Overdose, Nov.2009 by chrstphr

VIEWS: 62 PAGES: 8

									                                                 OVERDOSE / POISONING 1 of 8

TITLE: OVERDOSE / POISONING

 A.   PRESENTATION

      1. HISTORY/POSSIBLE CAUSES
            - Route, type, time, quantity of exposure
            - Accidental, intentional
            - Bystander action prior to arrival
            - Emesis
            - Any antidote given
            - Current medications
            - Allergies
            - Depression or suicidal history
            - Previous overdose/poisonings
            - History of drug/alcohol abuse
            - Dizziness
            - Confusion
            - Drowsiness
            - Blurred vision
            - Unresponsiveness
            - Anxiety
            - Agitation


      2. SIGNS/ SYMPTOMS
            Tricyclic Antidepressants (TCA)

             -   Anticholinergic effects
             -   Altered mental status (agitation, confusion, lethargy)
             -   Resting sinus tachycardia
             -   Dry mucous membranes
             -   Mydriasis
             -   Fever
             -   Cardiac effects
             -   Hypertension (early and transient, should not be treated)
             -   Tachycardia
             -   Orthostasis and hypotension
             -   Arrhythmia/ECG changes
             -   Central nervous system effects
             -   Coma
             -   Seizure
             -   Myoclonic twitches/tremor
             -   Hyperreflexia
             -   Pulmonary effects - Hypoventilation resulting from CNS depression
             -   Gastrointestinal tract effects - Decreased or absent bowel sounds




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         OPIOIDS

         -   Mild-to-moderate heroin overdose and other heroin toxicity manifest
             as analgesia, drowsiness, reduced physical activity, and difficulty in
             mentation.
         -   In massive overdoses, the coma is profound, and the patient is
             unresponsive to external stimuli.
         -   Agitated delirium and convulsions may occur in patients with
             concomitant sympathomimetic overdose, hypoxia, hypoglycemia, and
             CNS injury.
         -   Delirium may also be noted in overdoses with certain narcotics (eg,
             dextromethorphan, meperidine, codeine). Convulsions occur with
             meperidine, fentanyl, pentazocine, or propoxyphene overdoses.
         -   Respiratory
         -   Respiratory depression is also a hallmark of opioid toxicity and is the
             result of CNS depression.
         -   Opioids, including heroin, reduce the brain's responsiveness to
             changes in PCO2. With high doses, they also depress the brain's
             response to hypoxia. This results in severe respiratory depression
             progressing to apnea.
         -   Tachypnea may result from concomitant sympathomimetic
             intoxication, hypoxia, hypoglycemia, CNS injury, and as a result of
             poisoning with other opioids (eg, pentazocine, meperidine).
         -   Tachypnea may also result from noncardiogenic pulmonary edema,
             which is a relatively common complication of heroin overdoses that
             are accompanied by respiratory arrest.
         -   Noncardiogenic pulmonary edema carries a 5-9% risk of mortality and
             has been reported in 50-90% of autopsies performed on patients found
             dead at the scene. The condition is not specific to heroin overdoses and
             may occur with any narcotic, but it occurs most commonly in the
             setting of heroin, methadone, propoxyphene, and codeine overdoses.
         -   While the cause of this complication remains uncertain, hypoxia-
             induced lung damage is likely to play a major role in the development
             of pulmonary edema. Other mechanisms that have been suggested
             include acute anaphylaxis, neurogenic effects, humoral effects,
             immune-complex deposition, and depressed myocardial contractility.
         -   On auscultation, the lungs are initially clear. Tachypnea, tachycardia,
             and development of bilateral rales herald the onset of pulmonary
             edema.
         -   Wheezing due to bronchospasm may be evident. Wheezing may also
             indicate bronchospasm secondary to histamine release.
         -   The presence of localized rales and wheezing should raise suspicion of
             aspiration pneumonia.
         -   Eyes:
         -   The presence of miosis in the setting of overdose is highly suggestive
             of opioid toxicity, including poisoning caused by heroin.



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         -   The absence of miosis does not exclude opioid toxicity because
             mydriasis may develop when severe hypotension, acidosis, and anoxia
             have occurred.
         -   Mydriasis may also be noted in patients with mixed overdoses and in
             patients with overdoses of meperidine, propoxyphene, diphenoxylate
             with atropine, dextromethorphan, and codeine.
         -   Cardiovascular:
         -   Effects of heroin and other opioids on the myocardium are not
             significant but include mild bradycardia and mild hypotension.
         -   Mild peripheral vasodilation occurs with reduced peripheral resistance
             and inhibition of baroreceptor reflexes.
         -   Blood pressure is usually well maintained unless the body is stressed
             by hypoxia, hypovolemia, or acidosis.
         -   Hypotension due to opioid overdose is generally attributable to
             histamine release and is observed in a number of opioids, including
             heroin, morphine, meperidine, and fentanyl.
         -   Hypertension and tachycardia may occur with pentazocine and
             meperidine overdoses and in the setting of hypoxia, acidosis,
             hypoglycemia, and co-ingestions.
         -   Propoxyphene may cause ventricular arrhythmias.
         -   Gastrointestinal:
         -   Heroin and other opioids decrease gastric motility, thereby prolonging
             gastric emptying time by as much as 12 hours.
         -   Heroin can also inhibit acetylcholine's effect on the small intestine and
             diminish the colonic propulsive waves, thereby delaying colonic
             emptying and resulting in constipation.
         -   Skin:
         -   Heroin and other opioids cause vasodilation of the cutaneous blood
             vessels, resulting in flushing.
         -   The vasodilatory effect may be enhanced by histamine release, which
             also results in pruritus.
         -   Examination of the skin may reveal patterns of heroin use such as
             track marks, fresh puncture wounds, and “skin-popping” marks.

         COCAINE

         -   Cardiac and chest pain
         -   Cardiopulmonary complaints are the most common presenting
             manifestations of cocaine abuse. Cardiac complications associated
             with cocaine use include chest pain (frequently observed in long-term
             use or overdose), MI, arrhythmias.
         -   Of individuals with cocaine-associated MI, median times to onset of
             chest pain vary with route of cocaine use. The median time to onset is
             30 minutes for intravenous use, 90 minutes for crack, and 135 minutes
             for intranasal use.




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         -   Chest pain may be observed in as many as 40% of patients presenting
             to the emergency department after admitted cocaine use. In a study of
             urban and suburban emergency departments, cocaine or its metabolites
             were found in 17% of patients presenting with chest pain. This stands
             in stark contrast to the pretest estimate of 2-4% prevalence for the
             suburban study site and the 10% approximation for the urban sites.
             The mean age of patients with chest discomfort and positive assays for
             cocaine was 36 years.
         -   Vascular:
         -   Include cocaine in the differential diagnosis of any acute vascular
             problem.
         -   Vascular spasm may cause blindness, renal infarction, limb ischemia,
             and intestinal ischemia.
         -   Aortic dissection also may be observed.
         -   Hypertension occurs frequently.
         -   Pulmonary edema
         -   Exacerbation of asthma
         -   CNS stimulant effects (eg, neurogenic pulmonary edema, respiratory
             depression in overdose or postictal state, abnormal hypoxic response in
             infants of cocaine-abusing mothers, sudden infant death syndrome
             (SIDS), and pulmonary hypertension)

         CALCIUM CHANNEL BLOCKERS

         -   Focus the physical examination on mental status and cardiovascular
             assessment.
         -   Hypotension
         -   Bradycardia, with variable degrees of heart block
         -   Altered mental status or seizures secondary to hypotension
         -   Types:
         -   Verapamil
         -   Nifedipine (eg, Procardia, Procardia XL, Adalat, Adalat CC) is
             representative of the dihydropyridine class, which produces profound
             hypotension with less heart block.
         -   Diltiazem (Cardizem), the only CCB in the benzothiazepine class,
             produces significant antidromotropic effects.
         -   Patients ingesting diltiazem typically present with heart block and
             lesser degrees of hypotension.
         -   Bepridil (Vascor), used for refractory angina, is a unique calcium
             channel blocker with some sodium channel blocking activity.




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     B.    STABILIZATION

           BLS- General Overdose
                    1. A-B-C’s: Initially open airway using jaw trust maneuver if
                        indicated. Maintain airway as needed, consider OPA, NPA.
                    2. Monitor SaO2
                    3. Administer oxygen:
                              SaO2 <95% administer O2 at 10-15 LPM NRB mask.
                              SaO2 >95% administer O2 at 2-6 LPM by N/C

           ALS- General Overdose
                    1. Control airway as appropriate
                    2. Apply Cardiac monitor
                    3. Perform a 12 Lead EKG
                    4. Evaluate blood glucose level, treat as appropriate (see
                        diabetic protocol)
                    5. Establish IV access X 2 IVs (one large bore with NS at
                        KVO in the AC and an additional reseal is preferred).
                    6. Perform Blood draw, specialized gray top tube.
                    7. Complete a neurological assessment
                    8. Initiate proper treatment according to type of drug ingested
                        (see below)
                    9. Transport to the appropriate facility

     B2.   INGESTION SPECIFIC STABILIZATION
                 TRICYCLIC ANTI-DEPRESSANTS

                     1. Anticipate airway compromise resulting from possible rapid
                        deterioration of neurologic and cardiovascular functions.
                     2. Administer Sodium Bicarbonate IVP in patients presenting
                        with cardiotoxicity: Prophylactic use in a patient displaying
                        no signs of cardiotoxicity is not indicated.
                     3. Adults: Sodium Bicarbonate- Initial bolus: 1-2 mEq/kg IV
                        push over 1-2 min; not to exceed 100 mEq / dose
                        Follow-up infusion: 100-150 mEq in 1 L 0.9% Normal
                        Saline infused at 100-200 mL/h IV (using a dial-a-flow).
                     4. Pediatrics: Sodium Bicarbonate- Prepare infusions as in
                        adults; infuse at 1.5- to 2-times maintenance fluid
                        requirements.
                     5. Treat Seizure activity with Diazepam (Valium) as
                        appropriate.
                     6. Adults: Valium- Adult: 2-10 mg very slowly titrated to
                        patient needs. Valium should not be diluted.
                     7. Pediatrics: 0.2 mg/kg, not to exceed a 2 mg single dose.
                        Valium should not be diluted.
                     8. Treat hypotension as appropriate:



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                  9. Adults: With clear lung fields and signs of hypotension,
                      administer a 500ml Normal Saline fluid bolus and reassess.
                  10. Pediatrics: With clear lung fields and signs of hypotension,
                      administer 10-20ml/kg of Normal Saline and reassess.
                  11. Consider the placement of an appropriately sized NG/OG
                      tube.
                  12. Transport

     C.    TCA- SPECIAL CONSIDERATIONS

                   1. Careful attention to airway, breathing, circulatory, and
                   neurologic parameters are of utmost importance because of the
                   risk of rapid deterioration in patients. Decontamination
                   strategies should be used judiciously in selected patients.

     B3.   INGESTION SPECIFIC STABILIZATION
                OPIODS

                   1. Assess the need for aggressive airway control. Aggressive
                      airway control must take precedence over pharmacologic
                      reversal because the vast majority of morbidity and
                      mortality results from respiratory depression.
                   2. Apply appropriate physical restraint devices to all four
                      extremities.
                   3. Administer Naloxone for significant CNS and/or
                      respiratory depression.
                   4. Adult Naloxone: 0.1-2 mg/dose IV/IM (dose depends on
                      circumstances); may be repeated in 1- to 2-min intervals
                      following IV use and 10-min intervals following IM
                      administration; not to exceed 10 mg cumulative dose; 0.1-
                      to 0.2-mg increments recommended if opioid dependency
                      suspected; may need to repeat doses q20-60min
                      Discontinue treatment as soon as desired degree of opioid
                      reversal achieved.
                      Pediatric Naloxone: 0.01mg/kg IV/IM (2 to 2.5 times the
                      dose ET), may repeat every 2-3 minutes up to 3 doses if
                      needed
                      May need to repeat doses q20-60min; discontinue as soon
                      as desired degree of opioid reversal achieved
                   5. The best way to reverse respiratory depression and coma,
                      while avoiding precipitant withdrawal, is by gradual
                      measured administration of naloxone.
                   6. Consider the placement of an appropriately sized NG/OG
                      tube
                   7. Transport




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                                              OVERDOSE / POISONING 7 of 8



     C.    OPIOID-SPECIAL CONSIDERATIONS

                   1. Opioid toxicity characteristically presents with a depressed
                      level of consciousness. Opiate toxicity should be suspected
                      when the clinical triad of CNS depression, respiratory
                      depression, and pupillary miosis are present.
                   2. Pertinent history may be obtained from bystanders, family,
                      friends, or EMS providers. Pill bottles, drug paraphernalia,
                      or eyewitness accounts may assist in the diagnosis.
                      Occasionally a trial of naloxone by EMS is helpful to
                      establish the diagnosis in the prehospital setting. Ingestion
                      time, quantity, and co-ingestants are important aspects of
                      the history and should be ascertained.
                   3. The clinical half-life of naloxone is roughly 20-60 minutes,
                      with a duration period of 2-3 hours. Some variation exists
                      because of dosage and route.
                   4. In cases where a patient displays hallucinations and is
                      deemed combative as a result of a known heroin overdose,
                      consider sedation with Valium 5-10mg IV/IM.

     B3.   INGESTION SPECIFIC STABILIZATION
                COCAINE

                   1. Assess the need for aggressive airway control.
                   2. Treat hyperthermia as appropriate.
                   3. Treat Convulsions with Valium as appropriate:
                      Aggressively treat recurrent seizures because they may
                      worsen hyperthermia, hypoxia, and acidosis.
                   4. Adults: Valium- Adult: 2-10 mg very slowly titrated to
                      patient needs. Valium should not be diluted.
                      Pediatrics: 0.2 mg/kg, not to exceed a 2 mg single dose.
                      Valium should not be diluted.
                   5. Myocardial ischemia and infarction: The administration of
                      oxygen, nitrates, and aspirin are recommended in all
                      patients with cocaine-induced myocardial ischemia (see
                      chest pain protocol).
                   6. Treat isolated confirmed cocaine-induced hypertension as
                      appropriate: Cocaine-induced hypertension commonly
                      responds to benzodiazepines (must call for an order).
                      Benzodiazepines have been shown to be effective in the
                      treatment of cocaine-induced hypertension, with or without
                      chest pain or tachycardia.
                   7. When benzodiazepines fail to control hypertension cocaine-
                      induced hypertension, contact medical control for an order
                      of SL nitrates.



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                                            OVERDOSE / POISONING 8 of 8

                 8. Supraventricular tachycardias: Consider electrical
                     cardioversion in all unstable patients (see SVT protocol).
                 9. Ventricular tachycardias: Perform defibrillation in all
                     patients with pulseless ventricular tachycardia (see VT
                     protocol).
                 10. Ventricular arrhythmias: When ventricular arrhythmias
                     occur shortly after cocaine use, they are thought to be due
                     to the effects of cocaine on the sodium channels. These
                     arrhythmias may respond to sodium bicarbonate, the
                     general antidote for sodium channel blockers. Sodium
                     bicarbonate may be considered in patients with
                     tachycardias associated with QRS durations greater than
                     100 milliseconds. As in tricyclic antidepressant (TCA)
                     toxicity (see TCA overdose protocol).
                 11. Transport

     C.   COCAINE- SPECIAL CONSIDERATIONS

                 1. Initial assessment: Assessment and stabilization of the
                    airway must be performed early in the course of poisoning,
                    and mechanical ventilation with oxygenation must be
                    provided immediately when the airway is threatened. The
                    infusion of dextrose 50% in water (D50W) and thiamine as
                    part of the advanced cardiac life support (ACLS) protocol
                    also are appropriate first steps of resuscitation if
                    unresponsiveness is the initial mental status presentation.
                 2. Ventricular arrhythmias that occur several hours after
                    cocaine use may be due to myocardial ischemia and,
                    therefore, should be treated accordingly




Nov-09

								
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