Rosen & Barkin's 5-Minute Emergency Medicine Consult (765 page)

Patients with shunt complications usually require neurosurgical consultation and admission. An ICU or other monitored setting is often needed.

When shunt malfunction is ruled out, disposition depends on alternate diagnosis and patient condition.

• Avoid “tunnel vision” in a patient with a shunt and consider other causes for the presentation
  
• Severe constipation may cause increased intra-abdominal pressure and decrease drainage resulting in increased ICP:
  
  • Treatment of constipation may ameliorate the apparent “shunt malfunction”
    

• Barnes NP, Jones SJ, Hayward RD, et al. Ventriculoperitoneal shunt block: What are the best predictive clinical indicators?
  Arch Dis Child
  . 2002;87:198–201.
  
• Madsen MA. Emergency department management of ventriculoperitoneal cerebrospinal fluid shunts.
  Ann Emerg Med
  . 1986;15:1330–1343.
  
• Martínez-Lage JF, Martos-Tello JM, Ros-de-San Pedro J, et al. Severe constipation: An under-appreciated cause of VP shunt malfunction: A case-based update.
  Childs Nerv Syst
  . 2008;24:431–435.
  
• Moza K, McMenomey SO, Delashaw JB Jr. Indications for cerebrospinal fluid drainage and avoidance of complications.
  Otolaryngol Clin North Am
  . 2005;38:577–582.
  
• Stein SC, Guo W. Have we made progress in preventing shunt failure? A critical analysis.
  J Neurosurg Pediatr.
  2008;1(1):40–47.
  

CODES

• V45.2 Presence of cerebrospinal fluid drainage device
  
• 996.63 Infection and inflammatory reaction due to nervous system device, implant, and graft
  
• 996.75 Other complications due to nervous system device, implant, and graft
  

BASICS

• A wide complex tachydysrhythmia with a quasirandom signal (QRS) >120 and a rate >100
  
• Rapid and regular depolarization of the ventricles independent of the atria and the normal conduction system
  
• Re-entry:
  
  • Structural heart disease most common
    
  • Seen in dilated cardiomyopathy, ischemia, and infiltrative heart disease, previous MI, scarring
    
  • May be pharmacologically induced
    
  • Usually produces a regular and monomorphic rhythm
    
• Triggered automaticity:
  
  • Minority of ventricular tachycardia (VT)
    
  • Caused by repetitive firing of a ventricular focus
    
• Torsades de pointes:
  
  • Polymorphic form of VT
    
  • Alternating electrical polarity and amplitude
    
  • Prolongation in repolarization necessary
    
  • Usually pharmacologically induced
    
• Regardless of the mechanism, all VT may degenerate to ventricular fibrillation (VF).
  

• Wide complex tachycardia:
  
  • 80% likelihood of being VT
    
  • 20% supraventricular tachycardia (SVT) with a baseline left bundle branch block (LBBB) or aberrancy
    
• Wide complex tachycardia and a history of MI:
  
  • >98% likelihood of being VT
    
  • Age >35: 80% risk of VT
    
  • Age <35: 75% risk of SVT
    
• Incidence of nonsustained VT:
  
  • 0–4% in the general population
    
  • Up to 60% of patients with dilated cardiomyopathy
    
• Associated with increased risk for sudden cardiac death (SCD)
  

DIAGNOSIS

• Asymptomatic
  
• Syncope/near syncope
  
• Lightheadedness/dizziness
  
• Shortness of breath
  
• Palpitations
  
• Chest discomfort/pain
  
• Diaphoresis
  
• Cannon A-waves
  
• Hypotension
  
• CHF
  
• Beat-to-beat variability of systolic BP
  
• Variability in heart tones, especially S1
  

• Establish presence of pulses, mental status and vital sign abnormalities.
  
• Auscultation of heart will reveal tachycardia.
  

• EKG:
  
  • Most important initial test to differentiate VT from SVT with aberrancy or LBBB
    
• VT definition:
  
  • ≥3 consecutive QRS complexes with a ventricular rate over 100 bpm and a QRS duration >120 msec
    
• Torsades de pointes:
  
  • Polymorphic VT that rotates its axis every 10–20 beats
    
• Criteria to determine VT:
  
  • Atrial ventricular (AV) dissociation (present in 60–75%)
    
  • Fusion beats (P-wave partially activates ventricle in advance of next VT cycle), capture beats (P-wave totally activates ventricle)
    
  • Uniform morphology (except in the case of torsades)
    
  • Extreme axis deviation (–90° to +180°)
    
  • QRS >140 msec, with right bundle branch block (RBBB) morphology; or QRS >160 msec, with LBBB morphology, but >160 suggests VT regardless of bunch branch morphology
    
  • QRS concordance in the precordial leads
    
  • RBBB pattern V1 with R > R’ is VT 50:1.
    
  • LBBB pattern with Q or QS pattern in V 6 is VT 50:1.
    
  • Brugada criteria defines VT in wide complex tachycardia:
    
    • 99% sensitivity, 97% specificity
      
    • Only need to meet 1 criterion
      
    • AV dissociation
      
    • R-S interval absent in all precordial leads
      
    • QRS onset to the nadir of S >100 msec in any precordial lead
      
    • V1 R-wave >30 msec; R-S interval >70 msec, slurred, notched S
      
    • Wide QRS with LBBB in precordium
      
  • Indicators of SVT with aberrancy include:
    
    • Normal-axis QRS <140 msec
      
    • Absence of Q-waves
      
    • RBBB in V1 with rsR′ triphasic pattern
      
    • AV nodal blockade: Slowing of impulse conduction velocity seen with antiarrhythmic drugs is more pronounced at faster rates, so may result in wide complex SVT (SVT with aberrancy)
      

• Cardiac enzymes
  
• Electrolytes, BUN, creatinine, glucose
  
• Magnesium level
  
• Calcium level
  
• Digoxin level if toxicity suspected
  

CXR:

• Cardiomegaly or other cardiac anomalies may be apparent.
  

ECHO:

• Structural disease may be identified.
  

Esophageal pacing catheters:

• May be able to detect atrial activity to establish AV dissociation and therefore diagnose VT
  
• Catheters can then be used to overdrive pace if refractory to cardioversion/antiarrhythmics.
  

• SVT with aberrancy or baseline LBBB
  
• Proarrhythmia secondary to antidysrhythmia medications; suspect if:
  
  • VT morphology is different than previous episodes of VT
    
  • Medications have recently been started or changed
    
  • QT interval is >440 msec.
    
  • Torsades de pointes
    
  • If VT continues to recur after cardioversion
    

TREATMENT

• Cautions:
  
  • Transport stable patients suspected of being in VT without attempting to convert them.
    
  • Synchronized
    cardioversion for unstable patients with a pulse
    
  • Defibrillation for pulseless VT
    
• Controversies:
  
  • Lidocaine:
    
    • No benefit in the prevention of VT in patients with isolated premature ventricular contractions, regardless of the frequency
      

Pulseless VT: Defibrillate immediately and follow the VF treatment plan.

• Unstable patient:
  
  • Definition:
    
    • Chest pain
      
    • Hypotension
      
    • Evidence of worsening heart failure
      
  • Initiate immediate synchronized cardioversion with 100 J, quickly progressing to 200 J, 300 J, and 360 J if no response.
    
    • If the VT is polymorphic, begin cardioversion at 200 J.
      
  • Sedate the patient before cardioversion if at all possible.
    
  • If unable to terminate the VT, administer lidocaine and repeat the cardioversion.
    
  • Antitachycardia overdrive pacing if torsades
    
  • After successful return of sinus rhythm, begin amiodarone.
    
• Stable patient, monomorphic VT:
  
  • Normal cardiac function at baseline:
    
    • Procainamide
      or
      sotalol; may also consider amiodarone or lidocaine
      
    • Avoid sotalol if evidence of prolonged QT or known long QT syndrome.
      
  • Impaired cardiac function at baseline:
    
    • Amiodarone bolus, then infusion
      or
      lidocaine, then synchronized cardioversion
      
• Stable patient, polymorphic VT:
  
  • Normal QT interval at baseline:
    
    • Correct electrolyte abnormalities.
      
    • Treat ischemia if present.
      
    • Then begin
      1
      of the following: b2-blockers, lidocaine, amiodarone, procainamide, or sotalol.
      
  • Prolonged QT Torsades de pointes:
    
    • Correct electrolytes.
      
    • Magnesium sulfate
      or
      overdrive pacing
      or
      1 of the following: Isoproterenol, phenytoin, lidocaine
      
    • Isoproterenol is used to overdrive the tachycardia if the patient has no history of coronary artery disease or long QT syndrome.
      
    • Temporizing measure until external pacing available
      
  • Impaired cardiac function at baseline
    
  • Amiodarone bolus
    or
    lidocaine bolus then synchronized cardioversion