The Journal of Emergency Medicine, Vol. 8, pp. 295-297, 1990 Printed in the USA * Copyright 0 1990 Pergamon Press plc

FATAL MYOCARDITIS SECONDARY TO SALMONELLA SEPTICEMIA IN A YOUNG ADULT

Carolyn R. Burt, DO,* Jeffrey C. Proudfoot, DO,* Mont Roberts, MD, FACEP,* R.H. Horowitz, MD, FAcPt

*Department of Emergency Medicine, Michigan State University Emergency Medicine Residency Program and tDepartment of Laboratories, Section of Pathology, Sparrow Hospital, Lansing, Michigan

Reprint address: Jeffrey C. Proudfoot, DO, Emergency Medicine Department, Sparrow Hospital, 1215 E. Michigan Avenue, Lansing, MI 48909

0 Abstract - A 29-year-old white male with a recent history of gastroenteritis sustained a cardiac arrest at home. He was found to be in ventricular fibrillation and could not be resuscitated. Pathologic findings included focal aggregates of histiocytes, lymphocytes and occasional neutrophils in the myocardium as well as inilammatory changes in the colon, liver, and spleen. Blood cultures were positive for Salmonelhz heidelberg. The patient was seen 3 times by emergency departments prior to his demise. Death from Salmonella is rare except when associated with septi- cemia. The severity of iBness and prognosis are often related to the site of infection and underlying disease processes.

0 Keywords - myocarditis; salmonella septicemia; Salmonelk heidelberg; gastroenteritis; cardiac arrest

INTRODUCTION

Salmonellosis is primarily a disease of children. The largest number of outbreaks occur because of mishan- dling of food. Poultry, meat, eggs, and dairy products have been the most important vehicles of transmission, although person-to-person and pet-to-person exposures are also significant. Most cases of salmonella gastroen- teritis are self-limited. We report a fatal case of salmo- nella septicemia associated with gastroenteritis and myo- carditis .

CASE REPORT

A 29-year-old white male presented to a small commu- nity emergency department (ED) complaining of low back pain after lifting 80 pounds at home. He was diagnosed as a low back strain and started on Flexerilm and ibuprofen and placed off work for 48 hours. He

returned 24 hours later complaining of diarrhea with low abdominal pain and flatus. Vital signs were temperature 36.5 “C, pulse 120, respirations 20, and blood pressure 102/64 mmHg. Physical examination was unremarkable, and no laboratory studies were performed. The diagnosis of gastroenteritis was made, and the patient was in- structed to stop taking the previously prescribed medi- cations.

The patient presented ambulatory to our ED 72 hours later still complaining of persistent nonbloody diarrhea without vomiting. He was able to take clear liquids but had had no solid food for the prior 5 days. He was taking Immodium@ prescribed per phone by his family doctor. Vital signs were temperature 38°C pulse 116, respira- tions 24, and blood pressure 1 lo/70 mmHg. Physical examination was unremarkable except for the tachycar- dia and diffuse abdominal tenderness. Bowel sounds were present and there was no guarding, rebound or costovertebral angle tenderness. Rectal exam was posi- tive for trace blood.

An IV of DS/Lactated Ringers was started and the patient given 1000 cc over 30 minutes and then an additional 250 cc in the next hour. Additional laboratory studies were as follows: WBC 5,400/mm3 (segs 49, bands 13, lymphocytes 24, monocytes 13, and eosino- phils l), hemoglobin 15.7 gm/dL, hematocrit 44%, sodium 134 mEq/L, potassium 3.2 mEq/L, chloride 96 mEq/L, bicarbonate 28.3 mEq/L, and glucose 128 mg%. The patient was given 40 mEq KC1 orally and discharged after 3 hours and 45 minutes in the depart- ment with a diagnosis of gastroenteritis and instructed to follow up with his family doctor in 48 hours. The patient was unable to produce a stool sample while in the depart ment. Five hours after discharge the patient became

RECEIVED: 28 June 1989; ACCEPTED: 22 September 1989 0736-4679190 $3.00 + .OO 295

296 C. R. Burt, J. C. Proudfoot, Mont Roberts, R. H. Horowitz

suddenly unresponsive at home. Paramedics arrived within 4 minutes to find him apneic, and pulseless, with CPR in progress by fire department personnel. The patient was endotracheally intubated and ventricular fibrillation noted on the monitor. There was no response to successive defibrillations, and ACLS protocol was continued throughout transport to the ED. On arrival at the ED the patient remained in ventricular fibrillation unresponsive to all further defibrillations and adminis- tered antidysrhythmics.

An autopsy was performed and significant findings included mild hepatosplenomegaly. The liver was 1950 grams and the spleen 310 grams. Gross examination of the heart revealed no atheromatous infiltrates and normal coronary arteries. Significant microscopic findings in- cluded focal aggregates of histiocytes, lymphocytes, plasma cells, and occasional neutrophils adjacent to the intramyocardial veins and myocardial fibers. There were no gross abnormalities of the stomach or gastrointestinal tract. There were moderate cellular infiltrates composed of mature plasma cells, occasional eosinophils and histiocytes evident in the lamina propria of the colon. The mucosa was free of these infiltrates. Blood cultures were positive for Salmonella heidelberg. HIV antibody was negative, and a comprehensive drug screen revealed only lidocaine at 8.8 mcg/dL. The patient’s daughter was subsequently culture positive for Salmonella heidelberg and was treated without incident.

DISCUSSION

The actual incidence of salmonella infections in the U. Se is unknown but estimated to be approximately two million cases annually (1). Only approximately 40,000 cases per year are actually reported to the CDC, suggest- ing widespread underreporting (2). Likewise, the mor- tality and morbidity is seriously underestimated. Salmonella bacteremia has been shown to be a relatively common event. Salmonellosis has a seasonal pattern with the highest incidence in summer months and is related to inadequate food preparation/storage procedures. lnfec- tion depends on the mode and to some extent the vehicle of transmission. Human disease is caused by 10 sero- types, 6 of which are common to animal reservoirs. Salmonella heidelberg is the most common nontyphoid species responsible for infection. The organism itself is resistant to freezing and dessication and can remain viable when removed from host tissues (3). Although more than 50% of cases are in children under 5 years of age, any individuals with predisposing illnesses or ma- lignancies are more susceptible to infection (45). Trans- mission can be person-to-person or pet-to-person, although in most cases the mechanism is never found.

Clinically the disease can manifest as intestinal symp- toms (ie, enterocolitis), as enteric fever, or as extraint- estinal disease. Enterocolitis usually presents as severe diarrhea 12 to 48 hours post exposure. Death from intestinal involvement is rare and occurs at the extremes of age. Affected individuals may be carriers postinfec- tion, and this condition is thought to be prolonged by antimicrobial therapy. A significant percentage of inoc- ulated individuals may be asymptomatic, which contrib- utes to underreporting of extraintestinal disease. Septicemia often results from uncomplicated enterocolitis. Focal infections are also related to unique populations (ie, osteomyelitis in sickle cell disease, mycotic aortic aneu- rysms in the elderly). Of extraintestinal disease, 25% occurs in structures related to the gastrointestinal tract (6). Focal infections after untreated bacteremia range as high as 25% (7). A review of the literature reveals a paucity of reports of death secondary to septicemia in the young adult population.

The mainstay of therapy is symptomatic, with fluid and electrolyte replacement. Antibiotics have not been shown beneficial in limiting the duration or severity of infection (8,9). There is also evidence that in vitro susceptibility testing may not correlate with in vivo response for certain antibiotics (10). Treatment with antidiarrheal agents has been thought to prolong the course and intensify the symptoms via reduced gut motility (11,12). Whether this predisposes the patient to development of septicemia, as in this case, is unknown, since the exact mechanism and portal of entry for development of bacteremia has yet to be delineated. This is suspected to be mucosal invasion of the bowel (13). The microscopic findings in this patient showed aggre- gates of histocytesflymphocytes with plasma cells inlil- trating the myocardial tissue-pathology characteristic for salmonella infection (13,14). No erythrophagocyto- sis was noted, which is another histologic marker of salmonella infections. The characteristic leukopenia with paradoxical bradycardia in the febrile patient was not observed in this case. Cardiac arrest was judged to be secondary to myocarditis caused by the salmonella septicemia.

SUMMARY

Diarrhea with nonspecific abdominal pain is a common presenting complaint in the emergency department. Emer- gency physicians should be attuned to etiologies that may lead to increased morbidity. Unfortunately, there are few objective criteria that will alert the physician to these cases, and we must rely on the occurrence of unscheduled return visits to raise our level of suspicion for poor outcomes and to increase attention to close

Fatal Myocarditis

follow-up. Salmonellosis is one such underreported yet and can be fatal. Great care should be used in treating relatively common cause for gastrointestinal complaints diarrhea with agents that may reduce intestinal motility.

REFERENCES

1.

2.

3.

4.

5.

6.

I.

Cohen ML, Gangarosa ET. Nontyphoid salmonellosis. South Med J. 1978;71:1540-5. Chalker RB, Blaser MJ. A review of human salmonellosis: III. Magnitude of salmonella infection in the United States. 1988;lO: 111-24. Davidson CM, Boothroyd M, Georgala DL. Thermal resistance of Salmonella senjienberg. Nature.. 1966;212:1060. Han T, Sokal JE, Neter E. Salmonellosis in disseminated malig- nant diseases. N Engl J Med. 1967;276:1045. Cherubin CE, Neu HC, Imperato PJ, Harvey RP, Bellen N. Septicemia with nontyphoid Salmonella. Medicine. 1974;53:365- 76. Saphra I, Winter JW. Clinical manifestation of salmonellosis in man. N Engl J Med. 1957;256:1128. Black PH. Kunz LJ, Swartz MN. Salmonellosis-a review of

8.

9.

10.

11.

12.

13.

14.

some unusual aspects. N Engl J Med. 1960;262:813. Askeroff BA, Bennett JV. Effect of therapy in acute salmonellosis on salmonellae in feces. N Engl J Med. 1969;281:3-7. Rosenthal SI, Exacerbation of salmonella enteritis due to ampicil- lin. N Engl J Med. 1969;280:147-8. Dawkins AT, Homick RB Evaluation of antibiotics in a typhoid model. Antimicrob Agents Chemother. 1966;6:6-10. DuPont HL, Homick RB. Adverse effect of Lomotil therapy in shigellosis. JAMA. 1973;226:1525-8. Sprinz H. Pathogenesis of intestinal infection. Arch Path01 Lab Med. 1969;87:556-62. Robbins SL, Cotran RS. Pathologic Basis of Disease. 2nd ed. Philadelphia: W.B. Saunders Co. 1979:390-393. Horowtiz RH. Pathology report A-435-88,Sparrow Hospital, Lan- sing, MI.