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

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