Neuroendocrine tumors (NETS) of the Gallbladder or the biliary tree are rare. Most of the current guidelines and protocols are derived from the experience of managing Lung small cell neuroendocrine carcinoma (SCNEC) or gastrointestinal (GI) NETS. But the overall outcome of Gallbladder NETS (GB NETS) seems worse than similarly staged lung NETS and adenocarcinoma of the gallbladder. This may be due to its rarity and lack of literature for a focused approach towards its treatment. Hence the need for a specifically designed approach might help improve the results of treatment for these rare tumours. We share our experience of two patients with GB NETS and their 5-year outcome.
A 28-year-old male presented to us with new onset refractory status epilepticus. Prior to his seizures, he had a history of fever, headache and blurring of vision, for which he was admitted elsewhere. No cause was found; he was treated symptomatically and was discharged as his symptoms had abated. Post-discharge, he started having multiple seizures. Neuro-imaging suggested encephalitis. He progressed to status epilepticus and was referred to our center. We intensified the anti-epileptic medications but owing to no response, he had to be put under coma with thiopental, yet the seizures persisted. Workup for the etiology of his seizures was negative except for CSF TB-PCR (Gene Xpert) being positive and hence anti-tuberculous therapy was initiated. By this time, he developed rhabdomyolysis, and thereafter renal failure with dyselectrolytemia, and thus there was a plan to initiate dialysis. But before this could be done, he succumbed to a cardiac arrest secondary to ventricular tachyarrhythmias. We believe this to be the first reported case of new onset refractory status epilepticus secondary to tuberculosis of the central nervous system.
A 56-year-old woman with a medical history of hypertension presented to our hospital with back pain, abdominal pain, vomiting and elevated blood pressure. The laboratory parameters including evaluation for secondary hypertension were within normal ranges at the time of presentation. During her hospitalisation, fluctuations in her blood pressure and pulse were observed which were attributed to autonomic disturbances, the cause of which was unknown. On the seventh day after presentation to the hospital, the patient developed focal seizures and slurred speech which was believed to be secondary to hyponatraemia detected at that time. Hyponatraemia improved with hypertonic saline and she experienced no further seizures. On the eighth day of her admission, she developed acute flaccid paralysis of all her limbs and respiratory distress. We concluded this to be secondary to Guillain-Barre syndrome (GBS). She responded to plasmapheresis.The presence of dysautonomia and hyponatraemia before the onset of paralysis makes this a rare presentation of GBS.
A 14-year-old boy presented with a painful swelling topped by a bruise overlying the skin of the right inguinal region without peritonitis. This was the area of impact of bicycle handlebar while riding 6 days ago. On contrast-enhanced CT scan, we found a traumatic abdominal wall hernia (handlebar hernia) near the right deep ring without any solid organ, bowel or urinary bladder injury. Inguinal exploration revealed a defect in transversus abdominis and internal oblique muscle which was repaired and meshplasty was done.Delayed presentation and ignorance towards ‘handlebar sign’ is associated with visceral injury (haematoma/perforation) will incur the risk of rising morbidity and mortality. With CT scan we can assess the abdominal cavity to rule out associated visceral or vascular injury. Surgical repair for restoring disrupted anatomy with or without meshplasty is the preferred approach.
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