ABSTRACT
We describe a patient who presented with mechanical obstruction of the small bowel secondary to impaction of the ileocecal valve from a gallstone. The stone impaction of the ileocecal valve was confirmed by colonoscopy. Although the stone was disimpacted, it could not be trapped and extracted during colonoscopy. Thereafter, the patient's small bowel obstruction was relieved with no further intervention. Even though surgery is the gold standard for the management of gallstone ileus. colonoscopy can be useful in management of patients with gallstone ileus in whom surgery is contraindicated. A review of the literature is also presented.
Subject(s)
Cholelithiasis/complications , Colonoscopy , Ileal Diseases/etiology , Ileocecal Valve/pathology , Intestinal Obstruction/diagnosis , Intestinal Obstruction/etiology , Aged , Aged, 80 and over , Cholelithiasis/diagnosis , Female , Follow-Up Studies , Humans , Ileal Diseases/diagnosis , Ileal Diseases/therapy , Intestinal Obstruction/therapyABSTRACT
New Zealand white rabbits were used to determine whether the changes in the Vth cranial nerve sensory root after compression were associated with the loss of a specific subclass of Vth cranial nerve ganglion cells, the disappearance of a distinct subset of primary afferent terminals in Vth cranial nerve nucleus caudalis, and/or injury to a specific axonal fiber type. There was no significant difference in the size of surviving ganglion cells after Vth cranial nerve compression, as measured 2 to 3 months after injury (P > 0.5, n = 4). Densitometric analysis of the nerves of rabbits that survived > 2 months after compression showed no significant difference in the immunoreactivity of substance P and calcitonin gene-reactive protein between compressed and control sides (P > 0.1, n = 4). Fink-Heimer staining of the Vth cranial nerve subnucleus caudalis revealed that transganglionic degeneration was most dense in the deeper layers, which are the sites of termination of large myelinated fibers. Ultrastructural evaluation of the type of myelinated axons injured by Vth cranial nerve compression in rabbits killed 7, 14, 37, and 270 days after injury was studied, and morphometric analysis was performed. The frequency distribution of axon diameters was significantly different for injured and control areas. The injured areas had higher ratios of small (< 3-microns diameter) to large-diameter axons compared to control distribution. These data indicate that balloon compression results in loss of fibers from the Vth cranial nerve sensory root and extensive transganglionic degeneration in the Vth cranial nerve brain stem complex. Cell size measurements and immunocytochemical data suggest that there is no specific loss of small ganglion cells or fine-caliber primary afferents. These experiments suggest that balloon compression relieves trigeminal pain by injuring the myelinated axons involved in the sensory trigger to the pain.
Subject(s)
Axons/pathology , Catheterization, Peripheral/instrumentation , Catheterization/instrumentation , Nerve Degeneration/physiology , Nerve Fibers, Myelinated/pathology , Trigeminal Ganglion/pathology , Trigeminal Neuralgia/therapy , Trigeminal Nuclei/pathology , Afferent Pathways/pathology , Animals , Female , Immunoenzyme Techniques , Male , Microscopy, Electron , Nerve Regeneration/physiology , Neurotransmitter Agents/analysis , Pressure , Rabbits , Trigeminal Nerve/pathology , Trigeminal Neuralgia/pathologyABSTRACT
The histopathological and autonomic effects of percutaneous trigeminal ganglion compression for trigeminal neuralgia were studied in New Zealand White rabbits. Drops in mean arterial blood pressure of 38% and in heart rate of 30% were observed during compression (p less than 0.0001). Corneal reflex, pinprick sensation, and mastication strength were intact in 13 of 14 rabbits after compression. These findings resembled the effects of percutaneous compression in humans and suggested that the New Zealand White rabbit is a useful model for the study of percutaneous compression. Trigeminal sensory roots and ganglia from 14 rabbits killed at intervals from 1 to 84 days after percutaneous compression were sectioned and stained using immunoperoxidase for neurofilaments, hematoxylin and eosin, luxol fast blue, and cresyl echt violet. Focal axonal damage and demyelination were present 7 days after compression. No difference could be detected in the perikaryonal distribution of neurofilaments between compressed and control trigeminal ganglia. Focal demyelination and Schwann cell proliferation preceding remyelination were present in the trigeminal sensory root at 84 days. Differential injury of axons compared to trigeminal ganglion cell bodies suggests that axonal regeneration is possible and may contribute to the recovery of motor and sensory function in patients after percutaneous compression.
