DIAGNOSIS & TREATMENT - PART 10 docx

Amphetamines, Ecstasy, Cocaine■ Essentials of Diagnosis • Sympathomimetic clinical scenario: anxiety, tremulousness, tation, tachycardia, hypertension, diaphoresis, dilated pupils, mus-c

Acute Otitis Media

• Most common organisms in both children and adults include

Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and group A streptococcus

• Complications include mastoiditis, skull base osteomyelitis, moid sinus thromboses, meningitis, brain abscess

sig-■ Differential Diagnosis

• Bullous myringitis (associated with mycoplasmal infection)

• Acute external otitis

• Otalgia referred from other sources (especially pharynx)

Reference

Damoiseaux RA et al: Primary care based randomized, double blind trial ofamoxicillin versus placebo for acute otitis media in children aged under 2years BMJ 2000;320:350 [PMID: 10657332]

21

Endolymphatic Hydrops (Meniere’s Syndrome)

• Benign positioning vertigo

• Posterior fossa tumor

• Low-salt diet and diuretic

• Antihistamines, diazepam, and antiemetics may be given enterally for acute attacks

par-• Aminoglycoside ablation of unilateral vestibular function via dle ear infusion

mid-• Surgical treatment in refractory cases: decompression of lymphatic sac, vestibular nerve section, or labyrinthectomy ifprofound hearing loss present

Benign Positioning Vertigo

■ Essentials of Diagnosis

• Acute onset of vertigo, nausea, tinnitus

• Provoked by changes in head positioning rather than by nance of a particular posture

mainte-• Nystagmus with positive Bárány test (delayed onset of symptoms

by movement of head with habituation and fatigue of symptoms)

Acute Sinusitis

■ Essentials of Diagnosis

• Nasal congestion, purulent discharge, facial pain, and headache;teeth may hurt or feel abnormal in maxillary sinusitis; history ofallergic rhinitis, acute upper respiratory infection, or dental infec-tion often present

• Fever, toxicity; tenderness, erythema, and swelling over affectedsinus; discolored nasal discharge and poor response to deconges-tants alone

• Clouding of sinuses on imaging or by transillumination

• Coronal CT scans have become the diagnostic study of choice

• Pain not prominent in chronic sinusitis—a poorly defined entity

• Typical pathogens include Streptococcus pneumoniae, other tococci, Haemophilus influenzae, Staphylococcus aureus, Mor- axella catarrhalis; aspergillus in HIV patients

strep-• Complications: orbital cellulitis or abscess, meningitis, brainabscess

Allergic Rhinitis (Hay Fever)

■ Essentials of Diagnosis

• Seasonal or perennial occurrence of watery nasal discharge, ing, itching of eyes and nose

sneez-• Pale, boggy mucous membranes with conjunctival injection

• Eosinophilia of nasal secretions and occasionally of blood

• Positive skin tests often present but of little value in most instances

• Oral antihistamines; oral or inhaled decongestants

• Short-course systemic steroids for severe cases

• Nasal corticosteroids and nasal cromolyn sodium often effective

if used correctly

■ Pearl

A Wright’s flambé of secretions is the best way to demonstrate phils: stain the smear, ignite it, decolorize it, and the cells will be seen readily at low power.

eosino-Reference

Corren J: Allergic rhinitis: treating the adult J Allergy Clin Immunol 2000;105(6 Part 2):S610 [PMID: 10856166]

21

■ Essentials of Diagnosis

• Sudden onset of stridor, odynophagia, dysphagia, and drooling

• Muffled voice, toxic-appearing and febrile patient

• Cherry-red, swollen epiglottis on indirect laryngoscopy; pharynxtypically normal or slightly injected

• Should be suspected when odynophagia is out of proportion tooropharyngeal findings

ob-• Parenteral antibiotics active against Haemophilus influenzae and

short burst of systemic corticosteroids

21

External Otitis

■ Essentials of Diagnosis

• Presents with otalgia, often accompanied by pruritus and lent discharge

puru-• Usually caused by gram-negative rods or fungi

• Often a history of water exposure or trauma to the ear canal

• Movement of the auricle elicits pain; erythema and edema of theear canal with a purulent exudate on examination

• When visualized, tympanic membrane is red but moves normallywith pneumatic otoscopy

■ Differential Diagnosis

• Malignant otitis externa (external otitis in an mised or diabetic patient with osteomyelitis of the temporal bone);pseudomonas causative in diabetes

immunocompro-■ Treatment

• Prevent additional moisture and mechanical injury to the ear canal

• Otic drops containing a mixture of an aminoglycoside or lones and a corticosteroid

quino-• Purulent debris filling the canal should be removed; occasionally,

a wick is needed to facilitate entry of the otic drops

Viral Rhinitis (Common Cold)

■ Essentials of Diagnosis

• Headache, nasal congestion, watery rhinorrhea, sneezing, scratchythroat, and malaise

• Due to a variety of viruses, including rhinovirus and adenovirus

• Examination of the nares reveals erythematous mucosa andwatery discharge

• Supportive treatment only

• Phenylephrine nasal sprays (should not be used for more than 5–7 days) and decongestants may be useful

• Secondary bacterial infection suggested by a change of rhea from clear to yellow or green; cultures are useful to guideantimicrobial therapy

Acute Sialadenitis (Parotitis, Submandibular Gland Adenitis)

• Often seen in severe dehydration

• Examination shows erythema and edema over affected gland andpus from affected duct

• Leukocytosis

• Complications: parotid or submandibular space abscess

■ Differential Diagnosis

• Salivary gland tumor

• Facial cellulitis or dental abscess

22 Poisoning

Acetaminophen (Tylenol; Many Others)

■ Essentials of Diagnosis

• Nausea and vomiting after ingestion; may be no signs of toxicityuntil 24–48 hours after ingestion

• Serum acetaminophen levels measured 4 hours after ingestion or

at initial evaluation if longer than 4 hours since ingestion; levelshould be obtained in all drug overdoses

• Hepatic and renal injury not apparent until after 36–72 hours

• Striking elevations in aminotransferases; in some cases, nant hepatic necrosis

fulmi-• Patients may not realize that combination analgesics (eg, Tylenol

No 3, Vicodin, Darvocet) contain acetaminophen

• Gastric lavage if less than 1 hour since ingestion

• Acetylcysteine (140 mg/ kg orally, followed by 70 mg/ kg every

4 hours) if serum level is higher than toxic line on standard gram

nomo-■ Pearl

A serum acetaminophen should be obtained in all overdoses: once hepatotoxicity ensues, therapy is valueless, and the depressed suicidal patient tends to ingest multiple drugs.

Reference

Salgia AD et al: When acetaminophen use becomes toxic Treating acute dental and intentional overdose Postgrad Med 1999;105:81 [PMID:102123088]

acci-481

Copyright 2002 The McGraw-Hill Companies, Inc Click Here for Terms of Use

Amphetamines, Ecstasy, Cocaine

■ Essentials of Diagnosis

• Sympathomimetic clinical scenario: anxiety, tremulousness, tation, tachycardia, hypertension, diaphoresis, dilated pupils, mus-cular hyperactivity, hyperthermia

agi-• With cocaine in particular, stroke and myocardial infarction fromvasospasm

• Psychosis, seizures

• Metabolic acidosis may occur

• Urine toxicology screen

• Ecstasy (MDMA) associated with serotonin syndrome (see depressants) and malignant hyperthermia

anti-■ Differential Diagnosis

• Anticholinergic poisoning

• Functional psychosis

• Exertional heat stroke

• Other stimulant overdose (eg, ephedrine, phenylpropanolamine)

■ Treatment

• Activated charcoal for oral ingestions

• Gastric lavage if less than 1 hour since ingestion

• Chemistry panel and creatine kinase for metabolic acidosis, renalfailure, and rhabdomyolysis

• For agitation or psychosis: sedation with benzodiazepines(lorazepam or diazepam)

• For hyperthermia: remove clothing, cool mist spray, coolingblanket

• For hypertension: phentolamine, nifedipine, nitroprusside, orlabetalol (not propranolol because it may generate unopposedalpha-adrenergic effects and worsen hypertension)

• For tachyarrhythmias or tachycardia, use esmolol— the shorthalf-life allows rapid dissipation of effect if necessary

Antidepressants: Atypical Agents (Serotonin Syndrome)

■ Essentials of Diagnosis

• Trazodone, bupropion, venlafaxine, and the SSRIs (fluoxetine, traline, paroxetine, fluvoxamine, and citalopram); well-tolerated inpure overdoses, high toxic-to-therapeutic ratios

ser-• History of ingestion paramount

• Serotonin syndrome: changes in cognition or behavior sion, agitation, coma), autonomic dysfunction (hyperthermia, dia-phoresis, tachycardia, hypertension), and neuromuscular activity(myoclonus, hyperreflexia, muscle rigidity, tremor, ataxia)

• Cardiac monitoring and ECG based on specific agent

• Benzodiazepines initially; bupropion, venlafaxine, and SSRIsassociated with seizures

• Serotonin syndrome typically self-limited; stop all offendingagents

• Cyproheptadine (an antiserotonergic agent) in serotonin drome (4–8 mg orally, repeated once in 2 hours if no response)

syn-■ Pearl

Serotonin syndrome is more frequently due to the combination of an SSRI and another serotonergic agent: rave participants increase the risk by taking an SSRI (“preloading”) followed by ecstasy.

Reference

Carbone JR: The neuroleptic malignant and serotonin syndromes Emerg MedClin North Am 2000;18:317 [PMID: 10767887]

22

• Central antimuscarinic effects: agitation, delirium, confusion,hallucinations, slurred speech, ataxia, sedation, coma

• Cardiotoxic effects from voltage-dependent sodium channel bition: PR and QRS interval widening, right axis deviation of terminal 40 ms (terminal R in aVR, S in lead I), depressed con-tractility, heart block, hypotension, ectopy; QT prolongation frompotassium channel antagonism

inhi-• Generalized seizures from GABA-A receptor antagonism

• Toxicity can occur at therapeutic doses in combination with otherdrugs (antihistamines, antipsychotics)

• Gastric lavage if less than 1 hour since ingestion

• Urine screen for other ingestions; qualitative TCA screen

• Electrocardiographic and cardiac monitoring

• Sodium bicarbonate for QRS > 100 ms, refractory hypotension,

or ventricular dysrhythmia (1–2 meq/kg boluses to goal serum

pH 7.50–7.55, then infuse D5W with three ampules sodium bonate at 2–3 mL/kg/h)

bicar-• Benzodiazepines for seizures

nee-22

• Abdominal x-ray may demonstrate metallic ingestion

• Differential may reveal relative eosinophilia; smear may showbasophilic stippling of red cells

• ECG shows prolonged QT interval, especially in chronic toxicity

■ Differential Diagnosis

• Septic shock

• Other heavy metal toxicities, including thallium and mercury

• Other peripheral neuropathies, including Guillain-Barré syndrome

• Addison’s disease

• Hypo- and hyperthyroidism

■ Treatment

• Gastric lavage for acute large ingestion

• Activated charcoal may adsorb other ingested toxins

• Whole-bowel irrigation if radiopaque material visible on inal x-ray

abdom-• Chelation therapy of dimercaprol in acute symptomatic ingestions

• Oral succimer (DMSA) preferred and less toxic agent for stablepatients with suspected chronic toxicity

• Twenty-four-hour urinary arsenic levels

■ Pearl

A gaseous form (arsine) produces acute hemolytic anemia; treatment differs from that of poisoning with inorganic compounds.

Reference

Graeme KA et al: Heavy metal toxicity, Part I: arsenic and mercury

J Emerg Med 1998;16:45 [PMID: 9472760]

22

• Calcium antagonist overdose

• Digitalis or other cardiac glycoside ingestion

• Tricyclic antidepressant toxicity

■ Treatment

• Gastric lavage if less than 1 hour since ingestion

• Activated charcoal

• Electrocardiographic and cardiac monitoring

• For bradycardia and hypotension, if refractory to normal salinebolus, then glucagon bolus (0.05–0.15 mg/ kg) followed by intra-venous infusion (0.075–0.15 mg/ kg/ h)

• If glucagon insufficient or unavailable, then dopamine or nephrine infusion

norepi-• Isoproterenol, magnesium, correction of hypokalemia, sodiumbicarbonate, overdrive pacing, or aortic balloon pump

• Supportive therapy for coma or seizures

Calcium Antagonists (Calcium Channel Blockers)

■ Essentials of Diagnosis

• Bradycardia, hypotension, atrioventricular block

• Cardiac arrest or cardiogenic shock

• Decreased cerebral perfusion leads to confusion or agitation,dizziness, lethargy, seizures

• Electrocardiographic and cardiac monitoring

• Monitor electrolytes for acidosis, hyperkalemia, hypocalcemia

• Supportive therapy for coma, hypotension, and seizures

• To reverse cardiotoxic effects: fluid boluses, then calcium chlorideboluses to obtain ionized calcium of 2–3 meq/ L; if ineffective,then glucagon (0.1 mg/ kg intravenous bolus, then 0.1 mg/ kg/ hinfusion); if refractory, then dopamine or norepinephrine

• To improve rate and contractility, there may be roles for none, atropine, high-dose insulin with dextrose, or aminopyri-dine; rescue methods include slow (50 beats/min) cardiac pacing,aortic balloon pump, hemoperfusion, and bypass

• Specific treatment depends on clinical symptoms

• Remove from exposure

• Maintain airway and assist ventilation; intubation may be essary

nec-• 100% oxygen by nonrebreathing face mask

• Hyperbaric oxygen if response limited or in the setting of loss ofconsciousness, myocardial ischemia, or a pregnant patient

Cardiac Glycosides (Digitalis)

■ Essentials of Diagnosis

• Accidental ingestion, single large ingestion, or chronic use

• Age, coexisting disease, electrolyte disturbance (hypokalemia,hypomagnesemia, hypercalcemia), hypoxia, and other cardiacmedications (including diuretics) increase potential for digitalistoxicity

• Acute overdose: nausea, vomiting, severe hyperkalemia, visual turbances, syncope, confusion, delirium, bradycardia, supraven-tricular or ventricular dysrhythmias, atrioventricular block

dis-• Chronic toxicity: nausea, vomiting, ventricular arrhythmias

• Elevated serum digoxin level in acute overdose; level may benormal with chronic toxicity

■ Differential Diagnosis

• Cardiotoxic plant or animal ingestion: oleander, foxglove, lily ofthe valley, rhododendron, toad venom

• Beta-blocker toxicity

• Calcium blocker toxicity

• Tricyclic antidepressant ingestion

• Clonidine overdose

• Organophosphate insecticide poisoning

■ Treatment

• Activated charcoal

• Gastric lavage if less than 1 hour since ingestion

• Electrocardiographic and cardiac monitoring

• Maintain adequate airway and assist ventilation as necessary

• Correct hypomagnesemia, hypoxia, hypoglycemia, hyperkalemia

or hypokalemia; calcium is contraindicated, as it may generateventricular arrhythmias

• Lidocaine, phenytoin, magnesium for ventricular arrhythmias;avoid quinidine, procainamide, and bretylium

• Atropine, pacemaker for bradycardia or atrioventricular block

• Ventricular arrhythmias, unresponsive bradyarrhythmias, andhyperkalemia with digoxin toxicity are indications for usingdigoxin-specific antibodies (Digibind); base dosing on esti-mated ingestion

cya-• Absorbed rapidly by inhalation, through skin, or nally

gastrointesti-• Symptoms shortly after inhalation or ingestion; some compounds(acetonitrile, a cosmetic nail remover) metabolize to hydrogencyanide, and symptoms may be delayed

• Dose dependent toxicity; headache, breathlessness, anxiousness,nausea to confusion, shock, seizures, death

• Disrupts the ability of tissues to use oxygen; picture mimicshypoxia, including profound lactic acidosis

• High oxygen saturation of venous blood; retinal vessels bright red

• Odor of bitter almonds on patient’s breath or vomitus

■ Differential Diagnosis

• Carbon monoxide poisoning

• Hydrogen sulfide poisoning

• Other sources of acidosis in suspected ingestion: methanol, ene glycol, salicylates, iron, metformin

ethyl-■ Treatment

• Remove patient from the source of exposure, decontaminate skin;100% oxygen by face mask; intensive care

• For ingestion, gastric lavage, activated charcoal

• Inhaled amyl nitrite or intravenous sodium nitrite plus sodiumthiosulfate antidote; nitrites may exacerbate hypotension or causemassive methemoglobinemia

• When the diagnosis is uncertain, significant hypotension traindicates empirical nitrite use; sodium thiosulfate alone (with100% oxygen) may be effective

con-• Also hydroxocobalamin, dicobalt edetate, nol—all given with thiosulfate

• Hepatic failure the most dangerous adverse reaction to chronic use

• Substantial genetic variability in the rate at which people olize INH

metab-■ Differential Diagnosis

• Salicylate, cyanide, carbon monoxide, or anticholinergic overdose

• In the patient with seizures, acidosis, and coma, consider sepsis,diabetic ketoacidosis, head trauma

• Hepatitis due to other cause

• Benzodiazepines as adjunct in seizure control

• Supportive therapy for coma, hypotension

■ Pearl

Ten to 20 percent of patients using INH for chemoprophylaxis will have elevated serum aminotransferases; 1% overall will progress to overt hepatitis; the former have no symptoms, the latter have those of typical hepatitis.

Reference

Romero JA et al: Isoniazid overdose: recognition and management Am FamPhysician 1998;57:749 [PMID: 9490997]

22

• Ataxia, confusion, obtundation, seizures

• Peripheral blood smear may show basophilic stippling and chromic microcytic anemia; renal insufficiency common

hypo-• Bone radiographs in children show lead bands; abdominal graphs show radiopaque material in intestine

radio-• Blood lead > 10 µg/dL toxic, > 70 µg/dL severe

• Elevation of free erythrocyte protoporphyrin in chronic exposure

■ Differential Diagnosis

• Other heavy metal toxicity (arsenic, mercury)

• Tricyclic antidepressant, anticholinergic, ethylene glycol, or bon monoxide exposure

car-• Other sources of encephalopathy: alcohol withdrawal, hypnotic medications, meningitis, encephalitis, hypoglycemia

sedative-• Medical causes of acute abdomen (eg, porphyria, sickle cell crisis)

• For chronic toxicity: depression, iron deficiency anemia, learningdisability

irri-• Chelation therapy based on presentation and blood lead levels

• Investigate the source and test other workers or family memberswho might have been exposed

■ Essentials of Diagnosis

• Classic triad: painless rigidity, tremor, hyperreflexia

• Multiple medications increase the risk of lithium toxicity (ACEinhibitors, benzodiazepines, caffeine, loop diuretics, NSAIDs,tricyclic antidepressants, haloperidol), as do renal failure, volumedepletion, gastroenteritis, and decreased sodium intake

• Worsening hand tremor, vertical or rotatory nystagmus, ataxia,dysarthria, polyuria (nephrogenic diabetes insipidus), delirium,stupor, rigidity, coma, seizures

• Acute ingestions cause more gastrointestinal symptoms (nausea,vomiting, diarrhea, abdominal pain)

• Elevated serum lithium levels (> 1.5 meq/L); acute ingestionslead to higher serum levels than chronic overdose

• U waves, flattened or inverted T waves, ST depression, and cardia may be seen on ECG

brady-■ Differential Diagnosis

• Neurologic disease (cerebrovascular accident, postictal state,meningitis, parkinsonism, tardive dyskinesia)

• Other psychotropic drug intoxication

• Neuroleptic malignant syndrome

• Aggressive normal saline hydration with close management ofvolume and electrolytes

• Airway protection, ventilatory and hemodynamic support asindicated

• Hemodialysis for severely symptomatic patients

Methanol, Ethylene Glycol, & Isopropanol

■ Essentials of Diagnosis

• Methanol is found in solvents, record cleaning solutions, and paintremovers; ethylene glycol in antifreeze; isopropanol (rubbingalcohol) in solvents, paint thinners

• Elevated serum osmolality and osmolar gap occur initially, lowed by development of anion gap metabolic acidosis

fol-• Methanol and ethylene glycol poisoning progress to confusion,convulsions, coma; ethylene glycol may produce tachycardia,hypocalcemia, with tetany, prolonged QT

• Diplopia, blurred vision, visual field constriction, and blindnesswith methanol; oxalate crystalluria and renal failure with ethyleneglycol; hemorrhagic gastritis and ketonemia without glycosuria orhyperglycemia with isopropanol

• Urine may fluoresce under Wood’s lamp in ethylene glycol tions

acti-• Maintain adequate airway and assist ventilation

• Supportive therapy for coma and seizures

• Sodium bicarbonate in presence of metabolic acidosis due tomethanol or ethylene glycol ingestion

• Ethanol infusion to level of 100–150 mg/dL to prevent metabolism

of methanol and ethylene glycol (not necessary for isopropanol);alternatively, fomepizole (4-methylpyrazole) may be used

• Hemodialysis for severe toxicity

abnor-• Methemoglobin cannot bind oxygen

• Dizziness, nausea, headache, dyspnea, anxiety, tachycardia, andweakness at low levels to myocardial ischemia, arrhythmias,decreased mentation, seizures, coma

• Cyanosis unchanged by O2; saturation fixed at 85% even insevere hypoxemia

• Definitive diagnosis is by co-oximetry (may be from a venoussample); routine blood gas analysis may be falsely normal

• Blood may appear chocolate brown (compare with normal blood);urine may also turn brown

inges-• Discontinue offending agent; high flow oxygen

• Intravenous methylene blue for symptomatic patients with highmethemoglobin levels; patients with G6PD deficiency (higherincidence in black males and patients of Mediterranean ancestry)may develop hemolysis in response to methylene blue

• If methylene blue therapy fails or is contraindicated, then change transfusion or hyperbaric oxygen

■ Essentials of Diagnosis

• Euphoria, drowsiness, and constricted pupils in mild intoxication

to somnolence, ataxia, hypotension, bradycardia, respiratory pression, apnea, coma, and death with more severe intoxication

de-• Signs of intravenous drug abuse (needle marks, a tourniquet)

• Some (propoxyphene, tramadol, dextromethorphan, meperidine)may cause seizures

• Noncardiogenic pulmonary edema

• Detectable in urine, though not all opioids produce positive sults on general toxicology screens

re-• Meperidine or dextromethorphan plus monoamine oxidase hibitor may produce serotonin syndrome

• Congestive heart failure

• Infectious or metabolic encephalopathy

• Hypoglycemia, hypoxia, postictal state

■ Treatment

• Naloxone for suspected overdose

• Gastric lavage for very large ingestions presenting within 1 hour

• Activated charcoal for oral ingestion

• Maintain adequate airway and assist ventilation, including tubation

in-• Supportive therapy for coma, hypothermia, and hypotension

• Benzodiazepines for seizures

sys-• Mild acute ingestion: nausea, vomiting, gastritis

• Moderate intoxication: hyperpnea, diaphoresis, tachycardia, nitus, elevated anion gap metabolic acidosis

tin-• Severe intoxication: agitation, confusion, proteinuria, lation, seizures, pulmonary edema, cardiovascular collapse, hyper-thermia, hypoprothrombinemia

hyperventi-• Chronic pediatric ingestion: hyperventilation, volume depletion,acidosis, hypokalemia, metabolic acidosis, respiratory alkalosis;

in adults: hyperventilation, confusion, tremor, paranoia, memorydeficits

■ Differential Diagnosis

• Carbon monoxide poisoning

• Any cause of anion gap metabolic acidosis (eg, methanol or ylene glycol ingestion)

• Maintain adequate airway and assist ventilation

• Supportive therapy for coma, hyperthermia, hypotension, andseizures; correct hypoglycemia and hypokalemia

• Intravenous fluid resuscitation with normal saline; urinary linization with sodium bicarbonate to enhance salicylate excretion

alka-• Hemodialysis for severe metabolic acidosis, markedly alteredmental status, or clinical deterioration despite supportive care

■ Essentials of Diagnosis

• Mild intoxication: nausea, vomiting, tachycardia, tremulousness

• Severe intoxication: tachyarrhythmias (premature atrial and tricular contractions, multifocal atrial tachyarrhythmia, atrial fib-rillation and flutter, runs of ventricular tachycardia), hypokalemia,hyperglycemia, metabolic acidosis, hallucinations, hypotension,seizures

ven-• Chronic intoxication: vomiting, tachycardia, and seizures, but ically no hypokalemia or hyperglycemia

typ-• Elevated serum theophylline concentration

sustained-• Activated charcoal; repeated doses may enhance elimination

• Ranitidine for vomiting

• Oxygen; maintain adequate airway and assist ventilation

• Monitor for arrhythmias; correct hypokalemia

• Treat seizures with benzodiazepines

• Hypotension and tachycardia may respond to beta-blockade(esmolol, labetalol)

• Hemodialysis or hemoperfusion for patients with status cus or markedly elevated serum theophylline levels (> 100mg/mL after acute overdose or > 60 mg/mL with chronic intoxi-cation)

epilepti-■ Pearl

Inappropriate sinus tachycardia in a patient with COPD may be the only clue to the diagnosis: once seizures occur, the prognosis worsens appreciably.

Reference

Vassallo R et al: Theophylline: recent advances in the understanding of its mode

of action and uses in clinical practice Mayo Clinic Proc 1998;73:346 [PMID:9559039]

22