PAIN & SEDATION MANAGEMENT IN ICU

DR.S.SREENIVASARAO MD,C.C.P.P.M, ASSIST PROFESSOR, DEPT.OF ANAESTHESIA, S.V.R.R.G.G.H.&S.V.M.C, TIRUPATI

DEFINITION OF PAIN ?

WHAT IS PAIN?
DEFINITION: An unpleasant sensory and emotional experience associated with actual or potential damage or described in terms of such damage -International Association for the Study of Pain, 1979

PAIN IS SUBJECTIVE REACTION TO AN OBJECTIVE STIMULUS WHAT THE PATIENT SAYS HURTS

5TH VITAL SIGN..

PATHWAYS & PATHOPHYSIOLOGY

PATHOPHYSIOLOGY
Pain: Involves four physiological processes: - Transduction - Transmission - Modulation - Perception

PAIN PATHWAYS & PATHOPHYSIOLO

Perception

DESCENDING

Transmission (conduction by nerve fibers) ASCENDING

Modulation(Modification with spinal corel)

Transduction (Generation & electrical impulses) Noxious stimulus Release of inflammatory substances

WHY WE ARE WORRIED ABOUT PAIN.?

30%-70% of patients are bothered by pain during their ICU stay 50% complain of moderate, severe, or excruciating pain Need to determine the etiology of pain, treat it, and eliminate potential barriers to adequate pain control

FACTORS PAIN PERCEPTION

FEAR IN STRANGE SURROUNDINGS INABILITY TO REMEMBER OR UNDERSTAMD THE SITUATION ANXIETY & UNCERTAINITY ABOUT ONESELF,ONES FAMILY AND ABOUT PRESENT & FUTURE BACKGROUND AGGREVATIONSNOICE,ALARMS ONGOING ACTIVITY THROUGH OUT THE NIGHT INABILITY TO COMMUNICATE LACK OF SLEEP FATIGUE AFTER SURGERY BOREDOM & LACK OF DISTRACTION

REASONS FOR PAIN IN ICU

REASONS FOR PAIN IN ICU

PAIN IN ICU..

REASONS FOR PAIN IN ICU

Primary pathology such as burns,traumatic injuries,fractures,wounds(surgical or traumatic) Complications of original condition or new problems such as bowel perforation,ichemic boel,pancreatitis Other symptoms such as abscesses,skin inflammation,wuond infection Support systems & monitoringperipheral,central venous line insertions,catheters,drains,regulalar suctioning,dressing changes,phyaiotharapy Tissue hypoxia as a result of low cardiac output,low o2 saturation,fall in hb result in mi Painfull joints,pressure points,pain on changing,position in bed

WHAT HAPPENS IF YOU ARE NOT TREATED ADEQUATELY.?

WHAT HAPPENS IF YOU ARE NOT TREATED ADEQUATELY.?

MANAGEMENT OF PAIN

Assessment Goal Therapy

HOW TO ASSESS.?

DIFFICULTY IN PAIN ASSESSMENT AND MANAGEMENT IN ICU

Unable to communicate effectively Cognitive impairment Sedation Paralysis Mechanical ventilation

HOW TO ASSESS.?

The behavioral pain assessment scale for patients unable to provide self-report of pain.

Erdek M A , Pronovost P J Int J Qual Health Care 2004;16:59-64

International Society for Quality in Health Care and Oxford University Press 2004; all rights reserved

MODIFIED BEHAVIORAL PAIN SCALE FASCIAL EXPRESSION

Relaxed Partially tightened (brow lowered) Fully tightened (lid closing or tightened, cheek raised) Grimacing (nose wrinkle, upper lip raise) 1 2 3 4

UPPER LIMBS
No movement Partially bent Fully bent(fingers flexed),making a fist Permanent retraction(even after stimulus removed) 0 1 2 3

COMPLIANCE WITH VENTILATOR

Tolerating movement Coughing ,but tolerating vent most of the times Fighting vent,alarms high pressure,but settles down 0 1 2

Unable to controle vent,does not settle down,requires manual ventilation 3 Choose the appropriate score from each of the three categories and add together to get the patients total score; maximum score is 10.

PAIN ASSESSMENT

Unparalyzed patient with altered mental status:

0 1 2 3 4 Painful stimuli necessary to gain No grimacing or guarding with repositioning Grimacing or guarding with Grimacing or guarding with greater than 1 min for the Grimacing or guarding at rest; attention or solicit movement spontaneous movement or vigorous movement slight movement, takes patient to relax not able to relax despite rest

PAIN MAP

VAS7/10 10-6-2012

METHODS OF DRUG ADMINISTRATION

METHODS OF DRUG ADMINISTRATION

Oral Intramuscular Intravenous Per rectal-suppositories Subcutaneous-patches Oral Transmucosal-lolly pops Inhalational Nasal spray Regional blocks Epidural

ROLE OF PCA

ROLE OF PCA

From: Rosenburg, Grande, Bernstein. Pain Management and Regional Anesthesia in Trauma. WB Saunders, 2000

DISPOSABLE PCA PUMPS

HOW TO MANAGE?
ANALGESIA ONLY ? SEDATION ONLY ? SEDOANALGESIA !!!!!!!!

ANALGESIA

PRINCIPLES OF SEDATION AND ANALGESIA Consider individual patient characteristics when selecting analgesic and sedativemedications Correct underlying conditions Considering underlying metabolic/excretion capacities Considering adverse effects of sedatives/ Analgeiscs

PRINCIPLES OF SEDATION AND ANALGESIA

Using an algorithm or guideline to assist the practitioners Tools to assess sedative/pain status Prompting several questions related to patient characteristics When/how to do / what need to do

Exclusion of treatable causes of discomfort Exclusion of warning signs Goal of sedation/ analgesia should be established Priority of pain management is highlighted Re-assessment of sedation/ analgesia Analgesics are not 100% of sedatives, and vice versa

GUIDELINE: BENEFIT!

Evidence-based; "best practice" Standardize care Reduce variability Reduce complications Can decrease costs

PRINCIPLES OF PAIN MANAGEMENT

PRINCIPLES OF PAIN MANAGEMENT

Anticipate pain Recognize pain Ask the patient Look for signs Find the source Quantify pain / Assess the pain Set the goal Treat: Quantify the patients perception of pain Correct the cause where possible Give appropriate analgesics regularly as required Remember, most sedative agents do not provide analgesia ReassessReassessReassess

SIGNS OF PAIN IN ICU Hypertension Tachycardia Lacrimation Sweating Pupillary dilation

ANALGESIA
PHARMACOLOGICAL OPIOIDS NSAIDS LOCAL ANAESTHETICS ALPHA2 AGONISTS NONPHARMACOLOGICAL

NONPHARMACOLOGIC INTERVENTIONS
Proper position of the patient Stabilization of fractures Elimination of irritating stimulation Proper positioning of the ventilator tubing to avoid traction on endotracheal tube

OPIOIDS

OPIOIDS

Activating opioid receptors in the midbrain & turning on the Descending inhibitory system Activating opiod receptors on the second order pain transmission cells to prevent the Ascending transmission of pain signals Activating opioid receptors at the central terminals of C fibers in the spinal cord Activating opioid receptors in the periphary to inhibit the activation of nociceptors & to inhibit cells that may release inflmmatoy mediators

OPIOIDS
BENEFITS Relieve pain or the sensibility to noxious stimuli Sedation trending toward a change in sensorium, especially with more lipid soluble forms including morphine and hydromorphone. RISKS Respiratory depression NO amnesia Pruritus Ileus Urinary retention Histamine release causing venodilation predominantly from morphine Morphine metabolites which accumulate in renal failure can be analgesic and anti-analgesic. Meperidine should be avoided due to neurotoxic metabolites which accumulate, especially in renal failure, but also produces more sensorium changes and less analgesia than other opioids

OPIOID ANALGESICS
CLASSIFICATION AGONIST MORPHINE CODEINE,OXYCODONE DIHYDROCODEINE OXYMORPHONE PETHIDINE,METHADONE HYDROMORPHONE FENTANYL DIAMORPHINE(HEROIN) TRAMADOL TAPENTADOL AGONIST-ANTAGONIST PENTAZOCINE BUTORPHANOL NALBUPHINE DEZOCINE MEPTAZINAL PARTIAL AGONIST BUPRENORPHINE ANTAGONIST NALOXONE NALTREXONE

From: Marino. The ICU Book, 2nd Ed. Lippincott Williams & Wilkins, 1998.

METHODS OF ANALGESIA: PCA

METHODS OF ANALGESIA: EPIDURALS

NSAIDS

NSAIDS
Salicylates-Aspirin p-amino phenol derivatives-Paracetamol Propionic acid derivatives-Ibuprofen Acetic acid derivativesIndomethacin,Diclofenac,Ketorolac Oxicam derivatives-Piroxicam,Meloxicom Fenamic acid derivatives-Mefeamic acid Cox-2 inhibitors-Celecoxib,Valdecoxib Sulphonanilides-Nimmesulide Others-Licofelone

RISK STRATAGY WITH NSAID

IF ORAL NSAIDS ARE TAKEN FOR 2 MONTHS

RISK OF ENDOSCOPIC ULCER IS 1 IN 5 SYMPTAMATIC ULCER IS 1 IN 70 BLEEDING ULCER IS 1 IN 150 DEATH FROM BLEEDING ULCER 1 IN 1300

PARACETAMOL

Central antinociceptive effect & potential mechanisms for this include inhibition of a CNS COX-2 Inhibition of a central cyclooxygenase COX-3 that is selectively susceptible toparacetamol, Modulation of inhibitory descending serotinergic pathways Prevent PG production at the cellular transcriptional level, independent of cyclooxygenase activity
1. Piguet V et al. Eur J Clin Pharmacol 1998;53:321-4. 2. Carlsson KH et al. Pain 1988;32:313-26. 3. Flower RJ et al. Nature 1972;240:410-1. 4. Tjlsen A et al. Eur J Pharmacol 1991;193:193-201. 5. Plissier T et al. JPET 1996;278:8-14.

Activatio n of opioid receptor s

PARACETAMOL METABOLISM

(N-acetylbenzoiminoquinone)

Metabolism of acetaminophen (Ac) to hepatotoxic metabolites. (GSH, glutathione; GS, glutathione moiety; Ac*, reactive intermediate.)

Paracetamol safety benefits

No centrally mediated side-effects1 (e.g. sedation, constipation, nausea, vomiting, respiratory depression) n No effect on platelet aggregation, bleeding, or uric acid excretion2 3 n No gastrointestinal side effects 4 5 n Good renal and hepatic safety n Few contra-indications and drug interactions
n 1. Lechat P et al. Thrapie 1989;44:337-54. 2. Insel PA. Analgesic-antipyretic and antiinflammatory agents and drugs employed in the treatment of gout. In: Goodman & Gilman eds. ,The pharmacological basis of therapeutics. McGraw Hill, 9th edition, 1996:617-57. 3. Singh G. Am J Therapeut 2000;7(2):115-21. 4. Whelton A. Am J Therapeut 2000;7(2):63-74. 5. Whitcomb DC et al. JAMA 1994;272(23):1845-50.

DOSAGE

ADULTS1GM UP TO 4 TIMES DAILY,MINIMUM INERVAL BETWEEN EACH ADMINISTRATION IS 4 HRS (6HRS IN RENAL,HEPATIC IMPAIREMENT) CHILDREN UPTO 33KG15MG/KG 4 TIMES A DAY, INTERVAL IS 6 HRS, MAX DAILY DOSE NOT EXCEEDING 60MG/KG IN NEONATES LESS THAN 10 DAYS 7.5MG/KG,4 TIMES A DAY

LOCAL ANAESTHETICS
ACTIONBLOCK THE Na CHANNELS IMPULSE CONDUCTION ROUTES ORAL,INFILTRATION,SPINAL,EPIDURAL,S C PATCHES,TOPICAL etc

A MAJOR DRAWBACK ANALGESIA TREATMENT IS TACHYPHYLAXIS DRUGSLIGNOCAINE,BUPIVICAINE TOXIC EFFECTS CNS & CVS

SERRATIOPEPTIDASE
Serratiopeptidase or serrapeptase is a protein (proteolytic) enzyme isolated from the non-pathogenic enterobacteria Serratia E15 found in silkworms Swelling caused by inflammation can cause tissue to press against sensitive nerves and cause pain. Serratiopeptidases ability to reduce and drain fluid from the inflamed area can reduce swelling and pain. Serratiopeptidase also reduces pain through its ability to block the release of pain-inducing amines from inflamed tissues. Unlike NSAID pain medications, serratiopeptidase does not cause dangerous internal bleeding nor is it addictive like many pain medications

MISCELLANEOUS

VASODILATORSRAYNAUDS PHENOMENON BUERGERS DISEASE,CRPS etc DRUGS ARE NIFEDIPINE,XANTHINOL NICOTINATE,PENTOXYPHYLLINE

MUSCLE RELAXANTS ACUTE MUSCLE SPASM, FIBROMYALGIA,NOCTURNAL LEG CRAMPS DRUGS ARETIZANIDINE,BACLOFEN,DANTROLENE,DIAZEPAM

SEDATION

NEED FOR SEDATION

ANXIETY PAIN ACUTE CONFUSIONAL STATE MECHANICAL VENTILATION TREATMENT OF DIAGNOSTIC PROCEDURES PSYCHOLOGICAL RESPONSE TO STRESS

GOALS OF SEDATION
PATIENT COMFORT CONTROLE OF PAIN ANXIOLYSIS AND AMNESIA BLUNTING ADVERSE AUTONOMIC AND HEMODYNAMIC RESPONSES FACILITATE NURSING MANAGEMENT FACILITATATE MECHANICAL VENTILATION AVOID SELF EXTUBATION REDUCE OXYGEN CONSUMPTION

IDEAL SEDATION AGENT

LACK OF RESPIRATORY DEPRESSION ANALGESIA RAPID ONSET, TITRABLE, SHORT ELIMINATION HALF-TIME SEDATION WITH EASE OF ORIENTATION & AROUSABILITY ANXIOLYTIC HEMODYNAMIC STABILITY

CHALLENGES OF ICU SEDATION

ASSESSMENT OF SEDATION ALTERED PHARMACOLOGY TOLERANCE DELAYED EMERGENCE WITHDRAWAL DRUG INTERACTION

BEFORE STARTING DRUGS.

When patients exhibit signs of anxiety or agitation, the first priority is to identify and treat any underlying physiological disturbances, such as hypoxemia, hypoglycemia, hypotension, pain, and withdrawal from alcohol and other drugs. Sedation of agitated critically ill patients should be started only after providing adequate analgesia and treating reversible physiological causes. (Grade C)

Assessment Goal Therapy

ASSESSMENT OF SEDATION

AN IDEAL SEDATION SCALE

Good reliability and validity
Determination of the degree of sedation and agitation, Behavioral descriptors,

Applicability
Require minimal training Easy to score For diverse patient population

Guide the titration of therapy to a defined sedation endpoint

SUBJECTIVE METHODS

The Ramsay Scale The Glasgow Coma Scale modified by Cook and Palma, GCSC The Sedation Agitation Scale, SAS The Richmond Agitation and Sedation Scale, RASS The Bloomsbury sedation scale the Adaptation to the Intensive Care Environment (ATICE) scale The Avripas sedation scale the Comfort scale for pediatric patients.

OBJECTIVE METHODS

Pharmacokinetic methods Physiologic parameters lower oesophageal sphincter contractility measurement heart rate variability measurement Neurophysiologic methods Frontalis muscle electromyograms auditory evoked potentials, AEP Electroencephalography, EEG Bispectral Index, BIS Patient State Index, PSI Entropy Narcotrend

The Ramsay Scale Scale

1
2 3 4 5 6

Description
Anxious and agitated or restless, or both
Cooperative, oriented, and tranquil Response to commands only Brisk response to light glabellar tap or loud auditory stimulus Sluggish response to light glabellar tap or loud auditory stimulus No response to light glabellar tap or loud auditory stimulus

THE RIKER SEDATION-AGITATION SCALE

Score Description 7 6 5
Dangerous agitation Very agitated Agitated

Definition
Pulling at endotracheal tube, trying to strike at staff, thrashing side to side Does not calm despite frequent verbal commands, biting ETT Anxious or mildly agitated, attempting to sit

4
3

Calm and cooperative

Sedated

Calm, awakens easily, follows commands

Difficult to arouse, awakens to verbal stimuli, follows simple commands

2
1

Very sedated
Unarousable

Arouse to physical stimuli, but does not communicate spontaneously

Minimal or no response to noxious stimuli

SAS, SEDATION-AGITATION SCALE

Stratification of agitation in more categories than the Ramsay scale

BLOOMSBURY SEDATION SCALE

Clinical Status
agitated and restless

Score
3

awake and uncomfortable

aware but calm roused by voice, remains calm roused by movement or stimuli roused by painful stimuli Unrousable natural sleep

2
1 0 -1 -2 -3 A

Recommendations for dosing sedatives reliability not tested

GCSC, GLASGOW COMA SCALE MODIFIED BY COOK AND PALMA

useful in mechanically ventilated patients

Absence of agitation scoring Unuseful to monitor sedation in agitated patients

ATICE, THE ADAPTATION TO THE INTENSIVE CARE ENVIRONMENT SCALE

AVRIPAS SEDATION SCALE

the predetermined standardized sedation goals based on the patients weaning classification

GOAL
Mechanical ventilation
Pressure support ventilation, CPAP, SIMV
good pt cooperation Ramsay 2, GCSC 13-15, SAS 4, RASS 0

Assisted controlled
Ramsay 3, GCSC 8-12, SAS 3, RASS -1~-3

Pressure controlled
Ramsay 4-5, GCSC 8-12, SAS 2, RASS -4

Agitation and delirium

Ramsay 2-3, SAS 3-4, RASS 0~-2

IICP
Ramsay 5, SAS 1, RASS -5

SEDATION

Causes for Agitation

Sedatives

UNDERSEDATION
Sedatives

Causes for Agitation

Agitation & anxiety Pain and discomfort Catheter displacement Inadequate ventilation Hypertension Tachycardia Arrhythmias Myocardial ischemia Wound disruption Patient injury

OVERSEDATION
Causes for Agitation

Prolonged sedation Delayed emergence Respiratory depression Hypotension Bradycardia Increased protein breakdown Muscle atrophy Venous stasis Pressure injury Loss of patient-staff interaction Increased cost

Sedatives

CHOOSE THE RIGHT DRUG

Benzodiazepines Propofol Brbiturates Ketamine -2 agonists

SEDATION OPTIONS: BENZODIAZEPINES (MIDAZOLAM AND LORAZEPAM)

Pharmacokinetics/dynamics Lorazepam: onset 5 - 10 minutes, half-life 10 hours, glucuronidated Midazolam: onset 1 - 2 minutes, half-life 3 hours, metabolized by cytochrome P450, active metabolite (1-OH) accumulates in renal disease Benefits Anxiolytic Amnestic Sedating

RISKS

Delirium NO analgesia Excessive sedation: especially after long-term sustained use Propylene glycol toxicity (parenteral lorazepam): significance uncertain
Evaluate when a patient has unexplained acidosis Particularly problematic in alcoholics (due to doses used) and renal failure

Respiratory failure (especially with concurrent opiate use) Withdrawal

PROPOFOL

Pharmacology: GABA agonist Pharmacokinetics/dynamics: onset 1 - 2 minutes, terminal half-life 6 hours, duration 10 minutes, hepatic metabolism Benefits Rapid onset and offset and easily titrated Hypnotic and antiemetic Can be used for intractable seizures and elevated intracranial pressure

RISKS

Not reliably amnestic, especially at low doses NO analgesia! Hypotension Hypertriglyceridemia; lipid source (1.1 kcal/ml) Respiratory depression Propofol Infusion Syndrome Cardiac failure, rhabdomyolysis, severe metabolic acidosis, and renal failure Caution should be exercised at doses > 80 mcg/kg/min for more than 48 hours Particularly problematic when used simultaneously in patient receiving catecholamines and/or steroids

Onset Propofol 30-60 sec

Peaks 2-5 min

Duration short

3-5 g/kg/min antiemetic 5-20 g/kg/min anxiolytic 20-50 g/kg/min sedative hypnotic >100 g/kg/min anesthetic

MEDICATIONS FOR SEDATION

Barbiturates Infusion doses are subhypnotic Thiopental: 1-5 mg/min Methohexital: 0.5-2.5 mg/min Prolonged infusion of methohexital is associated with a more rapid recovery than thiopental because the clearance rate of methohexital is 34xs higher, resulting in a shorter elimination half-life

MEDICATIONS FOR SEDATION

Ketamine Low dose infusions (5-25 mcg/kg/min) effective for sedation in the ICU and for local or regional anesthetic procedures Significantly decreases the opioid analgesic requirement when used for ICU sedation Effective for burn care May need to pretreat with a benzodiazepine

TASK FORCE OF THE AMERICAN COLLEGE OF CRITICAL CARE MEDICINE - 1995

Recommendations: Sedation Midazolam and propofol for short term (<24 hours) Lorazepam for long term Analgesia MSO4 for most patients Fentanyl for hemodynamically unstable patients

MEDICATIONS FOR SEDATION: INFUSION

From: Marino. The ICU Book, 2nd Ed. Lippincott Williams & Wilkins, 1998.

SEDOANALGESIA

ALPHA2 AGONISTS

ALPHA 2 RECEPTORS

Alpha 2A adrenoceptor subtypes appears to couple in an inhibitory fashion to the L-type calcium channel in the locus coeruleus In the vasculature, the alpha 2B adrenoceptor subtype couples in an excitatory manner to the same effector mechanism . Activation of the receptors in the brain and spinal cord inhibits neuronal firing, causing hypotension, bradycardia, sedation, and analgesia. anesthesiologic viewpoint, neuronal hyperpolarization is a key element in the mechanism of action of 2adrenoceptor agonists

Presynaptic activation of the 2adrenoceptor inhibits the release of norepinephrine, terminating the propagation of pain signals Postsynaptic activation of 2 adrenoceptors in the central nervous system (CNS) inhibits sympathetic activity and thus can decrease blood pressure and heart rate. Combined, these effects can produce analgesia, sedation, and anxiolysis

NECHANISM OF ACTION

Activation of G1-protein-gated potassium channels results in membrane hyperpolarization, decreasing the firing rate of excitable cells in the CNS. Direct regulation of calcium entry through N-type voltage-gated calcium channels ( independent of cAMP and protein phosphorylation & is mediated by G0 proteins.) results reduction of calcium conductance into cells, thus inhibiting neurotransmitter release These 2 mechanisms represent 2 very different ways of effecting analgesia: ---- in the first, the nerve is prevented from ever firing, and ---- in the second, it cannot propagate its signal to its neighbor.

SUPRASPINAL

Highest densities of 2 receptors has been detected in the locus coeruleus, the predominant noradrenergic nucleus in the brain and an important modulator of vigilance. The hypnotic and sedative effects of 2-adrenoceptor activation have been attributed to this site in the CNS The locus coeruleus is also the site of origin for the descending medullospinal noradrenergic pathway, known to be an important modulator of nociceptive neurotransmission. In this region of the brain, 2-adrenergic and opioidergic systems have common effector mechanisms, indicating that dexmedetomidine has a supraspinal site of action.

SPINAL
It stimulate 2 receptors directly in the spinal cord, thus inhibiting the firing of nociceptive neurons The substantia gelatinosa of the dorsal horn of the spinal cord contains receptors , When stimulated, inhibit the firing of nociceptive neurons stimulated by peripheral A and C fibers And also inhibit the release of the nociceptive neurotransmitter substance P

In the heart, the dominant action of alpha-2 agonists is a decrease in tachycardia (through block of the cardio-accelerator nerve) and bradycardia (through a vagomimetic action). In the peripheral vasculature there is both a vasodilatory action via sympatholysis and vasoconstriction mediated through the receptors in the smooth muscle cells. The mechanism for both the anti-shivering and diuretic actions have yet to be firmly established.

HEMODYNAMIC EFFECTS

Combination of effects mediated by: Reduction of central SNS activity (alpha-2a) Reduction of presynaptic NE release (alpha-2a and c) Stimulation of VSM cells (alpha-2b) Stimulation of endothelium Stimulation of central imidazoline receptors Some vagomimetic activity

EFFECTS OF ALPHA-2 AGONISTS

Endocrine

NE release insulin release cortisol release GH release

Baroreflexes stay intact (reset) Normal response to vasoactive drugs Attenuates stress response

EFFECTS OF ALPHA-2 AGONISTS

No effect on ICP Reduces IOP No effect on relaxants Prolongs local anesthetic action Decreases metabolism Decreases oxygen consumption

SIDE EFFECTS
Sinus pause/arrest Orthostatic hypotension/Rebound hypertension on withdrawal Dry mouth Vasoconstriction

DEXMEDETOMIDINE

An intravenous anesthetic agent

Selective 2 receptor agonist. (2:1 1620:1) Provides -Sedation -Anxiolysis -Analgesia

Mechanism of Action of Dexmedetomidine

NE release decreased

SEDATION, SYMPATHOLYSIS
Binding on alpha2 receptor ANALGESIA

Inhibit Firing rate & Substance P release

107

ANALGESIA

PHARMACOLOGICAL POFILE
Rapid redistribution: 6 min Elimination half-life: 2 h Protein binding: 94% Metabolism: biotransformation in liver to inactive metabolites + excreted in urine No accumulation after infusions 12-24 h Pharmacokinetics similar in young adults + elderly

SPECIAL CONSIDERATIONS
Hypovolemic patients With other vasodilators or negative chronotropic agents dexmedetomidine have an additive effect With renal or hepatic impairment, metabolites may accumulate and dose reductions may be necessary

CONTRAINDICATIONS
In obstetric procedures , cesarean section deliveries, as the safety has not been studied Patients with pre-existent severe bradycardia and related bradydysrhythmias (advanced heart block) Patients with impaired ventricular functions (ejection fraction <30%). Infusion over 24 hours ???

ADMINISTRATION OF DEXMEDITOMIDINE
Loading dose 1g/kg 0.5ml[50g] diluted as10ml 10min. Maintenance 0.3-0.6g/kg/hr 1.5ml[150g] diluted in 500ml NS solution conc-0.3g/ml infusion-16 to32drops/min Recovery 10-12mins after cessation.

SEDOANALGESIA
Opioid + Hypnotic Infusion

Fentanyl + Midazolam or Propofol

Analgesia

Amnesia Anxiolysis Hypnosis

Decision tree for analgesia and sedation in critically ill patients. Possibility of verbal / nonverbal communication with the critically ill patient No yes Yes Pain No Agitation Assessment with sedation scale Painful behavior

Coma

Assessment with VAS / NRS

Exlusion of treatable causes Exclusion of OPIOIDS of discomfort Consider wake up tes treatable causes Aim: VAS < 30 / NRS < 3 Assessment with of agitation Regular assessme Re-assessment sedation scale (at least every 4 ho after 10-15 minutes OPIOIDS, Aim: reduced agitation Adjustment opioids Re-assessment after 10-15 minutes Re-assessment SEDATIVES after 10-15 Adjustment opioids Aim: short wake-up times minutes VAS < 30 / NRS < 3 Re-assessment after 10-15 minutes Re-assessment with VAS / NRS (at least every 4 hours Re-assessment with sedation scale (at least every 4 hours except night or wake-up test every 24 hours)

Assessment with Behavioral GCS&Sedation pain scale scale

Ajustment sedatives (and opioids)

OVERVIEW OF SCCM ALGORITHM

ALGORITHM FOR SEDATION AND ANALGESIA OF M ECHANICALLY VENTILATED PATIENTS
Is the Patient Comfortable & at Goal?
Y es No

Rule out and Correct Reversible Causes

Reassess goal daily, Titrate and taper therapy to maintain goal, Consider daily w ake-up, Taper if > 1 w eek high-dose therapy & monitor f or w ithdraw al Hemodynamically Unstable Fentanyl 25 - 100 mcg IVP Q 5-15 min, or Hydrom orphone 0.25 - 0.75 mg IVP Q 5 - 15 min Hemodynamically stable Morphine 2 - 5 mg IVP Q 5 - 15 min Repeat until pain controlled, then scheduled doses + prn

IVP Doses more of ten than Q 2hr?

Use Non-pharmacologic Treament, Optimize the Environment

Y es

Use Pain Scale to Assess f or Pain

Set Goal f or Analgesia

Consider continuous infusion opiate or sedative

Use Sedation Scale to Assess for Agitation/Anxiety

**

Set Goal f or Sedation

Acute Agitation # Midazolam 2 - 5 mg IVP Q 5 - 15 min until acute event controlled

Lorazepam via infusion? Use a low rate and IVP loadi ng doses

> 3 Days Propof ol?

(except neuro pt.)

Ongoing Sedation # Lorazepam 1 - 4 mg IVP Q 10-20 min until at goal then Q 2 - 6 hr scheduled + prn, or Propofol start 5 mcg/kg/min, titrate Q 5 min until at goal Convert to Lorazepam

Benzodiazepine or Opioid: Taper Inf usion Rate by 10-25% Per Day

Y es

Use Delirium Scale *** to Assess f or Delirium

Set Goal f or Control of Delirium

Haloperidol 2 - 10 mg IVP Q 20 - 30 min, then 25% of loading dose Q 6hr x 2-3 days, then taper

Doses approxim ate for 70kg adult

Jacobi J, Fraser GL, Coursin D, et al. Crit Care Med. 2002;30:119-141.

Guidelines for Sedation and Analgesia During Mechanical Ventilation General Overview, J Trauma. 2007;63:945950. The Journal of TRAUMA Injury, Infection, and Critical Care

SEDOANALGESIA !!!!!!!!!!

PATIENT IN ICU

SEDATION

ANALGESIA

THANK YOU