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analgesia and sedation
in I.C.U
what is your options ?
Dr. Mohamed El Sayed
Lecturer of Anesthesia and intensive care
ALS provider –ACLS provider –ATLS provider
Sedation
Analgesia
Sedation
Analgesia
Analgeia
• Treating pain in critically ill patients reliable
pain assessment tool adequacy ofpain relief
A horizontal numeric rating scale
• 10 equally-spaced divider markings, numbered
• 1 (no pain) to 10 (maximal pain).
• The patient points to one of the numbered markings to
indicate the severity of pain.
• A score of 3 or less indicates adequate pain control.
Behavioral-pain
scale
• Patient cannot
express himself
Factors reducing analgesic requirements
Opoid analgesia
• Most popular  fentanyl – morphine –
hydromorphine - remifentanyl
• Sedation - euphoria – analgesia – no amnesia
• Morphine  potent +histamine +metabolites
• Fentanyl  600 more potent + no (metabolites-
histamine)
• Hydro-morphine  more potent + no
metabolite + safe in renal
• Remifentanyl
– Ultra-short acting
– Analgesia 8 – 10 min
– No dose adjustment in renal and hepatic
– Used in patients needing frequent evaluation of
brain functions TBI
– Combining remi-fentanil with a longer-acting
opioid. To safe guard against withdrawal .
Adverse effects of opioid
• Respiratory depression  dose dependant
• Hemodynamic adverse effects  rarly needs
treatment
• Decrease intestinal motility
• Nausea and vomiting CTZ ++
Dosing
Non-Opioid Analgesia
Few non-opioid alternatives
Ketorolac
• (NSAID) 350 times more potent thanaspirin
• side effects GIT blrrding + inhibition of platlet
aggregation limited to 5 days
Ibuprofen
• Like ketorolac
• short-term pain control 24–48 h
• No limit time for treatment
Acetaminophen
• short-term treatment of pain and fever in
postoperative patient
• opioid-sparing effect
• no anti-inflammatory activity = major disadvantage
• Daily dose limitation of 4 grams
Oral agents for neuropathic pain
• Non-opioid analgesia  gabapentin, pregabalinand
carbamazepine
Ketamine
• analgesic adjunct in cases where patients fail to
respond to escalating doses of opioids(e.g., in
chronic opioid users).
Sedation
• Exaggerated feelings of fear
• Absence sense of wellbeing
• Agitation  anxiety with increase motor
activity
• Delirium  acute confusional state that may,
or may not, have agitation as a component.
• Sedation-Agitation Scale (SAS) and the
Richmond Agitation-Sedation Scale (RASS)
 assess sedation
Benzodiazepines ( midazolam –lorazepam )
Midazolam
• Once the most popular sedative drugs in the ICU
• drug accumulation + prolonged sedation =
recently  less popular
• Midazolam  rapid onset 1-2 min
• Accumulation in tissues + short duration of action
• Continuous infusion  prolonged sedation 
limit its use to 48 h
• Midazolam  active metabolite kidneys
Lorazepam (Ativan )
• longer-acting drug than midazolam
lasting up to 6 hours after i.v injection
• intermittent IV injections, or by
continuous IV infusion
• dosing has a maximum allowable dose
(2 mg for bolus doses, and 10 mg/hr
for continuous infusions).
• no active metabolites.
• PROPYLENE GLYCOL added to
lorazepam to increase solubility in
plasma .
BZ advantages
• Amnesia  dose related + anti-grade
• Anticonvulsant effect
• Drug of choice in alcohol and opioid withdrawal .
BZ disadvantages
• Prolonged sedation
• Deleriuim  GABA receptors binding
• Withdrawal symptoms  not common in ICU
• PROPYLENE GLYCOL TOXICITY  Toxidrome
– Metabolic (lactic) acidosis,
– Delirium (with hallucination).
– Hypotension.
– (in severe cases) multi-organ failure.
Propofol
• Rapidly-acting general anesthetic
• GABA receptor binding
• Rapid onset and offset
• Infusion only  awakening after 10 -15 min
even with prolonged infusion
• Lipid emulsion = intralipid  1 kcal/ml
• Green urine  harmless phenolic metabolites
Adverse effect
• Respiratory depression = M.V
• Hypotension = carful in hypotensive patient
• Hyper-triglycemia  not harmful
• Anaphylactoid reaction
• Propofol infusion syndrome 
– poorly understood condition
– abrupt onset of bradycardic heart failure, lactic
acidosis, rhabdomyolysis, and acute renal failure
– high-dose Propofol infusions (>4–6 mg/kg/hr for
longer than 24–48 hrs)
– The mortality 30%
Dexmedetomidine
• Selectivealpha-2 adrenergic agonist that has
sedative,amnestic, and mild analgesic effects,
yetdoes not depress ventilation
• Arousal is maintained, despite deeplevels of
sedation. 6 – 10 min.
• Lower prevalence of delirium
• Adverse effect 
– Hypotension or hypotension
– Bradycardia
Haloperidol
• first-generation antipsychotic
• blocking dopa-mine receptor
in CNS.
• IV bolus dose sedation in
10–20 min,
• Lasts 3–4 hours
• No resp. Depression
• no hypotension
• Adverse effects 
– Extra-pyramidal
– Neuroleptic malig. Syndrome
– Prolongation of the QT interval
References
• Barr J, Fraser GL,PuntilloK, etal.Clinical practice
guidelines for the management of
pain, agitation, and delirium in adult
patients in the intensive care unit. Crit
Care Med 2013;41(1):263– 306.
• Critical Care Medicine at a Glance, Third Edition.
Richard Leach. © 2014 John Wiley & Sons, Ltd.
Published 2014 by John Wiley & Sons, Ltd.
Sedation and analgesia

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Sedation and analgesia

  • 1. analgesia and sedation in I.C.U what is your options ? Dr. Mohamed El Sayed Lecturer of Anesthesia and intensive care ALS provider –ACLS provider –ATLS provider
  • 3. Analgeia • Treating pain in critically ill patients reliable pain assessment tool adequacy ofpain relief A horizontal numeric rating scale • 10 equally-spaced divider markings, numbered • 1 (no pain) to 10 (maximal pain). • The patient points to one of the numbered markings to indicate the severity of pain. • A score of 3 or less indicates adequate pain control.
  • 6. Opoid analgesia • Most popular  fentanyl – morphine – hydromorphine - remifentanyl • Sedation - euphoria – analgesia – no amnesia • Morphine  potent +histamine +metabolites • Fentanyl  600 more potent + no (metabolites- histamine) • Hydro-morphine  more potent + no metabolite + safe in renal
  • 7. • Remifentanyl – Ultra-short acting – Analgesia 8 – 10 min – No dose adjustment in renal and hepatic – Used in patients needing frequent evaluation of brain functions TBI – Combining remi-fentanil with a longer-acting opioid. To safe guard against withdrawal .
  • 8. Adverse effects of opioid • Respiratory depression  dose dependant • Hemodynamic adverse effects  rarly needs treatment • Decrease intestinal motility • Nausea and vomiting CTZ ++
  • 10. Non-Opioid Analgesia Few non-opioid alternatives Ketorolac • (NSAID) 350 times more potent thanaspirin • side effects GIT blrrding + inhibition of platlet aggregation limited to 5 days Ibuprofen • Like ketorolac • short-term pain control 24–48 h • No limit time for treatment
  • 11. Acetaminophen • short-term treatment of pain and fever in postoperative patient • opioid-sparing effect • no anti-inflammatory activity = major disadvantage • Daily dose limitation of 4 grams Oral agents for neuropathic pain • Non-opioid analgesia  gabapentin, pregabalinand carbamazepine Ketamine • analgesic adjunct in cases where patients fail to respond to escalating doses of opioids(e.g., in chronic opioid users).
  • 12. Sedation • Exaggerated feelings of fear • Absence sense of wellbeing • Agitation  anxiety with increase motor activity • Delirium  acute confusional state that may, or may not, have agitation as a component. • Sedation-Agitation Scale (SAS) and the Richmond Agitation-Sedation Scale (RASS)  assess sedation
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  • 16. Benzodiazepines ( midazolam –lorazepam ) Midazolam • Once the most popular sedative drugs in the ICU • drug accumulation + prolonged sedation = recently  less popular • Midazolam  rapid onset 1-2 min • Accumulation in tissues + short duration of action • Continuous infusion  prolonged sedation  limit its use to 48 h • Midazolam  active metabolite kidneys
  • 17. Lorazepam (Ativan ) • longer-acting drug than midazolam lasting up to 6 hours after i.v injection • intermittent IV injections, or by continuous IV infusion • dosing has a maximum allowable dose (2 mg for bolus doses, and 10 mg/hr for continuous infusions). • no active metabolites. • PROPYLENE GLYCOL added to lorazepam to increase solubility in plasma .
  • 18. BZ advantages • Amnesia  dose related + anti-grade • Anticonvulsant effect • Drug of choice in alcohol and opioid withdrawal . BZ disadvantages • Prolonged sedation • Deleriuim  GABA receptors binding • Withdrawal symptoms  not common in ICU • PROPYLENE GLYCOL TOXICITY  Toxidrome – Metabolic (lactic) acidosis, – Delirium (with hallucination). – Hypotension. – (in severe cases) multi-organ failure.
  • 19. Propofol • Rapidly-acting general anesthetic • GABA receptor binding • Rapid onset and offset • Infusion only  awakening after 10 -15 min even with prolonged infusion • Lipid emulsion = intralipid  1 kcal/ml • Green urine  harmless phenolic metabolites
  • 20. Adverse effect • Respiratory depression = M.V • Hypotension = carful in hypotensive patient • Hyper-triglycemia  not harmful • Anaphylactoid reaction • Propofol infusion syndrome  – poorly understood condition – abrupt onset of bradycardic heart failure, lactic acidosis, rhabdomyolysis, and acute renal failure – high-dose Propofol infusions (>4–6 mg/kg/hr for longer than 24–48 hrs) – The mortality 30%
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  • 22. Dexmedetomidine • Selectivealpha-2 adrenergic agonist that has sedative,amnestic, and mild analgesic effects, yetdoes not depress ventilation • Arousal is maintained, despite deeplevels of sedation. 6 – 10 min. • Lower prevalence of delirium • Adverse effect  – Hypotension or hypotension – Bradycardia
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  • 24. Haloperidol • first-generation antipsychotic • blocking dopa-mine receptor in CNS. • IV bolus dose sedation in 10–20 min, • Lasts 3–4 hours • No resp. Depression • no hypotension • Adverse effects  – Extra-pyramidal – Neuroleptic malig. Syndrome – Prolongation of the QT interval
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  • 28. References • Barr J, Fraser GL,PuntilloK, etal.Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Crit Care Med 2013;41(1):263– 306. • Critical Care Medicine at a Glance, Third Edition. Richard Leach. © 2014 John Wiley & Sons, Ltd. Published 2014 by John Wiley & Sons, Ltd.