Biomedical subjects
Publications and source records attributed to G J Todd.
The records of more than 1,000 patients who underwent colonoscopy were reviewed. The study group consisted of 55 of these 1,000 patients who had persistent unexplained bleeding per rectum and negative radiographic examinations. Colonoscopy was helpful in defining the site of bleeding in approximately 50 per cent of the patients studied.
Although it is clear that there is a significant frequency of recurrent volvulus after cecopexy, there is no evidence from either this series or previous reports that resection is associated with a lower recurrence rate than tube cecostomy. In the absence of data suggesting a clear superiority of colon resection, it appears that tube cecostomy should be the treatment of choice for cases of cecal volvulus that are not complicated by vascular compromise.
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A retrospective review of 1,000 elective cholecystectomies was undertaken to identify factors associated with wound infection. The technic of wound drainage appears to influence the incidence of infectious wound complications to a significant degree.
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A retrospective study of 18 episodes of upper gastrointestinal (UGI) bleeding secondary to Mallory-Weiss syndrome occuring in 16 patients is presented. Reported cases published since 1969 have been summarized and compared with earlier collected series. It is evident that the clinical spectrum, prognosis, and opinion regarding etiology and treatment of the syndrome have changed in the last decade. Increased awareness of gastroesophageal lacerations secondary to emesis as well as other causes of significantly increased intraesophagogastric pressures, and widespread utilization of fiberoptic endoscopy have resulted in identification of Mallory-Weiss syndrome with increasing frequency. Less severe lacerations which are healing with medical therapy are being recognized. It is recommended that endoscopy by performed in all cases of UGI hemorrhage and that patients with Mallory-Weiss syndrome be managed medically unless hemorrhage is massive or persistent since nearly three of four patients can be successfully treated without operation.
During reperfusion, functional and metabolic recovery of the isolated working rat heart from one hour of ischemia was best in hearts selectively cooled at the onset of the ischemic interval by perfusion with 5 to 10 ml. of 10 degrees C. or 15 degrees C. Krebs-Henseleit buffer. Hearts similarly perfused at 4 degrees C., 20 degrees C. recovered significantly less well or not at all. Immediately after the hour of ischemia and prior to reperfusion, the absolute levels of glycogen and high-energy phosphates were best in the hearts perfused at 4 degrees C. However, metabolic function was best preserved in those perfused at 10 degrees C. and 15 degrees C., as evidenced by rapid recovery of high-energy phosphates and glycogen to control levels compared to metabolic deterioration in the 4 degrees C. group.
Interruption of coronary flow during cardiac surgical procedures provides a bloodless flaccid heart and allows precise and rapid correction of complex cardiac defects. However, myocardial damage occurs in direct proportion to the duration of the ischemia. As the induction of cardioplegia simulataneous with the initiation of cardiac ischemia helps to preserve cardiac energy reserves and thus myocardial integrity, the identification of a consistently reliable cardioplegic technique is desirable. Isolated perfused working rat hearts were made ischemic for one hour by aortic cross-clamping and were compared with hearts rendered cardioplegic at the onset of ischemia by the intracoronary administration of 5 ml of a hypothermic solution: 1) Krebs-Henseleit buffer, 2) Ringer's lactate, 3) tetrodotoxin, 4) potassium chloride, or 5) potassium citrate. Cardiac output, heart rate, aortic pressure and coronary flow were determined pre and post-ischemia. When compared to time-matched controls and hearts arrested with potassium or tetrodotoxin, the ischemia and ischemia-Ringer's lactate groups showed significant post cross-clamp depression of all measured parameters. Intracoronary Ringer's lactate, although often used as an adjunct to ischemic arrest, was not of significant value. In contrast, hearts arrested with tetrodotoxin, potassium chloride or potassium citrate showed no significant post-ischemic functional or histologic deficit. Perfusion with hypothermic Krebs-Henseleit buffer protected the myocardium better than did Ringer's lactate but less well than the tetrodotoxin or isotonic high potassium solutions. The induction of hypothermic metabolic arrest of the heart by briefly perfusing the coronary arteries via the aortic root with isotonic buffered solutions results in markedly improved myocardial tolerance to one hour of ischemia and avoids the problems of low cardiac output and ventricular irritability previously reported with hypertonic potassium citrate arrest.
Intracoronary injection of 14 mcg. of tetrodotoxin into the ischemic isolated rat heart resulted in immediate cessation of mechanical activity. Upon reperfusion with oxygenated, modified Krebs-Henseleit bicarbonate buffer in a modified Langendorff apparatus, all hearts recovered normal rate, rtythm, and contractile vigor after up to 60 minutes of ischemia. In contrast, all hearts not administered tetrodotoxin showed bradycardia, irregular rhythm, and weak contraction upon reperfusion after 30 and 45 minutes of ischemia; after 60 minutes, no mechanical activity was evident. The improved cardiac function following ischemia in the tetrodotoxin-treated hearts was associated with persistence of normal adenosine triphosphate (ATP) levels after up to 30 minutes of ischemia and normal or elevated creatine phosphate (CP) levels after up to 60 minutes of ischemia. On the other hand, ATP and CP levels progressively declined to reach 50 per cent of normal values after 30 minutes in the ischemic hearts without tetrodotoxin. These findings indicate that postarrest ATP and CP levels play an important role in myocardial recovery after ischemic arrest.
To determine the reasons for clinical failure of Melrose solution, potassium arrest was studied in isolated working rat hearts. Eight control hearts were stable for 2-1/2 hours. After 1/2 hour of work, 42 experimental hearts were subjected to 1 hour of ischemis by aortic cross-clamping with unmodified ischemia in eight hearts and ischemia with simultaneous intracoronary injection of 5 ml. of 4 degrees C. (1)Krebs-Henseleit buffer in seven hearts (2)potassium chloride buffer in six hearts, (3)potassium citrate buffer in eight hearts (both 26 mEq. per liter of K, approximately 300 mOsm. per liter), (4)Melrose solution in seven hearts (greater than 200 mEq. per liter of K, greater than 400 mOsm. per liter), (5)hypertonic potassium citrate buffer in six hearts (26 mEq. per liter of K, greater than 400 mOsm. per liter). The pH of all solutions was 7.8 plus or minus 0.1. After recovery isotonic potassium citrate- and potassium chloride-arrested hearts and time-matched control hearts showed no significant differences in cardiac output, coronary flow, systolic pressure, or heart rate. Hypertonic potassium citrate decreased the recovery of cardiac function after arrest and Melrose arrest was not significantly different from unmodified ischemia. Intracoronary cold isotonic Krebs-Henseleit buffer was better than Melrose arrest but inferior to 26 mEq. er liter of potassium arrest. Arrest with 26 mEq. per liter of potassium augments perfusion hypothermia and prevents significant functional and histologic myocardial damage during 1 hour of ischemis. Previous authors assumed that hypertonicity and citrate were responsible for poor results with Melrose solution, but high potassium concentration is the major deleterious factor with hypertonicity playing a contributory role.
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