Limits...
Spontaneous erosion of a lost intra-abdominal gallstone through the back eight months following laparoscopic cholecystectomy.

Memon MA, Jenkins HJ, Fitzgibbons RJ - JSLS (1997 Apr-Jun)

Bottom Line: The purpose of this study was to determine the incidence of this complication in our patients.The number of perforations resulting in loss of stones in the abdominal cavity was 16% (165 patients).Of these 165 patients, only a single patient could be identified as having a long-term complication.

View Article: PubMed Central - PubMed

Affiliation: Department of Surgery, Creighton University School of Medicine, Omaha, Nebraska 68131, USA.

ABSTRACT

Background and objectives: Gallbladder perforation during laparoscopic cholecystectomy with spillage of bile and gallstones occurs in up to 40% of patients. Several reports have recently been published describing complications related to these lost gallstones. The purpose of this study was to determine the incidence of this complication in our patients.

Methods: A prospectively maintained database of 856 laparoscopic cholecystectomies performed between 1989 and 1996 by a single surgeon was analyzed.

Results: The number of perforations resulting in loss of stones in the abdominal cavity was 16% (165 patients). Of these 165 patients, only a single patient could be identified as having a long-term complication.

Conclusions: Intra-abdominal lost gallstones can produce complications secondary to migration and erosion. It is prudent to make a concerted effort to remove spilled gallstones by every possible means but conversion to laparotomy is not justifiable.

Show MeSH

Related in: MedlinePlus

Postero-anterior and lateral chest films showing no active pathology expect for granulomatous disease on the right side.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3021273&req=5

Figure 1: Postero-anterior and lateral chest films showing no active pathology expect for granulomatous disease on the right side.

Mentions: Two months after his laparoscopic cholecystectomy, the patient presented with complaints of intermittent pyrexia and abdominal pain. Physical examination was within normal limits except for an elevated temperature of 102.4° and a large tender lump in the right axilla. Laboratory evaluation at the time revealed a hemoglobin of 11.3 gm/dl, hematocrit of 34.1%, platelet count of 261 k/μl and white cell count of 5.4 k/μl with differential of 83% granulocytes (45-80%), 10% lymphocytes (15-40) and 6% monocytes (2-11%). Erythrocyte sedimentation rate was elevated at 70 mm/hr. Routine coagulation screening, urea and electrolytes, creatinine, total protein, albumin, calcium, phosphate, cholesterol and uric acid were all within normal limits. Liver function tests revealed normal bilirubin and lactic dehydrogenase but slightly raised alkaline phosphatase, AST and GGT. Amylase was also slightly elevated. Blood cultures were negative. Postero-anterior and lateral chest films revealed no active disease expect for granulomatous disease on the right side (Figure 1 A & B). The patient underwent an ultrasound scan of the whole abdomen which raised the suspicion of a poorly defined fluid collection in the area of the gallbladder fossa measuring 3 × 4 × 4 cm (Figure 2). The possibility of an abscess was entertained. However, computerized tomography (CT) scan of the abdomen with contrast failed to substantiate the findings of ultrasonography as no fluid collection was seen (Figure 3). As the patient continued to spike a temperature, a technetium-99m HMPAO white cell scintigraphy was arranged which did not demonstrate any evidence of focal inflammation or infection (Figure 4) which could account for his pyrexia. In view of these negative findings the patient was started on a course of antibiotics, erythromycin 500 mg qid. This failed to resolve his pyrexia after seven days of treatment and therefore he was switched to cefuroxime 250 mg bd for a further three days but without any improvement. He was then given Augmentin 500 mg tid for two weeks which led to the gradual return of the temperature to normal. Repeat liver function tests and amylase showed normal values. It was concluded that the patient's pyrexia may have been secondary to inflammation of the RUQ due to a hematoma or other low grade inflammatory process. Following the normalization of his temperature and laboratory workup, the patient was discharged back to his family practitioner. At the time of discharge the right axillary node had decreased quite significantly and was non-tender. It was speculated that this enlarged node represented reactive phenomenon related to his pyrexia of unknown origin.


Spontaneous erosion of a lost intra-abdominal gallstone through the back eight months following laparoscopic cholecystectomy.

Memon MA, Jenkins HJ, Fitzgibbons RJ - JSLS (1997 Apr-Jun)

Postero-anterior and lateral chest films showing no active pathology expect for granulomatous disease on the right side.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3021273&req=5

Figure 1: Postero-anterior and lateral chest films showing no active pathology expect for granulomatous disease on the right side.
Mentions: Two months after his laparoscopic cholecystectomy, the patient presented with complaints of intermittent pyrexia and abdominal pain. Physical examination was within normal limits except for an elevated temperature of 102.4° and a large tender lump in the right axilla. Laboratory evaluation at the time revealed a hemoglobin of 11.3 gm/dl, hematocrit of 34.1%, platelet count of 261 k/μl and white cell count of 5.4 k/μl with differential of 83% granulocytes (45-80%), 10% lymphocytes (15-40) and 6% monocytes (2-11%). Erythrocyte sedimentation rate was elevated at 70 mm/hr. Routine coagulation screening, urea and electrolytes, creatinine, total protein, albumin, calcium, phosphate, cholesterol and uric acid were all within normal limits. Liver function tests revealed normal bilirubin and lactic dehydrogenase but slightly raised alkaline phosphatase, AST and GGT. Amylase was also slightly elevated. Blood cultures were negative. Postero-anterior and lateral chest films revealed no active disease expect for granulomatous disease on the right side (Figure 1 A & B). The patient underwent an ultrasound scan of the whole abdomen which raised the suspicion of a poorly defined fluid collection in the area of the gallbladder fossa measuring 3 × 4 × 4 cm (Figure 2). The possibility of an abscess was entertained. However, computerized tomography (CT) scan of the abdomen with contrast failed to substantiate the findings of ultrasonography as no fluid collection was seen (Figure 3). As the patient continued to spike a temperature, a technetium-99m HMPAO white cell scintigraphy was arranged which did not demonstrate any evidence of focal inflammation or infection (Figure 4) which could account for his pyrexia. In view of these negative findings the patient was started on a course of antibiotics, erythromycin 500 mg qid. This failed to resolve his pyrexia after seven days of treatment and therefore he was switched to cefuroxime 250 mg bd for a further three days but without any improvement. He was then given Augmentin 500 mg tid for two weeks which led to the gradual return of the temperature to normal. Repeat liver function tests and amylase showed normal values. It was concluded that the patient's pyrexia may have been secondary to inflammation of the RUQ due to a hematoma or other low grade inflammatory process. Following the normalization of his temperature and laboratory workup, the patient was discharged back to his family practitioner. At the time of discharge the right axillary node had decreased quite significantly and was non-tender. It was speculated that this enlarged node represented reactive phenomenon related to his pyrexia of unknown origin.

Bottom Line: The purpose of this study was to determine the incidence of this complication in our patients.The number of perforations resulting in loss of stones in the abdominal cavity was 16% (165 patients).Of these 165 patients, only a single patient could be identified as having a long-term complication.

View Article: PubMed Central - PubMed

Affiliation: Department of Surgery, Creighton University School of Medicine, Omaha, Nebraska 68131, USA.

ABSTRACT

Background and objectives: Gallbladder perforation during laparoscopic cholecystectomy with spillage of bile and gallstones occurs in up to 40% of patients. Several reports have recently been published describing complications related to these lost gallstones. The purpose of this study was to determine the incidence of this complication in our patients.

Methods: A prospectively maintained database of 856 laparoscopic cholecystectomies performed between 1989 and 1996 by a single surgeon was analyzed.

Results: The number of perforations resulting in loss of stones in the abdominal cavity was 16% (165 patients). Of these 165 patients, only a single patient could be identified as having a long-term complication.

Conclusions: Intra-abdominal lost gallstones can produce complications secondary to migration and erosion. It is prudent to make a concerted effort to remove spilled gallstones by every possible means but conversion to laparotomy is not justifiable.

Show MeSH
Related in: MedlinePlus