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A Fatal Case Of Toxic Associated With J Am Board Fam Pract: first published as 10.3122/jabfm.5.5.523 on 1 September 1992. Downloaded from Group A Streptococcal

David M. Whittiker, M.D.

The patient in presents an imposing Case Report challenge to the physician's clinical skills; therapy The patient was a 38-year-old woman, a re­ must be initiated often before important data are formed intravenous amphetamine user and obtained to assure optimal outcome for these very former prostitute, who came to the office one ill patients. For the past several decades the term morning complaining of an abrupt onset of septic shock has been virtually synonymous with weakness, , left-sided abdominal pain, gram-negative sepsis, as this is most and difficulty breathing that began 48 hours frequently caused by the endotoxin sometimes earlier. Her history included bilateral breast im­ expressed by gram-negative organisms. In suscep­ plants S years previously, laser ablation of a tible individuals this endotoxin can cause hypo­ rectal carcinoma 2 years before, a total ab­ tension, mental obtundity, decreased left ven­ dominal hysterectomy and bilateral oophorec­ tricular function, acute renal impairment, tomy for persistently positive Papanicolaou vascular instability, severe hematological de­ smears 18 months before, and amphetamine rangements, and, in 2 S percent of cases, death.! abuse. Medications included regular injections The early 1980s introduced us to a relatively new of estrogens and a benzodiazepine for anxiety. player in sepsis: Staphylococcus ourem and the toxic During a brief examination in the office the shock syndrome. A series of cases was defined in pa tient was exceedingly weak but awake and alert, relation to vaginal use, but since then unable to speak because of her weakness. Her toxic shock has occurred also in the presence of was 80/50 mmHg, pulse 110 beats other staphylococcal .2 Recently an­ per minute, respirations were 28/min, and her other gram-positive bacterium has reportedly temperature was 35.SoC (96°F). Her throat was been associated with sepsis and shock. This or­ clear as were her lungs, and she had no heart ganism is well known to office-based family phy­ murmur. Her abdomen was slightly tender in the sicians as the cause of many soft tissue infections left lower quadrant, but the bowel sounds were thought until recently to be "routine": acute normal. There were bullous lesions on the dor­ pharyngitis, otitis media, acute sinusitis, cellu­ sum of the right hand. She denied recent use of http://www.jabfm.org/ litis, and . The organism is group A ~­ illicit drugs. hemolytic (GABHS), and there is She was sent immediately to the intensive care an increasing number of reports of sepsis and unit in the local hospital for further evaluation death occurring as complications of one of these and treatment. There her blood pressure was so-called routine infections.3-6 These findings are 80/S0 mmHg, pulse 120 beats per minute, respi­ of great importance to office-based family physi­ rations 40/min and rectal temperature 35°C on 1 October 2021 by guest. Protected copyright. cians, because many affected patients have (9S°F). There were no abnormal findings on a been young, otherwise healthy individuals with­ pelvic examination, but a rectal examination out predisposing immune deficiency or debilitat­ showed a stool grossly positive for occult blood. ing illnesses. The following is a report of septic Though she continued to be weak, there were no shock that recently occurred in my patient. lateralizing neurological signs. Her skin was mot­ tled, and there was peripheral cyanosis. Her right Submitted, revised,10 December 1991. hand was pale, cold, and painful. From the Wichita Falls Family Practice Residency Program, Laboratory studies disclosed the following val­ Department of Family Practice and Community Medicine, Uni­ ues: her white cell count was IS.9 X 1091L versity of Texas Southwestern Medical Center, Dallas, and The 3 Southwest Medical Clinic, Wichita Falls, TX. Address reprint (1S,900/mm ) with 0.32 segmented neutrophils requests to David M. Whittiker. M.D., Six Eureka Circle, and O.SO band forms. The hemoglobin was 10.7 Wichita Falls, TX 76308. mmollL (17.2 gIL) and the hematocrit was O.SO;

Toxic Shock 523 J Am Board Fam Pract: first published as 10.3122/jabfm.5.5.523 on 1 September 1992. Downloaded from platelets were 245 X 1091L (245,000/mm3). The amounts. The body was sent for an autopsy, where prothrombin time was 18 seconds with a control an "intense inflammatory infiltrate" and "large of 11 seconds. The sodium was 128 mmollL (128 numbers of gram-positive cocci" in microscopic mEqlL), potassium 6.6 mmollL (6.6 mEqlL), sections of the right-hand wound were found. The chloride 90 mmollL (90 mEqlL), bicarbonate 8 final autopsy diagnosis was death from complica­ mmollL (8 mEqlL), blood urea nitrogen 14.6 tions of cellulitis caused by GABHS. mmollL (41 mglL), and creatinine 398 IJ.mollL The culture specimen was sent to the labora­ (4.5 mglL). The blood glucose was initially meas­ tory of Dennis L. Stevens, M.D., at the Veterans ured at 0.6 mmollL (10 mglL), but this value was Administration Medical Center in Boise, ID, for judged clinically to be an artifact and a recheck identification and assay for presence of . had normal blood glucose readings. The urinaly­ The Streptococcus organism that was responsible sis showed a specific gravity of 1.010, a large for this patient's death was of M Type 22 and T amount of blood, a pH of 5.5, protein 1 gIL (100 Type 12, and it produced streptococcal pyrogenic mglL), and red cells and white cells too numerous exotoxin B. to count, with frequent bacteriuria. Arterial blood gases on admission showed a pH of 6.94, pC02 Discussion 4.4 kPa (33 mmHg), p02 14.3 kPa (107 mmHg), Gram-positive organisms were the most com­ and base excess - 1.37 mmollL (- 27 mEqlL). mon cause of sepsis and shock at the beginning The aspartate aminotransferase was 3.22 IJ.katIL of this century. Mter the introduction of effec­ (3217 nmollLlsec) (193 UIL), lactic dehydro­ tive in the 1930s and 1940s, the rate genase 11.55 IJ.katIL (11,550 nmoVsecJL) (693 of serious suppurative and nonsuppurative com­ UIL), urate 547 IJ.mollL (9.2 mglL), and creatine plications of gram-positive infections declined kinase was 174.03 IJ.katIL (174,044 nmoVsecJL) to where such cases became the exception.7 In (10,440 UIL). The fibrinogen was 3.14 gIL (314 the early 1980s the toxic shock syndrome was mglL), and fibrin split products were greater than defmed as a predictable "new" of 40 IJ.g/mL. A Gram stain of the fluid in the staphylococcal infections in susceptible individ­ right-hand bullae showed moderate gram­ uals.2 There have been reports during the past positive cocci in chains. Blood alcohol was not few years of resurgent virulence displayed by measurable, and the serum drug test showed certain group A streptococci,3-s In 1987 Cone, only the benzodiazepine, but the urine drug test et a1.4 reported two cases of streptococcal cellu­ contradicted the earlier history of no recent litis that were complicated by sepsis and shock. s drug use: there were amphetamines in the One patient died. In 1988 Bartter, et al. re­ http://www.jabfm.org/ urine. When confronted with this evidence, the ported three similar cases marked by the pres­ patient confirmed that she had been injected ence of streptococcal soft tissue , hypo­ by others with intravenous amphetamine into tension, and renal failure, and they coined her right hand. Other studies included an echo­ the term toxic strep syndrome, postulating an cardiogram with normal findings, an electro­ exotoxin-mediated process that can go un­ cardiogram that showed only sinus tachycardia, derdiagnosed and be confused with staphylo­ on 1 October 2021 by guest. Protected copyright. a normal chest radiograph, and an analysis of coccal toxic shock. Stevens, et al,3 reported in her cerebrospinal fluid that showed her protein 1989 a series of 20 patients in the Rocky Moun­ level was 0.31 gIL (3.1 gIL), but no other ab­ tain area who had streptococcal infections. normality. Samples of the cerebrospinal fluid, Nineteen developed sepsis and shock, and blood, urine, and fluid obtained from the bullae 6 died. The patients in all these cases were on the dorsum of the right hand were sent for young (aged 29 to 66 years) and otherwise culture. healthy, and most complained of soft tissue in­ Despite early institution of intravenous fluids, fections, such as cellulitis, pharyngitis, myositis, pressor agents, broad-spectrum antibiotics, and or fasciitis. Such cases have now been described bicarbonate, the patient's course deteriorated, and in Great Britain and in various regions of the she died 6 hours after admission. Cultures of all , suggesting not only an increased fluids were negative except that from the bullae rate but also a widespread occurrence of this on the right hand, which grew GABHS in great dangerous organism.

524 JABFP Sept.-Oct. 1992 Vol. 5 No.5 The toxic strep syndrome is probably medi­ infected area is required, because only a small J Am Board Fam Pract: first published as 10.3122/jabfm.5.5.523 on 1 September 1992. Downloaded from ated by produced by certain serotypes number of organisms can produce sufficient toxin ofGABHS.7-9 These toxins, streptococcal pyro­ to be clinically important. The toxins are not genic exotoxin-A (SPE-A), SPE-B and SPE-C, dialyzable, nor is there an antitoxin available. It have been analyzed and bear some structural might be wise, if GABHS infection is suspected, similarities to the toxin produced by the staphy­ to include aqueous in addition to the lococci that cause toxic shock syndrome. to The broad-spectrum antibiotics usually prescribed.8 serotypes associated with toxin production were The antistaphylococcal are active more widespread before the 1950s, and SPE-A against GABHS also, though much less so than has been implicated as the causative factor of penicillin. Other supportive measures, such as rheumatic , in decline since that time. It intravenous fluid therapy, central venous pres­ has further been proposed that a shift in the sure monitoring, acid-base management, and number of these virulent serotypes is responsi­ treatment of specific organ system dysfunction, ble for the emergence of the toxic strep syn­ are identical to such treatment rendered to drome, as well as the recent increase in rheu­ patients with gram-negative or staphylococcal matic fever reported in some areas.7.9 toxic shock. The syndrome can strike persons of any age. Primary care physician awareness of the toxic The most common complaint is an acute onset strep syndrome is crucial, for treatment must be of skin or other soft-tissue infection, usually initiated often before appropriate consultation accompanied by fever, , weakness, and can be obtained. It has been postulated that the other symptoms referrable to the specific infec­ present generation, treated as they have been with tion. 'Within hours multi organ changes occur, effective antibiotics for common streptococcal producing , acute renal failure, infections, could be without actively acquired mental status changes, decreased left ventricu­ immunity and therefore could be more sus­ lar function, severe acidemia, hematologic de­ ceptible to this dangerous organism and its rangements, vascular instability, and eventually toxins.9 If, as has been suggested, the rate of these death. Poor is presaged by early onset virulent serotypes is increasing, then the role of acute renal failure and hypotension. Labora­ played by the well-informed family physician will tory fmdings are not specific to this syndrome be pivotal. but reflect the severe organ dysfunction that occurs. Blood cultures can be negative, as it is less the presence of the organisms themselves References http://www.jabfm.org/ than the toxins they elaborate that cause the 1. Root RK, Jacobs R. Septicemia and septic cellular changes leading to this syndrome.ll shock. In: Wilson JD, Braunwald E, Isselbacher Cultures of the infected tissues should grow KJ, Petersdorf RG, Martin JB, Fauci AS, GABHS, but the time required for such cultures et a!., editors. Harrison's principles of internal to be completed limits their usefulness in the medicine. 12th ed. New York: McGraw-Hili, 1991:502-7. acute early stages of the illness. A Gram stain

2. Chesney PJ, Davis JP, Purdy WI<, Wand PJ, on 1 October 2021 by guest. Protected copyright. of infected tissues will often show the gram­ Chesney RW. Clinical manifestations of toxic shock positive cocci, giving weight to the diagnosis of syndrome.JAMA 1981; 246:741-8. sepsis or toxemia caused by GABHS. Caution 3. Stevens DL, Tanner MH, Wmship], Swarts R, Ries should be used, as it is often difficult to distin­ KM. Schlieven PM, et al. Severe group A strepto­ coccal infections associated with a toxic shock-like guish between streptococcal and staphylococcal syndrome and toxin A. N Engl J Med infections using Gram stain alone. 1989; 321:1-7. Effective treatment requires early suspicion 4. Cone LA, Woodard DR, Schlievert PM, Tomory for GABHS and prompt attention to the tissues GS. Clinical and bacteriologic observations of a toxic that can harbor the toxin-producing organisms. shock-like syndrome due to . Evaluation of patients with possible sepsis should N Engl] Med 1987; 317:146-9. 5. Bartter T, Dascal A. Carroll K, Curley FJ. "Toxic include a complete examination of the skin and strep syndrome.· A manifestation of group A strep­ other soft tissues for evidence of infection. Ifsuch tococcal infection. Arch Intern Med 1988; 148: an infection is suspected, then debridement of the 1421-4.

Toxic Shock 525 6. Group A beta-hemolytic streptococcal bacteremia­ 9. Schwartz B, Facklam R, Breiman RI. Changing epi­ J Am Board Fam Pract: first published as 10.3122/jabfm.5.5.523 on 1 September 1992. Downloaded from Colorado, 1989. MMWR 1990; 39:3-6, 11. demiology of group A streptococcal infection in the 7. Stollerman GR. Changing group A streptococci. USA. Lancet 1990; 336:1167-71. The reappearance of streptococcal "toxic shock." 10. Marrack P, Kappler J. Staphylococcal enterotoxins Arch IntemMed 1988; 148:1268-70. and their relatives. Science 1990; 248:705-11. 8. Sanderson P. Do streptococci cause toxic shock? 11. Bisno AL. Group A streptococcal infections and acute BMJ 1990; 301:1006-7. . NEnglJ Med 1991; 325:783-93.

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526 JABFP Sept.-Oct. 1992 Vol. 5 No.5