- Email: [email protected]
Fatal Toxic Shock Syndrome From an Intrauterine Device
INFECTIOUS DISEASE/CASE REPORT
Fatal Toxic Shock Syndrome From an Intrauterine Device Cameron D. Klug, MD C. Ryan Keay, MD Adit A. Ginde, MD, MPH
From the Division of Emergency Medicine, Denver Health Medical Center, Denver, CO (Klug, Keay); and the Department of Emergency Medicine, University of Colorado Denver School of Medicine, Aurora, CO (Ginde).
Toxic shock syndrome is a rare toxin-mediated condition that can rapidly produce multiorgan failure and severe shock. Toxic shock syndrome has been previously recognized in various clinical situations relating to surgery, nasal packing, abscesses, burns, and most notably menstrual-related cases. This case report describes a previously healthy 33-year-old woman presenting to the emergency department with complaints of nausea, vomiting, and diarrhea; vital signs at triage were normal. Within hours, she developed shock and cardiopulmonary arrest. The patient met all 6 of the Centers for Disease Control and Prevention diagnostic criteria for toxic shock syndrome, and her intrauterine device grew out Staphylococcus aureus. To our knowledge, this is the first reported case in the medical literature of fatal toxic shock syndrome related to an intrauterine device. [Ann Emerg Med. 2009;54:701-703.] 0196-0644/$-see front matter Copyright © 2009 by the American College of Emergency Physicians. doi:10.1016/j.annemergmed.2009.05.030
INTRODUCTION Toxic shock syndrome is a rare systemic toxin-mediated infection that can rapidly progress to multiorgan failure. The annual incidence of staphylococcal toxic shock syndrome is 1 to 2 cases per 100,000.1 Toxic shock syndrome was originally described in children in the late 1970s2 and then gained national attention when menstrual-related causes began to affect healthy young women.3 More recently, toxic shock syndrome has been recognized in a variety of clinical situations relating to postoperative patients, after nasal packing, in abscesses, and burns. To our knowledge, there have been only 2 reported cases of toxic shock syndrome related to an intrauterine device (IUD).4,5 Both of these cases were nonfatal and neither is described in the emergency medicine literature. In this case report, we describe a previously healthy 33-year-old woman who presented to the emergency department (ED) with a prodrome of nausea, vomiting, and diarrhea, and rapidly developed fatal shock. Her IUD grew out heavy Staphylococcus aureus (S aureus), with negative blood and urine culture results. The patient met all 6 of the Centers for Disease Control and Prevention (CDC) diagnostic criteria for the diagnosis of toxic shock syndrome.
CASE REPORT A 33-year-old previously healthy woman presented to the ED, complaining of 2 days of diffuse abdominal cramping, diarrhea, nausea, and vomiting. Her emesis and diarrhea were nonbloody. She denied fevers, vaginal discharge or bleeding, sick contacts, or recent travel. Her triage vital signs were blood pressure 145/92 mm Hg, pulse 67 beats/min, respiratory rate 18 breaths/min, and temperature 37.2°C (99° F). The physical examination demonstrated dry oral mucosa; normal Volume , . : November
cardiopulmonary systems; a soft, nontender, nondistended abdomen; and a normal rectal examination. Her pelvic examination was notable for the presence of an IUD and no cervical motion tenderness. Her skin examination revealed no petechia, pallor, or rash. Because of dehydration and nausea, she received 1 L normal saline solution and 4 mg of intravenous ondansetron, which improved her symptoms. During the next several hours, the patient became lightheaded, diaphoretic, lethargic, and ill appearing. Her systolic blood pressure was 80 mm Hg, pulse rate 156 beats/min, respiratory rate 45 breaths/min, and rectal temperature 40°C (104° F). A repeated physical examination revealed a soft, nontender abdomen and normal cardiopulmonary result (aside from her tachycardia and tachypnea). Bedside ultrasonography of the chest and abdomen demonstrated tachycardia and a grossly normal cardiac output without pericardial effusion; there was no evidence of free peritoneal fluid. Because the cause of her rapid deterioration was unknown, intravenous cefepime and vancomycin were administered to cover a potential infection with Gram-positive, Gram-negative, or methicillin-resistant S aureus organisms. A 2-L bolus of normal saline solution provided only minimal improvement in her vital signs; therefore, a central venous line and arterial catheter were placed. The patient’s initial central venous pressure was 1 mm Hg. On repeated examination, the patient remained lethargic but verbally interactive, reporting that she felt improved. Despite continued aggressive fluid resuscitation (5 L total), her systolic blood pressure decreased to 70 mm Hg, prompting the initiation of vasopressor support. Approximately 90 minutes into the resuscitation, she developed pulseless electrical activity Annals of Emergency Medicine 701
Fatal Toxic Shock Syndrome arrest. Compressions and advanced cardiac life support were initiated. The patient was promptly intubated, and intravenous atropine, epinephrine, and calcium chloride were administered. Because all laboratory values were pending, sodium bicarbonate was administered, first because of the assumption of severe sepsis with significant metabolic acidosis, and second to improve response to vasopressor therapy. These maneuvers resulted in prompt return of spontaneous circulation. After stabilization, a computed tomography scan of the abdomen and pelvis was obtained, demonstrating no focal infection or abscess; an IUD was visualized within the uterus. Although initially stable while in the radiology suite, the patient experienced another pulseless electrical activity arrest soon after completion of her imaging. She responded promptly to intravenous epinephrine and sodium bicarbonate; however, the patient remained hypotensive despite multiple vasopressors, requiring the addition of stress dose corticosteroids. Given the diagnostic concern for toxic shock syndrome, clindamycin was administered because of its effects on toxin synthesis in group A Streptococcus infection. At this time, the prearrest laboratory results became available, including potassium 3.3 mmol/L, bicarbonate 7 mmol/L, blood urea nitrogen 25 mg/dL, creatinine 3.9 mg/dL, lactate 15 mmol/L, WBC count 11.3/mm3, hemoglobin 15.8 g/dL, and platelets 266/mm3. The hepatic panel revealed a total bilirubin level of 2.9 units/dL, aspartate aminotransferase 428 units/dL, and alanine aminotransferase 163 units/dL. The pregnancy test result was negative, and urinalysis revealed 30 to 75 WBCs per high power field, 5 to 10 RBCs per high power field, and occasional bacteria. An arterial blood gas reading, obtained after her first pulseless electrical activity arrest and sodium bicarbonate administration, showed a pH of 7.14, PCO2 20 mm Hg, and PO2 217 mm Hg. The patient was admitted to the ICU for further treatment. The gynecology service was consulted for emergency removal of the IUD, and the device was sent for culture. During hospital day 1 in the ICU, a desquamating rash developed on the patient’s bilateral upper thighs. During her hospital course, the patient became progressively more hypotensive despite maximum doses of norepinephrine, dopamine, phenylephrine, epinephrine, and vasopressin. Her total intravenous fluid resuscitation included 36 L of normal saline solution. Despite aggressive treatment, the patient developed multiple-system organ failure. Urine and blood cultures were negative for bacterial growth, and the IUD culture grew out Peptostreptococcus and heavy S aureus. Intravenous antibiotics (ciprofloxacin, clindamycin, vancomycin, and piperacillin/tazobactam) were maintained and continuous venovenous hemofiltration was instituted on hospital day 2. Unfortunately, the patient continued to deteriorate, and she developed acute respiratory distress syndrome, necrosis of her digits, and massive sloughing of her skin by hospital day 3. On hospital day 4, care was withdrawn in accordance to family wishes and the patient died. 702 Annals of Emergency Medicine
Klug, Keay & Ginde
DISCUSSION Staphylococcal toxic shock syndrome was first described in 1978 by Todd et al2 in a group of 7 children who presented with high fever, headache, vomiting, diarrhea, confusion, conjunctival hyperemia, scarlatiniform rash, subcutaneous edema, refractory hypotension, and acute renal failure. All patients had S aureus isolated from mucosal or sequestered sites, but not from their blood. The recognition of this syndrome peaked in the early 1980s, when menstrual-related cases associated with highly absorbent tampons obtained national attention,3 prompting the withdrawal of several brands of highly absorbent tampons, resulting in a dramatic decrease in the incidence of toxic shock syndrome. The syndrome is caused by a strain of S aureus that produces toxic shock syndrome toxin-1, which acts as a superantigen. Superantigens stimulate T-cell proliferation independent of antigen-specific binding, resulting in massive cytokine production.6 Toxic shock syndrome toxin-1 has multiple other effects on the immune system, including neutrophil chemotaxis suppression and blockage of the reticuloendothelial system.7 The cumulative effects manifest as hypotension and shock in the severely affected patient, which can be unresponsive to large amounts of intravenous fluid administration. The CDC has developed criteria for the diagnosis of toxic shock syndrome based on physical examination and basic laboratory analysis (Figure).1 This patient met all 6 of the criteria: fever, hypotension, rash, evidence of multisystem dysfunction (nausea and vomiting at onset of illness, increased blood urea nitrogen and creatinine levels, and total bilirubin and transaminase levels greater than twice normal), desquamation, and negative cultures (both blood and urine), making this a “confirmed” case. The culture of her IUD grew out heavy S aureus, which most likely represents the source of her fatal infection. The patient’s rapid deterioration, with normal vital signs at triage and developing cardiopulmonary arrest within hours, also suggests toxic shock syndrome because rapid onset of severe shock and multisystem involvement is a hallmark of superantigen-mediated infection. Toxic shock syndrome from IUD use has been reported in the literature.4,5 However, to our knowledge, there has never been a documented fatal case, and this is the first reported in the emergency medicine literature. Although not a known risk factor for developing toxic shock syndrome, IUDs can cause disruption of the cervical mucosa, allowing for bacterial infection and systemic spread. A small study found that 4% of IUDs are colonized with S aureus,8 and there has been a case report of staphylococcal septicemia after insertion of an IUD.9 Even though IUDs rarely cause significant infection, emergency physicians should consider this device as a possible source in reproductive-aged women with the clinical features of toxic shock syndrome. Prompt removal of the device and antimicrobials that cover both Staphylococcus and Volume , . : November
Klug, Keay & Ginde
Fatal Toxic Shock Syndrome Streptococcus are essential treatment for this rare but potentially fatal condition.
I. Fever: temperature ⬎38.9°C II. Rash: diffuse macular erythroderma III. Hypotension: systolic blood pressure ⬍90 mm Hg (adults) or ⬍5th percentile for age (children younger than 16 years), or orthostatic hypotension, dizziness, or syncope IV. Multisystem dysfunction: at least 3: A. Gastrointestinal: vomiting or diarrhea at onset of illness B. Muscular: severe myalgias, or serum creatine phosphokinase level (CPK) greater than twice the upper limit of normal C. Mucous membranes: vaginal, oropharyngeal, or conjunctival hyperemia D. Renal: blood urea nitrogen or creatinine level greater than twice the upper limit of normal, or pyuria (⬎5 leukocytes per high-power field), in the absence of urinary tract infection E. Hepatic: total serum bilirubin or transaminase level greater than twice the upper limit of normal F. Hematologic: platelets ⬍100,000/L G. Central nervous system: disorientation or alteration in consciousness but no focal neurologic signs at a time when fever and hypotension are absent. V. Desquamation: One to 2 weeks after the onset of illness (typically palms and soles) VI. Evidence against an alternative diagnosis: If obtained: 1. negative culture results for blood, throat, or cerebrospinal fluid 2. absence of an increase in antibody titers to the agents of leptospirosis, measles, or Rocky Mountain spotted fever. *“Confirmed” case meets all 6 criteria; “probable” case meets 5 of the 6. † Blood culture may be positive for S aureus. Figure. Toxic shock syndrome: case definition*
Supervising editor: Kathy J. Rinnert, MD, MPH Funding and support: By Annals policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article that might create any potential conflict of interest. The authors have stated that no such relationships exist. See the Manuscript Submission Agreement in this issue for examples of specific conflicts covered by this statement. Publication dates: Received for publication November 28, 2008. Revisions received February 28, 2009, and May 13, 2009. Accepted for publication May 26, 2009. Available online July 3, 2009. Reprints not available from the authors. Address for correspondence: Cameron D. Klug, MD, Division of Emergency Medicine, Denver Health Medical Center, Denver, CO 80204; 303-436-7142, Fax 303-436-7541; E-mail [email protected].
REFERENCES 1. Centers for Disease Control and Prevention. Case definitions for infectious conditions under public health surveillance. MMWR Morb Mortal Wkly Rep. 1997;46:39. 2. Todd J, Fishaut M, Kapral F, et al. Toxic-shock syndrome associated with phage-group-I staphylococci. Lancet. 1978;2:1116-1118. 3. Davis JP, Chesney PJ, Want PJ, et al. Toxic-shock syndrome. N Engl J Med. 1980;303:1429-1435. 4. Herzer CM. Toxic shock syndrome: broadening the differential diagnosis. J Am Board Fam Pract. 2001;14:131-136. 5. Gisser JM, Fields MC, Pick N, et al. Invasive group A streptococcus associated with an intrauterine device and oral sex. Sex Transm Dis. 2002;29:483-485. 6. Schlievert PM. Role of superantigens in human disease. J Infect Dis. 1993;167:997-1002. 7. Lauter CB. Recent advances in toxic shock syndrome. Contemp Intern Med. 1994;6:11-16, 19-22. 8. Lewis R. A review of bacteriological culture of removed intrauterine contraceptive devices. Br J Fam Plann. 1998;24:95-97. 9. Geddes AM. Staphylococcal septicaemia after insertion of an intrauterine contraceptive device. BMJ. 1980;281:1639.
Did you know? You can personalize the new Annals of Emergency Medicine Web site to meet your individual needs.
Visit www.annemergmed.com today to see what else is new online!
Volume , . : November
Annals of Emergency Medicine 703
Fatal Toxic Shock Syndrome From an Intrauterine Device Cameron D. Klug, MD C. Ryan Keay, MD Adit A. Ginde, MD, MPH
From the Division of Emergency Medicine, Denver Health Medical Center, Denver, CO (Klug, Keay); and the Department of Emergency Medicine, University of Colorado Denver School of Medicine, Aurora, CO (Ginde).
Toxic shock syndrome is a rare toxin-mediated condition that can rapidly produce multiorgan failure and severe shock. Toxic shock syndrome has been previously recognized in various clinical situations relating to surgery, nasal packing, abscesses, burns, and most notably menstrual-related cases. This case report describes a previously healthy 33-year-old woman presenting to the emergency department with complaints of nausea, vomiting, and diarrhea; vital signs at triage were normal. Within hours, she developed shock and cardiopulmonary arrest. The patient met all 6 of the Centers for Disease Control and Prevention diagnostic criteria for toxic shock syndrome, and her intrauterine device grew out Staphylococcus aureus. To our knowledge, this is the first reported case in the medical literature of fatal toxic shock syndrome related to an intrauterine device. [Ann Emerg Med. 2009;54:701-703.] 0196-0644/$-see front matter Copyright © 2009 by the American College of Emergency Physicians. doi:10.1016/j.annemergmed.2009.05.030
INTRODUCTION Toxic shock syndrome is a rare systemic toxin-mediated infection that can rapidly progress to multiorgan failure. The annual incidence of staphylococcal toxic shock syndrome is 1 to 2 cases per 100,000.1 Toxic shock syndrome was originally described in children in the late 1970s2 and then gained national attention when menstrual-related causes began to affect healthy young women.3 More recently, toxic shock syndrome has been recognized in a variety of clinical situations relating to postoperative patients, after nasal packing, in abscesses, and burns. To our knowledge, there have been only 2 reported cases of toxic shock syndrome related to an intrauterine device (IUD).4,5 Both of these cases were nonfatal and neither is described in the emergency medicine literature. In this case report, we describe a previously healthy 33-year-old woman who presented to the emergency department (ED) with a prodrome of nausea, vomiting, and diarrhea, and rapidly developed fatal shock. Her IUD grew out heavy Staphylococcus aureus (S aureus), with negative blood and urine culture results. The patient met all 6 of the Centers for Disease Control and Prevention (CDC) diagnostic criteria for the diagnosis of toxic shock syndrome.
CASE REPORT A 33-year-old previously healthy woman presented to the ED, complaining of 2 days of diffuse abdominal cramping, diarrhea, nausea, and vomiting. Her emesis and diarrhea were nonbloody. She denied fevers, vaginal discharge or bleeding, sick contacts, or recent travel. Her triage vital signs were blood pressure 145/92 mm Hg, pulse 67 beats/min, respiratory rate 18 breaths/min, and temperature 37.2°C (99° F). The physical examination demonstrated dry oral mucosa; normal Volume , . : November
cardiopulmonary systems; a soft, nontender, nondistended abdomen; and a normal rectal examination. Her pelvic examination was notable for the presence of an IUD and no cervical motion tenderness. Her skin examination revealed no petechia, pallor, or rash. Because of dehydration and nausea, she received 1 L normal saline solution and 4 mg of intravenous ondansetron, which improved her symptoms. During the next several hours, the patient became lightheaded, diaphoretic, lethargic, and ill appearing. Her systolic blood pressure was 80 mm Hg, pulse rate 156 beats/min, respiratory rate 45 breaths/min, and rectal temperature 40°C (104° F). A repeated physical examination revealed a soft, nontender abdomen and normal cardiopulmonary result (aside from her tachycardia and tachypnea). Bedside ultrasonography of the chest and abdomen demonstrated tachycardia and a grossly normal cardiac output without pericardial effusion; there was no evidence of free peritoneal fluid. Because the cause of her rapid deterioration was unknown, intravenous cefepime and vancomycin were administered to cover a potential infection with Gram-positive, Gram-negative, or methicillin-resistant S aureus organisms. A 2-L bolus of normal saline solution provided only minimal improvement in her vital signs; therefore, a central venous line and arterial catheter were placed. The patient’s initial central venous pressure was 1 mm Hg. On repeated examination, the patient remained lethargic but verbally interactive, reporting that she felt improved. Despite continued aggressive fluid resuscitation (5 L total), her systolic blood pressure decreased to 70 mm Hg, prompting the initiation of vasopressor support. Approximately 90 minutes into the resuscitation, she developed pulseless electrical activity Annals of Emergency Medicine 701
Fatal Toxic Shock Syndrome arrest. Compressions and advanced cardiac life support were initiated. The patient was promptly intubated, and intravenous atropine, epinephrine, and calcium chloride were administered. Because all laboratory values were pending, sodium bicarbonate was administered, first because of the assumption of severe sepsis with significant metabolic acidosis, and second to improve response to vasopressor therapy. These maneuvers resulted in prompt return of spontaneous circulation. After stabilization, a computed tomography scan of the abdomen and pelvis was obtained, demonstrating no focal infection or abscess; an IUD was visualized within the uterus. Although initially stable while in the radiology suite, the patient experienced another pulseless electrical activity arrest soon after completion of her imaging. She responded promptly to intravenous epinephrine and sodium bicarbonate; however, the patient remained hypotensive despite multiple vasopressors, requiring the addition of stress dose corticosteroids. Given the diagnostic concern for toxic shock syndrome, clindamycin was administered because of its effects on toxin synthesis in group A Streptococcus infection. At this time, the prearrest laboratory results became available, including potassium 3.3 mmol/L, bicarbonate 7 mmol/L, blood urea nitrogen 25 mg/dL, creatinine 3.9 mg/dL, lactate 15 mmol/L, WBC count 11.3/mm3, hemoglobin 15.8 g/dL, and platelets 266/mm3. The hepatic panel revealed a total bilirubin level of 2.9 units/dL, aspartate aminotransferase 428 units/dL, and alanine aminotransferase 163 units/dL. The pregnancy test result was negative, and urinalysis revealed 30 to 75 WBCs per high power field, 5 to 10 RBCs per high power field, and occasional bacteria. An arterial blood gas reading, obtained after her first pulseless electrical activity arrest and sodium bicarbonate administration, showed a pH of 7.14, PCO2 20 mm Hg, and PO2 217 mm Hg. The patient was admitted to the ICU for further treatment. The gynecology service was consulted for emergency removal of the IUD, and the device was sent for culture. During hospital day 1 in the ICU, a desquamating rash developed on the patient’s bilateral upper thighs. During her hospital course, the patient became progressively more hypotensive despite maximum doses of norepinephrine, dopamine, phenylephrine, epinephrine, and vasopressin. Her total intravenous fluid resuscitation included 36 L of normal saline solution. Despite aggressive treatment, the patient developed multiple-system organ failure. Urine and blood cultures were negative for bacterial growth, and the IUD culture grew out Peptostreptococcus and heavy S aureus. Intravenous antibiotics (ciprofloxacin, clindamycin, vancomycin, and piperacillin/tazobactam) were maintained and continuous venovenous hemofiltration was instituted on hospital day 2. Unfortunately, the patient continued to deteriorate, and she developed acute respiratory distress syndrome, necrosis of her digits, and massive sloughing of her skin by hospital day 3. On hospital day 4, care was withdrawn in accordance to family wishes and the patient died. 702 Annals of Emergency Medicine
Klug, Keay & Ginde
DISCUSSION Staphylococcal toxic shock syndrome was first described in 1978 by Todd et al2 in a group of 7 children who presented with high fever, headache, vomiting, diarrhea, confusion, conjunctival hyperemia, scarlatiniform rash, subcutaneous edema, refractory hypotension, and acute renal failure. All patients had S aureus isolated from mucosal or sequestered sites, but not from their blood. The recognition of this syndrome peaked in the early 1980s, when menstrual-related cases associated with highly absorbent tampons obtained national attention,3 prompting the withdrawal of several brands of highly absorbent tampons, resulting in a dramatic decrease in the incidence of toxic shock syndrome. The syndrome is caused by a strain of S aureus that produces toxic shock syndrome toxin-1, which acts as a superantigen. Superantigens stimulate T-cell proliferation independent of antigen-specific binding, resulting in massive cytokine production.6 Toxic shock syndrome toxin-1 has multiple other effects on the immune system, including neutrophil chemotaxis suppression and blockage of the reticuloendothelial system.7 The cumulative effects manifest as hypotension and shock in the severely affected patient, which can be unresponsive to large amounts of intravenous fluid administration. The CDC has developed criteria for the diagnosis of toxic shock syndrome based on physical examination and basic laboratory analysis (Figure).1 This patient met all 6 of the criteria: fever, hypotension, rash, evidence of multisystem dysfunction (nausea and vomiting at onset of illness, increased blood urea nitrogen and creatinine levels, and total bilirubin and transaminase levels greater than twice normal), desquamation, and negative cultures (both blood and urine), making this a “confirmed” case. The culture of her IUD grew out heavy S aureus, which most likely represents the source of her fatal infection. The patient’s rapid deterioration, with normal vital signs at triage and developing cardiopulmonary arrest within hours, also suggests toxic shock syndrome because rapid onset of severe shock and multisystem involvement is a hallmark of superantigen-mediated infection. Toxic shock syndrome from IUD use has been reported in the literature.4,5 However, to our knowledge, there has never been a documented fatal case, and this is the first reported in the emergency medicine literature. Although not a known risk factor for developing toxic shock syndrome, IUDs can cause disruption of the cervical mucosa, allowing for bacterial infection and systemic spread. A small study found that 4% of IUDs are colonized with S aureus,8 and there has been a case report of staphylococcal septicemia after insertion of an IUD.9 Even though IUDs rarely cause significant infection, emergency physicians should consider this device as a possible source in reproductive-aged women with the clinical features of toxic shock syndrome. Prompt removal of the device and antimicrobials that cover both Staphylococcus and Volume , . : November
Klug, Keay & Ginde
Fatal Toxic Shock Syndrome Streptococcus are essential treatment for this rare but potentially fatal condition.
I. Fever: temperature ⬎38.9°C II. Rash: diffuse macular erythroderma III. Hypotension: systolic blood pressure ⬍90 mm Hg (adults) or ⬍5th percentile for age (children younger than 16 years), or orthostatic hypotension, dizziness, or syncope IV. Multisystem dysfunction: at least 3: A. Gastrointestinal: vomiting or diarrhea at onset of illness B. Muscular: severe myalgias, or serum creatine phosphokinase level (CPK) greater than twice the upper limit of normal C. Mucous membranes: vaginal, oropharyngeal, or conjunctival hyperemia D. Renal: blood urea nitrogen or creatinine level greater than twice the upper limit of normal, or pyuria (⬎5 leukocytes per high-power field), in the absence of urinary tract infection E. Hepatic: total serum bilirubin or transaminase level greater than twice the upper limit of normal F. Hematologic: platelets ⬍100,000/L G. Central nervous system: disorientation or alteration in consciousness but no focal neurologic signs at a time when fever and hypotension are absent. V. Desquamation: One to 2 weeks after the onset of illness (typically palms and soles) VI. Evidence against an alternative diagnosis: If obtained: 1. negative culture results for blood, throat, or cerebrospinal fluid 2. absence of an increase in antibody titers to the agents of leptospirosis, measles, or Rocky Mountain spotted fever. *“Confirmed” case meets all 6 criteria; “probable” case meets 5 of the 6. † Blood culture may be positive for S aureus. Figure. Toxic shock syndrome: case definition*
Supervising editor: Kathy J. Rinnert, MD, MPH Funding and support: By Annals policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article that might create any potential conflict of interest. The authors have stated that no such relationships exist. See the Manuscript Submission Agreement in this issue for examples of specific conflicts covered by this statement. Publication dates: Received for publication November 28, 2008. Revisions received February 28, 2009, and May 13, 2009. Accepted for publication May 26, 2009. Available online July 3, 2009. Reprints not available from the authors. Address for correspondence: Cameron D. Klug, MD, Division of Emergency Medicine, Denver Health Medical Center, Denver, CO 80204; 303-436-7142, Fax 303-436-7541; E-mail [email protected].
REFERENCES 1. Centers for Disease Control and Prevention. Case definitions for infectious conditions under public health surveillance. MMWR Morb Mortal Wkly Rep. 1997;46:39. 2. Todd J, Fishaut M, Kapral F, et al. Toxic-shock syndrome associated with phage-group-I staphylococci. Lancet. 1978;2:1116-1118. 3. Davis JP, Chesney PJ, Want PJ, et al. Toxic-shock syndrome. N Engl J Med. 1980;303:1429-1435. 4. Herzer CM. Toxic shock syndrome: broadening the differential diagnosis. J Am Board Fam Pract. 2001;14:131-136. 5. Gisser JM, Fields MC, Pick N, et al. Invasive group A streptococcus associated with an intrauterine device and oral sex. Sex Transm Dis. 2002;29:483-485. 6. Schlievert PM. Role of superantigens in human disease. J Infect Dis. 1993;167:997-1002. 7. Lauter CB. Recent advances in toxic shock syndrome. Contemp Intern Med. 1994;6:11-16, 19-22. 8. Lewis R. A review of bacteriological culture of removed intrauterine contraceptive devices. Br J Fam Plann. 1998;24:95-97. 9. Geddes AM. Staphylococcal septicaemia after insertion of an intrauterine contraceptive device. BMJ. 1980;281:1639.
Did you know? You can personalize the new Annals of Emergency Medicine Web site to meet your individual needs.
Visit www.annemergmed.com today to see what else is new online!
Volume , . : November
Annals of Emergency Medicine 703