Detection of left ventricular thrombi by computerized tomography

ABSTRACTS Peter Rosen, MD - - Editor

Frank J. Baker II, MD - - Assistant Editor Associate Professor and Director Department of Emergency Medicine University of Chicago Hospitals and Clinics

Director

Division of Emergency Medicine Denver General Hospital

DMSO

C u r r e n t s t a t u s of d i m e t h y l s u l f o x i d e ( D M S O ) Calesnick B Am Fam Physician 23:167-168

Apt 1981

DMSO is a dipolar aprotic hydroscopic solvent obtained as a byproduct of wood pulp. It is highly water soluble. Its various uses include analgesia, anti-inflammatory activity, bacteriostasis, diuresis, muscle relaxation, choline esterase inhibition, and the relief of symptoms of interstitial cystitis {the only FDA-approved indication). When applied over the skin, absorption into the blood stream is very rapid and reaches maximal serum levels in 4 to 8 hours. Its half life is 11 to 14 hours. It cannot be detected in the serum concentrations after 36 to 72 hours. The breath and skin odor in patients taking DMSO have a characteristic garlic-like odor. Side effects include skin irritation, dysuria, headache, transient change in color perception, photophobia and, in animals, it has been reported to induce ocular lens opacities. It is contraindicated in pregnancy. DMSO has a potential as a vehicle for transport of other drugs into the skin. [Editor's n o t e : There was great hope that this drug, highly touted as an almost universal solvent, would assist management in such diverse conditions as arthritis and cerebral edema. To date its indications in humans remain to be established.] David Bar-Or, MD

due to a decreased usage of formulas containing more than 20 mEq/L sodium and less use of boiled skim milk and electrolyte solutions. A low water intake in the presence of only a moderate sodium intake can result in hypernatremia. When water intake is normal, a solution of 30 mEq sodium per liter can be tolerated without causing hypernatremia; but if the same solution is administered in reduced amounts, an increase in serum sodium occurs. It is recommended that in infants less than 2 to 3 years of age a daily fluid intake of at least 50 ml/kg is required to prevent dehydration; and if intake is below this level, fluids administered should contain little or no sodium. When positive water balance is restored, solutions containing more than 17 mEq/L sodium may be introduced. Undiluted cows' milk or electrolyte solutions containing 30 mEq sodium per liter should not be administered until calculations of intake and output, and demonstrated weight gain, assure that rehydration is occurring. [Editor's llote: This presumes a source of fluid loss. The other side of this problem is the hyponatremia induced by u~knowledgeable mothers or babysitters who give infants large volumes of water with no electrolytes.] Tony Tercier, MD

COMPUTERIZED TOMOGRAPHY, DETECTION OF VENTRICULAR THROMBI; THROMBUS, VENTRICULAR, DETECTION BY COMPUTERIZED TOMOGRAPHY

Detection of left ventricular thrombi by c o m p u t e r i z e d t o m o g r a p h y

HYPERNATREMIA, IN INFANTS; PEDIATRIC, DIARRHEA, HYPERNATREMIA

Nair CK, Sketch MH, Mahoney PD, et al Br Heart J 45:535-541

1981

Sodium and w a t e r c o n t e n t of feedings for u s e in i n f a n t s w i t h d i a r r h e a Walker SH, Gahol VP, Quintaro BA Clin Pediatr 20:199-204

Mar 1981

Hypernatremia became frequent in the United States when oral electrolyte solutions containing 50 mEq sodium per liter were utilized in the management of diarrhea. This study compares the water and sodium intakes of a group of infants admitted for diarrhea and dehydration in 1972-1973, when hypematremia was common, with a group treated in 1978-1979, when it was rare. There was found to be a considerable difference in the incidence of hypematremia, with 23 of 63 patients in the 1972-1973 group having serum sodiums of greater than 145 mEq/L versus 2 of 74 cases in the 1978-1979 group. The difference was felt to be primarily

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Noninvasive diagnosis of left ventricular (LV) mural thrombi using M-mode and two-dimensional echocardiography has not proven reliable, the latter technique having identified only half of the angiographically Or surgically proven lesions in one series. This study was undertaken to assess the ability of rapid scanning computerized tomography (CT) to diagnose LV mural thrombi. Sixteen patients were studied who had suffered previous transmural myocardial infarctions. Fifteen were suspected of having LV mural thrombi because of ventricular aneurysms, and one had had systemic emboli. All were studied with M-mode and twodimensional echocardiography and CT; eight underwent cardiac catheterization and five had surgical aneurysmectomy. Results showed that M-mode echocardiography was of no value in the detection of LV mural thrombi. Cineangiography and CT correctly identified the presence or ab-

Annals of Emergency Medicine

11:7 July 1982

sence of mural thrombi in all five patients who underwent surgery. Two-dimensional echocardiography demonstrated thrombi in eight of the 10 patients diagnosed by CT, but failed to identify LV mural thrombi in three patients who had cleary defined LV filling defects seen by CT. One of these three had a surgically documented thrombus. The results indicate CT may be a promising noninvasive technique for diagnosing LV mural thrombi. The authors suggest a larger study using surgical confirmation of the findings to validate its usefulness. /Editor's note: It should be remembered, however, that echocardiography is an accurate w a y to diagnose atrial tumors which also m a y be a source of embolism.] Ted W. Larremore, MD

LIDOCAINE

Effect of lidocaine on e s c a p e rate in patients with complete atrioventricular block: B. Proximal His bundle block

HYPOTHERMIA, AND INFECTIONS

Kuo CS, Reddy CP Am J Cardio! 47:1315-1320 Jun 1981

Infections in hypothermic patients Lewis S, Brettman LR, Holzman, RS Arch Intern Med 141:920-925 Jun 1981

Infections in patients with hypothermia secondary to exposure were studied retrospectively in a group of 59 adults admitted with a rectal temperature less than 35 C. Alcoholism was the most common condition leading to hypothermia. Criteria for inclusion in the infected group included positive blood cultures, chest roentgenographic evidence of pneumonia, clinical evidence of cellulitis, positive urine culture, or bacteria isolated from' a normally sterile body fluid. Patients not fitting these criteria and without other clinical evidence of infection were considered uninfected. Fifty-nine percent (35) of the patients had no infection present on admission; four in this group were erroneously diagnosed as having infections, and ten of these received antibiotics on the first day of hospitalization. Forty-one percent (24) of the patients had 32 infections; nine had undiagnosed occult infections on admission, eight of whom did not receive antibiotics initially. Symptoms and signs of infection in this subset developed during the 72 hours after admission. Factors separating infected from uninfected patients were altered mental status, decreased total lymphocyte counts, and greater m a x i m u m t e m p e r a t u r e following admission; other clinical data including admission vital signs, concomitant illnesses, arterial pH, total WBC count, hematocrit, and BUN were not significantly different in the two groups. Respiratory and soft tissue infections with Gram-positive pyogenic cocci were most common. Mortality in the uninfected group was 3%, compared with 21% in the infected group. Although prompt antibiotic therapy did not decrease overall mortality, the authors conclude that patients with hypothermia due to exposure should receive empiric antibiotic therapy after initial clinical evaluation

11:7 July 1982

and appropriate cultures have been obtained. If all cultures are negative after 72 hours and no clinical evidence of infection has developed, antibiotic therapy may safely be discontinued. [Editor's note: Since hypothermia hides the appearance of infection, it is hard to argue with the authors' suggestion to treat empirically, especially in the alcoholic population. O n e should r e m e m b e r that metabolic failure, as well as environment, m a y cause hypothermia.] Mont R. Roberts, MD

The authors attempt to assess the effect of lidocaine on the atrioventricular (AV) junctional escape pacemaker in patients with acute myocardial infarction and complete AV block, and test the hypothesis that lidocaine depresses ischemic myocardium selectively. Lidocaine was administered intravenously (a loading dose of 1.5 mg/kg followed by a 3 mg/min infusion) to 10 patients with complete AV block proximal to the His bundle (as demonstrated by His bundle electrogram) and AV junctional escape rhythm. All patients had a right ventricular pacemaker in place. The 10 patients were divided into 2 groups: 7 patients in whom AV block was not due to an acute myocardial infarction (group 1), and 3 patients in whom AV block was secondary to an acute myocardial infarction (group 2). Lidocaine caused no change in the QRS pattern, the duration of the QRS complex, or the HV interval, nor did it cause any consistent change in the atrial rate of the 10 patients studied. Lidocaine was found to have either no or only a slight depressant effect on the rate of the escape pacemaker in all patients in group 1, but caused severe bradycardia or asystole in two of three patients in group 2. The results suggest that lidocaine selectively depresses conduction in ischemic or depolarized myocardium, which has been demonstrated in prior animal studies, and that therapeutic doses of lidocaine may cause severe bradycardia or asystole in patients with complete AV block due to acute myocardial infarction. The authors also point out that the use of lidocaine without prior insertion of a pacemaker is unsafe in patients with acute myocardial infarction and complete AV block proximal to the His bundle. [Editor's note: The urge to scratch the lidocaine itch m a y be very dangerous, as these authors point out. This is especially easy to trip over in field m a n a g e m e n t of the early

MI.]

Annals of EmergencyMedicine

James Bemer, MD

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