Cleveland Clinic ERAS Protocol (Pain)

Reference:

Chakravarthy, V., Yokoi, H., Manlapaz, M. and Krishnaney, A. (2019). Enhanced Recovery in Spine Surgery and Perioperative Pain Management. Neurosurgery Clinics of North America, 31(1), pp.81-91.

European Society of Cardiology: recommended treatment strategies for hypertensive emergencies

REFERENCE:

van den Born B-JH, Lip GYH, Brguljan-Hitij J, et al. Esc Council on hypertension position document on the management of hypertensive emergencies. Eur Heart J Cardiovasc Pharmacother 2019;5:37–46.

Checklist: Hypertensive Emergency Work-up

Proposed diagnostic studies in patients with suspected hypertensive emergency

Proposed evaluation in patients with suspected hypertensive emergency

History taking

  • Symptoms (headache, confusion, somnolence, visual disturbance, seizures, focal neurological deficits).
  • Pre-existing hypertension, current treatment, withdrawal, compliance, previous control.
  • Over-the-counter medication use (eg, nonsteroidal anti-inflammatory drugs, sympathomimetics).
  • Recent corticosteroid exposure.
  • Recreational drug use (eg, cocaine).
  • Comorbidities (eg, kidney disease, renal artery stenosis).

Diagnostic examination

  • BP both arms.
  • Radiofemoral delay.
  • Signs of heart failure (gallop rhythm, raised jugular venour pulse, bibasal crepitations, peripheral oedema).
  • Detailed neurological exam.
  • Funduscopy (papilloedema, haemorrhages).
  • ECG (ischaemia, arrhythmias, left ventricular
  • hypertrophy).
  • Urinalysis (proteinuria, haematuria)

Further investigations as indicated

  • Troponin-T, creatine kinase (CK), CK-MB.
  • Peripheral blood smear (for assessment of schistocytes).
  • Chest X-ray (volume overload).
  • Transthoracic echocardiography (cardiac structure and function).
  • CT/MRI-brain (intracerebral haemorrhage).
  • CT-angiography of thorax and abdomen (acute aortic disease).
  • Renal ultrasound (postrenal obstruction, kidney size, asymmetry suggestive of renal artery stenosis).
  • Secondary hypertension workup (renal profile, 24 hours urine metanephrines/catecholamines or spot plasma metanephrines, plasma renin and aldosterone, 24 hours urinary cortisol, thyroid-stimulating hormone)

Reference:

Kelly, D., & Rothwell, P. (2019). Blood pressure and the brain: the neurology of hypertension. Practical Neurology, practneurol-2019-002269. doi: 10.1136/practneurol-2019-002269.

Neurological Basis of Hypertension

Cardiovascular Center (medulla):

  • regulates cardiac output (modified heart rate, stroke volume, vascular tone via sympathetic / parasympathetic stimulation).
  • responds to baroreceptor signals (stretch) and chemoreceptors signals (PO2 / PCO2)

Rostral Ventrolateral Medulla and upper cervical spinal cord region:

  • play a key role in central BP control
  • High cervical SCI associated with very erratic BP
  • Dysregulated neural net rows dynamics in caudal pressors regions implicated in development of HTN

Higher Brain Regions:

  • I.e. cerebral cortex, hypothalamus, Lim nic system
  • Modulates brainstem control centers
  • Based on studies of patients undergoing intraoperative stimulation of insula before temporal lobe tiny for seizure control:
    • Stimulation of L insular cortex – produces bradycardia and depressor responses
    • Stimulation of R insular cortex – produces tachycardia and pressor effects (i.e. R dominance for sympathetic cardiovascular effects)
  • R MCA infarction May disinhibition insular function –> increased sympathetic cardiovascular tone

*NOTE TO SELF: short term rise in BP after stroke – compensatory, no need to treat. Chronic high blood pressure – likely renally mediated, requires treatment. (?)

Reference:

Kelly, D., & Rothwell, P. (2019). Blood pressure and the brain: the neurology of hypertension. Practical Neurology, practneurol-2019-002269. doi: 10.1136/practneurol-2019-002269.

Neurological Basis of Hypertension

Cardiovascular Center (medulla):

  • regulates cardiac output (modified heart rate, stroke volume, vascular tone via sympathetic / parasympathetic stimulation).
  • responds to baroreceptor signals (stretch) and chemoreceptors signals (PO2 / PCO2)

Rostral Ventrolateral Medulla and upper cervical spinal cord region:

  • play a key role in central BP control
  • High cervical SCI associated with very erratic BP
  • Dysregulated neural net rows dynamics in caudal pressors regions implicated in development of HTN

Higher Brain Regions:

  • I.e. cerebral cortex, hypothalamus, Lim nic system
  • Modulates brainstem control centers
  • Based on studies of patients undergoing intraoperative stimulation of insula before temporal lobe tiny for seizure control:
    • Stimulation of L insular cortex – produces bradycardia and depressor responses
    • Stimulation of R insular cortex – produces tachycardia and pressor effects (i.e. R dominance for sympathetic cardiovascular effects)
  • R MCA infarction May disinhibition insular function –> increased sympathetic cardiovascular tone

*NOTE TO SELF: short term rise in BP after stroke – compensatory, no need to treat. Chronic high blood pressure – likely renally mediated, requires treatment. (?)

Reference:

Kelly, D., & Rothwell, P. (2019). Blood pressure and the brain: the neurology of hypertension. Practical Neurology, practneurol-2019-002269. doi: 10.1136/practneurol-2019-002269.

Neurological Basis of Hypertension

Cardiovascular Center (medulla):

  • regulates cardiac output (modified heart rate, stroke volume, vascular tone via sympathetic / parasympathetic stimulation).
  • responds to baroreceptor signals (stretch) and chemoreceptors signals (PO2 / PCO2)

Rostral Ventrolateral Medulla and upper cervical spinal cord region:

  • play a key role in central BP control
  • High cervical SCI associated with very erratic BP
  • Dysregulated neural net rows dynamics in caudal pressors regions implicated in development of HTN

Higher Brain Regions:

  • I.e. cerebral cortex, hypothalamus, Lim nic system
  • Modulates brainstem control centers
  • Based on studies of patients undergoing intraoperative stimulation of insula before temporal lobe tiny for seizure control:
    • Stimulation of L insular cortex – produces bradycardia and depressor responses
    • Stimulation of R insular cortex – produces tachycardia and pressor effects (i.e. R dominance for sympathetic cardiovascular effects)
  • R MCA infarction May disinhibition insular function –> increased sympathetic cardiovascular tone

*NOTE TO SELF: short term rise in BP after stroke – compensatory, no need to treat. Chronic high blood pressure – likely renally mediated, requires treatment. (?)

Reference:

Kelly, D., & Rothwell, P. (2019). Blood pressure and the brain: the neurology of hypertension. Practical Neurology, practneurol-2019-002269. doi: 10.1136/practneurol-2019-002269.

CDAD in Neurocritical Care Unit (Data Collection)

Incidence of CDAD:

  1. general ICU setting – rates between 1 and 13%
  2. in Neurocritical Care Unit = 0.6% [1] or 0.4% [2]

DEFINITION: adult patient developing diarrhea with (+) EIA >48h after admission to neurocritical care unit

DATA COLLECTION:

Clinical Data:

  • Age
  • Gender
  • Admit date to unit
  • Diagnosis on admission
  • APACHE II scores
  • Date of CDAD diagnosis

Method of Diagnosis:

  • Stool cytotoxin assay
  • Stool EIA
  • Histology
  • Endoscopy

DISEASE SEVERITY: (UK Health Protection Agency Definition for diarrhea and disease severity)

  • MILD – normal WBC and ❤ type 5-7 stools per day (Bristol stool chart)
  • MODERATE – raised WBC <15 and loose motions (i.e. 3-5 type 5-7 stools/day)
  • SEVERE – WBC >15, T >38.5, acute rise in plasma creatinine (>50% baseline) and clinical/radiological signs of severe colitis
  • LIFE THREATENING – hypotension, partial / complete ileus or toxic megacolon / CT evidence of severe colitis

 

Risk Factors associated with C. difficile infection:

  • antibiotic use
    • Prophylactic – cephalosporin / etc
    • Treatment – cephalosporin / PCN / MNZ, vancomycin / quinolone / AG / etc
      • Microbiological cultures
      • Other causes of sepsis
  • laxative use
  • nasogastric feeding
  • antisecretory drugs (PPI / antihistamines)
  • steroid use
  • GI stimulants (metoclopramide / erthromycin)

Risk factors associated with ICU-associated CDAD:

  • advanced age > 65y
  • length of hospital stay
  • colonization pressure (duration of time and number of infectious contacts a susceptible patient is exposed to
  • antibiotic use
  • vancomycin resistant enterococci
  • use of medical devices (mech ventilation, urinary catheters, central lines)

Treatment:

  • None
  • MNZ
  • Vancomycin
  • Both

Complications:

  • Nonresponse
  • Toxic megacolon

Outcome:

  • ICU outcome
    • Discharge
    • Mortality
  • Hospital outcome 
    • Discharge
    • Mortality

Reference:

[1] Musa, S., Robertshaw, H., Thomson, S., Cowan, M., & Rahman, T. (2010). Clostridium difficile-Associated Disease Acquired in the Neurocritical Care Unit. Neurocritical Care13(1), 87-92. doi: 10.1007/s12028-010-9374-x

[2] Tripathy, S., Nair, P. and Rothburn, M. (2013). Clostridium difficile Associated Disease in a Neurointensive Care Unit. Frontiers in Neurology, 4.