Dural sinus thrombosis

Dural sinus thrombosis

568 AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 20, Number 6 • October 2002 10. Spiller HA, Schroeder SL, Ching DS: Hemiparesis and altered ment...

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568

AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 20, Number 6 • October 2002

10. Spiller HA, Schroeder SL, Ching DS: Hemiparesis and altered mental status in a child after glyburide ingestion, J Emerg Meal 1998;16:433-5 11. Montgomery DAD: The insulins. Practitioner 1979;222:34956 12. Silas JH, Grant DS, Maddocks JL: Transient hemiparetic attacks due to unrecognized nocturnal hypoglycemia. Br Med J 1981 ;282:132

DURAL SINUS THROMBOSIS To the Editor:--Headache is a common complaint in the emergency department (ED), It makes up 4% of all ED visits. Most of these patients have a benign headache process, however around 4% have serious or secondary pathology.~ Dural sinus thrombosis (DST) is an uncommon but potentially dangerous cause of headache. We report a case of a 30-year-old woman with systemic lupus erythematosus (SLE) who presented to the ED complaining of headache, nausea, and vomiting. This article reviews the pathophysiology and clinical features of DST and those individuals most at risk. A 30-year-old woman with SLE presented to the ED complaining of headache and vomiting for 2 weeks. This was her third ED visit for similar complaints. Each time, the physical examination was unremarkable. She had a computed tomography (CT) scan without contrast of the head, which was read as normal. The patient's headache was retro-orbital, sharp, and constant. She denied fever, chills, or neurologic symptoms. She had no carbon monoxide exposure, tick bites, head injury, meningitis exposure, oral contraceptive, or tobacco use. Past medical history was significant for SLE with no pertinent family or social history. The patient was afebrile with stable vital signs. Cranial nerves II-XII were grossly intact without any focal deficits. She had papilledema bilaterally but no temporal artery tenderness. The remainder of the examination was unremarkable. A lumbar puncture was performed revealing an opening pressure greater than 20 cm of water. The cerebrospinal fluid, electrolytes, and blood count studies were normal. The /3-HCG was negative. The patient was admitted and underwent a magnetic resonance venogram, which revealed a left transverse sinus thrombosis with no blood flow distal to the lesion. Her hypercoagulable work-up was positive for Lupus anticoagulant and anticardiolipin antibody. The patient was treated with heparin and warfarin. She had an uncomplicated hospital stay and was discharged home on warfarin and enoxaparin. The first diagnosis of DST was made by Ribes in 1825 during a post mortem examination, but until recently, was rarely diagnosed. 2 DST is an uncommon but dangerous cause of headache that can be misdiagnosed as a benign headache process like pseudotumor cerebri or migraine. Because of increased awareness and availability of advanced imaging studies the diagnosis of DST has risen in the last 10 years? DST is attributable to an imbalance of prothrombotic and thrombolytic processes, leading to clot formation within the dural sinuses. DST is found in the superior sagittal sinus 72% of the time, the lateral sinuses 70%, and more than one sinus about one-third of the time. 4 The slow growth of the thrombus and good collateral flow of the venous system allows for some compensation and may account for the insidious onset of headache that is characteristic of DST. Risk factors for DST are systemic inflammatory diseases and any coagulation disorders (activated protein C resistance, factor V Leiden mutation, infection, and malignancy). Oral contraceptive

Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2006-0017535.00/0 doi:10.1053/ajem.2002.35503

use and the puerperium period have been implicated more frequently in the past few years. 5.6 Our patient had SLE, a prothrombotic condition in which the lupus anticoagulant and anticardiolipin antibodies can manifest themselves clinically with recurrent venous or arterial clotting. DST can present with a wide spectrum of signs and symptoms. Headache is the presenting symptom in 70% to 90% of cases and most commonly evolves over a period of days to weeks. 7 It is most frequently associated with nausea, vomiting, and vision changes. Seizures, cranial nerve syndromes, neurologic deficits, and confusion are also common presentations. 2,6,8,9 Headache, nausea, and pyramidal signs can present with a rapid decline of consciousness to eventual coma followed by death, if the deep cerebral veins are involved. The classic triad of DST is headache, papilledema, and high opening cerebrospinal fluid (CSF) pressure. This makes diagnosis difficult to distinguish because more benign entities such as pseudotumor cerebri present in a similar fashion. 2-3.5.6 Treatment of DST is IV heparin, warfarin, or thrombolysis. There are very few randomized controlled studies on the treatment of DST but most investigators favor IV heparin in the acute phase, l° Oral anticoagulation is also administered and the patient can be discharged home on warfarin once therapeutic levels are attained. DST is a rare but potentially lethal cause of headache. Systemic inflammatory disorders and any hypercoagulable state are risk factors associated with DST. Headache, papilledema, and high opening CSF pressures are characteristic of DST. The initial presentation of headache and its work-up, including CT and lumbar puncture (LP), do not differentiate DST from other benign headache processes. Magnetic resonance imaging (MRI) with MRV is considered the gold standard for diagnosing DST, whereas the gold standard of treatment is heparin followed by warfarin. DST must be included in the differential diagnosis of headache when a patient presents to the ED with hypercoagulable risk factors, a negative CT scan, and normal CSF with high opening pressure. MICHAEL S. BEESON, MD

JULIE A. VESCO, DO BETH A. REILLY, MD

KENDALLJ. LITTLE,MD Summa Health System Northeastern Ohio Universities College of Medicine Department of Emergency Medicine Akron, OH

References 1. Ramirez-LassepasM, Espinosa CE, CiceroJJ, et al: Predictors of intracraial pathologic findings in patients who seek emergency care because of headache. Arch Neurol 54:1506, 1997 2. Wasson J, Redenburaugh J: Transverse sinus thrombosis: An unusual cause of headache. Headache 1997;37:457-9 3. Allroggen H, Abbott R: Central venous sinus thrombosis. Postgrad Med J 2000; 76:12-5 4. Bousser M-G, Chiras J, Bodes J, et al: Cerebral venous thrombosis - - A review of 38 cases. Stroke 1985;16:199-213 5. Lefebvre P, Lierneux B, Lenaerts L, et al: Cerebral venous thrombosis and procoagulant factors: A case study. Angiology 1998; 49:563-71 6. Kuehnen J, Schwartz A, Neff W, et al: Cranial nerve syndrome in thrombosis of the transverse/sigmoid sinuses: Brain 1998;121: 381-8 7. Ameri A, Bousser MG: Cerebral venous thrombosis. Neurol Clin 1992;10:87-111 8. Leker R, Steiner h Features of dural sinus thrombosis simulating pseudotumor cerebri. Eur J Neurol 1999;6:601-4 9. Bruijn S, Stam J, Koopman M, et al: Case-control study of risk of cerebral sinus thrombosis in oral contraceptive users who are carriers of hereditary prothrombotic conditions: Br Med J 1998; 316:589-92

• CORRESPONDENCE

10. Cipri S, Gangemi A, Campolo F, et al : High-dose heparin plus warfin administration in non-traumatic dural sinuses thrombosis: J Neurosurg Sci 1998; 42:23-32

THE USE OF PHYSOSTIGMINE IN DIPHENHYDRAMINE OVERDOSE To the Editor:--Diphenhydramine (DPH) is a non-prescription medication used to treat allergy, cold symptoms, and insomnia. Although DPH overdose has been often reported, no study has determined the best treatment. The standard approach to therapy has been supportive care, including observation and benzodiazepines.~ We present a case of DPH overdose and the safe use of physostigmine as both a diagnostic and therapeutic agent. A 31-year-old white man was brought to the ED because of altered mental status after a minor motor vehicle crash. The patient was awake and alert but agitated with incoherent speech. He stared aimlessly when asked questions. No meaningful information was obtainable. He was a healthy-appearing male in no obvious distress. His temperature was 99.0°F, blood pressure 145/80 mmHg, pulse of 140 beats/min, and respiratory rate of 16 breaths/min. His skin was warm and dry, but not flushed. Head was without trauma. Eyes revealed symmetric pupils at 4 mm and reactive bilaterally. Oropharynx revealed very dry mucous membranes. Lungs were clear. Cardiac examination revealed a regular tachycardia at 140 beats/min without murmurs or rubs. The abdomen was soft and nontender. Neurologic examination was normal. Electrocardiogram showed sinus tachycardia at a rate of 138 beats/min, normal intervals, axis and ST segments. Complete blood count, serum electrolytes, anion gap, glucose, renal and liver function tests were normal. Screen for amphetamines, opiates, cocaine, ethanol, THC, acetaminophen, and salicylates was negative. We suspected anticholinergic toxicity and administered 2 mg of physostigmine intravenously. Five minutes after the infusion his mental status improved and he was able to tell us that he took approximately 750mg of diphenhydramine daily for months. His heart rate decreased to 120 beats/min. An additional 1 mg dose of physostigmine was administered 90 minutes after the first because of return of altered mental status. After 6 hours of observation, the patient had normal vital signs, was eating, drinking and voiding and had normal mental status. DPH is well absorbed orally and reaches peak plasma concentrations in 2 to 3 hours with duration of action ranging from 6 to 24 hours. It reversibly binds the H~ histamine receptors in both the central nervous system and the peripheral tissues. Although numerous agents can cause the anticholinergic toxidrome, DPH is a common cause of anticholinergic toxicity. 2,3 Physostigmine is a carbamate that inhibits cholinesterases both centrally and peripherally, allowing acetylcholine to accumulate in the neuronal synapse. The accumulation of acetylcholine antagonizes the anticholinergic effects of the offending substances. Poorly absorbed orally, physostigmine is best administered via the intravenous route. Its onset is rapid, within 2 minutes, but peak effect is not observed until almost an hour and a half. 4 Side effects are usually mild--salivation and lacrimation, relative bradycardia, and anxiety. However, seizures and asthma exacerbations can occur. !

Physostigmine was implicated in causing asystole in 2 cases of tricyclic antidepressant (TCA) overdose. 5 This association has led many practitioners to assume that physostigmine has no role in the treatment of anticholinergic poisoning. The likely explanation of the cases of asystole is that physostigmine augmented vagal tone

Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2006-0018535.00/0 doi:l 0.1053/ajem.2002.34958

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and cardiac conduction defects induced by the sodium channel blocking effects of the T f A s . 6,7 In fact, physostigmine has been shown in several case reports to be safe and effective in anticholinergic poisoning, s-12 The controversy surrounding the use of physostigmine has led to under use of the drug. American poison centers reported in 1997 that only 2% of patients with moderate to severe symptoms received treatment with physostigmine.13 Probably most anticholinergic-poisoned patients are treated with benzodiazepines. Burns and coauthors retrospectively compared the efficacy of physostigmine versus benzodiazepines in 52 consecutive patients diagnosed with anticholinergic poisoning. The results favored the use of physostigmine to control agitation and delirium. =4 Indications for use of physostigmine include the presence of central and peripheral manifestations of anticholinergic toxicity. Generally accepted contraindications to physostigmine use include prolonged PR or QRS intervals and history of exposure to toxins that may cause intraventricular conduction delays (Ia or Ic antidysrhytmics, TCAs). 9 The initial dose of physostigmine for adults is 1 to 2 mg by slow intravenous infusion (over 3 to 5 minutes). Patients should be closely monitored for dysrhythmias and seizures. Physostigmine also has been safely and effectively used in children; the dose is 0.5 mg initially. =5.~6 Administration of physostigmine can be repeated, usually at 10 minute intervals until the signs and symptoms of toxicity resolve. Once the patient is asymptomatic a period of observation and cardiac monitoring is necessary. Six hours is a reasonable observation period. Our use of physostigmine allowed a rapid diagnosis and discharge from the ED after a brief observation period. Management with observation and benzodiazepines would have delayed an accurate diagnosis and likely hospital admission for observation. From our own experience with this case, as well as the other reports on this subject, we encourage use of physostigmine as a safe and reliable treatment for suspected anticholinergic poisoning. R. BRIAN PADILLA, M D

MAgc L. POLLACK,MD, PHD Department of Emergency Medicine York Hospital York, PA

References 1. Delaney KA: Anticholinergics, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen's Emergency Medicine: Concepts and Clinical Practice (ed 5). St. Louis; Mosby, 2002, pp 2081-6 2. Klein-Schwartz W, Oderda OM: Jimson weed intoxication in adolescents and young adults. Am J Dis Child 1984;138:737-9 3. Martin B, Howell PR: Physostigmine: g o i n g . . , going •.. gone? Two cases of central anticholinergic syndrome following anaesthesia and its treatment with physostigmine. Eur J Anaesthesiol 1997;14:467-70 4. Howland MA: Antidotes in Depth: Physostigmine, in Goldfrank LR, Flowerbaum NE, Lewin RS, et al (eds): Goldfrank's Toxicologic Emergencies (ed 6). Stamford, CT, Appleton and Lange, 1998, pp 614-7 5. Pentel P, Peterson CD: Asystole complicating physostigmine treatment of tricyclic antidepressant overdose• Ann Emerg Med 1980;9:588-90 6. Jeevaratnam K, Dasgupta S, Pravin Kumar, et al: Physiological, biochemical, and histological changes due to physostigmine in monkeys. Indian J Physiol Pharmacol 1998;42:25-38 7. Nilsson E, Meretoja OA, Neuvonen P: Hemodynamic responses to physostigmine in patients with drug overdose• Anesth Analg 1983;62:885-8 8. Beaver KM, Gavin TJ: Treatment of acute anticholinergic poisoning with physostigmine. Am J Emerg Med 1998;16:505-7 9. Lazarus P: Therapy of the anticholinergic syndrome in poisonings. Z Gesamte Inn Med 1987;42:187-90 10. Lang K, Sigusch H, Muller S: An anticholinergic syndrome with hallucinatory psychosis after diphenhydramine poisoning• Dtsch Med Wochenschr 1995;120:1695-8