CORRESPONDENCE

et al raises an important philosophic as well as practical question. A number of articles recently have appeared which stress cost effectiveness and search for adequate treatment at the expense of optimum treatment. Physicians should never forget that their commitment is primarily to the patient of the immediate moment. Herd statistics indi- cating a yield of 1 in 100 would be a poor excuse ff they resulted in the lack of a test causing a missed diagnosis or a delayed therapy. In an era when "acute remunerative liti-

gany" seems to complicate many missed diagnoses, physi- cians are poorly served to base their management of seizure disorders on herd statistics.

Marvin L Weil, MD Division of Pediatric Neurology Department of Pediatrics Harbor-UCLA Medical Center Torrance, California

Ischernic Stroke Made Worse With Intravenous Glucose

To the Edl"tor: While updating our county emergency medical techni-

cian - paramedic (EMT-P) standing orders protocol, I re- searched the use of administering IV glucose to patients who are unconscious or present with a neurologic deficit. I was surprised to find the literature replete with data that hyperglycemia certainly does not protect the insulted brain and may, in fact, cause harm.

Siemkowicz and Hansen~ noted that a controlled cerebral ischemia in experimental animals causes a reduced restitu- tion in hyperglycemic animals when compared to their normoglycemic or hypoglycemic controls. Myers and Yamagnchi2 recognized the ischemic brain tissue of their hyperglycemic animals to have greater lactacidosis than the normoglycemic counterparts. Siemkowicz and Gjedde 3 sug- gest that this increased cerebral cellular lactacidosis is the damaging factor in the hyperglycemic animal with cerebral ischemia.

Pulsinelli and coworkers 4 report in a prospective study that patients who present with ischemic stroke with high blood sugar levels have significantly worse neurologic out- comes. They state that it seems wise to maintain blood glucose levels in the near-normal range in diabetic patients with a high risk of stroke or with any symptoms suggesting impending or evolving cerebral ischemia. They recommend avoiding IV glucose in the treatment of patients with acute

or progressive stroke. I was not able to find evidence in the literature that hypo-

glycemia causes worsening of the cerebral ischemia or in- creased permanent neurologic deficit. For those patients who present with neuologic compromise (who are not in obvious insulin shock), perhaps our best avenue of care would be to administer glucose-containing fluids on/y after we prove the patient is hypoglycemic.

Robert Louis Stauter, MD Department of Emergency Medicine Trumbull Memorial Hospital Warren, Ohio

1. Siemkowicz E, Hansen AJ: Clinical restitution following cere- bral ischemia in hypo-, normo-, and hyperglycemic rats. Acta Neurol Scand 1978;58:1-8.

2. Myers RE, Yamagushi M: Effects of serum glucose concentra- tion on brain response to circulatory arrest. J Neuropath Exp Neurol 1976;35:301.

3. Siemkowicz E, Gjedde A: Post-ischemic coma in rat: Effect of different pre-ischemic blood glucose levels on cerebral metabolic recovery after ischemia. Acta Physiol Scand 1980;110:225-232.

4. Pulsinelli WA, Levy DE, et al: Increased damage after ischemic stroke in patients with hyperglycemia with or without estab- lished diabetes mellitus. Am J Med 1983;74:540-544.

Clostridial Myonecrosis Reviewed

To the Editor: Emergency medicine is indebted to Cline and Turnbull

for their zealous review of clostridial myonecrosis [May 1985; 14:459-466]. I am particularly pleased that they defined clostridial myonecrosis concisely and clearly distinguished it from other forms of so-called "gas gangrene." They laid a number of ghosts to rest. I wish, however, that they had chosen to put greater emphasis on the following points that they mentioned only briefly: 1. Clostridial myonecrosis may be a "well-recognized com- plication of war wounds," but the majority of cases are seen today in civil practice. 2. Common, relatively minor, and clean lacerations can re- sult in gas gangrene if muscle is exposed, and infection su- pervenes with other organisms. 3. The "striking scarcity" of leukocytes on Gram stain has been challenged, ~ and is clearly demonstrated in illustra- tions. 2

4. As alternatives to pencillin, metronidazol and erythromy- cin are good alternatives; cephalothin and clindamycin are not.3-6 5. But the major error in the review is the tabular summa- tion of diagnostic features and the algorithmic recommen- dation for management.

Pain out of proportion to physical findings and tachycar- dia out of proportion to fever are frequently quoted, but do not match my clinical experience nor have I seen good data to support the authors' impressions that they are charac- teristic findings.

Bronze erythema is a giveaway if it is present, but it is my impression that magenta is more common. Bullae often are not present, and they are not the best source for the Gram stain if they are. A Gram stain diagnostic for clostridial myonecrosis requires a swab from inside muscle.

Many would question the validity of the conclusion that

186/i121 Annals of Emergency Medicine 15:9 September 1986