V entriculoperitoneal shunt insertion is a wellestablished technique for permanent CSF diversion to treat a variety of intracranial pathological conditions most often resulting in hydrocephalus, but it is also used to treat other disorders causing intractable intracranial hypertension. Usually, the distal catheter is inserted by performing a small laparotomy in the right paraumbilical, right subcostal, or median supraumbilical region. Despite advances in shunt technology and implant materials, a myriad of various complications continue to be reported, some most unusual.2 It is estimated that within 1 year of shunt placement 25%-40% of patients experience shunt complications. The risk reduces to 4%-5% annually thereafter. The mean survival of a shunt is approximately 5 years. 16 We present a case of CSF galactorrhea as the sole presenting symptom of a delayed proximal subcutaneous migration of the intraabdominal portion of a VP shunt. Case ReportHistory and Examination. A 46-year-old woman presented with a 6-year history of headaches and progressive visual loss diagnosed as idiopathic intracranial hypertension. All imaging failed to reveal a cause. The only observed risk factor was moderate obesity; the patient had a BMI of 31 kg/m 2 . After medical therapy failed and a left optic nerve sheath fenestration was unsuccessful, she was referred for CSF shunting as definitive treatment. She was scheduled for a VP shunt.Operation. An image-guided right frontal approach was chosen and the peritoneal cavity was entered via a standard right subcostal minilaparotomy by using a muscle-splitting technique through the rectus abdominus. The peritoneum was closed with a purse-string suture after a 90-cm peritoneal catheter connected to a PS Medical Strata II programmable valve (Medtronic, Inc.) was passed freely into the peritoneal cavity. The procedure was without complication and the patient's postoperative imaging revealed intraabdominal placement of the catheter.Postoperative Course. Six weeks after the shunt was implanted, the patient presented with painless, spontaneous clear fluid leakage from her right nipple; on compression it originated from a single duct in a jetlike fashion (Fig. 1). There was no palpable subcutaneous fluid collection along the course of the shunt catheter, and both breasts appeared symmetrical without deformity or sign of injury. She denied any recurrence of her previous symptoms to suggest a shunt malfunction. A sonogram was diagnostic for a subcutaneous fluid collection starting at the abdominal incision and extending to the inferior medial quadrant of the breast. A shunt series demonstrated the path of the distal catheter medial to the breast shadow and complete proximal migration of the peritoneal catheter into the subcutaneous tissues just at the level of the abdominal incision (Fig. 2).This migration was treated by repositioning of the distal end of the migrated catheter into the peritoneal cavity. In addition to a new peritoneal entry site, a subfascial tunnel under the anterior rectus sheat...
Ten years after placement of a spinal cord stimulator (SCS) and resolution of pain, this patient presented with progressive paraplegia, worsening thoracic radicular pain at the same dermatome level of the electrodes, and bowel and bladder incontinence. Computed tomographic myelogram confirmed thoracic spinal cord central canal stenosis at the level of electrodes. After removal of the fibrotic tissue and electrodes, the patient had resolution of his thoracic radicular pain and a return of his pre-SCS pain and minimal neurologic and functional return. To the authors' knowledge, no studies have been identified with thoracic SCS lead fibrosis in the United States causing permanent paraplegia. Only one other case has been reported in Madrid, Spain. Patients with SCS presenting with loss of pain relief, new-onset radicular or neuropathic pain in same dermatome(s) as SCS electrodes, worsening neuromuscular examination, or new bladder or bowel incontinence need to be evaluated for complications regarding SCS implantation causing spinal stenosis and subsequent cord compression to avoid permanent neurologic deficits.
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