medical study: January 2009

Saturday, January 24, 2009

CAROTID SINUS SYNDROME

CAROTID SINUS SYNDROME - Jeremy Golding, MD
BASICS
DESCRIPTION
• In carotid sinus syndrome, stimulation of one or both of the hypersensitive carotid sinuses at the bifurcation of the common carotid arteries produces brief episodes of faintness or loss of consciousness. 4 types are described
- Cardioinhibitory: Vagally mediated, causing bradycardia, sinus arrest, or atrioventricular block for >3 seconds
- Vasodepressor: A sudden drop of peripheral vascular resistance leads to a >50 mm Hg decrease in systolic blood pressure (BP) without change in heart rate or to a >30 mm Hg symptomatic drop in systolic BP.
- Mixed: Combined cardioinhibitory and vasodepressor changes
- Cerebral: Extremely rare; carotid sinus hypersensitivity occurs without bradycardia or hypotension.
• System(s) Affected: Cardiovascular; Nervous
• Synonym(s): Hypersensitive carotid sinus syndrome; Carotid sinus syncope; Carotid sinus hypersensitivity
ALERT
Geriatric Considerations
• More likely to occur in elderly
• Associated with atheromata secondary to coronary artery disease. Should be considered in elderly patients with frequent falls.
GENERAL PREVENTION
• Avoidance of pressure on the neck
• Support hose may be helpful for some patients with vasodepressor type.
EPIDEMIOLOGY
• Predominant age: Elderly
• Predominant sex: Male > Female
Incidence
64 of 132 consecutive patients (48.5%) >65 evaluated for dizziness, falls, or syncope were found to have carotid sinus-type sensitivity.
RISK FACTORS
• Diffuse atherosclerosis
• Wearing tight collars
• Shaving over region of carotid sinus
• Emotional upheaval
• Head movement
ETIOLOGY
• Unknown etiology
• Stimulation of the hypersensitive baroreceptors in the carotid sinus affects vagus and sympathetic nerve outflow.
• Carotid body tumors
• Inflammatory and malignant lymph nodes in the neck
• Metastatic cancer
• Coronary artery disease
ASSOCIATED CONDITIONS
• Sick sinus syndrome
• Atrioventricular block
• Coronary artery disease

DIAGNOSIS
SIGNS AND SYMPTOMS
Paroxysmal
Dizziness
Syncope
Falls
Blurred vision
Vertigo
Tinnitus
Bradycardia
Hypotension
Pallor
Sweating
Tachypnea
No postictal symptoms
TESTS
Special tests
• With the patient in the supine position and while the ECG is monitored, manual pressure ("massage") of the carotid sinus causes asystole of >3 seconds (cardioinhibitory) and/or a drop in systolic BP as described in Description. Diagnostic yield may be increased by combining with tilt-table testing.
Diagnostic Procedures/Surgery
• Unilateral carotid sinus pressure ("massage") (check for potential contraindications before performing massage, including carotid bruits, known carotid hypersensitivity, and demonstrated carotid artery disease). Direct steady pressure is applied over the carotid sinus for 10 seconds.
• Orthostatic vital signs (exclude orthostatic hypotension)
• Electrophysiologic studies
• ECG
• Carotid duplex scan
DIFFERENTIAL DIAGNOSIS
• Vasovagal syncope
• Postural hypotension
• Primary autonomic insufficiency
• Hypovolemia
• Arrhythmias
• Sick sinus syndrome
• Syncope secondary to reduced cardiac output (e.g., aortic stenosis)
• Cerebrovascular insufficiency
• Emotional disturbances
• Other causes of syncope
TREATMENT
Outpatient. No treatment is required for asymptomatic individuals.
GENERAL MEASURES
Cardiac pacing (dual chamber) is the treatment of choice for recurrent episodes.
Diet
No special diet
Activity
No restrictions
MEDICATION (DRUGS)
First Line
• Anticholinergics: Atropine (acutely) for the cardioinhibitory type
• Sympathomimetics: Ephedrine
• Theophylline
• In one study, selective serotonin reuptake inhibitors were successful in controlling symptoms.
• Contraindications: Refer to manufacturer's instructions.
• Precautions: Concomitant usage of digitalis, -blockers, clonidine, and -methyldopa may accentuate response to carotid sinus massage.
• Significant possible interactions: Refer to manufacturer's instructions.
Second Line
Fludrocortisone has been used in clinical trials for patients with vasodepressor carotid sinus syndrome.
SURGERY
• Carotid sinus denervation by surgery or radiation therapy for selected patients
• Implantation of a permanent pacemaker helps prevent recurrent symptoms in patients with cardioinhibitory component.
• Surgery for selected patients with atheromata
FOLLOW-UP
DISPOSITION
Admission Criteria
Syncope of uncertain etiology
PROGNOSIS
May be serious if syncope is associated with atheromatous narrowing of sinus artery or basilar artery
COMPLICATIONS
• Prolonged confusion
• Frequent falls, leading to injuries and fractures
PATIENT MONITORING
Follow as an outpatient.
REFERENCES
1. ACC/AHA/NASPE 2002 Guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: Summary article. A report of the American College of Cardiology/American Heart Association task force on practice guidelines (ACC/AHA/NASPE committee to update the 1998 pacemaker guidelines). Circulation. 2002;106:2145.
2. Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia: WB Saunders, 2001.
3. Isselbacher KJ, et al., eds. Harrison's Principles of Internal Medicine, 14th ed. New York: McGraw-Hill, 1998.
4. McIntoch SJ, Lawson J, Kenny RA. Clinical characteristics of vasopressor, cardioinhibitory, and mixed carotid sinus syndrome in the elderly. Am J Med. 1993;95:203-208.
MISCELLANEOUS
• See also: Atherosclerosis
• It is clinically important to distinguish carotid sinus syndrome from sick sinus syndrome.

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CAROTID SINUS SYNDROME

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CARDIOMYOPATHY, END-STAGE

CARDIOMYOPATHY, END-STAGE - Tim Fitzgibbons, MD; Theo E. Meyer, MD, DPhil
BASICS
DESCRIPTION
In 1995, the WHO defined cardiomyopathy as a "disease of the myocardium associated with cardiac dysfunction." They proposed a classification system based on pathophysiology. Each class may be caused by many disorders, and some disorders may overlap classes.
• Classification of cardiomyopathy
- Dilated (systolic)
 Characterized by dilation and reduced systolic function of one or both ventricles
- Hypertrophic (diastolic)
 Left and or right ventricular hypertrophy with normal to reduced end diastolic volumes
 May include asymmetric septal hypertrophy
 Cause of SCD in young athletes
- Restrictive (diastolic)
 Restrictive filling and reduced diastolic volume of either or both ventricles
 Systolic function may be near normal
 Etiology: Idiopathic, amyloidosis, etc.
- Arrhythmogenic right ventricular (RV) dysplasia
 Fibrofatty replacement of the RV
 May present with arrhythmia or SCD in the young
- Unclassified
 Cases that do not fit easily into 1 group (i.e., non compacted myocardium)
- Specific: Includes patients with cardiomyopathy in association with a known systemic disorder, for example
 Ischemic
 Valvular
 Hypertensive
 Inflammatory
 Metabolic
 Peripartum
• "End-stage" cardiomyopathy patients have "Stage D" heart failure, or severe symptoms at rest refractory to standard medical therapy.
• System(s) Affected: Cardiovascular; Renal
ALERT
Pediatric Considerations
Etiology: Idiopathic, viral, congenital heart disease, and familial.
Pregnancy Considerations
May occur in women postpartum
GENERAL PREVENTION
Reduce salt and water intake; home blood pressure measurement and a daily weight
EPIDEMIOLOGY
Predominant age: Ischemic cardiomyopathy is the most common etiology; predominantly patients >50 years. Consider uncommon causes in young.
Incidence
• 60,000 patients 65 die each year from end-stage heart disease.
• From 35,000-70,000 of the population might benefit from cardiac transplant or chronic support.
Prevalence
Most rapidly growing form of heart disease
RISK FACTORS
• Hypertension
• Hyperlipidemia
• Obesity
• Diabetes mellitus
• Smoking
• Physical inactivity
• Excessive alcohol intake
• Dietary sodium
Genetics
Hypertrophic, dilated cardiomyopathy, and arrhythmogenic RV dysplasia may present as familial syndromes with autosomal dominant inheritance.
ETIOLOGY
• Ischemic heart disease: Most common etiology; up to 66% of patients
• Hypertension
• Familial cardiomyopathies
• Congenital heart disease
• Peripartum/postpartum
• Toxic/metabolic causes
- Alcoholism
- Radiation
- Beriberi
- Kwashiorkor
- Cobalt
- Selenium deficiency
- Hemosiderosis
- Thyrotoxicosis
• Infectious causes
- Viral (e.g., HIV, coxsackievirus)
- Diphtheria
- Toxoplasmosis
- Trichinosis
- Trypanosomiasis
- Acute rheumatic fever
• Inherited disorders of metabolism
- Glycogen storage disease
- Pompe disease
- Hurler syndrome
- Hunter syndrome
- Fabry disease
• Inherited neuromuscular disorders
- Duchenne muscular dystrophy
- Friedreich ataxia
• Drugs
- Chemotherapy: Anthracyclines, cyclophosphamide, Herceptin
• Inflammatory causes
- Giant cell myocarditis
- Loeffler eosinophilia
- Sarcoidosis
• Idiopathic
• Other causes
- Tachycardia-mediated cardiomyopathy
- Amyloidosis
- Valvular heart disease
- Endomyocardial fibrosis

DIAGNOSIS
SIGNS AND SYMPTOMS
• Dyspnea at rest or with exertion
• Paroxysmal nocturnal dyspnea
• Orthopnea
• Postprandial dyspnea
• Fatigue
• Syncope
• Tachypnea
Physical Exam
• Low pulse pressure
• Cool extremities
• Jugular venous distention
• Bibasilar rales
• Tachycardia
• S3 gallop
• Hepatosplenomegaly
• Ascites
• Edema
TESTS
• ECG: LV hypertrophy, interventricular conduction delay, atrial fibrillation, evidence of prior Q-wave infarction.
• Cardiopulmonary exercise testing: Maximal oxygen consumption 10 mL/kg/mm correlates with 50% 1-year mortality, and >18 mL/kg/mm correlates with >90% 1-year survival. Used in stable outpatients to estimate prognosis and prior to cardiac transplant referral.
Lab
• Hyponatremia
• Prerenal azotemia
• Anemia
• Elevated BNP or pro-BNP
• Mild hyperbilirubinemia
• Elevated liver function tests
• Elevated uric acid
Imaging
• Chest radiograph
- Cardiomegaly
- Increased vascular markings to the upper lobes
- Pleural effusions may or may not be present
• ECG
- In dilated cardiomyopathy 4-chamber enlargement and global hypokinesis are present.
- In hypertrophic cardiomyopathy, severe left ventricular (LV) hypertrophy is present.
- Segmental abnormalities in contraction of the LV are indicative of previous localized myocardial infarction.
• Cardiac MRI
- May be useful to characterize particular nonischemic cardiomyopathies
Diagnostic Procedures/Surgery
Cardiac catheterization:
• Helpful to rule out ischemic heart disease
• PA catheters may be reasonable in patients with refractory HF to help guide management (3)[C].
DIFFERENTIAL DIAGNOSIS
• Severe pulmonary disease
• Primary pulmonary hypertension
• Recurrent pulmonary embolism
• Hypothyroidism
• Some advanced forms of malignancy
TREATMENT
GENERAL MEASURES
• Reduction of filling pressures
• Treatment of electrolyte disturbances
Diet
Low fat, low salt, fluid restriction
MEDICATION (DRUGS)
First Line
• Systolic failure syndromes
- ACE inhibitors
 Lisinopril 5-40 mg/d or captopril 6.25-50 mg t.i.d. (3)[A]
- Loop diuretics
 May need to be given IV initially, and then orally as patient stabilizes
 Furosemide 40-120 mg/d or t.i.d.(3)[A]
- -Blockers:
 Use with caution in acutely decompensated or low cardiac output states
 Metoprolol succinate 12.5-200 mg/d, carvedilol 3.125-25 mg b.i.d., or bisoprolol 1.25-10 mg/d (3)[A]
- Aldosterone antagonists
 Patients with NYHA III-IV CHF, EF35%, on standard therapy
 Spironolactone 12.5-25 mg/d (3)[A]
- Digoxin 0.125-0.250 mg/d for symptomatic patients on standard therapy (3)[A]
- BiDil (hydralazine/nitrates)
 BiDil 1 tablet t.i.d is recommended in addition to standard treatment in African American patients with Class III-IV symptoms (3)[A]
• Diastolic failure
- Few evidence-based therapies for diastolic heart failure. Empiric management goals include
 Management of hypertension
 Reduction of congestive states (i.e., diuretics)
 Prevention of progression of LVH (i.e., RAAS blockade)
 Maintenance of sinus rhythm
• Contraindications
- -Blockers: Low cardiac output, 1st- or 2nd-degree heart block
- Aldosterone antagonists: Oliguria, anuria, renal dysfunction
- Loop diuretics: Hypokalemia, hypomagnesemia
- ACE inhibitors: Pregnancy, angioedema
• Precautions
- In patients with CKD, digoxin dosage should be 0.125 mg/d, and drug levels followed carefully.
- Closely monitor electrolytes
- ACE inhibitors: Initiate with care if blood pressure is low. Begin with low-dose captopril, such as 6.25 mg t.i.d.
- -Blockers: Avoid in patients with evidence of poor tissue perfusion; they may further depress systolic function.
- Milrinone, amrinone: Contraindicated for long-term use due to increased mortality
Second Line
• Nesiritide .01 mcg/kg/min IV for 48 hours in HF patients with dyspnea at rest (3)[C]
• Angiotensin receptor blockers as an alternative to, or in addition to ACE inhibitors
SPECIAL THERAPY
• Prophylactic ICD should be considered for patients with an LVEF 30% (3)[A].
• Biventricular pacing should be considered for patients with QRS interval >120 ms, LVEF 35%, and Class III CHF despite medical therapy(3)[A].
• Patients with severe, refractory HF with no reasonable expectation of improvement should not be considered for an ICD (3)[C].
FOLLOW-UP
DISPOSITION
Issues for Referral
• Consider referral to a heart failure center.
• Management by a heart failure team improves outcomes and facilitates early transplant referral.
PROGNOSIS
20-40% of patients in New York functional class IV die within 1 year. With a transplant, a 1-year survival is as high as 94%.
COMPLICATIONS
Worsening congestive heart failure, syncope, arrhythmias, or sudden death
REFERENCES
1. Richardson P. Report of the 1995 WHO on the definition and classification of cardiomyopathies. Circulation. 1996;93:841-842.
2. Noria A, Stevenson LW. Medical management of advanced heart failure. JAMA. 2002;287:628-640.
3. Hunt SA, et al. ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in adults. J Am Coll Cardiol. 2005;46:1116-1143.
MISCELLANEOUS
See also: Alcohol use disorders; Amyloidosis; Diabetes mellitus, type 1; Diabetes mellitus, type 2; Hypertension; Hypothyroidism, adult; Idiopathic hypertrophic subaortic stenosis; Malnutrition, protein-calorie; Rheumatic fever; Sarcoidosis

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CARDIAC TAMPONADE

CARDIAC TAMPONADE - Keith Medeiros, MD
BASICS
DESCRIPTION
• Rapid or slow compression of cardiac chambers by pressure on the heart secondary to an increase in pericardial fluid.
• Tamponade can be acute or subacute depending on the etiology.
• As fluid accumulates, pressure primarily affects the compliant cardiac wall and transmits the pressure transmurally, resulting in increased ventricular pressure. This decreases ventricular filling and reduces cardiac output by reducing stroke volume.
• The compensatory mechanisms for tamponade are increased peripheral resistance, central venous pressure, and heart rate.
• In some patients, pulsus paradoxus (10 mm Hg drop in systolic blood pressure between inspiration and expiration) and equalization of pressures may not occur, the absence of which does not rule out tamponade.
• In patients with elevated left ventricular (LV) diastolic pressures (as with chronic hypertension), resistance to LV filling is constant. Throughout the cardiac cycle, equalization of pressures in these patients may only be noted in the right heart chambers, with LV pressures being higher than right ventricular (RV) pressures.
• Variants include low pressure and regional tamponade.
• System(s) Affected: Cardiovascular
RISK FACTORS
Cardiac tamponade should be suspected in the hemodynamically unstable patient
• With known pericarditis
• Following blunt or penetrating chest trauma
• Following open heart surgery or cardiac catheterization
• With known or suspected intrathoracic neoplasm
• With suspected dissecting aortic aneurysm
• With renal failure on dialysis
PATHOPHYSIOLOGY
Fluid accumulation in the pericardial space leading to compression of cardiac chambers as the heart has to compete with increased pericardial contents for the fixed intrapericardial space. Cardiac filling is reduced, limiting cardiac output and eventually causing hypotension and shock. This can occur rapidly in cases of acute tamponade, usually resulting from trauma or surgery, or over weeks to months with slowly developing effusions that allow the pericardial compliance to increase gradually (1)[A].
ETIOLOGY
• Uremia
• Neoplasm: Breast, lung, lymphoma, leukemia
• Occurs in 1% of fibrinolytic-treated acute MI and is associated with increased 30-day mortality (2)[A].
• Postoperative
• HIV
• Other viruses: Coxsackie group B, influenza, ECHO, herpes
• Bacterial infection: Staphylococcus aureus, Mycobacterium tuberculosis, Streptococcus pneumoniae (rare)
• Fungal infection: Histoplasmosis capsulatum
• Lupus and rheumatologic disease
• Trauma
• Placement of central venous catheter, pacer wires
• Hypothyroidism
• Drug effects
ASSOCIATED CONDITIONS
• Myocardial infarction
• Aortic aneurysm

DIAGNOSIS
SIGNS AND SYMPTOMS
• Acute
- Patients may complain of chest pain or dyspnea
- Markedly elevated JVP
- Signs of cardiogenic shock: Cyanosis, cool extremities, and oligouria
• Subacute
- Most common complaints are intolerance to minimal activity and dyspnea. Agitation, central nervous system depression, coma, and cardiac arrest may develop later.
History
History of renal failure, surgery, neoplasm, or trauma
Physical Exam
• Beck triad: Distant heart sounds, hypotension, distended neck veins
• Narrow pulse pressure
• Pulsus paradoxus: >10 mm Hg drop in systolic blood pressure between inspiration and expiration
• Neck veins may be distended and reveal a rapid systolic (X) descent and attenuated or absent diastolic (Y) descent
• Tachycardia: A compensatory mechanism to maintain output
• Right upper quadrant tenderness due to hepatic engorgement
• Increased area of cardiac dullness outside the apical point of maximum impulse
TESTS
ECG
• May show sinus tachycardia, low-voltage QRS complexes, diffuse ST segment elevation, and PR segment depression of pericarditis
• Electrical alternans (QRS and/or R wave variation from beat to beat) seen in 10-20% of cases of tamponade; 50-60% of these are neoplastic in origin
Lab
• CBC
• Sedimentation rate
• Cardiac enzymes to rule out acute myocardial infarction
• Antinuclear antibodies
• Rheumatoid factor
• BUN/creatinine
• Pericardial fluid for culture of bacteria, fungus, mycobacteria, Gram stain, hematocrit, cell count, cytology, glucose, protein, rheumatoid factors, complement levels
Imaging
• Chest radiograph: May show enlargement of cardiac shadow (if >200 mL fluid present)
• Echocardiogram:
- Diagnostic of cardiac compression
 RA collapse is a sensitive sign of increased intrapericardial pressure but, diastolic RV collapse is more specific for tamponade (3,4)[A].
- Doppler: May show respiratory variation in transvalvular flow velocities, LV ejection, and LV isovolumetric times (3,4)[A].
Diagnostic Procedures/Surgery
Right heart catheterization:
• Equalization (within 2-3 mm) of right atrial, pulmonary artery diastolic, pulmonary capillary wedge, left atrial, and left ventricular diastolic pressures
• The intracardiac diastolic pressure will approximate the intrapericardial pressure.
• The dip and plateau pattern of constriction or restriction pericardial disease is absent.
• Loss of Y descent on atrial waveform
Pathological Findings
Pericardial blood usually does not clot, but occasionally will.
DIFFERENTIAL DIAGNOSIS
• Tension pneumothorax
• Acute RV failure
• COPD
• Constrictive pericarditis
• Acute acceleration of chronic bronchitis
• Acute pulmonary embolus
• Fat embolus
• Excessive or rapid administration of fluids
• Abdominal distention from ascites or ileus
• Increased intrathoracic pressure from pneumothorax, hemothorax, airway obstruction, or mechanical ventilation
• Administration of vasopressors
TREATMENT
STABILIZATION
Inpatient
GENERAL MEASURES
• Maintain hemodynamic stability until definitive correction of the pericardial tamponade
• All patients should have BP, heart rate, and at a minimum, central venous pressure measurement every 15 minutes. Strong consideration should be given to placement of a Swan-Ganz catheter if time allows.
• Fluids may be of temporary benefit, but rising filling pressures may further compromise coronary perfusion
Diet
As tolerated
Activity
Bed rest
MEDICATION (DRUGS)
Inotropic support with or without vasodilators is controversial partly due to maximal endogenous inotropic stimulation present during acute tamponade (1)[A].
SURGERY
Pericardiocentesis:
• Indications
- Rapid deterioration of hemodynamic function
- A delay in operation for traumatic effusion
- Diagnosis
• If rapid reaccumulation is anticipated (as in malignancy), it may be helpful to insert a long-term drainage catheter. Also consider instillation of sclerosing agents.
• Surgery should be performed under the most optimal circumstances available, as the patient's condition allows.
• Blind pericardiocentesis should be performed only in life-threatening emergencies.
• Ideally, echocardiography can be brought to the bedside to assist in needle placement and progress of fluid removal.
• Invasive monitoring is also helpful to follow decrease in pericardial pressures.
• Fluoroscopy may also be used.
• ECG guidance using the "V" lead to avoid contact with the epicardium may be useful.
• 20% of patients with tamponade will have a negative tap because the pericardial sac contains coagulated material. Hemorrhagic pericardial effusions usually do not clot.
FOLLOW-UP
Follow-up echocardiography should be used to evaluate for recurrence of effusions (3,4)[A].
PROGNOSIS
Good results are expected with the appropriate treatment.
COMPLICATIONS
• Cardiac perforation and/or laceration at time of pericardiocentesis
• Pneumothorax at time of pericardiocentesis
• Constriction of pericardium
PATIENT MONITORING
Close monitoring until stable with telemetry to monitor for cardiac arrhythmia
REFERENCES
1. Spodck DH, Acute cardiac tamponade. N Engl J Med 2003 Aug 14;349(7):684-690.
2. Patel MR et al. Cardiac tamponade in the fibrinolytic era: Analysis of 100,000 patients with ST-segment elevation myocardial infarction. Am Heart J 2006 Feb;151(2):316-322.
3. Cheitlin MD, et al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: Summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines for the Clinical Application of Echocardiography, Circulation. 2003;108:1146.
4. Cheitlin MD, et al, ACC/AHA Guidelines for the Clinical Application of Echocardiography. Circulation 1997;95:1686-1744.

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CARDIAC ARREST

CARDIAC ARREST - Bobby Peters, MD, FAAEM
BASICS
DESCRIPTION
• Absence of effective mechanical cardiac activity
• This section is not a substitute for an American Heart Association-approved Advanced Cardiac Life Support (ACLS) course and is intended only as a quick reference.
• Synonym(s): Code Blue
ALERT
Geriatric Considerations
Poor risk for survival and long-term outcome
Pediatric Considerations
Bradycardia is the most common initial form of cardiac arrest. Most frequently, it is a response to underlying pulmonary disease and hypoxia. Adequate oxygenation and ventilation are especially important.
Pregnancy Considerations
• Displace the uterus either manually or by placing a rolled towel or pad under the right hip. If the patient cannot be resuscitated within 5-15 minutes, consider emergency C-section to relieve uterine obstruction and increase blood return to the heart. This may also be done to save the fetus if at a viable age.
• Consider amniotic fluid embolism or eclampsia-related seizures as precipitating factors.
GENERAL PREVENTION
Treat underlying disease
EPIDEMIOLOGY
• Predominant age: Increases with age
• Predominant sex: Male > Female
Prevalence
In the United States: 200:100,000 (per year)
RISK FACTORS
• Male gender
• Increasing age
• Hypercholesterolemia
• Hypertension
• Cigarette smoking
• Family history of atherosclerosis
• Diabetes
ETIOLOGY
• Asystole (confirm in two leads; 11% actually fine ventricular fibrillation [VF])
• VF
• Pulseless ventricular tachycardia (VT)
• Pulseless electrical activity (PEA, previously known as electrical mechanical dissociation [EMD])
ASSOCIATED CONDITIONS
• Coronary artery disease (cardiac arrest may be first presenting symptom)
• Valvular heart disease
• Hypertension

DIAGNOSIS
SIGNS AND SYMPTOMS
• Loss of consciousness secondary to central nervous system hypoperfusion
• Absence of pulses in large arteries
• Apnea or agonal breathing
• Cyanosis or pallor
History
Find out how patient coded
• Witness or unwitnessed?
• Seizure activity?
• History or risk factors?
Physical Exam
• Check pupils: Dilated may indicate drug overdose
• Check pulse, hydration status, diaphoretic? (i.e., reasons for tachycardia)
• Check lungs (i.e., did person have respiratory decline before cardiac decline?)
TESTS
ECG
Lab
• Arterial blood gases
• Electrolytes
• CBC
• Drug levels (check toxicology screen, Tylenol level, also digoxin level or antiepileptic levels of history of specific medication use, etc.)
• Prothrombin time (international normalized ratio), partial thromboplastin time, type, and cross, if indicated
• Lab results may be altered by
- Digoxin toxicity: May cause hyperkalemia
- Hypo- or hyperventilation: Changes oxygen partial pressure and carbon dioxide partial pressure
- Acidosis: Increases serum potassium
Imaging
Chest radiograph for endotracheal tube (ET) placement, pneumothorax; consider echocardiogram for pericardial effusion
Diagnostic Procedures/Surgery
• If PEA secondary to tamponade, may need paracardiocentesis
• If coding, probably needs airway intubation
• May need central line for IV access
• May need chest tube for pneumothorax
Pathological Findings
Based on underlying cause
DIFFERENTIAL DIAGNOSIS
• Adverse reaction to drugs: Barbiturates, narcotics, calcium channel blockers, beta-blockers, and tricyclic antidepressants
• Shock: Septic or blood-loss induced
• Hypothermia
• Pulmonary embolism
• Cardiac tamponade
• Pneumothorax
• Acidosis
• Electrolyte abnormality
• Carbon monoxide poisoning
TREATMENT
STABILIZATION
• Prehospital emergency medical service personnel, ED, "cardiac arrest team," intensive care setting
• If response time is >5 minutes, improved outcome noted in patients when CPR started before defibrillation in Vfib. (1)[A]
GENERAL MEASURES
• Perform defibrillation 1st
- Adults: 200, 300, or 360 J
- Children: Use largest paddles that will fit on child, even adult size if good contact can be achieved.
- Defibrillate at 2 J/kg once. Increase to 4 J/kg twice.
• Administer 100% oxygen by bag-valve-mask or ET (preferred)
• Start 2 IV lines as close to the heart as possible (central line okay, but do not waste time). Large-bore peripheral lines can deliver fluid more quickly than a central line, especially important in PEA secondary to hypovolemia.
• Perform CPR, including closed-chest compression. Intermittent abdominal compression and active compression/decompression show no survival advantage.
• Keep patient, especially a child, warm if possible.
• Monitor pulse after 3 initial defibrillations. Check monitor between each defibrillation and after any intervention.
• Use an end-tidal CO2 monitor to assess gas exchange, if available. Esophageal intubation will produce a very low end-tidal CO2 and requires proper reintubation.
MEDICATION (DRUGS)
First Line
• Lidocaine, atropine, naloxone, and epinephrine may all be given by ET. Follow with 10 mL of normal saline or sterile water, followed by bagging.
• Epinephrine: 1 mL = 1 mg (1:1,000); 1 mL = 0.1 mg (1:10,000)
• Adults: VT and pulseless VT. Use in order listed below
- Defibrillate (nonsynchronized setting) 3 times at 200, 300, and 360 J
 Check monitor rhythm.
 Follow each drug administration with repeated defibrillation at 360 J.
 Check monitor and pulses after each subsequent intervention.
• Epinephrine: 1 mg IV every 3-5 minutes or a vasopressin 40 U IV single dose, 1 time only; may choose to resume epinephrine if no response after a single dose of vasopressin (high-dose epinephrine is permissible, but discouraged and may actually worsen outcomes).
• Amiodarone: 300 mg IV push may be used prior to lidocaine
• Lidocaine: 1.5 mg/kg IV, repeat in 5 minutes to total dose of 3 mg/kg
• Magnesium sulfate: 1-2 mg IV in suspected torsades de pointes or refractory VF/VT
• Procainamide: 30 mg per minute IV in refractory VF/VT (maximum dose: 17 mg/kg) is permissible. However, because the time to a useful level by infusion is so long, it is discouraged and is unlikely to be of any benefit. No improvement in survival to discharge.
• Bicarbonate: 1 mEq/kg IV only in known preexisting bicarbonate-responsive acidosis or to alkalinize the urine in known tricyclic overdose
Adults: Asystole
• CPR
• Confirm in 2 leads.
• Consider possible causes, including hypoxia, hyperkalemia, hypokalemia, preexisting acidosis, drug overdose, and hypothermia.
• Consider defibrillation, as for VT/VF, since VF may be mistaken for asystole.
• Consider immediate transcutaneous pacing.
• Epinephrine: 1 mg IV push repeated q3-5min; may use intermediate-dose or high-dose epinephrine (2-5 mg IV or 0.1 mg/kg IV) q3-5min
• Atropine: 1 mg IV push q3-5min to total dose of 0.04 mg/kg; shorter atropine dosing intervals acceptable (q1-2min)
• Consider termination of efforts if no reversible underlying cause is found.
For Pulseless Electrical Activity
• Includes EMD, idioventricular rhythms, ventricular escape rhythms, bradycardic-asystolic rhythms, and postdefibrillation idioventricular rhythms
• Assess blood flow by Doppler ultrasound if available.
• Consider possible reversible causes: Cardiogenic shock (weak pump), cardiac tamponade, tension pneumothorax, severe hypovolemia, pulmonary embolism (consider thrombolytics), hypothermia, hypoxia, acidosis, hyperkalemia, or overdose of drugs such as beta-blockers, calcium channel blockers, tricyclics, and digoxin (pnemonic 5H and 5Ts).
• Epinephrine: 1 mg IV push and repeat q3-5min; may use intermediate-dose or high-dose epinephrine (2-5 mg IV or 0.1 mg/kg IV, respectively) q3-5min, but this shows no proven improvement in survival
• Atropine: 1 mg IV q3-5min to total dose of 0.04 mg/kg if absolute bradycardia (60 beats per minute) or relative bradycardia; may decrease interval to 1-2min if desired
Children (drugs listed in alphabetical order):
• Amiodarone for pulseless VF/VT, 5 mg/kg IV or intraosseous (IO) rapid bolus; for perfusing tachyarrhythmias, loading dose of 5 mg/kg IV or IO over 20-60 minutes, maximum dose 15 mg/kg/d
• Atropine: 0.01-0.02 mg/kg per dose; minimum dose is 0.1 mg, maximum single dose is 0.5 mg in child, 1.0 mg in adolescent
• Epinephrine
- For bradycardia: 0.01 mg/kg IV/IO or 0.1 mg/kg ET (1:1,000)
- For asystolic or pulseless arrest: 1st dose is 0.01 to 0.03 mg/kg IV/IO. Doses as high as 0.2 mg/kg may be effective.
- Infusion: 0.1 ug/kg per minute. Titrate to desired effect (0.1-1.0 ug/kg per minute).
• Lidocaine:
- Bolus: 1 mg/kg per dose (maximum 3 mg/kg)
- Infusion: 20-50 ug/kg per minute
• Sodium bicarbonate: 1 mEq/kg per dose or 0.3  kg  base deficit; infuse slowly and only if ventilation is adequate
• Contraindications and precautions
- There are contraindications during an arrest.
- Calcium may be used if known (preexisting) hyperkalemia precipitated arrhythmia; calcium is contraindicated in hyperkalemia secondary to digoxin.
- Magnesium is relatively contraindicated in renal failure, but given the consequences of not terminating rhythm; this is only a relative contraindication in this setting.
Second Line
Asystole: Aminophylline 250 mg IV bolus has been effective in uncontrolled trials, but should be used only when conventional therapy has failed.
SURGERY
If indicated
• Pericardiocentesis to treat cardiac tamponade
• Needle decompression (second intercostal space midclavicular line), then chest tube insertion to treat tension pneumothorax
FOLLOW-UP
PROGNOSIS
• Outcome is related to underlying disease, age, duration of arrest, and other factors.
• Outcome is poor if
- >4 minutes to CPR or >8 minutes to ACLS
- Arrest occurs in field
- Resuscitation effort >30 minutes
• About 14% survive in-hospital arrest, fewer after field arrest
COMPLICATIONS
• Significant neurologic, hepatic, renal, or cardiac ischemic injury
• Rib fractures or pneumothorax from CPR
PATIENT MONITORING
Intensive care setting on continuous monitor to look for precipitating cause, including serial ECGs and enzymes to rule out myocardial infarction
REFERENCES
1. Wik L, Hansen TB, Fylling F, et al. Delaying defibrillation to give basic cardiopulmonary resuscitation to patients with out-of-hospital ventricular fibrillation: A randomized trial. JAMA. 2003;289(11):1389-1395.
2. Graber MA. Emergency medicine. In: Graber MA, Lanternier ML, Graber M, eds. The Family Practice Handbook. St. Louis, MO: Mosby-Yearbook; 1997.
3. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2000;102(suppl 8):I95-I104.
MISCELLANEOUS
Make sure patient is not listed as Do Not Resuscitate.

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CARBON MONOXIDE POISONING

CARBON MONOXIDE POISONING - Felix B. Chang, MD
BASICS
DESCRIPTION
• Carbon Monoxide (CO) is the leading cause of poisoning death in the us CO is an odorless, tasteless, colorless, gas, produced by combustion of carbon-containing compounds.
• CO inhalation leads to displacement of oxygen from binding sites on hemoglobin.
• CO has about 250 times the affinity for hemoglobin that oxygen has.
• Detrimental effects are related to tissue hypoxia from decreased oxygen content and a shift of the oxyhemoglobin dissociation curve to the left.
• CO binds to cytochrome oxidase, impairing mitochondrial function and to cytochrome oxidase, affecting muscle function.
• CO binding to myoglobin affects muscle activity.
• System(s) Affected: Cardiovascular; Musculoskeletal; Nervous
ALERT
Tissue hypoxia includes the fetus. CO poisoning may cause significant fetal abnormalities, depending on the developmental stage. However, adult hemoglobin holds to oxygen less tightly than does fetal hemoglobin. Therefore, a pregnant mother potentially may be unaffected while the fetus is affected.
EPIDEMIOLOGY
• 40,000 emergency department visits annually
• 5,000 to 6,000 deaths annually in the US
• Inadvertent CO poisoning likely causes 500 deaths annually.
• Unintended poisoning is most common during winter month in cold climates.
• 10,000 individuals miss 1 or more days of work due to CO poisoning.
RISK FACTORS
• Cigarette smoking
• Smoke inhalation
• Being in a closed space with a faulty furnace or stove or running engine
• Employment in coal mine, as an auto mechanic, paint stripper, or in the solvent industry
• Improper vented fuel-burning devices
- Kerosene heaters, charcoal grills, camping stoves, gasoline-power generators, wood stoves
- Open air exposure to motorboat exhaust
- Underground utility electrical cable fires
PATHOPHYSIOLOGY
• CO is rapidly absorbed in lungs.
• CO binds to hemoglobin to form carboxyhemoglobin (COHb), resulting in impaired oxygen carrying capacity, utilization, and delivery.
- Leftward shift of the oxyhemoglobin dissociation curve occurs.
- CO interferes with peripheral oxygen utilization by inactivating cytochrome oxidase.
• Delayed neurologic sequelae, probably involves lipid peroxidation by toxic oxygen species generated by xanthine oxidase.
• The half-life of CO while the patient is breathing room air is ~300 minutes, while breathing high-flow oxygen via a nonrebreathing face mask is ~90 minutes, and with 100 % hyperbaric oxygen is ~30 minutes.
ETIOLOGY
• CO inhalation
• Inhaled or ingested methylene chloride (from paint remover) (dichloromethane) is metabolized to CO by the liver, causing CO toxicity in the absence of ambient CO.
ASSOCIATED CONDITIONS
CO and cyanide poisoning can occur simultaneously following smoke inhalation (synergistic effect).

DIAGNOSIS
• Acute CO poisoning is suggestive by history, physical examination, and an elevated COHb
• Chronic CO intoxication is difficult to diagnose.
• Pulse oximetry cannot screen for CO exposure, because it does not differentiate carboxyhemoglobin from oxyhemoglobin.
PRE HOSPITAL
Patients often present in clusters, with similar symptoms and a common environment.
SIGNS AND SYMPTOMS
• Headaches
• Tinnitus
• Nausea
• Dizziness
• Weakness
• Confusion
• Fatigue
• Flushing
• Vomiting
• Central nervous system depression
• Syncope
• Angina
• Tachycardia
• Tachypnea
• Cardiac dysrhythmias
• Nystagmus
• Ataxia
• Seizures
• Coma
• Diarrhea
• Cardiopulmonary arrest
Physical Exam
• A careful neurologic examination is crucial.
• In absence of trauma or burns, look for altered mental status.
• "Cherry red" appearance of the lips and skin
• Impaired judgment, respiratory depression, arrhythmias, hypotension
• Cyanosis
• Visual field defects, blindness, papilledema
TESTS
Lab
• Measurement of COHb.
• Check CO level via co-oximetry of arterial or venous blood.
• Check acid-base status on blood gas.
• EKG in all patients
• Cardiac enzymes in
-  65 years
- Patient with cardiac risk factors
- Younger patients with chest pain or symptoms suggestive of ischemia
Imaging
Head CT scan is helpful to rule out other causes of neurologic decompensation.
Pathological Findings
Hemorrhagic infarction of the globus pallidus and deep white matter have been reported (rare).
DIFFERENTIAL DIAGNOSIS
• Cyanide toxicity
• Acute viral syndrome
• Other causes of mental status changes: Metabolic, drugs, infectious, trauma
TREATMENT
STABILIZATION
• ED for mild poisoning
• Inpatient treatment for moderate or severe poisoning
GENERAL MEASURES
• Removal from offending source
• Rapid reduction in tissue hypoxia with 100% oxygen to reduce the half-time of elimination of CO to 40 minutes
• Supportive care as necessary
• Intubation and mechanical ventilation may be necessary for severe intoxication.
• Volume resuscitation
Activity
Rest until carboxyhemoglobin reduced and symptoms abate
SPECIAL THERAPY
• 100% oxygen by tight-fitting nonrebreathing mask
• Hyperbaric oxygen for severe poisoning
• For mild poisoning (carboxyhemoglobin levels 30%); no signs or symptoms of cardiovascular or neurologic dysfunction
- Treatment: Admission if carboxyhemoglobin >25%
- Symptomatic medication for headache
- 100% oxygen by nonrebreathing mask until carboxyhemoglobin 5%
- Patients with underlying heart disease should be admitted regardless of level of carboxyhemoglobin.
• For moderate poisoning (carboxyhemoglobin 30-40%); no signs or symptoms of cardiovascular or neurologic dysfunction
- Treatment: Admission
- Cardiovascular status should be followed closely, even in the absence of clear cardiac effects.
- Determination of acid-base status: Corrected by oxygen
- 100% oxygen by nonrebreathing mask until carboxyhemoglobin 5%
• For severe poisoning (carboxyhemoglobin >40%); cardiovascular or neurologic functional impairment at any carboxyhemoglobin level
- Treatment: Admission
- Cardiovascular function monitoring
- Acid-base status monitoring
- 100% oxygen by nonrebreathing mask until carboxyhemoglobin 5%
- Hyperbaric oxygen immediately if available; if unavailable, treat as in moderate poisoning
- If no improvement occurs in cardiovascular or neurologic function within 4 hours, transport the patient to the nearest facility with hyperbaric oxygen, regardless of distance.
MEDICATION (DRUGS)
First Line
• Institution of 100% oxygen by high-flow mask or endotracheal tube
• 100% normobaric oxygen for all suspected victims of CO poisoning, regardless of pulse oximetry or arterial PO2 (1)[B].
FOLLOW-UP
DISPOSITION
Admission Criteria
Patients whose symptoms do not resolve, who demonstrate ECG or laboratory evidence of severe poisoning, or who have other medical or social cause of concern should be hospitalized.
Discharge Criteria
Patient with mild symptoms from accidental poisoning can be managed in the ED and safely discharged.
PROGNOSIS
Most survivors recover completely, with only a minority developing chronic neuropsychiatric impairment.
COMPLICATIONS
• Myocardial infarction
• Pulmonary edema (CHF)
• Pneumonia (aspiration)
• Anoxic encephalopathy
• Long-term neuropsychiatric complications
- Intellectual deterioration
- Memory impairment
• Dysrhythmia
• Shock
• Rhabdomyolysis, personality changes
- Irritability
- Aggressiveness
- Violence
- Moodiness
ALERT
Geriatric Considerations
• Higher incidence of cardiovascular and neurologic disease, increasing complications.
• Atherosclerosis with chronic exposure
PATIENT MONITORING
• Measurement of carboxyhemoglobin levels
• Arterial blood gases
• Psychiatric evaluation and follow-up for intentional exposure
REFERENCES
1. Hampson NB, Scott KL, Zmaeff JL. Carboxyhemoglobin measurement by hospitals: Implications for the diagnosis of carbon monoxide poisoning. J Emerg Med. 2006;31:13.
2. Kao LW, Nanagas KA. Carbon monoxide poisoning. Emerg Med Clin North Am. 2004;22:985.
3. Satran D, Henry CR, Adkinson C, et al. Cardiovascular manifestations of moderate to severe carbon monoxide poisoning. J Am Coll Cardiol. 2005;45:1513.
ADDITIONAL READING
• Internet resources available at: www.cpsc.gov.
• Insufficient evidence to establish usefulness of hyperbaric oxygen for carbon monoxide poisoning. Cochrane Library 2005;1:CD002041.
• Juurlink D, Buckley N, Stanbrook M, et al. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev 2005;CD002041.

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CANDIDIASIS

CANDIDIASIS - Brock D. Lutz, MD; Ronald A. Greenfield, MD
BASICS
DESCRIPTION
Candida albicans and related species cause a variety of infections
• Cutaneous syndromes include erosio interdigitalis blastomycetica, folliculitis, balanitis, intertrigo, paronychia, onychomycosis, diaper rash, perianal candidiasis, and the syndromes of chronic mucocutaneous candidiasis.
• Mucous membrane infections include oral candidiasis (thrush), esophagitis, and vaginitis.
• The most serious manifestations of candidiasis are candidemia and hematogenously disseminated invasive candidiasis.
The remainder of this chapter discusses candidemia and hematogenously disseminated candidiasis.
GENERAL PREVENTION
• Polyenes, azoles, and echinocandins reduce the incidence of candidiasis in patients undergoing induction therapy for acute leukemia or bone marrow or stem cell transplantation. (4)[A]
• Fluconazole prophylaxis in high-risk ICU patients reduces the incidence of invasive candidiasis. (6)[A]
EPIDEMIOLOGY
• Predominant age: All ages are susceptible to hematogenously disseminated candidiasis; premature neonates are at particularly high risk.
• Predominant sex: Male = Female (hematogenously disseminated candidiasis)
Incidence
20/100,000 persons per year
RISK FACTORS
• Neutropenia
• Corticosteroid treatment
• HIV infection
• Diabetes mellitus
• Mucocutaneous colonization/infection
• Broad-spectrum antibacterial chemotherapy
• Indwelling intravascular access devices
• Cardiothoracic or abdominal surgery
• Parenteral nutrition
• Prolonged hospital stay
• ICU stay
• Burns
• Premature birth
PATHOPHYSIOLOGY
An acute suppurative infection in which polymorphonuclear host defense is the critical element.
ETIOLOGY
• Candida albicans is the most frequent pathogen. Other important human pathogens include C. tropicalis, C. krusei, C. stellatoidea, C. pseudotropicalis, C. guilliermondi, C. parapsilosis, C. lusitaniae, C. rugosa, C. lambica, and C. glabrata.
• Candida species colonize human mucocutaneous surfaces; most infections are endogenously acquired from this reservoir.
• Human-to-human transmission of Candida occurs in some settings.
ASSOCIATED CONDITIONS
See "Risk Factors."

DIAGNOSIS
SIGNS AND SYMPTOMS
• Fever
• Malaise
• Tachycardia
• Hypotension
• Altered mental status
• Hepatosplenomegaly
• Maculopapular or nodular skin rash
ALERT
Pediatric Considerations
For an infant with thrush, be sure to also check for candidal diaper dermatitis. Also, there is often a concomitant infection.
TESTS
• The diagnosis is established by isolating the causative organism from blood cultures or other normally sterile body sites, or by demonstration of organisms in histopathologic specimens of normally sterile tissues.
• Isolation of Candida from multiple sites should raise the diagnostic suspicion of hematogenously disseminated invasive candidiasis.
• Candida species isolated from a normally sterile site should be identified to the species level. (4)[A]
• Because fluconazole-resistant C. albicans and particularly non-albicans species are reported with increasing frequency, fluconazole susceptibility testing should be performed before treatment with fluconazole. (4)[B]
Imaging
• Generally not specifically useful in diagnosis of hematogenously invasive disseminated candidiasis.
• In the syndrome of hepatosplenic candidiasis (chronic systemic candidiasis) imaging of the liver and spleen by liver scan, ultrasound, CT, or MRI may suggest this syndrome as the cause of persistent fever and liver dysfunction in patients who have recently recovered from neutropenia.
Diagnostic Procedures/Surgery
• If blood cultures remain consistently negative, aspiration or excisional biopsy of sites of focal infection may be useful in diagnosis.
• Aspiration and biopsy of skin lesions occasionally seen with hematogenously disseminated candidiasis are also useful.
Pathological Findings
Characteristic histopathology of lesions of Candida invasion of visceral organs is microabscess formation.
DIFFERENTIAL DIAGNOSIS
Includes a variety of cryptic bacterial infections and, in the neutropenic host, multiple opportunistic infections.
TREATMENT
Inpatient for hematogenously disseminated invasive candidiasis
GENERAL MEASURES
• Fluid and electrolyte therapy are often required.
• Hemodynamic and respiratory support may be required in seriously ill patients.
• The removal of potentially infected intravascular access devices is imperative.
Diet
No special diet
Activity
As tolerated
MEDICATION (DRUGS)
First Line
• Caspofungin
- An initial therapy of choice for any patient with candidemia (4)[A].
- Administer 70 mg IV dose on day 1 followed by 50 mg IV daily for 2 weeks after last positive sterile site culture if no evident metastatic infection
- Modify dose for severe hepatic insufficiency.
- C. parapsilosis has reduced sensitivity to echinocandins.
• Fluconazole
- An initial therapy of choice for some patients (4)[A]
- Because it is fungistatic rather than fungicidal, it should not be used for treatment of patients with severe neutropenia or severe immunosuppression.
- It should only be used after confirmation of in vitro susceptibility in patients with azole therapy in prior 3 months
- Should be used empirically only in institutions with a very low prevalence of resistance
- Useful for switch therapy after demonstration of in vitro susceptibility after initial therapy with amphotericin or an echinocandin.
- For 1st week, administer daily 400-800 mg intravenously, followed by additional IV or oral therapy at the same dose for 2 weeks after the last positive blood culture or last evidence of infection. Higher doses of fluconazole may be required if non-albicans species are known or suspected, because they carry a higher likelihood of drug resistance.
- C. krusei and many C. glabrata are resistant to fluconazole.
• Liposomal amphotericin B
- An initial therapy of choice for any patient with candidemia (4)[A]
- Usual dosage is 3 mg/kg IV daily.
- Substantially more expensive than conventional amphotericin B deoxycholate, but also substantially less toxic
- C. lusitaniae may be resistant.
- Consider higher doses for C. krusei or C. glabrata (5-10 mg/kg/day).
Second Line
• Although caspofungin is the only echinocandin approved by the FDA for this indication, preliminary data suggest that micafungin and anidulafungin have similar efficacy and safety for treatment of hematogenously disseminated invasive candidiasis. (B)
• Other azole antifungals depending on activity and safety (itraconazole and voriconazole). (B)
• Contraindications
- The safety of amphotericin B therapy in pregnant patients has not been established.
- Echinocandins are pregnancy category C.
• Precautions
- Liposomal amphotericin B
 The toxicity is less common than with conventional amphotericin B, but may still be formidable. Acute reactions (fever, rigors, and hypotension) may occur during the initiation of therapy. Ameliorate or eliminate by premedication with acetaminophen or ibuprofen. Use meperidine if needed to abort rigors.
 Azotemia may occur; there may be an indication for reducing dose in some patients (to reduce toxicity). Maintenance of optimal fluid status and prevention of dehydration help minimize the risk of azotemia. "Sodium loading" with 77 mEq (77 mmol) sodium daily (= 1 L half-normal saline) may decrease renal toxicity.
 Significant hypokalemia and renal tubular acidosis) may develop. Significant hypomagnesemia may worsen hypokalemia.
 Anemia commonly develops in patients on protracted therapy, but is almost always reversible.
 Headache and phlebitis are common.
 Leukopenia, thrombocytopenia, and liver function abnormalities are rarely encountered.
• Itraconazole, voriconazole, and caspofungin and other echinocandins do not enter the urinary stream in sufficient concentrations to treat UTIs.
• Significant possible drug-drug interactions
- Caspofungin and other echinocandins
 Potentially important interactions with carbamazepine, phenytoin, cyclosporine, tacrolimus, sirolimus, non-nucleoside reverse transcriptase inhibitors, and rifampin
- Liposomal amphotericin B
 Concomitant therapy with cyclosporine or other nephrotoxic agents, such as aminoglycosides or vancomycin, may increase the risk of amphotericin-induced nephrotoxicity.
- Fluconazole and other azoles
 Potentially important drug-drug interactions may occur in patients receiving oral hypoglycemics, coumarin-type anticoagulants, phenytoin, cyclosporine, rifampin, theophylline, or terfenadine or astemizole.
 These drug-drug interactions are more likely with itraconazole and voriconazole than with fluconazole.
FOLLOW-UP
Patients should receive followup visit approximately 6 weeks after end of therapy and be screened for metastatic infection complications by history and physical exam
PROGNOSIS
Overall mortality for patients with hematogenously disseminated candidiasis is 40-75%, with mortality attributable to candidemia being 15-37%.
COMPLICATIONS
• Systemic inflammatory response syndrome
• Pyelonephritis
• Endophthalmitis
• Endocarditis, myocarditis, pericarditis
• Arthritis, chondritis, osteomyelitis
• Pneumonitis
• Central nervous system infection
PATIENT MONITORING
• Evaluate CBC, serum electrolytes, and serum creatinine at least twice weekly in patients on liposomal amphotericin B therapy.
• If blood cultures are positive, they should be repeated until negative.
REFERENCES
1. Benjamin DK Jr., Stoll BJ, Fanaroff AA, et al. Neonatal candidiasis among extremely low birth weight infants: Risk factors, mortality rates, and neurodevelopmental outcomes at 18 to 22 months. Pediatrics. 2006;117:84-92.
2. Golan Y, Wolf MP, Pauker SG, Wong JB, Hadley S. Empirical anti-Candida therapy among selected patients in the intensive care unit: a cost-effectiveness analysis. Ann Intern Med. 2005;143:857-869.
3. Ostrosky-Zeichner L, Pappas PG. Invasive candidiasis in the intensive care unit. Crit Care Med. 2006;34:857-863.
4. Spellberg BJ, Filler SG, Edwards JE Jr. Current treatment strategies for disseminated candidiasis. Clin Infect Dis. 2006;42:244-251.
5. Uzon D, Anaissie EJ. Predictors of outcome in cancer patients with candidemia. Am Oncol. 2000;11:1517-1521.
6. Varadakas KZ, Samonis G, Michalopoulos A, et al. Antifungal prophylaxis with azole in high-risk, surgical intensive care unit patients: A meta-analysis of randomized, placebo-controlled trials. Crit Care Med. 2006;34:1216-1224.
MISCELLANEOUS
• Other candidal infections
- Intraperitoneal infection in patients with major abdominal surgery
- Biliary tract candidiasis
- Isolated lower UTI
• See also: Candidiasis; Mucocutaneous; Vulvovaginitis; Candidal

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CANDIDIASIS, MUCOCUTANEOUS

CANDIDIASIS, MUCOCUTANEOUS - Susan Louisa Montauk, MD
BASICS
DESCRIPTION
A mucocutaneous disorder caused by infection with various species of Candida. Areas include
• Candida vulvovaginitis: Vaginal mucosa and/or cutaneous aspects of the vulva
• Candidal Balanitis: Glans penis
• Candidal Paronychia: Nail bed of a digit
• Oropharyngeal candidiasis: Oral cavity (thrush) and/or pharynx
• Candida esophagitis: Esophagus (commonly associated with immunosuppression)
• Gastrointestinal candidiasis: Gastritis, sometimes with ulcers, usually associated with thrush; may affect the small and large bowel
• Angular cheilitis: Fissures at mouth corners
• System(s) Affected: Gastrointestinal; Skin/Exocrine; Genitourinary
• Synonym(s): Monilia; Thrush; Yeast
ALERT
Vaginal antifungal creams and suppositories can weaken condoms and diaphragms.
Pregnancy Considerations
• No known fetal complications of maternal Candida
• Miconazole is usually the drug of choice.
GENERAL PREVENTION
• Antibiotics may potentiate candidiasis.
• Candida overgrowth is more likely with pH changes from douching, chemicals (such as spermicides), or other vaginitides.
• Moist environments are conducive to overgrowth of Candida. Cotton underwear may help deter some Candida infections.
EPIDEMIOLOGY
• Common in the United States, very common in with immunodeficiency and/or uncontrolled diabetes
• Predominant age
- Infants and seniors for thrush and cutaneous infections (infant diaper rash)
- Women of childbearing age predominate for vaginitis. It is uncommon to see prepubertal or postmenopausal yeast vaginitis because of atrophic changes in the vaginal wall.
• Predominant sex: Female > Male (because of vaginitis)
Incidence
Not well studied, but some estimate 50/100,000
Prevalence
Candida colonizes more than 1/2 of U.S. population
RISK FACTORS
• Immunosuppression (includes chronic medications such as corticosteroids and immune modulators for transplants or rheumatologic dz
• Antibacterial therapy
• Douches, chemical irritants, and other vaginitides can predispose to yeast vaginitis
• Dentures
• Birth control pills
• Hyperglycemia
Genetics
• Chronic mucocutaneous candidiasis is a heterogeneous, genetic syndrome that usually presents in childhood, but it's mode of inheritance has not been clarified.
• Family analysis has identified an isolated form of mucocutaneous candidiasis, as well as its chromosomal region, which affects nails only.
ETIOLOGY
C. albicans and, less frequently, C. tropicalis
ASSOCIATED CONDITIONS
• HIV and other leukopenias
• Diabetes mellitus
• Cancer and other immunosuppressive disorders
• Disorders that call for steroids (oral or intranasal) (1) and other immunosuppressive chemotherapy

DIAGNOSIS
NOTE: Candida is normally present, in very small amounts, in the oral cavity, gastrointestinal tract, and female genital tract.
SIGNS AND SYMPTOMS
• In children
- Oral: White, raised, painless, distinct patches within the mouth
- Perineal: Erythematous maculopapular rash with white "satellite" pustules
- Angular cheilitispainful fissures in mouth corners
• In adults: Vulvovaginal lesions; thin to thick whitish "cottage cheese-like" discharge; erythematous patches in the vagina or on the perineum; symptoms range from none to intense pruritus with "burning" irritation
• In immunocompromised hosts
- Oral lesions: White, raised, painless, distinct patches; erythematous, slightly raised patches; thick, dark-brownish coating; deep fissures
- Esophagitis: Dysphagia, odynophagia, retrosternal pain; usually associated with thrush
- Gastrointestinal symptoms: Ulcerations, pain
- Balanitis: Erythema, linear erosions, scaling
- Angular cheilitis (see "In children")
TESTS
Lab
• Potassium hydroxide 10% microscopic slide preparation (KOH prep): Breaks down epithelial cell walls; allows yeast forms to be visualized
- Best if heated
- Lack of slide identification does not rule out
- A scant number of fungal forms without symptoms does not imply pathogenesis
• Culture: Blood or Sabouraud agar is present; a positive test may be the result of normal flora.
• Drugs that may alter lab results
- Douches and spermicides
- Inadequately dosed antifungal medications
• Disorders that may alter lab results: Other vaginitides (may obscure vaginal slide findings)
Imaging
Barium swallowesophageal candidiasis may reveal a "cobblestone" appearance, fistulas or esophageal dilatation (from denervation)
Diagnostic Procedures/Surgery
• KOH prepa sample of the discharge or "coating" of the infected area or ulcer is needed.
• Esophagitis may require an endoscopic biopsy.
• HIV seropositivity plus thrush with dysphagia relieved by antifungal treatment is acceptable criteria for the diagnosis of Caplital esophagitis.
Pathological Findings
Slide preparation: Mycelia (hyphae) or pseudomycelia (pseudohyphae) yeast forms; Candida does not induce a heightened polymorphonuclear leukocyte response
DIFFERENTIAL DIAGNOSIS
• Baby formula can mimic thrush.
• Hairy leukoplakiadoes not rub off to erythematous base; usually on lateral tongue.
• Bacterial vaginitis
• Angular Cheilitis from vitamin B or iron deficit, other microbes, or edentulous "over" closure
• Symptoms of Trichomonas vaginalis that are similar to those of Candida vaginalis include
- Initial symptoms appearing postmenstrually
- Marked vulvar irritation
- Labial erythema
- External dysuria
- Vaginal tenderness
• Iron deficiency and staph infections can mimic angular cheilitis
TREATMENT
GENERAL MEASURES
Screen both well infants and patients with severe immunodeficiency at routine visits.
Diet
A few authorities say rectal colonization may be decreased with active-culture yogurt or other live lactobacillus; evidence is not yet strong.
Complementary and Alternative Medicine
Probioticscertain gut bacteria, in particular species of Lactobacillus and Bifidobacterium, may exert beneficial effects in the oral cavity by inhibiting cariogenic streptococci and Candida sp. (2)
MEDICATION (DRUGS) (3,4,5) [A,B]
First Line
Vaginal (choose one):
• Miconazole (Monistat) 2% cream: One applicator or one 100-200 mg suppository, intravaginally q.h.s.  7 days
• Clotrimazole (Gyne-Lotrimin, Mycelex): Intravaginal tablets (100 mg q.h.s.  6-7 days, 200 mg q.h.s.  3 days; 500 mg daily  1), or 1% cream (one applicator q.h.s.  6-7 days)
• Nystatin (Mycostatin, Nilstat): 100,000 U/g cream (one applicator) or 100,000 U tablets (one tablet) intravaginally 1  day  7-14 days
• Fluconazole (Diflucan): 150 mg tablet  1
Oropharangeal
• Clotrimazole (Mycelex): 10 mg troche, suck on over 20 minutes 5  day  7-14 days*
• Nystatin pastilles: 1-2 q.i.d.  7-14 days*

*Two days after disappearance of thrush
Esophagitis
Fluconazole:100 mg/d  14-21 days, load w/200 mg)
Itraconazole (Sporanox)
• Solution: 1-200 mg daily  7-14 days
• Capsules: 200 mg/d (take with food)  2-3 weeks
Gastrointestinal
Therapy not well defined
• Contraindications
- Vaginal antifungal creams and suppositories can decrease protective aspects of condoms and diaphragms.
- Any drug is contraindicated if it causes a severe allergic response or severe adverse reaction.
- Ketoconazole, itraconazole, or nystatin (if swallowed): Severe hepatotoxicity
- Amphotericin B: Renal failure
• Precautions
- Miconazole: Usually pregnancy drug of choice
- Fluconazole: Renal excreted; rare hepatotoxicity; resistance has often been noted
- Itraconazole: Doubling the dosage results in ~3-fold increase in itraconazole plasma concentrations.
• Possible interactions (rarely seen with creams, lotions, or suppositories)
- Fluconazole
 Rifampin: Decreased fluconazole concentrations
 Tolbutamide: Decreased tolbutamide concentrations
 Warfarin, phenytoin, cyclosporine: Altered metabolism; check levels
• Itraconazole: This potent cytochrome P450 3A4 isoenzyme system (CYP3A4) inhibitor may increase plasma concentrations of the many drugs metabolized by that pathway and cause serious cardiovascular events. Carefully assess all co-administered medications.
Second Line
Oropharyngeal
• Nystatin oral suspension (100,000 U/mL): Children: 5-10 mL q.i.d.  10 days directly to oral lesions); Adults: Swish "for as long as reasonable" and swallow 5-10 mL q.i.d.  14 days); prophylaxis = above dosages 2-5  day.
• Fluconazole: 100 mg/d  7-14 days (load immunocompromised patient with 200 mg)
• Itraconazole (Sporanox) Suspension: 200 mg (20 mL) daily swish and swallow  7-14 days* Capsules: 200 mg/d (take with food)  2-4 wks*
• Amphotericin B (Fungizone) oral suspension (100 mg/mL): 1 mL q.i.d., swish "for as long as reasonable" and swallow; use between meals
• Ketoconazole: 200-400 mg PO daily for 14-21 days
Esophagitis: Amphotericin B (variable dosing)
Vaginal:
• Terconazole (Terazol), particularly for recurrent cases that may involve imidazole resistance: 0.4% cream (one applicator intravaginally q.h.s.  7 days); 0.8% cream/80 mg suppositories (1 applicator or 1 suppository intravaginally q.h.s.  3 days)
• Itraconazole 200 mg capsule 1 b.i.d.  1 day
• Any of the antifungal creams or suppositories can be tried every month for a few days near menses to help curb recurrent infections.

*Two days after disappearance of thrush
FOLLOW-UP
DISPOSITION
Issues for Referral
• Patients without obvious reasons for recurrent superficial candidal infections (e.g., HIV, diabetes) may have chronic mucocutaneous candidiasis.
• GI candidiasis
PROGNOSIS
For immunocompetent individuals, a benign course and excellent prognosis are the norm. In immunosuppressed persons, Candida may become an "AIDS-defining illness" by the Centers for Disease Control and Prevention criteria and chronicity may cause much morbidity.
COMPLICATIONS
• Major complications rarely develop in immunocompetent persons.
• In immunosuppressed persons, complications depend on the severity of the immune status. Moderate immunosuppression (e.g., CD4 200-500 cells/mm3) may be associated with chronic candidiasis. In severe immunosuppression (e.g., CD4 100 cells/mm3), thrush may lead to esophagitis, then a full-systemic infection involving every organ system, particularly renal.
PATIENT MONITORING
Immunocompromised persons may benefit from regular symptom evaluation plus "routine" KOH preps during vaginal and oral exams.
REFERENCES
1. Kyrmizakis DE, et al. Acute candidiasis of the oro- and hypopharynx as the result of topical intranasal steroids administration. Rhinology. 2000;38(2):87-89.
2. Strus M. et al. The in vitro activity of vaginal Lactobacillus with probiotic properties against Candida. Infect Dis Obstet Gynecol. 2005;13(2):69-75.
3. Rex JH, et al. Practice guidelines for the treatment of candidiasis. Infectious Diseases Society of America. Clin Infect Dis. 2000;30(4):662-678. Epub 2000 Apr 20.
4. Eggimann P, Garbino J, Pittet D. Management of Candida species infections in critically ill patients. Lancet Infect Dis. 2003;3(12):772-785. Review.
5. Pappas PG, et al. Guidelines for treatment of candidiasis. Clin Infect Dis. 2004;38:161-189.
6. Friedlander SF, Rueda M, Chen BK, Caceres-Rios, HW. Fungal, protozoal, and helminthic infections. In: Schachner LA, Hansen RC, eds. Pediatric Dermatology. Edinburgh: Mosby; 2003:1093.
ADDITIONAL READING
• Betts RF, et al. A Practical Approach to Infectious Diseases. Boston, MA: Little, Brown  Co; 2002.
• Kauffman CL, Barnhill RL, eds. Fungal infections. In: Textbook of Dermatopathology, New York, NY: McGraw-Hill; 2004.
MISCELLANEOUS
• Other notes
- Transmission from person to person is rare.
- Occasionally Candida vaginitis may be sexually transmitted.
- Rarely, oral Candida leukoplakia may be precancerous.
- Skin testing is positive in 70-85% of individuals randomly checked in studies.
• See also: Candidiasis; HIV Infection; AIDS; Vulvovaginitis; Candidal

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Thursday, January 22, 2009

BURSITIS

BURSITIS - John Herbert Stevenson, MD; Christopher Lutryzkowski, MD; Peter L. Hoth, MD
BASICS
DESCRIPTION
• A bursa is a sac that is formed or found in areas subject to friction, such as locations where tendons pass over bony landmarks. Most common sites are subdeltoid, olecranon, prepatellar, trochanteric, radiohumeral. They essentially lubricate the region with synovial fluid.
• Large bursae usually communicate with joints and are responsible for retaining the synovial fluid in place.
• Bursae are fluid-filled sacs that serve as a cushion between tendons and bones.
• Bywaters, an English rheumatologist, found at least 78 bursae symmetrically placed on each side of the body.
• System(s) Affected: Musculoskeletal
ALERT
Pediatric Considerations
Bursitis less common in the pediatric population.
GENERAL PREVENTION
• Appropriate warm-up and cool-down maneuvers, avoidance of overuse, or inadequate rest between workouts
• Range-of-motion exercises
• Maintain high level of fitness and general good health.
EPIDEMIOLOGY
Predominant age
• 15-50 years (most common in skeletally mature)
• Traumatic bursitis more likely in patients 35 years of age
Incidence
• Common
• Trochanteric pain: 1.8 per 1000 per year (6)[B]
RISK FACTORS
Individuals who engage in repetitive and vigorous training or others who suddenly increase their level of activity (e.g., "weekend warriors")
ETIOLOGY
• Bursitis may be acute or chronic.
• Many types of bursitis, including infectious, traumatic, inflammatory, and gouty
• Less often rheumatoid disease or tuberculosis as well as gout and pseudogout
ASSOCIATED CONDITIONS
• Tendinitis
• Sprains, strains
• Associated stress fractures

DIAGNOSIS
SIGNS AND SYMPTOMS
• Pain/tenderness
• Decreased range of motion of affected region (rare except at shoulder)
• Erythema if infection present
• Swelling
• Crepitus sometimes found
TESTS
ECG (if shoulder pain mimics cardiac pain)
Lab
• The following may help in differentiating soft-tissue disease from rheumatic and connective tissue disease
- CBC
- ESR
- Serum protein electrophoresis
- Rheumatoid factor
- Serum uric acid
- Phosphorus
- Alkaline phosphatase
- Blood testing for syphilis
- Joint fluid analysis and culture (when indicated)
• Drugs that may alter lab results
- ESR rate may be increased with coexistent use of methyldopa, methysergide, penicillamine, theophylline, vitamin A.
- ESR may be decreased with coexistent use of quinine, salicylates, and drugs that cause a high glucose level.
Imaging
• MRI may prove beneficial if diagnosis is unclear
• Calcific deposits may be seen on plain radiograph.
• Ultrasound (1)[B]
Diagnostic Procedures/Surgery
• Aspiration of swollen bursa and evaluation of synovial fluid
• The clinician must differentiate infected from inflammatory bursitis. Fluid analysis and culture help make the diagnosis. If the Gram stain and culture yield an infective cause, treat with appropriate antibiotics. If the etiology is inflammatory, give local care.
Pathological Findings
• Acute with early inflammation: Bursa is distended with watery or mucoid fluid.
• Infection: Purulent fluid
• Chronic
- Bursal wall is thickened, and inner surface is shaggy and trabeculated.
- The space is filled with granular, brown, inspissated blood admixed with gritty, calcific precipitations.
- Upper extremity tendonitis and bursitis are usually the result of repetitive microtrauma, probably resulting in disruption of fibers leading to pain, spasm, and disability.
DIFFERENTIAL DIAGNOSIS
• Septic arthritis
• Gout, pseudogout
• Rheumatic disorders
• Osteoarthritis
• Tendinitis, strains, and sprains
• Lyme arthritis
TREATMENT
Outpatient; refer only difficult cases.
GENERAL MEASURES
• Conservative therapy consists of rest, ice, and local care; elevation, gentle compression (often referred to as RICE therapy [rest-ice-compression-elevation]).
• Compression with Ace wrap or neoprene sleeve
• Bursa aspiration
• Corticosteroid injection if infectious etiology ruled out
• Treatment of any underlying infection
Diet
Consider changes if bursitis is directly related to obesity/crystalline deposition.
Activity
Rest and elevation of affected extremity
MEDICATION (DRUGS)
First Line
• NSAIDs or aspirin (2,4,5)[C], (9)[C]
• Antibiotic therapy if infection present; cover for staph and strep species (most common) (8)[B]
• Contraindications: Refer to manufacturer's profile of each drug.
• Precautions: Refer to manufacturer's profile of each drug.
• Significant possible interactions: Refer to manufacturer's profile of each drug.
Second Line
• Injectable corticosteroids once infectious etiology ruled out (2,4,5)[C], 3[B], (9)[B]
• Systemic steroids provide limited short-term benefit (7)[B].
SURGERY
Surgical excision in severe cases unresponsive to conservative treatments (8)[B]
FOLLOW-UP
PROGNOSIS
• Most bouts of bursitis heal without sequelae.
• Repetitive acute bouts may lead to chronic bursitis, necessitating repeated joint/bursal aspirations or eventually surgical excision of involved bursa.
COMPLICATIONS
• Septic bursitis may extend to the nearby joint.
• Acute bursitis may progress to chronic.
• Severe long-range limitation of motion
PATIENT MONITORING
• Discontinue NSAIDs as soon as possible to avoid side effects
• Some patients may require repeated injections (usually no more than 3) of a corticosteroid and lidocaine (2,4,5)[C].
REFERENCES
1. Finlay K, Friedman L. Ultrasonography of the lower extremity. Orthop Clin North Am. 2006;37(3):245-75,v.
2. Talia, Alfred H., Cardone, Dennis. Diagnostic and Therapeutic injection of the shoulder region. Am Fam Phys. 2003;67(6): 1271-1278.
3. Buchbinder R, et. al. Corticosteroid injection for shoulder pain. Cochrane Database Sys Rev. Jan. 1, 2003.
4. Cardone D, Tallia AH. Diagnostic and therapeutic injection of the elbow. Am Fam Phys. 2002;66(11):2097-3100.
5. Cardone D, Tallia AH. Diagnostic and therapeutic injection of the hip and knee. Am Fam Phys. 2003;67(10):2147-2153.
6. Lieviense A, et al. Prognosis of trochanteric pain in primary care. Br J Gen Pract. xxx;55(512): 199-204.
7. Buchbinder R, et. al. Short course prednisolone for adhesive capsulitis (frozen shoulder or stiff painful shoulder): A randomized, double blind, placebo controlled trial. Ann Rheum Dis. 2004;63(11):1460-1469.
8. Small LN. Suppurative tenosynovitis and septic bursitis. Infect Dis Clin North Am. 2005;19(4):991-1005, xi.
9. McFarland EG. Miscellaneous conditions about the elbow in athletes. Clin Sports Med. 2004;23(4):743-763, xi-xii.
MISCELLANEOUS
See also: Tendinitis

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BURNS

BURNS - Timothy L. Black, MD; James P. Miller, MD
BASICS
DESCRIPTION
• Tissue injuries caused by application of heat, chemicals, electricity, or irradiation to the tissue
• Extent of injury (depth of burn) is result of intensity of heat (or other exposure) and duration of exposure
- Partial thickness: 1st degree involves superficial layers of epidermis. 2nd degree involves varying degrees of epidermis (with blister formation) and part of the dermis.
- Full thickness: 3rd degree involves destruction of all skin elements with coagulation of subdermal plexus
• System(s) Affected: Endocrine/Metabolic; Skin/Exocrine
ALERT
Geriatric Considerations
• Prognosis poorer for severe burns
• Patients >60 years of age account for 11% of burns. (1)[C]
Pediatric Considerations Consider child abuse or neglect when dealing with hot water burns in children
• Observe distribution of burns.
• Pay attention to straight lines, especially if bilateral.
GENERAL PREVENTION
Skin grafts or newly epithelialized skin is highly sensitive to sun exposure and thermal extremes.
EPIDEMIOLOGY
• Predominant age: All ages
- Average age is 30 years
- 13% are infants, and 11% are >60 years of age
• Predominant sex: Males account for 70%
Incidence
Per year in US
• Total population: 1.2-2 million burns, 700,000 emergency room visits, 45,000-50,000 hospitalizations, 3,900 deaths due to burn-related complications (1,2)[C]
• In children: 250,000 burns, 15,000 hospitalizations, 1,100 deaths
• Estimated total cost of $2 billion annually for burn care in the United States (1)[C]
• 75% of burn related deaths are the result of house fires (1)[C]
RISK FACTORS
• Water heaters set too high
• Workplace exposure to chemicals, electricity, or irradiation
• Young children and elderly adults with thin skin are more susceptible to injury.
• Carelessness with burning cigarettes
• Inadequate or faulty electrical wiring
• Lack of smoke detectors
ETIOLOGY
• Open flame and hot liquid are most common (heat usually 15-45C)
• Caustic chemicals or acids (may show little signs or symptoms for the first few days)
• Electricity (may have significant injury with very little damage to overlying skin)
• Excess sun exposure
ASSOCIATED CONDITIONS
Smoke inhalation syndrome
• Occurs within 72 hours of burn
• Should be suspected in all burns occurring in an enclosed space
• Intubation, ventilation with positive end-expiratory pressure assistance

DIAGNOSIS
SIGNS AND SYMPTOMS
• 1st degree
- Erythema of involved tissue
- Skin blanches with pressure
- Skin may be tender
• 2nd degree
- Skin is red and blistered
- Skin is very tender
• 3rd degree
- Burned skin is tough and leathery
- Skin is not tender
History
• History of source of burn
• In children, check for consistency between the history and the burn's physical characteristics
Physical Exam
• Careful documentation of extent of burn and the estimated depth of burn
• Check for any signs suggestive of potential airway involvement: Singed nasal hair, facial burns, carbonaceous sputum, progressive hoarseness, or tachypnea
TESTS
• Children: Glucose (hypoglycemia may occur in children because of limited glycogen storage)
• Smoke inhalation: Arterial blood gas, carboxyhemoglobin
• Electrical burns: ECG, urine myoglobin, creatine kinase isoenzymes
Lab
• Hematocrit
• Type and cross
• Electrolytes, including blood urea nitrogen and creatinine
• Urinalysis
• Disorders that may alter lab results: Preexisting cardiac disease
Imaging
• Chest radiograph
• Xenon scan may be useful in suspected smoke inhalation.
• Other radiographs if other trauma involved
Diagnostic Procedures/Surgery
Bronchoscopy may be necessary in smoke inhalation to evaluate lower respiratory tract.
Pathological Findings
• 1st degree
- Devitalization of superficial layers of epidermis
- Congestion of intradermal vessels
• 2nd degree
- Coagulation necrosis of varying depths of epidermis
- Clefting of epidermis (blister)
- Coagulation of subdermal plexus
- Skin appendages intact
• 3rd degree
- Necrosis of all skin elements
- Coagulation of subdermal plexus
DIFFERENTIAL DIAGNOSIS
• Toxic epidermal necrolysis
• Scalded skin syndrome
TREATMENT
• Hospitalization for all serious burns
- 2nd-degree burns >10% body surface area, any 3rd-degree burn
- Burns of hands, feet, face, or perineum
- Electrical/lightning burns
- Inhalation injury
- Chemical burns
- Circumferential burn
• Transfer to burn center for (1,2,3)[C]
- 2nd- and 3rd-degree burns >10% body surface area in patients 10 years and >50 years of age
- 2nd-degree burns >20% body surface area and full thickness burns >5% BSA in any age range
- Burns of hands, feet, face, or perineum
- Electrical/lightning burns
- Inhalation injury
- Chemical burns
- Circumferential burn
- Chemical burns with threat of functional impairment
PRE-HOSPITAL (1)[C]
• Remove patient from source of the burn
• Extinguish and remove all burning clothing
• Remove all rings, watches, and jewelry
• Room-temperature water may be poured onto burn but only in the 1st 15 minutes following burn exposure
• Wrap patient to prevent hypothermia
• All patients should receive 100% O2 by face mask
GENERAL MEASURES
• Based on depth of burns and accurate estimate of total body surface area involved (rule of nines)
• Rule of nines (1)[C]
- Each upper extremity: Adult and child 9%
- Each lower extremity: Adult 18%; child 14%
- Anterior trunk: Adult and child 18%
- Posterior trunk: Adult and child 18%
- Head and neck: Adult 10%; child 18%
• Quick estimate (for smaller burns): The surface area of the patient's hand is ~1% of the body surface area.
• Tetanus prophylaxis (if not current)
• Remove all rings, watches, and other items from injured extremities to avoid tourniquet effect.
• Remove clothing and cover all burned areas with dry sheets.
• Flush area of chemical burn (for ~2 hours)
• 100% oxygen administration for all major burns; consider early intubation
• Do not apply ice to burn site.
• Nasogastric tube (high risk of paralytic ileus)
• Foley catheter
• Pain relief
- IV meperidine (Demerol), morphine, or methadone for severe pain
- Oral analgesics, such as acetaminophen (Tylenol) with codeine, acetaminophen with oxycodone (Percocet), or acetaminophen with hydrocodone (Lortab) for moderate pain
• ECG monitoring in 1st 24 hours following electrical burn
• Whirlpool hydrotherapy followed by silver sulfadiazine (Silvadene) occlusive dressings in severe burns
• Once- or twice-a-day cleansing with dressing changes
• Epilock or Elasto-Gel may be used as dressing in selected patients (especially useful for outpatient treatment of minor burns)
• Burn fluid resuscitation (1,2,3)[C]
- Calculate fluid resuscitation from time of burn, not from time treatment begins
- 2-4 mL Ringer's lactate  body weight (kg)  % body surface area burn (1/2 given in 1st 8 hours, 1/4 in 2nd 8 hours, and 1/4 in 3rd 8 hours). In children, this is given in addition to maintenance fluids and is adjusted according to urine output and vital signs.
- Colloid solutions are not recommended during the 1st 12-24 hours of resuscitation (1,2)[C], (4)[A]
• Other: Use of biological membranes or skin substitutes may be indicated for burn coverage.
Diet
• High-protein, high-calorie diet when bowel function resumes
• Nasogastric tube feedings may be required in early postburn period
• Total parenteral nutrition if NPO expected for >5 days
Activity
Early mobilization is the goal.
MEDICATION (DRUGS)
First Line
• Morphine small frequent IV doses (0.1 mg/kg/dose in children; 2.5-20 mg q2-6h in adults)
• Silver sulfadiazine (Silvadene) topically to burn site (can cause leukopenia)
• Electrical burn with myoglobinuria will require alkalinization of urine and mannitol
• No indication for prophylactic antibiotics.
• Consider H2 blockers (cimetidine, ranitidine, famotidine, or nizatidine) for stress ulcer prophylaxis in severely burned patients.
• Contraindications
- Specific drug allergies
• Precautions
- Be alert for respiratory depression with narcotics.
• Significant possible interactions
- Refer to manufacturer's profile for each drug.
Second Line
• Mafenide (Sulfamylon)full-thickness burn (caution: Metabolic acidosis)
• Silver nitrate 0.5% (messy, leaches electrolytes from burn, and causes water toxicity)
• Povidone-iodine (Betadine) may result in iodine absorption from burn, "tan eschar." Makes debridement more difficult.
• Travaseenzymatic debridement
SURGERY
• Escharotomy may be necessary in constricting circumferential burns of extremities or chest.
• Tangential excision with split-thickness skin grafts
FOLLOW-UP
PROGNOSIS
• 1st-degree burn: Complete resolution
• 2nd-degree burn: Epithelialization in 10-14 days (deep 2nd-degree burns will probably require skin graft)
• 3rd-degree burn: No potential for re-epithelialization, skin graft required
• Length of hospital stay and need for ICU care depend on extent of burn, smoke inhalation, and age
• A 50% survival rate can be expected with a 62% burn in ages 0-14 years, 63% burn in ages 15-40 years, 38% burn in age 40-65 years, 25% burn in patients >65 years (1,2,3)[C]
• 90% of survivors can be expected to return to an occupation as remunerative as their preburn employment.
COMPLICATIONS
• Gastroduodenal ulceration (Curling ulcer)
• Marjolin ulcersquamous cell carcinoma developing in old burn site
• Burn wound sepsisusually gram-negative organisms
• Pneumonia
• Decreased mobility with possibility of future flexion contractures
• Hypertrophic scarring common with burns
PATIENT MONITORING
According to extent of burn and treatment
REFERENCES
1. Teague H, Sweneki SA, Tang A. The burned patient: Assessment, diagnosis, and management in the ED. Trauma Reports. 2005;6:1-12.
2. Townsend C, Beauchamp RD, Evers BM, et al. eds. Sabiston Textbook of Surgery 17 ed. Philadelphia, PA: Elsevier Saunders, 2006.
3. Gillespie RW, Dimik AR, Hallberg PW. Advanced Burn Life Support Course Provider's Manual. Lincoln, NE: Nebraska Burn Institute; 1990.
4. Roberts I, Alderson P, Bunn F, et al. Colloids versus crystalloids for fluid resuscitation in critically ill patients (Review). Cochrane Database Sys Rev. 2006; Vol 1.

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BRUCELLOSIS

BRUCELLOSIS - Nancy Snapp, MD, MPH
BASICS
DESCRIPTION
• Systemic bacterial infection caused by Brucella species in infected animal products, or vaccine
• Incubation period usually 5-60 days, but highly variable and may be several months
• Characterized by intermittent or irregular fevers, with symptoms ranging from subclinical disease to infection of almost any organ system
• Bone and joint involvement common
• May be chronic or recurrent
• System(s) Affected: Cardiovascular; Endocrine/Metabolic; Gastrointestinal; Musculoskeletal; Nervous; Pulmonary; Renal/Urologic; Skin/Exocrine
• Synonym(s): Undulant fever; Malta fever
ALERT
Pediatric Considerations
May be mild, subclinical
Pregnancy Considerations
High rates of miscarriage or abortion (can occur in subclinical cases). Early antibiotic treatment is preventive.
GENERAL PREVENTION
• Avoid infected dairy products.
• For occupational exposure, use caution, animal vaccination, protective goggles, protective gloves. There is a possibility of future human vaccine.
• Postexposure prophylaxis same as treatment in large-scale exposure such as bioterrorism
• Susceptible to heat, disinfectant, but can survive in dust, soil, or water for weeks
EPIDEMIOLOGY
• Predominant age: All ages, but especially ages 20-60 years (occupational exposure), sometimes children (milk-related outbreaks)
• Predominant sex:
- Male > Female (occupational exposure)
- Female  Male (milk exposure)
Incidence
~100 per year (0.34/100,000), but probably underreported (1,2)
Prevalence
• Common in developing countries; consider in immigrants
• Highest rates in Hispanic population, along US-Mexico border
• Considered a potential biological terror agent in aerosolized form
• Reportable in all states except Nevada
RISK FACTORS
• In the US, from occupational exposure to infected animals (especially cattle, sheep) veterinarians, meat processors, farm workers who may experience accidental exposure to vaccine.
• Consumer exposure to unpasteurized milk products, cheese, especially in Hispanics along US-Mexico border
• Exposure while traveling in countries where endemic (Mediterranean, Middle East, North and East Africa, Central Asia, India, Mexico, and Central and South America)
• Worse in chronically ill, immunosuppressed, and malnourished
• Iron deficiency increases susceptibility
Genetics
• Some evidence for intrauterine transmission
• Some complications may have genetic predisposition (2)
ETIOLOGY
• Brucella ingestion from tissue or milk
• Worst disease: B. melitensis, B. suis; also B. canis, B. abortus. Enters through mucous membrane or broken skin; occasionally inhaled.
• Facultative intracellular parasite
• Person-to-person transmission rare; sexual, vertical, and possibly breast milk; case report of neonatal brucellosis from a blood transfusion
• Potential air-borne biologic weapon

DIAGNOSIS
SIGNS AND SYMPTOMS
• Fever (may be undulant, increased in afternoon and evening, maximum 101-104F daily); weakness; headache; sweating; chills; generalized aching; arthralgia (90%) (2)[A]
• Also common: Weight loss, depression, irritability, hepatosplenomegaly (20-30%)
• Hepatic dysfunction (abnormal liver function test): 30-60%
• Gastrointestinal symptoms (unusual)
• Lymphadenopathy, especially cervical, inguinal (12-21%)
• Orchitis, epididymitis (normal urinalysis) (2-40%)
• Nephritis, prostatitis (rare)
• Cystitis
• Pulmonarycough or other pulmonary symptoms; radiograph may be normal (15-25%)
• Cutaneousmany transient, nonspecific rashes have been described; also, purpura from thrombopenia (5%)
• Visual disturbances, eye pain
• Chronic fatigue syndrome and various neuropsychiatric symptoms described. Relationship is unclear.
• Also localized supurative infections (see "Complications")
• Malodorous perspiration (2)
History
Exposure
TESTS
Echocardiogram, depending on location
Lab
• Isolation of organism from blood, discharge, bone, or other tissue (3)[C]
- Fastidious and slow growing
- Watch for 3-4 weeks, with periodic subcultures
- Automated systems shorten time, but not all recognize brucellosis.
- Polymerase chain reaction (PCR) accurate, including nonblood samples, but not available in most clinical labs (3)[C]
- Skin tests not standardized, not recommended for diagnosis
• Acute illness: Blood culture positive 70%, bone marrow 90%
• May have thrombocytopenia, disseminated intravascular coagulation; granulopenia, lymphopenia, lymphocytosis. 30-60% with abnormal liver function test. Up to 70% may have normal labs.
• Serology: Use at least 2 tests to confirm (4)[C]
- Brucella standard tube agglutination paired sera, >1:160 or 4 rise (cheapest)
- Easy, accurate, and rapid dipstick for IgM now exists for developing countries
• More effective enzyme-linked immunosorbent assay (ELISA), indirect fluorescent antibody test, Coombs tests, immunocapture-agglutination (Brucellacapt). With ELISA, IgM, IgG, or IgA may be present at low levels >1 year even if treated
• IgM increased initially for several weeks, declines by 3 months
• IgG begins to rise in 2 weeks, may stay up (low levels) >1 year if treated or not treated (though IgM increase may be lower or gone by 6 months if treated, can also persist >1 year at low levels). IgG titer rises again with reinfection or reactivation. IgG and IgA titer >1:160 at 1 year implies ongoing disease. (4)[C]
• New research: Gene cloning and amplification for discriminatory markers detection and strain differences; PCR-ELISA
• Drugs that may alter lab results
- None
• Disorders that may alter lab results
- Serologic cross-reaction with F. tularensis, Yersinia enterocolitica, V. cholerae, or vaccinated patients
- Has been misdiagnosed in culture as Moraxella phenylpyruvica
Imaging
• Bone scan, CT, depending on location
• Chest radiographpleural effusion, lung cavitation
• Joint radiographs frequently normal, requiring scan or MRI
Diagnostic Procedures/Surgery
Biopsy, aspiration, depending on location
Pathological Findings
• Facultative intracellular Gram-negative coccobacillus; can survive inside phagocytic cells, circulate to regional lymph nodes, and into circulation
• Variable tissue reaction depending on site, organisms. Causes local microabscesses; noncaseating granulomas; (1) possibly some immune reaction in arthritis, including elevated C3, C4; antinuclear antibody, and rheumatoid factor.
DIFFERENTIAL DIAGNOSIS
• Many nonspecific systemic febrile illnesses; a great mimic
• Tularemia
• Psittacosis
• Rickettsial disease
• Tuberculosis
• Visceral leishmaniasis
• Other disease of infected organs
• HIV infection
TREATMENT
• Outpatient in mild cases, hospitalization in severe illness
• Cardiac care unit for patients with complicating cardiac disease
GENERAL MEASURES
• Supportive care
• In milk-related or occupational outbreak, look for other cases.
Diet
• No special diet
• May need to provide supplemental foods, such as milk shakes, to counter weight loss
Activity
Bed rest during febrile periods and restricted activity in acute cases
Nursing
Patient comfort, education
IV Fluids
If cardiac complications
MEDICATION (DRUGS)
First Line
• Optimal therapy includes 2 drugs, at least 1 with good intracellular penetration. In some cases, 3 drugs may give a better long-term cure.
• Longer courses (months) may improve relapse rate in complicated disease.
• Rifampin 600-900 mg and doxycycline 200 mg given together every day for at least 6 weeks (possibly for several months with severe complications); 5-10% relapse rate, not related to drug resistanceuse same drugs for relapse. Usual cause is localized sequestration of organisms or noncompliance with medication (5)[C].
• Steroids in Herxheimer reaction, severe illness, and pancytopenia
• Contraindications
- Avoid doxycycline in children and pregnant women (affects bone).
• Precautions:
- May get Herxheimer reaction when therapy initiated
• Significant possible interactions:
- Rifampin is a potent inducer for the hepatic P450 enzyme system, and may increase metabolism of many drugs metabolized by the liver.
- Doxycycline: Antacids, anticoagulants, barbiturates, carbamazepine, hydantoins, cimetidine, digoxin, insulin, iron salts, lithium, methoxyflurane, oral contraceptives, penicillins, sodium bicarbonate
Second Line
• In recent studies, ciprofloxacin 1 g daily and rifampin 600 mg/d for 30 days as effective as rifampin/doxycycline for 4-5 weeks (2,6)[A]
• Doxycycline PO b.i.d. and streptomycin by injectionvery effective (streptomycin currently not available in the US except by special request from Centers for Disease Control and Prevention); slightly more effective than doxycycline/rifampin, especially with spondylitis, but more toxic and less convenient (5)
• In children and pregnant women, rifampin 15 mg/kg for 4-5 weeks plus cotrimoxazole for 6 weeks or gentamicin for 7 days or netilmicin 5-6 mg/kg IM. Significant cotrimoxazole resistance in some countries (1,6)[C]
• Ofloxacin plus rifampin effective in recent study
• Sensitivities frequently don't reflect in vivo action (2)[C]
SURGERY
Specific complications may require surgical drainage or valve replacement (endocarditis).
FOLLOW-UP
PROGNOSIS
• Untreated case fatality 2%
• Most cases resolve with treatment in 2-3 weeks in acute uncomplicated cases, but at least 6 weeks treatment recommended
COMPLICATIONS
• Relapse rate overall: 5-10% (6)[C]
• Complications present 10-15% (4)[C]
• Localized suppurative infectionsosteo-articular (20-85%). Includes arthritis (possibly also immune effect), bursitis, tenosynovitis, osteomyelitis, sacroiliitis, vertebral or paraspinous abscess
• Endocarditisrare, but main cause of death in brucellosis
• Thrombophlebitis
• Neuro-brucellosismost are meningeal. Also peripheral neuritis (usually single; bilateral is possible), encephalitis, myelitis, radiculopathy. Possibly neuropsychiatric symptoms
• Intrinsic ocular lesionsuveitis, retinal thrombophlebitis, nummular keratitis
• Pneumonitis with pleural effusion
• Hepatitis
• Cholecystitis
• Chronic infection. Persistent (>1 year) signs of infection, elevated titers, occasional bacteria in blood or tissue. Chronic fatigue syndrome with everything negative is controversial.
PATIENT MONITORING
• Check serology at 6 months and 1 year for chronic disease (difficult to evaluate if continuing exposure).
• Investigate any evidence of complication or recurrence.
• PCR recently shown to be sensitive and specific for monitoring treatment relapse
REFERENCES
1. Sauret J, Vilissova N. Human brucellosis. J Amer Board Fam Pract. 2002;15:401-406.
2. Pappas, Georgios, et al. Brucellosis. N Eng J Med. 2005;352(22);2325-2336.
3. Al Dahouk S, Tomaso H, et al. Laboratory-based diagnosis of brucellosisa review of the literature. Part I: Techniques for direct detection and identification of Brucella spp. Clin Lab. 2003;49:487-505.
4. Al Dahouk S, Tomaso H, et al. Laboratory-based diagnosis of brucellosisa review of the literature. Part II: Serological tests for brucellosis. Clin Lab. 2003;49:577-589.
5. Montejo JM, et al. Open randomized therapeutic trial of six antimicrobial regimens in brucellosis. Clin Infect Dis. 1993;16:671-676.
6. Pappas, Georgios, et al. New approaches to the antibiotic treatment of brucellosis. Intl J Antimicrob Ag. 2005;26(2);101-105.
MISCELLANEOUS
See also: Abortion, Spontaneous; Chronic Fatigue Syndrome; Thrombosis, Deep Vein (DVT)

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