Medical Management of Kidney Stones

General Principles

  • Fluid intake that will achieve a urine volume of at least 2.5 liters daily
  • Pain control:
    • NSAIDS:
      • Any, but toradol has been given special interest. In one emergency department study, the narcotic-like analgesic effects of this agent were superior to the effects of meperidine
      • Contraindication to the use of extracorporeal shock wave lithotripsy, because of the increased risk of perinephric bleeding
      • Must balance with the presence of acute kidney injury
    • Narcotics: Codeine, morphine, hydromorphone, and meperidine are effective in suppressing pain
    • Medical Expulsive Therapy
      • Alpha blockers: tamsulosin: faster stone passage, fewer hospitalizations, fewer procedures
      • CCB: nifedipine – not as good as alpha-blockers

Stone-Specific Management

  • Calcium stones and low urinary citrate:
    • Potassium citrate to raise urine pH
    • Increase intake of fruits and vegetables and limit non-dairy animal protein
    • Thiazide diuretics to patients with high or relatively high urine calcium and recurrent calcium stones
  • Cystine stones:
    • Limit sodium and protein intake.
    • Potassium citrate to raise urine pH
  • Struvite stones: acetohydroxamic acid (AHA) to patients with residual or recurrent struvite stones only after surgical options have been exhausted
  • Calcium oxalate stones:
    • Limit intake of oxalate-rich foods and maintain normal calcium consumption
    • Give allopurinol to patients with recurrent calcium oxalate stones who have hyperuricosuria and normal urinary calcium
    • Oral calcium carbonate in doses up to 4 g/d is used for patients with enteric hyperoxaluria to bind oxalate within the gastrointestinal tract
  • Uric acid stones or calcium stones and relatively high urinary uric acid:
    • Limit intake of non-dairy animal protein
    • Potassium citrate to raise urine pH
    • Allopurinol is not first line therapy

Neuro-Behcet Disease

General Information

  • Excluding headaches, neurological complications of Behçet syndrome (neuro-Behçet syndrome) occur in less than 12% of cases, often a few years after the onset of the other systemic features.

Clinical Manifestations and Diagnosis

  • In parenchymal disease, meningoencephalitis occurs, with a mixed inflammatory cell infiltrate leading to necrosis and apoptotic neuronal loss. Inflammatory infiltration, rather than fibrinoid necrosis, is seen around small vessels.
    • The brainstem and mid-brain are the most commonly affected areas, but spinal cord lesions and cerebral involvement may also occur and, occasionally, neuro-Behçet syndrome presents as a pseudotumour cerebri.
    • Brainstem involvement usually presents subacutely, with headache, cranial neuropathies or cerebellar or corticospinal tract dysfunction.
    • Sensorineural hearing loss can occur, resulting in sudden deafness, balance disturbances and dizziness.
    • The characteristic MRI lesion in parenchymal neuro-Behçet syndrome is a unilateral upper brainstem lesion extending into the thalamus and basal ganglia.
    • Analysis of cerebrospinal fluid shows a neutrophilic (in early disease) or lymphocytic (in late disease) pleocytosis, but usually no oligoclonal bands.
  • Neurovascular disease accounts for approximately 20% of cases of neuro-Behçet syndrome and symptoms include dural sinus thrombosis, intracranial aneurysm and extracranial aneurysm and/or dissection.
    • The clinical findings are usually limited to those of intracranial hypertension (that is, headache, vomiting, altered levels of consciousness and papilloedema).
    • Intracranial hypertension may be present without MRI abnormalities and should be managed in the same way as idiopathic benign intracranial hypertension.
    • Aneurysms of the cerebral, vertebral and carotid arteries can also occur.


  • Headaches are often under-treated. An effort should be made to classify the type of headache and, in the case of migraine, agents such as pizotifen and β­blockers should be offered.
  • Parenchymal disease:
    • Initial Management: treated with high-dose steroids in the first instance, along with initiation of a DMARD, usually azathioprine.
      • Methotrexate, mycophenolate, cyclophosphamide, tacrolimus and IFN-­α are probably effective, although evidence is lacking.
      • Cyclosporin is potentially neurotoxic and should not be used for patients with a history of CNS disease.
    • The alternative therapeutic option for severe and aggressive disease is the early use of a biologic agent (i.e. anti-TNF therapy, like infliximab)
  • Neurovascular disease:
    • Cerebral vascular thrombosis and aneurysms also require aggressive immunosuppression.
    • Anti-coagulation for venous thrombosis needs to be assessed on a case-by-case basis.

Ambrose, N. L. & Haskard, D. O. Nat. Rev. Rheumatol. 9, 79–89 (2013); published online 25 September 2012; doi:10.1038/nrrheum.2012.156

“I can make $13,000 doing what!?!”

Continuing the recent trend of posting entries related to GI comes an article from The Washington Post about getting paid for donating your stool to be used for fecal transplants. The article focuses on the organization, OpenBiome, which collects these stool samples, processes, and delivers them all over the country. But they don’t just take any sample. It’s a rigorous screening process as one of the co-founders jokes it’s easier to get into M.I.T than to have your stool accepted. They want stool samples from very healthy individuals. Recent research has shown remarkable results in treating C. diff infections with donor feces. Click on the table below to read more about this!