Concomitant laparoscopic cholecystectomy and splenectomy for surgical management of hereditary spherocytosis.

Laparoscopic splenectomy is rapidly becoming a common treatment modality in the surgical management of hematological processes involving the spleen. Hereditary spherocytosis is the most common red blood cell membrane disorder, and its diagnosis is often associated with hemolytic crisis and premature cholelithiasis. This condition has not been successfully treated laparoscopically until recently, and to our knowledge, the technique of concomitant laparoscopic splenectomy and cholecystectomy described here is the first reported in U.S. literature. Our patients, a 16-year-old 5-foot 3-inch-tall 90 pound emaciated albino, presented with cholelithiasis, splenomegaly, and anemia. Because of persistent anemia and gastrointestinal symptoms, the patient underwent laparoscopic cholecystectomy and splenectomy. The cholecystectomy was performed in a standard laparoscopic fashion. An additional 12-mm trocar was utilized for takedown of the spleen. The umbilical incision was extended to 4.5 cm, and the spleen was extracted manually. Total operative time was 12 hours. Examination demonstrated a 15 x 10 x 5-cm spleen, which weighed 350 grams. The gallbladder microscopically showed cholecystitis and had several stones. In conclusion, we present a combined laparoscopic cholecystectomy and splenectomy for hereditary spherocytosis associated with splenomegaly, cholelithiasis, and cholecystitis.

Thrombolytic therapy in cardiogenic shock: effect of increased aortic pressure and rapid tPA administration.

OBJECTIVES: To investigate the effect of an increase in aortic pressure combined with rapid tissue plasminogen activator infusion on hemodynamic stability and patency of the infarct-related artery in patients with acute myocardial infarction complicated by profound hypotension or cardiogenic shock. BACKGROUND: Thrombolytic therapy improves mortality in relatively stable patients with acute myocardial infarction but not in patients with cardiogenic shock. Recent canine studies have demonstrated that a moderate increase in low aortic pressure improves thrombolysis. Conceivably, then, decreased thrombolytic efficacy in cardiogenic shock is due, at least in part, to a low aortic pressure impairing delivery of the thrombolytic agent. PATIENTS AND METHODS: For patients presenting within 6 h of an acute myocardial infarction complicated by profound hypotension or cardiogenic shock, an inotropic agent was rapidly administered to increase the systolic aortic pressure to approximately 110 mmHg, and 100 mg of tissue plasminogen activator was administered intravenously over 45 to 60 mins. RESULTS: Eight consecutive patients meeting the study criteria were treated over 18 months. In six of eight patients, the inotropic agent increased systolic blood pressure over 10 mins, from a mean of 64 +/- 12 mmHg to 102 +/- 12 mmHg. In the two patients whose blood pressure did not increase, early angiography in one demonstrated occlusion of the infarct-related artery, and both of the patients died. In the other six patients there was clinical and hemodynamic evidence of early reperfusion, and infarct-related arteries were patent on angiography. These six patients survived at least 30 days, with four having a favourable clinical outcome and two having a functional limitation due to heart failure. CONCLUSIONS: These results are consistent with experimental data indicating that an increase in aortic pressure combined with rapid tissue plasminogen activator infusion may increase thrombolytic efficacy when an acute myocardial infarction is complicated by profound hypotension or cardiogenic shock.

Cardiac masses: signal intensity features on spin-echo, gradient-echo, gadolinium-enhanced spin-echo, and TurboFLASH images.

Fifteen patients with cardiac or paracardiac masses underwent magnetic resonance (MR) imaging with spin-echo (n = 15), cine gradient-echo (n = 15), gadopentetate dimeglumine-enhanced spin-echo (n = 15), and TurboFLASH (fast low-angle shot) (n = 7) sequences. All masses had either histologic confirmation (n = 11) or confirmation with other imaging modalities (n = 4). Myxomas (n = 6) were characterized by an intermediate signal intensity (SI) on spin-echo (n = 6) and low SI on cine gradient-echo (n = 6) images and moderately high-SI contrast enhancement (n = 5). Percent contrast enhancement for myxomas was 57% +/- 11%. Thrombus (n = 4) had intermediate (n = 3) or high (n = 1) SI on spin-echo images and low (n = 2) or intermediate (n = 2) SI on gradient-echo images and did not show substantial contrast enhancement. Postcontrast first-pass TurboFLASH images were useful by clearly demonstrating the nonenhancing mass lesion in a high-SI blood pool. Other cardiac and paracardiac tumors (n = 5) showed variable pre- and postcontrast spin-echo SI; however, no other tumor showed low SI on cine gradient-echo images.

Coronary thrombolysis. Comparative effects of intracoronary administration of recombinant tissue plasminogen activator and urokinase.

We employed a canine model of coronary thrombosis, induced by injection of radioactive blood clot, via a catheter placed in the left anterior descending coronary artery, to compare effects of intracoronary administration of recombinant tissue plasminogen activator (rtPA) and urokinase (UK) on rate and extent of coronary thrombolysis. Two doses of UK, 15,000 U/kg (UK15) and 30,000 U/kg (UK30) and two doses of rtPA, 0.25 mg/kg (rtPA.25) and 0.75 mg/kg (rtPA.75) were given. Drugs were infused over 45 min. Compared with the other regimens, rate and extent of coronary thrombolysis were significantly increased with rtPA.75. Also, despite a much higher dose of UK, coronary thrombolysis was similar with UK30 and rtPA.25. Compared with UK15, rate and extent of coronary thrombolysis were increased with rtPA.25. These results indicate that intracoronary administration of rtPA is superior to intracoronary UK in inducing thrombolysis.

Coronary thrombolysis with recombinant tissue plasminogen activator. Intracoronary vs intravenous administration.

We employed a canine model of coronary thrombosis, induced by injection of radioactive blood clot, via a catheter placed in the left anterior descending coronary artery, to compare effects of recombinant tissue plasminogen activator (rtPA) administered intravenously and administered directly into the coronary circulation. A control group did not receive rtPA. Compared with controls, both rtPA regimens induced coronary thrombolysis. However, compared with intravenous administration, rate and extent of coronary thrombolysis were increased with intracoronary administration. Most likely, the enhanced thrombolysis with intracoronary administration is explained by an increase in delivery of the drug to the thrombus.

Randomized, placebo-controlled study of the effect of verapamil on exercise hemodynamics in coronary artery disease.

At cardiac catheterization, 16 patients with coronary artery disease (14 men and 2 women) were allocated by a random, double-blind method to intervention with placebo (saline solution) or verapamil (0.2 mg/kg total by bolus and by 10-minute infusion). In all patients, resting and exercise (3 minutes with a bicycle at 150 kg X m/min) hemodynamic values were obtained during a control period and after intervention. Subsequent left ventriculography and coronary arteriography revealed a mean ejection fraction of 52 and 53% and the mean number of diseased vessels (3-vessel scale) of 2.1 and 1.5 in the placebo and verapamil groups, respectively. In both groups of patients, exercise induced significant increased heart rate, mean arterial pressure, left ventricular end-diastolic pressure and cardiac index. Verapamil increased the heart rate and decreased the mean arterial pressure at rest and the arterial pressure during exercise. It did not affect exercise-induced increases in left ventricular end-diastolic pressure or cardiac index. These results support a role for peripheral mechanisms mediating the antianginal effects of verapamil.

The effects of shock energy, propranolol, and verapamil on cardiac damage caused by transthoracic countershock.

Myocardial damage by transthoracic countershocks was assessed by observation for electrocardiographic loss of R waves and elevation of ST segments, creatine kinase depletion, and histologic evidence of necrosis in damaged areas, and by excision and examination, 3 days later, of all tissue macroscopically observed to be damaged. When 4000 J of stored energy was passed across the chest of dogs anesthetized with pentobarbital sodium (30 mg/kg), more damage was caused when the energy was divided among 10 shocks than when it was applied in 20 or 40 shocks (at intervals of 0.5 min). The prior intravenous administration of verapamil (1 mg/kg) reduced the weight of damaged shocks. Propranolol (0.4 mg/kg) had no effect. These results give further evidence for the role of calcium accumulation in cardiac necrosis after direct current countershocks. Multiple low-energy shocks cause less cardiac damage than do a few high-energy shocks of similar total energy.

Response to programmed ventricular stimulation: sensitivity, specificity and relation to heart disease.

This prospective study of 100 patients evaluated the sensitivity and specificity of the repetitive ventricular response and ventricular tachycardia induced by programmed electrical stimulation for identifying patients with spontaneous ventricular tachyarrhythmias. The influence of underlying heart disease on such sensitivity and specificity was also evaluated. The repetitive ventricular response was sensitive (92 percent) for detecting patients with prior spontaneous ventricular tachyarrhythmias, but lacked specificity (57 percent); the rate of false positive responses was 43 percent. Inducible ventricular tachycardia was less sensitive (65 percent) but more specific (98 percent); the rate of false positive responses was only 3 percent. Among the 100 patients, 71 had heart disease, 29 did not. The presence of underlying heart disease had no significant effect on the sensitivity and specificity of repetitive ventricular responses or ventricular tachycardia induced by programmed stimulation; it did not increase the rate of false positive responses. It is concluded that (1) ventricular tachycardia induced with programmed ventricular stimulation is an excellent basis for guiding the management of clinically significant ventricular tachyarrhythmias, regardless of underlying heart disease; and (2) the repetitive ventricular response is not useful for this purpose because of its high rate of false positive responses among patients with or without significant heart disease.

The human sinus node electrogram: a transvenous catheter technique and a comparison of directly measured and indirectly estimated sinoatrial conduction time in adults.

To improve methods for evaluating human sinus node function (SNF), we developed a transvenous electrode catheter technique for direct recording of sinus node electrograms in adults. Sinus node electrograms (SNE) characterized by low-frequency, anatomically localized pre-P-wave potentials were obtained in 19 of 23 patients. The SNE configuration was similar to that previously found for endocardial SNE recordings in in vitro atrial preparations, in open-chest dogs and during human open heart surgery. In 16 patients with normal SNF, directly recorded sinoatrial conduction times (SACTs) were 46-116 msec. In three patients with sick sinus syndrome, SACT was 110-126 msec. In 15 of the 19 patients, SACT was estimated by the atrial premature stimulus technique and was compared with the directly measured SACT. When atrial premature depolarizations produced no sinus node depression, the mean differences between the direct and estimated SACT was 1.8 +/- 5.6 msec.

Current required for ventricular defibrillation.

The mean current required for ventricular defibrillation was measured and found to be 0.35 +/- SE 0.03 A/kg body weight, which is about one-third of that predicted from animal experiments. There was no apparent correlation between the current required and body weight (r = -0.007 +/- SE 0.213). There is no evidence of need for defibrillators storing more than 400 J.