Laparoscopic repair of a ruptured diaphragm secondary to blunt trauma.

The diagnosis of acute diaphragmatic rupture can be a challenge for even the most experienced clinician. The treatment of the rupture and its concomitant injuries, particularly in the elderly, can be associated with significant morbidity and mortality. The advent of laparoscopy for both the diagnosis and repair of this condition has allowed a more minimally invasive approach. We present the case of a 70-year-old woman who was hurt in a motor vehicle crash. On admission, her physical exam showed left upper quadrant tenderness and bruising. The chest radiograph was suggestive of a ruptured diaphragm. She was taken to the operating room and explored laparoscopically. After a thorough exploration of all the abdominal contents, a tear in the diaphragmatic hiatus to the right of the esophagus was noted. The stomach and small intestine were returned to the abdomen, and the diaphragmatic rupture was repaired. We conclude that laparoscopic exploration and repair of a ruptured diaphragm in a bluntly injured patient is a safe and effective option in selected cases.

Myocardial infarction after noncardiac surgery.

BACKGROUND: In this study, the authors intensively monitored isoenzyme and electric activity of the heart for the first 7 days after noncardiac surgery in a large group of patients at risk for postoperative myocardial infarction (PMI). METHODS: After institutional review board approval and written informed consent were received, 323 patients, aged 50 yr or older, who had ischemic heart disease and presented for noncardiac surgery, were enrolled in this prospective, blinded study. After operation, patients had daily clinical assessments, electrocardiograms, and measurements of creatine kinase (CK), CK-2 (mass and activity), and Troponin-T on the operative night, twice daily on postoperative days 1-4, and then daily on days 5-7. A diagnosis of PMI was made if the total CK was > 174 U/l and in the presence of two of the following: (1) CK-2/CK (mass or activity) > 5%, (2) new Q waves lasting > or = 0.04 s and 1 mm deep in at least two contiguous leads, (3) Troponin-T was > 0.2 microg/l, or (4) a positive result of pyrophosphate scan. RESULTS: Eighteen of the 323 patients (5.6%) had a PMI, of which 3 (17%) were fatal. Only 3 of 18 patients had chest pain, whereas 10 of 18 patients (56%) had other clinical findings. The electrocardiographic classification of the PMI was Q wave in 6, non-Q wave in 10, and indeterminate in 2. The PMIs occurred on the day of operation in 8, on day one in 6, on day two in 3, and on day four in 1 patient. CONCLUSIONS: This study determined that PMI was an early event, only occasionally associated with chest pain, and usually non-Q wave in nature.

Effectiveness of cholecystokinin-stimulated cholescintigraphy in the diagnosis and treatment of acalculous gallbladder disease.

We retrospectively reviewed the medical records of 107 patients in two community hospitals who had undergone cholecystokinin-stimulated cholescintigraphy with ejection fraction to determine whether this test is reliable in identifying patients whose symptoms will improve following cholecystectomy. Patients with cholelithiasis or incomplete medical records and patients who could not be interviewed were excluded from the study. Forty-two of 58 study patients (72%) had an abnormal ejection fraction (defined as 35% or less); 27 of 42 patients (64%) underwent cholecystectomy. Twenty-six of 27 (96%) reported lessening of or resolution of symptoms following cholecystectomy. Sixty-seven per cent of the surgical specimens from the 27 patients demonstrated chronic cholecystitis. Fifteen of 42 patients (36%) with abnormal ejection fractions did not undergo cholecystectomy; 12 of 15 (80%) also reported lessening or resolution of symptoms. Of the 16 of 58 patients with a normal ejection fraction, 2 underwent cholecystectomy and reported resolution of symptoms. Five of 14 (36%) with normal ejection fractions who did not undergo cholecystectomy reported improvement. In this series, most patients with an abnormal ejection fraction had lessening of symptoms regardless of whether they underwent cholecystectomy.

Temporary, catheter-induced block in accessory pathways.

Catheter-induced conduction delay or block in the accessory atrioventricular pathway of four patients with the preexcitation syndrome was observed. Block in the accessory pathway occurred during routine catheter placement and lasted from 90 seconds--14 hours. All of the pathways were in locations readily accessible to catheter trauma, located in the right anterior septal/paraseptal area in three patients, and in the posterior septum near the orifice of the coronary sinus in the fourth. The location of the acessory pathway was confirmed at surgery by endocardial mapping in three of the four patients. The fourth patient did not undergo survey. These findings suggest the need for caution in performing and interpreting electrode catheter studies which are undertaken to document the presence of accessory pathways.