- less likely to sudden develop in an adult

Todd’s paralysis: nonlocalizing but highly lateralizing sign- suggests a seizure from the contralateral hemisphere from the paralysis

Where are the eyes going? Active focal seizure will cause eyes to look contralateral to the seizure focus. After the stroke, you will often look ipsilateral to the seizure focus

Seizure precipitants: Metabolic and electrolyte abnormalities, fever/systemic infetion, stimulants, sedatives, ETOH w/d, sleep deprivation, nonadherence, stress, brain injury

Reminders:

  • Seizure mimics: migraine, stroke, parainsomnia, syncope

  • Syncope: convulsive movements are frequent during syncopal attacks

  • Encephalopathic patients can have nonfocal status

  • Nocturnal seizures: high stereotyped complex motor behavior

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