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.g.clonidine, propranolol)• pheochromocytoma• sympathomimetic drugs (cocaine, amphetamines, phencyclidine)• MAOI in combination with sympathomimetics or tyramine containing foods (cheese, red wine)• treatment: readminister sympathetic blocker if due to withdrawal (e.g.clonidine, propranolol)• avoid use of pure beta-blockers as they inhibit beta mediated vasodilation and leave alpha-adrenergic vasoconstriction unopposed• best agents are nicardipine, verapamil, fenoldopam.Phentolamine and nitroprusside are possible alternativesSTATUS EPILEPTICUS (see Neurology Chapter)❏ a single seizure/series of seizures that lasts > 30 min• generalized: tonic-clonic, tonic, clonic, myoclonic, absence• partial: simple, complex❏ etiology• drugs (anticonvulsant withdrawal, EtOH withdrawal),metabolic disorders, cerebrovascular disorders, infection, idiopathic❏ investigations• CBC, lytes, BUN, Cr, glucose, anticonvulsant levels, tox screen, prolactin (8), CT +/– MRI, EEG❏ treatment• diazepam 5-20 mg IV• Dilantin 15 mg/kg, given over 30 mins• phenobarbital 15 mg/kg IV• if above fail, Lidocaine 1.5 mg/kg IV; Pentothal 3 mg/kg IV OR midazolam and intubate• emergency EEG if no response after 15-20 minutesMCCQE 2002 Review NotesEmergency Medicine – ER31APPROACH TO COMMON ER PRESENTATIONS.CONT.SYNCOPE❏ sudden, transient loss of consciousness and postural tone with spontaneous recovery Etiology❏ usually caused by generalized cerebral hypoperfusion❏ cardiogenic: arrhythmia, outflow obstruction, MI• non-cardiogenic: peripheral vascular (hypovolemia), vaso-vagal, cerebrovascular disorders, seizure disordersHistory❏ gather details from witnesses❏ distinguish between syncope and seizure (see Neurology Chapter)• signs and symptoms of precyncope, syncope and postsyncope• past medical history, drugsPhysical❏ BP and pulses in both arms, posturals❏ cardiovascular exam and neuro examInvestigations❏ ECG❏ CBC, lytes, BUN, creatinine, glucose, ABG’s, Troponin, CKMB, Mg, Ca Disposition❏ cardiogenic syncope: admit to medicine/cardiology❏ non-cardiogenic syncope: discharge with follow-up of Holter or echo study SEXUAL ASSAULT AND DOMESTIC VIOLENCE❏ involve local/regional sexual assault team❏ 1 in 4 women and 1 in 10 men will be sexually assaulted in their lifetime General Management Principles❏ ABC’s❏ ensure patient is not left alone and ongoing emotional support provided❏ set aside adequate time for exam (usually 1 1/2 hours)❏ obtain consent for medical exam and treatment, collection of evidence, disclosure to police (notify police as soon as consent obtained)❏ Sexual Assault Kit (document injuries, collect evidence)❏ samples ––> labeled immediately ––> passed directly to police❏ offer community crisis resources (e.g.shelter, hotline)❏ do not report unless victim requests (legally required if metabolized by Cytochrome P450 ––> saturation of pathway ––> toxic metabolite (NAPQI) scavenged by glutathione (an antioxidant) (in non-overdose situations)• in OD: exhaustion of glutathione stores ––> NAPQI accumulates ––> binds hepatocytes and hepatic necrosis❏ toxic dose of acetaminophen > 150 mg/kg (~7.0 g)❏ increased risk of toxicity if chronic EtOH and/or anti-convulsant drugs❏ clinical: no symptoms• serum acetaminophen level• evidence of liver/renal damage (delayed > 24 hours)• increased AST, INR• decreased glucose, metabolic acidosis, encephalopathy (indicate poor prognosis)❏ management• decontamination• serum acetaminophen level 4 hours post ingestion• measure liver enzymes and INR, PTT• use the Rumack-Matthew Nomogram for acetaminophen hepatotoxicity• N-acetylcysteine (Mucomyst)• substitutes for glutathione as anti-oxidant to prevent liver damage• use according to dosing nomogram• best effect if started within 8 hrs post-ingestion, but therapy should be initiated regardless ASA Overdose❏ acute and chronic (elderly with renal insufficiency)❏ clinical• hyperventilation (central stimulation of respiratory drive)• increased AG metabolic acidosis (increased lactate)• tinnitus, confusion, lethargy• coma, seizures, hyperthermia, non-cardiogenic pulmonary edema, circulatory collapse❏ ABG’s possible: 1.respiratory alkalosis2.metabolic acidosis3.respiratory acidosis❏ management• decontamination• 10:1 charcoal:drug ratio• whole bowel irrigation (useful if enteric-coated ASA)• close observation of serum level, serum pH• alkalinization of urine as in Table 14 to enhance elimination and to protect the brain (want serum pH 7.45-7 [ Pobierz całość w formacie PDF ]
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.g.clonidine, propranolol)• pheochromocytoma• sympathomimetic drugs (cocaine, amphetamines, phencyclidine)• MAOI in combination with sympathomimetics or tyramine containing foods (cheese, red wine)• treatment: readminister sympathetic blocker if due to withdrawal (e.g.clonidine, propranolol)• avoid use of pure beta-blockers as they inhibit beta mediated vasodilation and leave alpha-adrenergic vasoconstriction unopposed• best agents are nicardipine, verapamil, fenoldopam.Phentolamine and nitroprusside are possible alternativesSTATUS EPILEPTICUS (see Neurology Chapter)❏ a single seizure/series of seizures that lasts > 30 min• generalized: tonic-clonic, tonic, clonic, myoclonic, absence• partial: simple, complex❏ etiology• drugs (anticonvulsant withdrawal, EtOH withdrawal),metabolic disorders, cerebrovascular disorders, infection, idiopathic❏ investigations• CBC, lytes, BUN, Cr, glucose, anticonvulsant levels, tox screen, prolactin (8), CT +/– MRI, EEG❏ treatment• diazepam 5-20 mg IV• Dilantin 15 mg/kg, given over 30 mins• phenobarbital 15 mg/kg IV• if above fail, Lidocaine 1.5 mg/kg IV; Pentothal 3 mg/kg IV OR midazolam and intubate• emergency EEG if no response after 15-20 minutesMCCQE 2002 Review NotesEmergency Medicine – ER31APPROACH TO COMMON ER PRESENTATIONS.CONT.SYNCOPE❏ sudden, transient loss of consciousness and postural tone with spontaneous recovery Etiology❏ usually caused by generalized cerebral hypoperfusion❏ cardiogenic: arrhythmia, outflow obstruction, MI• non-cardiogenic: peripheral vascular (hypovolemia), vaso-vagal, cerebrovascular disorders, seizure disordersHistory❏ gather details from witnesses❏ distinguish between syncope and seizure (see Neurology Chapter)• signs and symptoms of precyncope, syncope and postsyncope• past medical history, drugsPhysical❏ BP and pulses in both arms, posturals❏ cardiovascular exam and neuro examInvestigations❏ ECG❏ CBC, lytes, BUN, creatinine, glucose, ABG’s, Troponin, CKMB, Mg, Ca Disposition❏ cardiogenic syncope: admit to medicine/cardiology❏ non-cardiogenic syncope: discharge with follow-up of Holter or echo study SEXUAL ASSAULT AND DOMESTIC VIOLENCE❏ involve local/regional sexual assault team❏ 1 in 4 women and 1 in 10 men will be sexually assaulted in their lifetime General Management Principles❏ ABC’s❏ ensure patient is not left alone and ongoing emotional support provided❏ set aside adequate time for exam (usually 1 1/2 hours)❏ obtain consent for medical exam and treatment, collection of evidence, disclosure to police (notify police as soon as consent obtained)❏ Sexual Assault Kit (document injuries, collect evidence)❏ samples ––> labeled immediately ––> passed directly to police❏ offer community crisis resources (e.g.shelter, hotline)❏ do not report unless victim requests (legally required if metabolized by Cytochrome P450 ––> saturation of pathway ––> toxic metabolite (NAPQI) scavenged by glutathione (an antioxidant) (in non-overdose situations)• in OD: exhaustion of glutathione stores ––> NAPQI accumulates ––> binds hepatocytes and hepatic necrosis❏ toxic dose of acetaminophen > 150 mg/kg (~7.0 g)❏ increased risk of toxicity if chronic EtOH and/or anti-convulsant drugs❏ clinical: no symptoms• serum acetaminophen level• evidence of liver/renal damage (delayed > 24 hours)• increased AST, INR• decreased glucose, metabolic acidosis, encephalopathy (indicate poor prognosis)❏ management• decontamination• serum acetaminophen level 4 hours post ingestion• measure liver enzymes and INR, PTT• use the Rumack-Matthew Nomogram for acetaminophen hepatotoxicity• N-acetylcysteine (Mucomyst)• substitutes for glutathione as anti-oxidant to prevent liver damage• use according to dosing nomogram• best effect if started within 8 hrs post-ingestion, but therapy should be initiated regardless ASA Overdose❏ acute and chronic (elderly with renal insufficiency)❏ clinical• hyperventilation (central stimulation of respiratory drive)• increased AG metabolic acidosis (increased lactate)• tinnitus, confusion, lethargy• coma, seizures, hyperthermia, non-cardiogenic pulmonary edema, circulatory collapse❏ ABG’s possible: 1.respiratory alkalosis2.metabolic acidosis3.respiratory acidosis❏ management• decontamination• 10:1 charcoal:drug ratio• whole bowel irrigation (useful if enteric-coated ASA)• close observation of serum level, serum pH• alkalinization of urine as in Table 14 to enhance elimination and to protect the brain (want serum pH 7.45-7 [ Pobierz całość w formacie PDF ]