LHH ERAS Protocol for Spine Surgery

Pre-hospital phase (to be done by surgeon)

  • RISK FACTORS
    • Encourage smoking cessation x 1 month preop (consider concierge referral for smoking/tobacco cessation at Northwell Health)
    • BMI assessment
      • Discuss risks of obesity for BMI > 35
      • Consider referral to Bariatrics or to concierge Northwell Nutrition
  • LABS:
    • Glucose control
      • Check preop HgbA1C in diabetic patients
      • If HgBA1C >8 –> defer elective surgery or require endocrine optimization
    • Nutrition assessment: check albumin; assess for malnutrition low albumin
    • Assess Hct: if < 33 consider hematology consultation
  • OTHERS
    • Pain management consultation pre-op if chronic use of narcotics; arrange appropriate pre-opioid weaning if necessary
    • Consider allergy testing for PCN allergic patients if concern for anaphylaxis; test dose of cefazolin by anesthesia if patient states penicillin allergic
  • Arrange home and social support: Identify a home coach

Preop hydration:

  • No solid food on day of surgery
  • Clear liquids permitted until 3 hours before surgery
    • Nondiabetic: Carbohydrate loaded drink (Gatorade/Powerade) on way to hospital
    • Diabetic: 20 ounces of water 3-4 hours before surgery
  • NPO 3 hours prior to surgery
  • If in preop area >3 hours until surgery start time, can give Ensure Clear (8 ounces) in preop area (only if cleared by attending surgeon)
  • *If patient drinks anything other than clear liquids in the 8 hours prior to surgery, or drink clear liquids after 2 hours before surgery start time (other than a small sip with meds) the procedure will be postponed or cancelled

Preop medication (in holding):

  • Acetaminophen 1000mg PO (unless h/o liver disease or abnormal LFTs)
  • Aprepitant (Emend) 40mg PO
  • Gabapentin 300mg PO (hold if >70 y/o)
  • Celecoxib 200mg PO (optional)
  • *Patients on narcotics and gabapentin should take their home dose in AM of surgery

Intraoperative:

  • Dexamethasone 4-10mg IV pre-incision
  • Local Analgesia:
    • Lidocaine 1% before incision
    • Liposomal bupivacaine (Exparel) 20mg mixed with 20cc of 0.25% Marcaine (10cc of Marcaine if small incision) for local field block
    • Option for TLIP block by anesthesia instead of local field block
  • Fluid management
    • Maintain euvolemia throughout perioperative period
    • Prefer LR at 1-3 mL/Kg or another crystalloid
    • Replace fluid deficit (NPO, blood loss, urine, insensible) at discretion of anesthesiologist
  • Opioids:
    • Goal: minimize opiod use intraoperatively
    • Use of remifentanil with discretion by the anesthesiologist due to possible association with postop hyperalgesia
    • Titrate long acting opioids near end of case

Post-operative:

  • Medications: (if patient admitted)
    • Acetaminophen 1000mg q8h PO standing (IV if cannot take PO)
    • Methocarbamol (Robaxin) 500mg q8h standing
    • Pregabalin (Lyrica) 50mg TID po standing (hold if > 70 yrs old)
    • Oxycodone 5mg po PRN for severe pain (PAS of 7-10)
    • Ondansetron (Zofran) 4mg sublingual q6h standing
    • Metoclopramide (Reglan) 10mg IV or po q8h PRN nausea/vomiting (second line)
    • *Dexamethasone (Decadron) 4mg q6h IV x 6 doses standing (hold if diabetic) (optional)
  • Physical therapy/Occupational therapy
    • Start PT in PACU if appropriate
      • Elevate HOB 10 degrees q10 min as tolerated x 3 (up to 30 degrees)
      • Dangle with assistance from RN
      • If lightheaded, increase IVF before PT
      • Out of bed and ambulating within 4 hours of arrival to PACU
    • Start PT and OT on POD #1
  • Early nutrition
    • Clear liquids PACU tray (encourage liquids, withhold if nauseated, bloated, or somnolent)
      • 1 Ensure clear or Enlive
      • 1 lemon ice
      • 2 cups of hot water to make tea or broth
      • Caffeinated coffee (if requested)
    • Regular diet ordered (unless airway concerns)
  • Early removal of catheters / drains
    • Remove Foley catheter on AM of POD #1 for inpatients
    • Avoid Foley catheter use in OR for short procedures (or remove at end of case)

Discharge Medications

  • Acetaminophen (Tylenol) 500mg PO standing q8h x 1 week
  • Oxycodone/acetaminophen (Percocet) 5/325mg PO q6h PRN for severe pain
  • Methocarbamol (Robaxin) 500mg po q8h PRN muscle spasm
  • Pregabalin (Lyrica) 50mg TID x 1 month
  • *Gabapentin 300mg BID if unable to get pregabalin

REFERENCE:

  • Department of Neurosurgery, LHH

VISTA-ICH

Study published in Journal of Stroke and Cerebrovascular Diseases published Nov 2020 looking at the link between blood pressure and outcome in ICH patients using the data from the VISTA trials (Virtual International Stroke Trials Archive)

Retrospective analysis of VISTA-ICH trial. n=384. Results below.

 Odds of unfavorable outcome for blood pressure categories. Left: unadjusted ORs. Right: adjusted ORs.

Study concluded that elevated BP after ICH is associated with poor outcome and supports the practice of targeting SBP of 140 mm Hg.

Limitations of the study:

  1. observational nature
  2. small sample size
  3. study population skewed towards less disease severity

Note that ENLS (published 2017) changed guidelines:

…it may be reasonable to target a systolic blood pressure between 140 and 180 mmHg with the specific threshold determined based on patient comorbidities and level of chronic hypertension.

While AHA/ASA (published 2015) guidelines originally stated that: (prior to recent ICH trials being published)

For ICH patients presenting with SBP between 150 and 220 mmHg and without contraindication to acute BP treatment, acute lowering of SBP to 140 mmHg is safe (Class I; Level of Evidence A) and can be effective for improving functional outcome

References:

Claude Hemphill, J., & Lam, A. (2017). Emergency Neurological Life Support: Intracerebral Hemorrhage. Neurocritical Care27(S1), 89-101. doi: 10.1007/s12028-017-0453-0

Francoeur, C., & Mayer, S. (2020). Acute Blood Pressure and Outcome After Intracerebral Hemorrhage: The VISTA-ICH Cohort. Journal Of Stroke And Cerebrovascular Diseases30(1), 105456. doi: 10.1016/j.jstrokecerebrovasdis.2020.105456

Hemphill, J., Greenberg, S., Anderson, C., Becker, K., Bendok, B., & Cushman, M. et al. (2015). Guidelines for the Management of Spontaneous Intracerebral Hemorrhage. Stroke46(7), 2032-2060. doi: 10.1161/str.0000000000000069

COVID-19 Infectivity and Quarantine Recommendations

  1. most contagious –> right before and immediately following symptom onset
  2. Contagiousness rapidly decreases to near-zero after
    1. ~10 days from symptom onset (mild-moderately ill)
    2. 15 days (critically ill / immunocompromised)
    3. **longest duration of viral viability reported is 20 days
  3. Persistently positive SARS-CoV-2 RNA PCRs in recovered patients common
    1. associated with high Ct values = low viral loads
    2. do not indicate replication-competent virus
    3. not associated with contagiousness
  4. patients who have recovered but with alternating (+) and (-) PCR assays ==> reflect sampling variability and low levels of viral debris at the borderline of detection –> unlikely contagious
  5. Infection confers at least short-term immunity; duration of immunity unclear, cases of re-infection have now been confirmed

WHO and CDC Guidance for Discontinuing Isolation in Patients with Confirmed Covid-19 Infection and Approach to Persistent or Recurrent
Positive PCR Tests

Table enlarged below…

Note: WHO also allows for a test-based strategy to discontinue isolation based on clinical recovery and 2 sequential negative PCR tests >24 h apart.

CDC no longer recommends a test-based strategy, except to discontinue isolation earlier than outlined by the time-based strategy, or possibly in persons who are severely immunocompromised (in consultation with infectious disease experts).

CDC definitions (severity of illness criteria adapted from the NIH COVID-19 Treatment Guidelines)

Mild Illness: Individuals who have any of the various signs and symptoms of COVID-19 (eg, fever, cough, sore throat, malaise, headache, muscle pain) without shortness of breath, dyspnea, or abnormal chest imaging.

Moderate Illness: Individuals who have evidence of lower respiratory disease by clinical assessment or imaging, and a saturation of oxygen (SpO2) ≥94% on room air at sea level.

Severe Illness: Individuals who have respiratory frequency > 30 breaths per minute, SpO2 <94% on room air at sea level (or, for patients with chronic hypoxemia, a decrease from baseline of >3%), ratio of arterial partial pressure of oxygen to fraction of inspired oxygen (PaO2/FiO2) <300 mmHg, or lung infiltrates >50%

Critical Illness: Individuals who have respiratory failure, septic shock, and/or multiple organ dysfunction.

Severely Immunocompromised: chemotherapy for cancer, untreated HIV infection with CD4 T lymphocyte count <200, combined primary immunodeficiency disorder, and receipt of prednisone >20mg/day for more than 14 days.

Reference:

Rhee, C., Kanjilal, S., Baker, M., & Klompas, M. (2020). Duration of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infectivity: When Is It Safe to Discontinue Isolation?. Clinical Infectious Diseases. doi: 10.1093/cid/ciaa1249

IV Diclofenac Sodium for Central Fever

Dose:

  • initial bolus: 0.2 mg/kg in 100 ml of saline solution over 30 minutes
  • continuous infusion:
    • 75 mg in 50 ml NS
    • dosage 0.004–0.08mg/kg/hour titrated to body temperature
    • discontinued if temperature <37.5°C for more than 12 hours on a dose of 0.004 mg/kg/hour
  • Monitor BP, CBC, liver and kidney function
  • continuous monitoring of temperature with esophageal probe

Side effects: hypotension, reduced MAP. oliguria, reduced HR, CPP, PBtO2

Table. Studies on use of diclofenac in the ICU

Diclofenac sodium low dose IV infusion is not commonly used in the ICU for the treatment of central fever. Needs further studies and clinical experience. This method / dosing schedule is lifted from a case report on the successful treatment of central fever in a stroke patient. (reference below)

Reference:

Giaccari, L., Pace, M., Passavanti, M., Sansone, P., Esposito, V., Aurilio, C., & Pota, V. (2019). Continuous intravenous low-dose diclofenac sodium to control a central fever after ischemic stroke in the intensive care unit: a case report and review of the literature. Journal Of Medical Case Reports13(1). doi: 10.1186/s13256-019-2281-7

Hemorrhagic Transformation in Stroke – Predictive Scores

Published predictive scores of hemorrhagic transformations

  • HTI: Hemorrhagic Transformation Index Score
  • ASPECTS: Alberta Stroke Program Early CT Score
  • iScore: Ischemic Stroke Predictive Risk Score
  • HAT: hemorrhage after thrombolysis
  • HeRS: Hemorrhage Risk Stratification Score
  • SEDAN: Blood Sugar [glucose] on admission, Early infarct signs and [hyper] Dense cerebral artery sign on admission computed tomography [CT] head scan, Age, and NIHSS
  • SITS- SICH: Safe Implementation of Treatments in Stroke (SITS) Symptomatic Intracerebral Hemorrhage Risk Score
  • GRASPS: Get With The Guidelines–Stroke symptomatic intracerebral hemorrhage risk
  • MSS: Multicenter rt-PA Stroke Survey Group Score
  • SPAN-100: Stroke Prognostication using Age and NIH Stroke Scale

Summary of predictors of hemorrhagic transformation.

Reference:

ANDRADE, J., MOHR, J., LIMA, F., BARROS, L., NEPOMUCENO, C., PORTELA, L., & SILVA, G. (2020). Predictors of hemorrhagic transformation after acute ischemic stroke based on the experts’ opinion. Arquivos De Neuro-Psiquiatria78(7), 390-396. doi: 10.1590/0004-282×20200008

Steroids in Brain Abscess

Journal Article [1]:

  • There is no well-controlled, randomized clinical study evaluating the use of corticosteroids for controlling the cerebral edema surrounding brain abscesses; nevertheless, corticosteroids are recommended perioperatively for reducing intracranial pressure and avoiding acute brain herniation, but only in those patients that demonstrate signs of meningitis or disproportionate cytotoxic edema posing a life-threatening problem. [1]

UpToDate [2]:

  • Glucocorticoids should be used when substantial mass effect can be demonstrated on imaging.
    • Dexamethasone load 10 mg IV then 4 mg q6h
    • discontinue once mass effect and neurologic manifestations improved

CONS of steroids:

  • Reduction in contrast enhancement on CT scan
  • Slowing of capsule formation
  • Increasing the risk of ventricular rupture

Journal Article [3]

  • Steroid administration should be generally avoided unless the patient demonstrates signs of meningitis or disproportionate cytotoxic edema posing a life threatening problem.
  • Corticosteroids decrease enhancement of abscess wall on CT. Therefore reduction of ring enhancement should not be interpreted as resolution of abscess and indication of effectiveness of therapy.
  • Steroids reduce brain edema but diminish the effectiveness of the host defense mechanisms that assist in containment of infection.
  • Steroids inhibit collagen capsule formation and also inhibit migration of leucocytes.
  • They are therefore, avoided in the stages of early and late cerebritis.

Reference:

[1] Miranda, H., Castellar Leones, S., Elzain, M., & Moscote-Salazar, L. (2013). Brain abscess: Current management. Journal Of Neurosciences In Rural Practice04(S 01), S67-S81. doi: 10.4103/0976-3147.116472

[2] UpToDate. (2020). Retrieved 16 October 2020, from https://www.uptodate.com/contents/treatment-and-prognosis-of-bacterial-brain-abscess#H10

Brain-Heart-Lung Connection in SAH

How the brain, heart and lungs are connected in SAH.

Pathophysiology of cardiopulmonary complications in SAH. SAH leads to catecholamine surge, which activates alpha, alpha + beta, and beta receptors. This leads to pulmonary and myocardial dysfunction as well as platelet aggregation. Patients then develop neurogenic pulmonary edema, LV dysfunction and shock.

Reference:

Muehlschlegel, S. (2018). Subarachnoid Hemorrhage. CONTINUUM: Lifelong Learning In Neurology24(6), 1623-1657. doi: 10.1212/con.0000000000000679

Pathophysiology of Delayed Cerebral Ischemia (DCI)

Historically, DCI thought to be caused by cerebral vasospasm. Recent studies now indicates DCI may be caused by several factors, including early brain injury, microthrombosis, cortical spreading depolarizations and related ischemia, in addition to cerebral vasospasm.

Cerebral vasospasm may be an epiphenomenon, and underlying biochemical and biophysical changes that lead to DCI occur as early as SAH onset.

Supporting evidence? Endothelin 1 is strongest vasoconstrictor mediator in SAH. Administration of clazosentan (potent endothelin 1 receptor inhibitor) resulted in less angiographic vasospasm but did not decrease DCI nor lead to improvement in 90-day outcomes.

Reference:

Muehlschlegel, S. (2018). Subarachnoid Hemorrhage. CONTINUUM: Lifelong Learning In Neurology24(6), 1623-1657. doi: 10.1212/con.0000000000000679