Rosen & Barkin's 5-Minute Emergency Medicine Consult (544 page)

• CT sensitive for adrenal masses >1 cm (IV contrast may pose a slight risk):
  
  • 5% of incidental adrenal tumors seen on CT are pheos.
    
• MRI or positron emission tomography more sensitive in identifying adrenal pheos as well as identifying extra-adrenal tumors
  
• Metaiodobenzylguanidine (radionuclear scintiscan: High specificity for localization, but not sensitive enough to exclude pheo)
  
• Chest radiograph for pulmonary edema
  
• CT head for CVA/intracranial bleed
  

• Clonidine suppression test if diagnosis uncertain (levels not suppressed if pheo)
  
• Provocative testing with glucagon is not recommended.
  
• Fine-needle aspiration is contraindicated.
  
• Laparoscopic resection is feasible in many cases.
  

• Alcohol withdrawal syndrome
  
• Autonomic hyperreflexia
  
• Cerebral vascular accident
  
• Cocaine or amphetamine intoxication
  
• Hypertensive crisis
  
• Migraines/subarachnoid hemorrhage
  
• Panic attack
  
• Postural tachycardia syndrome
  
• Paroxysmal supraventricular tachycardia
  
• Posterior reversible encephalopathy syndrome
  
• Serotonin syndrome
  
• Thyrotoxicosis
  
• Toxemia
  

TREATMENT

• IV access, oxygen
  
• Continuous cardiac/BP monitoring
  
• Nitroglycerin 0.4 mg SL for chest pain and HTN
  

• Phentolamine: α-blockade:
  
  • 1 mg IV test dose
    
  • 2.5–5 mg IV bolus given at 1 mg/min repeat bolus every 5–15 min to BP control. Follow by infusion
    
  • Infusion starting at 0.1 mg/min titrated up to 1 mg/min
    
  • Vigorous fluid resuscitation required as vasoconstriction is relieved
    
  • Traditional approach, but Nicardipine or Nitroprusside drip may be more practical
    
• β-blockade:
  
  • Add to α-blockade for further BP control
    
  • If tachycardia develops during induction of α-blockade
    
  • NEVER USE ALONE: Institution of β-blockade without prior α-adrenergic blockade may exacerbate hypertension by antagonizing β-mediated vasodilation in smooth muscle.
    
  • Esmolol: Load 500 μg/kg over 1 min, followed by 50 μg/kg/min for 4 min; if adequate therapeutic effect not achieved within 5 min, repeat loading dose and increase infusion to 100 μg/kg/min; repeat loading dose and titrate infusion rate upward at 50 μg/kg/min q4–q5min as needed; omit further loading doses once nearing therapeutic target.
    
  • Labetalol: Begin with 10–20 mg IV; BP falls within 5 min, maximum effect at 10 min; can double IV dose q15–q30min until target reached (α-blockade inadequate to be relied on as a single agent).
    
  • Metoprolol: 5 mg IV q15min until response
    
• Resistance to α- and β-blockade or 1st-line option if unfamiliar with Phentolamine:
  
  • Nitroprusside:
    
    • Start at 0.5 μg/kg/min
      
    • Titrate by 0.5 μg/kg/min increments
      
    • Maximum dose 10, average needed 3–4
      
  • Nicardipine:
    
    • Start infusion at 5 mg/hr
      
    • Titrate up by 2.5 mg/hr every 15 min
      
    • 15 mg/hr maximum dose
      
  • Add β-blockade to vasodilator if needed
    
• Ventricular tachydysrhythmias:
  
  • Lidocaine:
    
    • 50–100 mg bolus
      
    • Repeat bolus q5min (5 mg/kg max.)
      
  • Esmolol 50–200 μg/kg/min infusion
    

• Phenoxybenzamine: Start at 10 mg BID orally, titrate up 10 mg every other day until desired effect (start at least 7 days preop).
  
• Other α-blockers (1st dose effect):
  
  • Doxazosin: 1–8 mg/d (start at 1 mg)
    
  • Terazosin: 1–10 mg/d (start at 1 mg)
    
• β-blocker added to control reflex tachycardia:
  
  • Metoprolol or atenolol: 25–100 mg/d
    

• Calcium-channel blockers:
  
  • Amlodipine, nicardipine, or nifedipine
    
• Inhibition of catecholamine synthesis:
  
  • Metyrosine: 250–500 mg q6h
    

• May be confused with toxemia, but proteinuria is usually absent
  
• MRI is the preferred imaging modality.
  
• Nitroprusside should not be used for hypertensive crisis, but all other BP medications are acceptable.
  
• Spontaneous vaginal delivery will likely precipitate hypertensive crisis, such that C-section should be planned.
  

FOLLOW-UP

• Suspicion of pheo in an ill or toxic patient with labile swings in BP
  
• Hypertensive urgency or crisis
  
• Cardiac arrhythmias
  
• End organ compromise: Congestive heart failure, myocardial infarction, renal insufficiency, CVA, abdominal pain
  

Stable patient with mild hypertension.

• Obtain plasma-free metanephrine during a hypertensive episode.
  
• Consider initiating doxazosin or terazosin or a calcium-channel blocker for BP control.
  
• Arrange close follow-up
  

• Paroxysms of severe hypertension, headache, intense diaphoresis, and palpitations comprise a tetrad very suggestive of pheo.
  
• Pallor and sweating, not flushing, is typical of pheo crisis.
  
• Orthostasis is common in pheo and it is further aggravated by α-blockade, unless volume repletion is not done concomitantly.
  
• Consider pheo in unexplained shock, multisystem organ failure, cardiomyopathy, new glucose intolerance with weight loss.
  
• Never administer β-blockers (even labetalol) before α-blockade in patients with pheo
  
• Plasma-free metanephrine during an attack is very sensitive but not specific in the diagnosis
  

• Anderson NE, Chung K, Willoughby E, et al. Neurologic manifestations of phaeochromocytomas and secretory paragangliomas: A reappraisal.
  J Neurol Neurosurg Psychiatry.
  2013;84:452–457.
  
• Donckier JE, Michel L. Pheochromocytoma: State-of-the-art.
  Acta Chir Belg.
  2010;110(2):140–148.
  
• Mannelli M, Lenders JW, Pacak K, et al. Subclinical pheochromocytoma.
  Best Pract Res Clin Endocrinol Metab.
  2012;26:507–515.
  
• Prejbisz A, Lenders JW, Eisenhofer G, et al. Cardiovascular manifestations of pheochromocytoma.
  J Hypertens.
  2011;29:2049–2060.
  
• Scholten A, Cisco RM, Vriens MR, et al. Pheochromocytoma is not a surgical emergency.
  J Clin Endocrinol Metab.
  2013;98(2):581–591.
  
• Yu R, Nissen NN, Chopra P, et al. Diagnosis and treatment of pheochromocytoma in an academic hospital from 1997 to 2007.
  Am J Med
  . 2009;122:85–95.
  

CODES

• 194.0 Malignant neoplasm of adrenal gland
  
• 227.0 Benign neoplasm of adrenal gland
  

BASICS

• True phimosis is the pathologic inability to retract the foreskin over the glans of the penis as a result of scarring.
  
• The inability to retract a normal, supple foreskin is not true phimosis.
  
• The foreskin is rarely retractable at birth due to normal adhesions between the glans and the inner prepuce.
  
• ∼90% are retractable by 3 yr of age, and 99% are retractable by 17 yr, as the epithelial cells that comprise smegma are shed.
  
• Parents should be instructed not to forcibly retract the foreskin.
  

Possible causes of true phimosis include:

• Trauma from forcible retraction of the foreskin
  
• Repetitive bouts of diaper dermatitis
  
• Recurrent balanoposthitis
  
• Poor hygiene
  
• Poorly performed circumcision
  
• Congenital anomalies
  

DIAGNOSIS