JUST THE FACTS IN EMERGENCY MEDICINE - PART 8 pot

412 SECTION 16 • HEMATOLOGIC AND ONCOLOGIC EMERGENCIES ANTITHROMBOTIC AGENTS ORAL ANTICOAGULANT • Warfarin inhibits vitamin K–dependent clotting factors (II, VII, IX, X). • Dosing is guided by the international normalized ratio (INR), derived from the prothrombin time (PT); the desired INR is usually between 2.0 and 2.5. Onset of anticoagulation occurs after 3 to 4 days. • Warfarin also affects proteins C and S, and for 24 to 36 h there may be a hypercoagulable effect; this is minimized by a starting dose of 5 mg/day. In situations where immediate anticoagulation is critical, a heparin product should be used until an adequate INR is achieved. Warfarin is contraindi- cated in pregnancy. PARENTERAL ANTICOAGULANTS • Unfractionated heparin forms a complex with antithrombin III (ATIII), which inhibits factors IXa and Xa. • Body weight–based IV dosing is recommended, typically 70 to 80 U/kg IV bolus, followed by IV infusion at 15 to 18 U/kg/h. Therapy is monitored by the activated partial thromboplastin time (aPTT); the therapeutic range is 1.5 to 2.5 times the normal value. • Low-molecular-weight (LMW) heparin fractions (enoxaparin, dalteparin, and ardeparin) are de- rived from unfractionated heparin. These agents are effective when administered SC once to twice daily. LMW heparin is used for both prophylaxis and treatment. • Enoxaparin is FDA-approved for the prophylaxis of deep venous thrombosis (DVT) and for treat- ment of DVT with or without pulmonary embo- lism (PE), non-Q-wave myocardial infarction (MI), and unstable angina. • For DVT, PE, and unstable angina, enoxaparin 1 mg/kg SC bid or dalteparin 100 IU/kg SC bid may be used. • The heparins and danaparoid may be used in preg- nancy. • LMW heparins and danaparoid produce minimal elevation in prothrombin time (PT) or aPTT; labo- ratory monitoring is not routinely necessary ex- cept in renal failure, where anti-Xa activity can be measured. PLATELET ACTIVATION BLOCKER • Aspirin blocks the enzyme cyclooxygenase, which results in inhibition of platelet activation. The in- hibitory effect is irreversible and lasts for the life span of the platelet (10 days). PLATELET AGGREGATION BLOCKERS • Platelet aggregation involves binding of fibrinogen to the platelet glycoprotein IIb-IIIa receptor. • The platelet membrane–altering agents ticlopi- dine and clopidogrel render the receptor ineffec- tive and block aggregation. These agents are gen- erally used in patients who are intolerant of or have failed aspirin therapy. Glycoprotein IIB-IIIa inhibitors (abciximab, eptifibatide, and tirofiban) have been found beneficial in patients with acute MI and unstable angina and those undergoing per- cutaneous angioplasty. FIBRINOLYTIC AGENTS • Fibrinolytics work by activating plasminogen to plasmin, which then dissolves the fibrin in thrombi. Streptokinase (SK) is usually administered as 1.0 to 1.5 million U over 60 min. • Anistreplase (APSAC) is derived from and has an effect similar to that of SK, but it can be admin- istered as a slow bolus (typically 30 mg over 5 min). • Tissue plasminogen activator (tPA), in theory, produces less systemic fibrinolysis and is more ‘‘clot specific.’’ In acute MI, a front-loaded regi- men is commonly used: a 15-mg bolus, then 0.75 mg/kg over 30 min (maximum 50 mg), and then 0.50 mg/kg over 60 min (maximum 35 mg). • Reteplase, a derivative of tPA, is administered as a double bolus (10-U bolus, repeated in 30 min). SK and APSAC are more antigenic than tPA or reteplase and therefore are more likely to produce allergic reactions. • Though administered infrequently, urokinase is used for indwelling catheter–associated throm- bosis. INDICATIONS FOR ANTITHROMBOTIC THERAPY ACUTE MYOCARDIAL INFARCTION • Fibrinolytic therapy should be initiated within 30 min of patient arrival at the emergency depart- ment (ED). In the appropriate clinical setting, cri- teria for fibrinolytic therapy include (1) presenta- tion within 12 h of symptom onset; (2) ST-segment elevation in two or more contiguous leads or new- CHAPTER 136 • EXOGENOUS ANTICOAGULANTS AND ANTIPLATELET AGENTS 413 onset left bundle-branch block; and (3) absence of contraindications (Table 136-1). • Angioplasty is preferred over fibrinolysis in car- diogenic shock. • Rapid initiation of fibrinolytic therapy is more important than the specific agent used. However, tPA is the agent of choice with a history of the following: (1) allergy to SK or APSAC; (2) treat- ment with SK in the previous 6 months or with APSAC in the previous 12 months; (3) streptococ- cal infection in the previous 12 months; or (4) hemodynamic instability. • Aspirin should be administered immediately. Un- fractionated heparin should be administered to patients who have received tPA. DEEP VENOUS THROMBOSIS AND PULMONARY EMBOLISM • Treatment can be initiated with either unfraction- ated or LMW heparin. • Selected patients may benefit from fibrinolytic therapy followed by heparin. ISCHEMIC STROKE • TPA may benefit some stroke patients if given within 3 h of symptom onset, although there is an increased risk of intracranial hemorrhage. • Thrombolytic agents should be withheld from pa- TABLE 136-1 Contraindications to Fibrinolytic Therapy ABSOLUTE Active or recent internal bleeding (Յ14 d) CVA Ͻ2–6 months or hemorrhagic CVA Intracranial or intraspinal surgery or trauma Ͻ2 months Intracranial or intraspinal neoplasm, aneurysm, or arteriovenous malformation Known severe bleeding diathesis On anticoagulants (warfarin, PT Ͼ15 s, heparin, increased aPTT) Uncontrolled hypertension (i.e., blood pressure Ͼ185/100 mmHg) Suspected aortic dissection or pericarditis Pregnancy RELATIVE Active peptide ulcer disease Cardiopulmonary resuscitation Ͼ10 min Hemorrhagic ophthalmic conditions Puncture of noncompressible vessel Ͻ10 d Advanced age Ͼ75 years Significant trauma or major surgery Ͼ2 weeks and Ͻ2 months Advanced kidney or liver disease Concurrent menses is not a contraindication In ischemic CVA, symptoms Ͼ3 h, severe hemispheric stroke, plate- lets Ͻ100/ȐL, and glucoseϽ50 or Ͼ400 mg/dL are additionalcontra- indications. tients with rapidly improving symptoms, pretreat- ment hypertension (Ͼ185/110 mmHg), and signs or history of hemorrhagic stroke. COMPLICATIONS OF ANTITHROMBOTIC THERAPY • Warfarin anticoagulation may be reversed by vita- min K 1 , fresh-frozen plasma (FFP), and coagula- tion factor concentrates. • Warfarin has many potential drug interactions, especially with antibiotics as well as drugs that affect the cytochrome P450 system; the most seri- ous interactions can markedly increase the PT and lead to bleeding complications. Another complica- tion of warfarin is skin necrosis, which primarily affects individuals with protein C deficiency. • Heparin-associated bleeding is first treated by stopping the infusion. In severe cases protamine (1 mg IV per 100 U of heparin in previous 4 h) reverses the effect of heparin. • LMW heparins cause less bleeding than unfrac- tionated heparin. Reversal of LMW heparins by protamine is compound-specific; enoxaparin is only partially reversed. • Heparin-induced thrombocytopenia (HIT) is a potentially deadly complication that affects 3 per- cent of patients on unfractionated heparin and fewer patients on LMW heparins. HIT is anti- body-mediated, causing platelet activation, thrombocytopenia, and thrombosis; onset is usu- ally 5 to 12 days into treatment. Heparin therapy is stopped as soon as HIT is recognized. Platelet counts usually recover in 4 to 6 days. • Aspirin-related life-threatening GI bleeding is un- common. Severe hemorrhage may respond to transfusion of functional platelets to increase the platelet count by 50,000/ȐL (6 U of platelets). • Fibrinolytic therapy–related bleeding can be mini- mized by avoiding administration to patients with absolute contraindications. External bleeding can be controlled by local pressure. Major hemorrhage mandates replacement of coagulation factors (see Chap. 135). Intracranial hemorrhage requires rapid coagulation factor replacement and immedi- ate neurosurgical consultation. B IBLIOGRAPHY Crowther MA, Ginsberg JB, et al: A randomized trial com- paring 5 mg and 10 mg warfarin loading doses. Arch Intern Med 159:48, 1999. 414 SECTION 16 • HEMATOLOGIC AND ONCOLOGIC EMERGENCIES Glover JJ, Morrill GB: Conservative management of overan- ticoagulated patients. Chest 108:987, 1995. Kasner SE, Grotta JC: Emergency identification and treat- ment of acute ischemic stroke. Ann Emerg Med 30:642, 1997. Laposta M, Green D, Van Cott EM, etal:Theclinical use and laboratory monitoring of low-molecular-weight heparin, danaproid, hirudin and related compounds, and argatro- ban. Arch Pathol Lab Med 122:799, 1998. Ryan TJ, Anderson JL, Antman EM, et al: ACC/AHA guidelines for the management of patients with acute myo- cardial infarction: Executive summary, American College of Cardiology. Circulation 94:2341, 1996. The GUSTO investigators: An international randomized trial comparing four thrombolytic strategies for acute myo- cardial infarction. N Engl J Med 329:673, 1993. The PURSUIT trial investigators: Inhibition of platelet gly- coprotein IIb/IIIa with eptifibatide in patients with acute coronary syndrome. N Engl J Med 339:436, 1998. White H: Unmet therapeutic needs in the management of acute ischemia. Am J Cardiol 80:2B, 1997. For further reading in Emergency Medicine: A Com- prehensive Study Guide, 5th ed., see Chap. 216, ‘‘Exogenous Anticoagulants and Antiplatelet Agents,’’ by Stephen D. Emond, John R. Cooke, and J. Stephen Stapczynski. 137 EMERGENCY COMPLICATIONS OF MALIGNANCY John Sverha SPINAL CORD COMPRESSION EPIDEMIOLOGY • Spinal cord compression most often occurs as a complication of multiple myeloma, lymphoma, breast cancer, prostate cancer, and lung cancer. PATHOPHYSIOLOGY • Neurologic symptoms are caused by direct pres- sure on the spinal cord by a primary tumor or by metastases. CLINICAL FEATURES • Back pain is typically progressive over weeks. • Neurologic symptoms include leg weakness or numbness and urinary retention. • Physical examination may reveal vertebral percus- sion tenderness, decreased rectal tone, saddle an- esthesia, and diminished lower extremity reflexes. DIAGNOSIS AND DIFFERENTIAL • All patients with back pain and a history of cancer should receive radiographs. • Patients with signs or symptoms of cord compres- sion require emergency magnetic resonance im- aging scanning or computed tomography (CT) with myelography. EMERGENCY DEPARTMENT CARE AND DISPOSITION • Patients with symptoms of cord compression should receive immediate administration of dexa- methasone 10 to 25 mg intravenously (IV). • Consultation is required to determine need for radiation therapy or surgical decompression. UPPER AIRWAY OBSTRUCTION EPIDEMIOLOGY • Upper airway obstruction is usually a late manifes- tation of a variety of tumors arising in the neck, oropharynx, or superior mediastinum. PATHOPHYSIOLOGY • Acute compromise often occurs when new bleed- ing, secretions, or infection obstructs an existing stricture. CLINICAL FEATURES • A change in voice often occurs in the weeks pre- ceding the obstruction. • The new onset of stridor indicates acute com- promise. CHAPTER 137 • EMERGENCY COMPLICATIONS OF MALIGNANCY 415 DIAGNOSIS AND DIFFERENTIAL • The presence of a foreign body or infection can produce symptoms similar to those of tumor expansion. • Soft tissue views of the neck and fiberoptic laryn- goscopy can be helpful. EMERGENCY DEPARTMENT CARE AND DISPOSITION • The airway should be suctioned and supplemental oxygen administered. Heliox may be used as a temporizing measure. • Patients with impending airway obstruction re- quire immediate intervention to create a secure and patent airway. Ideally, this should be in the operating room after otolaryngology consultation. Otherwise, bedside orotracheal intubation or cri- cothyroidotomy should be performed. MALIGNANT PERICARDIAL EFFUSION EPIDEMIOLOGY • Common causes of malignant pericardial effusion include breast carcinoma, lung carcinoma, and malignant melanoma. Pericardial effusions can also be caused by therapeutic irradiation and some chemotherapeutic agents. PATHOPHYSIOLOGY • The degree of cardiac dysfunction depends on the volume of the effusion and the speed of its accu- mulation. Sudden or large (Ͼ500 mL) effusions compress the right ventricle and reduce cardiac output. CLINICAL FEATURES • Classic features of tamponade include (a) hypo- tension and a narrowed pulse pressure, (b) jugular venous distention, (c) diminished heart sounds, (d) pulsus paradoxus Ͼ10 mmHg, (e) low QRS voltage or electrical alternans on electrocardio- gram (ECG), and (f) cardiomegaly without con- gestive heart failure on chest radiograph. DIAGNOSIS AND DIFFERENTIAL • The diagnosis should be considered in any cancer patient with dyspnea or hypotension. Definitive diagnosis is obtained through echocardiography. EMERGENCY DEPARTMENT CARE AND DISPOSITION • Patients in extremis should have emergency peri- cardiocentesis performed. Other patients with ma- lignant pericardial effusions should have their care plan developed in consultation with an oncologist. SUPERIOR VENA CAVA SYNDROME EPIDEMIOLOGY • Superior vena cava (SVC) syndrome is commonly associated with lung carcinoma, breast carcinoma, or lymphoma. PATHOPHYSIOLOGY • Superior vena cava syndrome may occur through tumor compression or invasion of the SVC. Super- imposed thrombosis within the SVC often occurs as well. CLINICAL FEATURES • The onset is typically insidious, and patients may complain of headache, edema of the face or arms, or a vague sensation of head fullness. With disease progression, an increase in intracranial pressure (ICP) can cause confusion, seizure, or coma. • Physical examination may reveal neck and upper chest vein distention, edema of the face or arms, facial telangiectasia, and sometimes a palpable su- praclavicular mass. Papilledema indicates criti- cally high ICP. DIAGNOSIS AND DIFFERENTIAL • Chest radiograph may reveal mediastinal widen- ing or a lung mass. Definitive diagnosis is through contrast-enhanced chest CT scan or venography. 416 SECTION 16 • HEMATOLOGIC AND ONCOLOGIC EMERGENCIES EMERGENCY DEPARTMENT CARE AND DISPOSITION • Administration of furosemide 40 mg IV and meth- ylprednisolone 120 mg IV may be effective tempo- rizing measures in patients with evidence of ele- vated ICP. • Chemotherapy and radiation therapy should be initiated after the specific tumor type is identified. HYPERCALCEMIA OF MALIGNANCY EPIDEMIOLOGY • Hypercalcemia of malignancy is typically associ- ated with multiple myeloma, lung carcinoma, breast carcinoma, renal cell carcinoma, and lymphoma. PATHOPHYSIOLOGY • Hypercalcemia of malignancy is usually produced by osteolysis caused by bony metastases. Patients without bony metastases can develop hypercalce- mia through the release of tumor-produced hor- mone-like substances. Squamous cell carcinoma of the lung is known to produce a parathyroid- like substance. CLINICAL FEATURES • Symptoms include nausea, constipation, abdomi- nal pain, weakness, confusion, and coma. Hyper- calcemia also causes a diuresis that results in dehy- dration. • The QT interval on the ECG may shorten as the calcium level rises. DIAGNOSIS AND DIFFERENTIAL • Serum calcium determinations should consider the albumin level or preferably measure ionized calcium directly as this best correlates with symp- toms. Patients tolerate greater degrees of hyper- calcemia if it is gradual in onset. EMERGENCY DEPARTMENT CARE AND DISPOSITION • If significant symptoms are present or if calcium levels are Ͼ14 mg/dL, treatment with normal sa- line (NS) infusion (1 to 2 L) and furosemide diure- sis (40 to 80 mg IV) is indicated. Other treatments such as phosphate, mithramycin, and prednisone are slower in onset and should be discussed with an oncologist before being initiated. TUMOR LYSIS SYNDROME EPIDEMIOLOGY • Tumor lysis syndrome is most commonly seen after chemotherapy of hematologic malignancies, especially Burkitt’s lymphoma. PATHOPHYSIOLOGY • Rapid destruction of tumor cells results in hyper- kalemia, hyperuricemia, and hyperphosphatemia. Hypocalcemia develops secondary to hyperphos- phatemia. CLINICAL FEATURES • Tumor lysis syndrome most commonly occurs 1 to 5 days after chemotherapy or radiation therapy. It is more common in patients with underlying renal insufficiency. • Hyperkalemia can cause life-threatening dys- rhythmias. • Hyperuricemia and hyperphosphatemia can cause renal failure. • Hypocalcemia can cause muscle cramps, confu- sion, and seizures. EMERGENCY DEPARTMENT CARE AND DISPOSITION • Vigorous hydration, urinary alkalinization, and al- lopurinol administration can all be used to pro- mote uric acid excretion. • Emergency hemodialysis should be considered in the setting of serum potassium Ͼ6.0 meq/L, uric acid Ͼ10.0 mg/dL, phosphate Ͼ10 mg/dL, creati- nine Ͼ10 mg/dL, or symptomatic hypocalcemia. SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE EPIDEMIOLOGY • Syndrome of inappropriate antidiuretic hormone (SIADH) is commonly associated with small cell lung carcinoma, primary and metastatic brain can- CHAPTER 137 • EMERGENCY COMPLICATIONS OF MALIGNANCY 417 cer, pancreatic adenocarcinoma, and prostate car- cinoma. PATHOPHYSIOLOGY • Antidiuretic hormone is secreted by tumor cells in the absence of an appropriate physiologic stim- ulus. This results in the production of concentrated urine despite euvolemic hyponatremia. CLINICAL FEATURES • The symptoms of SIADH are those of hypona- tremia. Depending on the degree of hypona- tremia, the patient may demonstrate nausea, vom- iting, weakness, confusion, seizures, and coma. DIAGNOSIS AND DIFFERENTIAL • The hallmarks of SIADH are hyponatremia, less than maximally dilute urine, and urine sodium concentration Ͼ30 meq/L in the setting of euvo- lemia. EMERGENCY DEPARTMENT CARE AND DISPOSITION • Mild hyponatremia can be treated with water re- striction. • Patients with serum sodium levels Ͻ115 meq/L and central nervous system (CNS) signs and symp- toms should be treated with hypertonic (3%) sa- line infusion. Care should be taken to correct so- dium levels no faster than 1 meq/L/h to avoid central pontine myelinolysis. HYPERVISCOSITY SYNDROME EPIDEMIOLOGY • Hyperviscosity syndrome is typically associated with Waldenstro ¨ m’s macroglobulinemia (most common cause), multiple myeloma, cryoglobuli- nemia, various leukemias, and polycythemia vera. PATHOPHYSIOLOGY • Severe increases in serum proteins (typically im- munoglobulins), red blood cell concentration, or white blood cell (WBC) concentration can cause a dangerous increase in blood viscosity. • Increased blood viscosity can result in sludging, stasis, and a reduction in microcirculatory blood flow. CLINICAL FEATURES • Early symptoms include fatigue, headache, and somnolence. • As viscosity increases, microthromboses may cause visual disturbances, deafness, seizures, stroke, and coma. Congestive heart failure and myocardial infarction have also been reported. DIAGNOSIS AND DIFFERENTIAL • Physical examination of the ocular fundi may re- veal ‘‘sausage-linked’’ retinal vessels, hemor- rhages, and exudates. • Patients with hyperviscosity due to erythrocytosis typically have a hematocrit Ͼ60 percent. Those with hyperviscosity due to leukocytosis typically have WBC concentrations Ͼ100,000 cells per mi- croliter. • Patients with hyperviscosity due to increased se- rum proteins may show evidence of rouleau for- mation on the peripheral blood smear. Serum or urine protein electrophoresis is diagnostic. EMERGENCY DEPARTMENT CARE AND DISPOSITION • Definitive treatment of symptomatic hyperviscos- ity due to increased serum proteins is emergency plasmapheresis. Temporizing measures include phlebotomy (2 U) and infusion of 1 to2LofNS. • Definitive treatment of symptomatic hyperviscos- ity due to leukocytosis is leukapheresis. Symptom- atic hyperviscosity caused by erythrocytosis is treated by phlebotomy (2 U) and infusion of 1 to 2LofNS. NEUTROPENIA AND INFECTION PATHOPHYSIOLOGY • Many chemotherapeutic agents cause myelosup- pression and result in neutropenia days after their administration. CLINICAL FEATURES • Patients with neutropenia and fever often do not have focal symptoms. 418 SECTION 16 • HEMATOLOGIC AND ONCOLOGIC EMERGENCIES DIAGNOSIS AND DIFFERENTIAL • Patients with an absolute neutrophil count Ͻ500 cells per microliter and a fever Ͼ38.3ЊC (100.9ЊF) are at high risk for infection. • Approximately two-thirds of cancer patients who are neutropenic with a fever will have a bacterial cause of their fever. • A thorough physical exam including examination for possible cellulitis and perirectal abscess should be performed. EMERGENCY DEPARTMENT CARE AND DISPOSITION • Patients should have blood and urine cultures ob- tained prior to antibiotic therapy. • All patients with an absolute neutrophil count Ͻ500 cells and a fever Ͼ38.3ЊC (100.9ЊF) should have empiric antibiotic therapy initiated. Addi- tional antibiotic coverage should be directed at any obvious sources of infection. • Monotherapy with a third-generation cephalo- sporin such as ceftazidime or cefepime is consid- ered adequate empiric antibiotic coverage. Van- comycin may be added on the basis of clinical suspicion or local institutional bacterial sensitiv- ities. B IBLIOGRAPHY DeAngelis LM, Posner JB: Neurologic complications in pa- tients with cancer, in Holland JF, Frei E III, Bast RC, et al (eds): Cancer Medicine, 4th ed. Baltimore, Williams & Wilkins, 1997. Friefeld AG, Pizzo PA, Walsh TJ: Infections in the cancer patient, in DeVita VT, Hellman S, Rosenberg SA (eds): Cancer: Principles and Practice of Oncology, 5th ed. Phila- delphia, Lippincott-Raven, 1997. Fuller BG, Heise J, Oldfield EH: Spinal cord compression, in DeVita VT, Hellman S, Rosenberg SA (eds): Cancer: Principles and Practice of Oncology, 5th ed. Philadelphia, Lippincott-Raven, 1997. Moore GP, Jorden RC (eds): Hematologic/oncologic emer- gencies. Emerg Med Clin North Am 11:2, 1993. Schamban N, Borenstein M: Oncologic emergencies, in Ro- sen P, Barkin R (eds): Emergency Medicine: Concepts and Clinical Practice, 4th ed. St. Louis, Mosby-Yearbook, 1998. Warrell RP Jr: Metabolic emergencies, in DeVita VT, Hell- man S, Rosenberg SA (eds): Cancer: Principles and Practice of Oncology, 5th ed. Philadelphia, Lippincott- Raven, 1997. For further reading in Emergency Medicine: A Com- prehensive Study Guide, 5th ed., see Chap. 217, ‘‘Emergency Complications of Malignancy,’’ by John Sverha and Marc Borenstein. Section 17 NEUROLOGY 138 HEADACHE AND FACIAL PAIN Philip B. Sharpless EPIDEMIOLOGY • Headaches are classified into the primary and sec- ondary causes noted in Table 138-1. • One study revealed that 3.8 percent of emergency department (ED) headache patients have serious or secondary pathology. • Subarachnoid hemorrhage (SAH) represents about 1 percent of all nontraumatic headaches 1 and accounts for up to 25 percent of all sudden, severe headaches. 2 • The prevalence of migraine is approximately 15 to 17 percent in women and 5 percent in men. 3 PATHOPHYSIOLOGY • Migraine auras are thought to be the result of a slowly spreading wave of neuronal hypoactivity with an associated secondary reduction in local blood flow. Since vascular territories are not re- spected, the cause of the aura is no longer consid- ered primarily vasospastic. 4 • The migraine headache is thought to result from sterile neurogenic inflammation of pain-sensitive intracranial structures (arteries, dura), and this promotes a secondary vasodilation. No consensus exists on the precise biochemical triggers that initi- ate the migraine. 4 419 CLINICAL FEATURES • Table 138-2 lists the findings on the patient’s his- tory and physical examination, which should alert the clinician to the possibility of a more serious secondary cause for the headache and prompt con- sideration of more extensive testing. • Focal or nonfocal neurologic findings in the pa- tient with a headache have a 39 percent predictive value for intracranial pathology. 1 • Migraine headaches are typically gradual in onset, unilateral, and throbbing; they last 4 to 72 h, with frequent nausea and vomiting. The majority (80 percent) present without an aura. The aura in the remainder develops over 5 to 20 min, lasts no more than 60 min, and may consist of visual changes (scintillating scotomas, flashes) or other neuro- logic symptoms (focal weakness, paresthesias, ver- tigo, etc.). • Tension headaches tend to be gradual in onset, bilateral, nonpulsating, and—unless very se- vere—without nausea and vomiting. Overlap with migrainous headache symptoms occurs. • Cluster headaches are rare, occur primarily in men, and are typified by intense, unilateral, perior- bital pain lasting 15 to 180 min. The headaches recur in ‘‘clusters,’’ often at the same time daily for weeks before remitting. Some combination of ipsilateral conjunctival injection, tearing, nasal congestion, or rhinorrhea is seen. • Subarachnoid hemorrhage (SAH) is most com- monly a sudden-onset, severe headache and is of- ten described as ‘‘the worst headache of my life.’’ The headache may be global or unilateral but is frequently occipital and radiates to the neck and back. 5 Syncope, mental status changes, vomiting, meningismus, focal cranial nerve deficits (typically oculomotor nerve), or other neurologic deficits Copyright 2001 The McGraw Hill Companies, Inc. Click Here for Terms of Use. 420 SECTION 17 • NEUROLOGY TABLE 138-1 Primary and Secondary Causes of Headache PRIMARY HEADACHE SYNDROMES Migraine Tension type Cluster SECONDARY CAUSES OF HEADACHE Vascular Subarachnoid hemorrhage Intraparenchymal hemorrhage Subdural or epidural hematoma Ischemia (stroke, TIA) Cavernous sinus thrombosis Arteriovenous malformation Temporal arteritis Carotid or vertebral artery dissection CNS infection Meningitis (bacterial, viral, other) Encephalitis Cerebral abscess Non-CNS infection Focal or systemic Sinusitis Herpes zoster of face or scalp Other CNS Tumor (benign or malignant) Pseudotumor cerebri Ophthalmic Glaucoma Iritis Optic neuritis Drug-related and toxic or metabolic Nitrates and nitrites MAOI drugs Chronic analgesic use and abuse Hypoxia or high altitude Hypercapnia Hypoglycemia Monosodium glutamate Carbon monoxide poisoning Alcohol withdrawal Miscellaneous Malignant hypertension Preeclampsia Pheochromocytoma Fever Post–lumbar puncture Dental (referred) Otic (referred) A BBREVIATIONS : CNS, central nervous system; MAOI, monoamine oxidase inhibitor; TIA. transient ischemic attack. may be present; however, almost half will have normal vital signs and exam. 6 Sentinel hemor- rhages or warning bleeds occur in 30 to 60 percent of patients presenting with SAH. Subhyaloid (pre- retinal) hemorrhages may be seen. • A family history of SAH increases the risk four- fold over the general population. 7 • Post–lumbar puncture headache is due to persis- tent cerebrospinal fluid (CSF) leak through the dural puncture and develops 1 to 2 days after the lumbar puncture (LP). It is characterized by intense pain on standing with significant improve- ment when supine. • Preeclampsia must be considered in the female patient with headache in the latter half of preg- nancy or early postpartum period. Hypertension, proteinuria, and edema are frequent additional findings. Eclampsia increases the risk of intracran- ial bleed. Dural sinus thrombosis tends to occur in the early postpartum period. • Meningitis often presents with fever, headache, meningismus, and photophobia. Sinusitis, influ- enza and other non–central nervous system infections may also present with fever and headache. • Intraparenchymal hemorrhage produces head- ache in 55 percent of patients, and neurologic signs and symptoms are found in the vast majority. • Subdural hematoma may present with headache, altered mental status, or focal neurologic abnor- malities. There may be a history of recent or relatively remote trauma (weeks). Those at risk include the elderly, chronic alcoholics, and patients on anticoagulants or with bleeding di- athesis. • Temporal arteritis is a systemic panarteritis, which produces headache in 60 to 90 percent, usually in the temporal region with a tender temporal artery. TABLE 138-2 High-Risk Findings in the Headache Patient History Headache pattern Severe, worst headache ever; sig- nificant change from prior headache Headache onset Sudden maximum severity at on- set; new headache in the elderly Associated symptoms Syncope, altered mental status, neck pain, fever, seizure, focal neurologic complaints or visual disturbance Other history Medications (MAOIs, anticoagu- lants), cocaine, bleeding diathe- sis, carbon monoxide exposure, pregnancy, hypertension, HIV, malignancy, recent or remote trauma, ventricular-peritoneal shunt, polycystic renal disease Family history Subarachnoid hemorrhage Physical examination Vital signs Fever, marked hypertension Head and neck Papilledema, subhyaloid hemor- rhage, absent ocular venous pul- sations, corneal edema, neck stiff- ness, and temporal artery tenderness Neurologic Any focal or nonfocal neurologic finding CHAPTER 138 • HEADACHE AND FACIAL PAIN 421 Table 138-3 Diagnosis of Migraine Headache For a headache to be classified as a migraine headache, the fol- lowing must be present: duration of 4-72 h (without treatment) and: At least 2 of the following: 1. Unilateral position 2. Pulsating quality 3. Moderate or severe intensity (inhibits or prohibits daily ac- tivities) 4. Aggravation by walking stairs or similar routine physical ac- tivity And at least one of the following: 1. Nausea, vomiting, or both 2. Photophobia and phonophobia In addition, to be classified as a migraine with aura, the following must be satisfied: 1. One or more fully reversible aura symptoms indicating brain dysfunction 2. At least one aura symptom develops gradually over more than 4 min or two or more symptoms occur in succession 3. No single aura symptoms lasts more than 60 min 4. Headache follows aura with a free interval of less than 60 min Almost all patients are over 50 years of age and have a sedimentation rate greater than 50. They may present with visual loss due to ischemic optic neuritis, jaw claudication, or symptoms of polymy- algia rheumatica. 9 Table 138-4 Differential Diagnosis of the Patient with Headache TYPE OF HEADACHE HISTORY/PHYSICAL FINDINGS Migraine headache Young at onset; lasts longer than 60 min; unilateral, pulsating, throbbing; ϩ/Ϫ visual aura; nausea and vomiting; precipitated by foods, drugs, alcohol, exercise or orgasm; ϩ family history Cluster headache Onset in 20s; predominantly male; brief episodes or pain (45–60 min); orbital/retroorbital pain; periodic and seasonal (spring/autumn); nasal congestion and conjunctival injection/tearing associated; Ϫ family history Tension-type headache Onset at any age; dull, nagging, persistent pain; progressively worse throughout day Subarachnoid headache Sudden onset, ‘‘worst headache ever,’’ loss of consciousness, meningismus, vomiting, occipitonuchal lo- cation Hypertensive headache Throbbing, occipital Meningitis Entire head, fever, meningismus Mass lesions Subdural hematoma Depressed mental status, variable-quality headache Epidural hematoma History of trauma, consciousness wtih headache followed by unconsciousness; fracture across groove of middle meningeal artery Brain tumor Pain on awakening or with Valsalva; new headache associated with nausea and/or vomiting Brain abscess Findings similar to those of mass lesions, fever Sinusitis Stabbing or aching pain, worse by bending or coughing, decreased in supine position Toxic/metabolic headache Bicranial; headache remits after removal from offending agent/environment Postconcussion headache History of trauma within hours to days; vertigo, nausea, vomiting, mood alterations, concentration diffi- culty associated Pseudotumor cerebri Obese young female; irregular menstrual cycles/amenorrhea; papilledema Acute glaucoma Nausea, vomiting, orbital pain, edematous/cloudy cornea, midposition pupil, conjunctival injection, in- creased intraocular pressure • Temporomandibular disorder (TMD) most often presents with pain localized to the temporoman- dibular joint (TMJ) and ear but may cause a more diffuse face and head pain. TMJ tenderness and palpable clicking are frequent findings, as is a his- tory of bruxism. • Trigeminal neuralgia (tic douloureux) produces paroxysms of brief lancinating pain on one side of the face. Trigger points on the cheek or gum are stimulated by light touch or chewing. DIAGNOSIS AND DIFFERENTIAL • Table 138-3 lists the diagnostic criteria for a mi- graine headache. • Table 138-4 summarizes selected clinical features in the differential diagnosis of headache. • Computed tomography (CT) without contrast is the test of choice for evaluating suspected SAH; new-generation scanners have a sensitivity greater than 93 percent in the first 24 h from symptom onset. 10 Sensitivity falls after 24 h. • For the patient with suspected SAH and a normal head CT, a LP is considered necessary to assist in ruling out SAH. Xanthochromia detected by spectrophotometry in the cerebrospinal fluid [...]... • The patient may first notice numbness and tingling in the lower extremities, which is followed by as- CHAPTER 144 • • • • • cending weakness of the legs, thighs, and upper extremities In classic cases, there is symmetric extremity weakness, more pronounced in the legs The hallmark physical examination finding is absent deep tendon reflexes In all forms of the disease, there is potential for developing... a rare autosomal dominant disorder involving the triad of weakness, psychosis, and abdominal pain The three symptoms occasionally occur together, but in most cases they arise independently • Medications such as phenytoin, barbiturates, sulfonamides, and estrogens may trigger flares • The major neurologic findings include weakness and diminished reflexes, particularly in the legs • The key management issue... neurologist • MENINGITIS, ENCEPHALITIS, AND BRAIN ABSCESS 146 443 MENINGITIS, ENCEPHALITIS, AND BRAIN ABSCESS O John Ma MENINGITIS EPIDEMIOLOGY • There are 25,000 cases of bacterial meningitis annually in the United States; two-thirds of these cases occur in children The mortality rate is 25 percent in neonates, 5 percent in children beyond infancy, and 25 percent in adults.1,2 • There is an increasing prevalence... neurologists and neurosurgeons in the United Kingdom BMJ 316:1709, 19 98 For further reading in Emergency Medicine: A Comprehensive Study Guide, 5th ed., see Chap 219, ‘‘Headache and Facial Pain,’’ by Michael Schull 139 • • • STROKE SYNDROMES Stefanie R Seaman EPIDEMIOLOGY • Stroke is the third leading cause of death and the leading cause of disability in the United States The incidence of stroke doubles... al: The international cooperative study on the timing of aneurysmal surgery: I Overall management results J Neurosurg 73: 18, 1990 7 Schieuink WI: Intracranial aneurysms N Engl J Med 336: 28, 1997 8 American College of Emergency Physicians: Clinical policy for the initial approach to adolescents and adults presenting to the emergency department with a chief complaint of headache Ann Emerg Med 27 :82 1,... prior to LP in order to determine the possible risks for transtentorial or tonsillar herniation associated with LP In these cases, antibiotic therapy must be initiated prior to patient transport to the radiology suite for CT scanning Antibiotic therapy should always be initiated in the emergency department (ED) and never be delayed for CT scanning or other studies • Presently, the antibiotic therapy of... indication in selected individuals (Table 13 9-3 ) Total dose of rt-PA is 0.9 mg/kg, with a maximum dose of 90 mg Ten percent of the dose should be administered as an initial bolus, followed by an infusion of the remainder over 60 min rt-PA is not indicated if the exact time of CHAPTER 139 • STROKE SYNDROMES 425 TABLE 13 9-3 Criteria for Use of rt-PA in Acute Ischemic Stroke and Management of Patients Following... nervous system Neurol Clin 2: 187 , 1 984 7 Wekre LL, Stanghalle JK, Lobben B, Oyhaugen S: The Norwegian polio study 1994: A nationwide survey of problems in long-standing poliomyelitis Spinal Cord 36: 280 , 19 98 For further reading in Emergency Medicine: A Comprehensive Study Guide, 5th ed., see Chap 226, ‘‘Chronic Neurologic Disorders,’’ by Edward P Sloan • Over two-thirds of bacterial meningitis cases are... pneumoniae, Neisseria meningitidis, and Haemophilus in uenzae.4 • Infection begins with entrance of bacteria into the subarachnoid space, usually by upper airway inoculation, and is followed by dissemination into the bloodstream and invasion across the bloodbrain barrier.4 Direct inoculation is also possible from infection of parameningeal structures (e.g., otitis media, brain abscess, sinusitis), neurosurgery,... readings 5–10 min apart: • Infuse sodium nitroprusside (0.5–1.0 Ȑg/kg/min); continuous arterial pressure monitoring advised • • • • onset of symptoms cannot be ascertained No aspirin or heparin therapy is given with the first 24 h of treatment Admission to an intensive care unit (ICU) setting is recommended Glucose-containing solutions are to be avoided because of increased neuronal damage in hyperglycemia . FOR ANTITHROMBOTIC THERAPY ACUTE MYOCARDIAL INFARCTION • Fibrinolytic therapy should be initiated within 30 min of patient arrival at the emergency depart- ment (ED). In the appropriate clinical setting, cri- teria. undergoing per- cutaneous angioplasty. FIBRINOLYTIC AGENTS • Fibrinolytics work by activating plasminogen to plasmin, which then dissolves the fibrin in thrombi. Streptokinase (SK) is usually administered. glycoprotein IIb-IIIa receptor. • The platelet membrane–altering agents ticlopi- dine and clopidogrel render the receptor ineffec- tive and block aggregation. These agents are gen- erally used in patients