- Email: [email protected]
Abdominal Pain and Multi-Organ Dysfunction Syndrome in a Young Woman
Abdominal Pain and Multi-Organ Dysfunction Syndrome in a Young Woman FONE-CHING HSIAO, MD; YI-JEN HUNG, MD; CHANG-HSUN HSIEH, MD; LING-YI WU, MD; KUANG-CHUNG SHIH, PHD; CHIH-TSUENG HE, MD
ABSTRACT: Thyroid storm is a rare but life-threatening condition caused by exaggerated thyrotoxic manifestations. Untreated thyroid storm is fatal, and the case fatality rate is 21% to 30%. The most important clinical management in thyroid storm is early recognition and treatment. We present the case of a previously healthy young woman in whom suspected gastrointestinal tract sepsis complicated by multi-organ dysfunction syn-
drome masked the major symptomatology of thyroid storm. This patient highlights the importance of a high clinical suspicion for potentially life-threatening conditions, such as thyroid storm, even in the absence of clinical clues (exophthalmos, lid lag, and goiter) or a history of thyrotoxicosis. KEY INDEXING TERMS: Abdominal pain; Multi-organ dysfunction syndrome; Thyroid storm. [Am J Med Sci 2007;334(5):399–401.]
T
normochromic normocytic anemia (Hb, 11.6 g/dL), a prolonged prothrombin time of 16 seconds (international normalized ratio, 1.93), mildly deranged liver and renal profiles (aspartate aminotransferases, 104 U/L; alanine aminotransferases, 46 U/L; total bilirubin, 1.3 mg/dL; creatinine, 1.2 mg/dL), an elevated amylase concentration of 626 U/L, and a normal lipase concentration of 25 U/L. Serum electrolytes included a Na⫹ level of 144 mEq/L, K⫹ of 5.0 mEq/L, and Cl– of 109 mEq/L. Arterial blood gas analysis on room air included a pH of 7.13, a PCO2 of 43 mm Hg, a PO2 of 89 mm Hg, and a measured HCO3⫺ of 14.8 mEq/L; the anion gap was 20.2 mEq/L. The serum lactic acid was 10 mmol/L (normal: 0.8 to 2.2). The serum and urine ketones were negative. The serum toxicology results were entirely negative. All other parameters were within normal limits. An electrocardiogram was interpreted as atrial fibrillation with a rapid ventricular rate of 120 to 150 beats per minute. Chest radiography demonstrated bilateral pulmonary infiltrates and pleural effusion. One hour after admission, the patient had cardiovascular collapse and shock developed. The patient became increasingly obtunded and dyspneic and required endotracheal intubation as well as mechanical ventilation for respiratory failure. After the blood pressure was stabilized via fluid resuscitation and administration of inotropic agents, emergent computed tomography (CT) of the abdomen (non– contrast-enhanced instead of contrast-enhanced due to the deteriorated renal function by hypotension) was performed and was unremarkable. On gastroscopy, only a mild esophagitis was identified. A transthoracic echocardiogram revealed four mildly dilated cardiac chambers in the absence of valvular defects or regional wall motion abnormalities. In the following 2 days of the patient’s admission, she remained febrile and tachycardic with alternating lethargy and agitation despite appropriate fluid resuscitation and empiric antibiotics administration. A diagnosis of thyroid storm was not achieved until the third day of admission, when the results of the thyroid function tests (ordered because of persistent atrial fibrillation) were available (Figure 1). The most stunning components of the panel included a thyroid-stimulating hormone level of 0.05 mU/L (normal: 0.3 to 5.0) and a free thyroxin level of 5.4 ng/dL (normal: 0.8 to 2.0). The standard treatment for thyroid storm was immediately administered and included oral propranolol (40 mg every 8 hours), intravenous hydrocortisone (100 mg every 8 hours), and oral propylthiouracil (200 mg every 4 hours) followed by Lugol’s solution (8 drops every 6 hours) 1 hour later. Within 24 hours, a
hyroid storm refers to the sudden onset of lifethreatening manifestations of thyrotoxicosis accompanied by systemic organ decompensation. Prompt recognition is the key to successful management. We discuss a patient in thyroid storm who lacked the tell-tale clinical signs (exophthalmos, lid lag, and goiter) at the time of initial assessment and did not give a medical history of thyroid disease. This case serves to illustrate the variable presentation of thyroid storm that may delay its diagnosis and initiation of life-saving treatment. Case Report
In September 2005, a 38-year-old woman presented to our hospital with a 1-week history of insomnia, dyspnea on exertion, and nonbloody diarrhea. Approximately 12 hours before admission, the patient’s dyspnea had worsened. Nausea, vomiting, and severe abdominal pain rapidly ensued. On physical examination, the patient was alert, irritable, febrile (38.3°C), tachypneic (28 breaths/min), and tachycardic (135 beats/min) but normotensive (125/70 mm Hg). The patient had prominent jugular venous distention. No exophthalmos, goiter, lid lag, or lid retraction was noted. No heart murmur was identified on auscultation, but rales were noted bilaterally. Tender distension with no rebounding pain in the epigastric region was identified, and bowel sounds were sluggish. Laboratory test results revealed a leukocytosis of 12.1⫻109/L (neutrophils, 43.7%),
From the Division of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. Submitted December 28, 2006; accepted in revised form April 27, 2007. Correspondence: Dr. Chih-Tsueng He, Division of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Sec. 2, Chenggong Road, Neihu District, Taipei City 114, Taiwan (E-mail: [email protected]). THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
399
Abdominal Pain Complicated by Multi-Organ Dysfunction Syndrome
Figure 1. Twelve-lead ECG demonstrating atrial fibrillation with a rapid ventricular rate of 150 to 200 beats/min.
dramatic clinical improvement was identified, particularly with reference to the patient’s level of the agitation, hyperthermia, and tachycardia. Within 1 week, mechanical ventilation was successfully weaned and the patient recovered uneventfully. All blood, urine, sputum, and stool cultures were negative for bacterial organisms. When last seen in October 2006, the patient was clinically and biochemically euthyroid and was continuing to take propranolol and propylthiouracil as directed.
Discussion Thyroid storm is a rare but life-threatening condition caused by exaggerated thyrotoxic manifestations, including advanced fever, marked tachycardia, gastrointestinal dysfunction, and central nervous system involvement, varying from confusion to coma.1 The pathogenesis of thyroid storm has not been determined. It has been suggested that the rate of the elevation of thyroid hormone levels is more important than the absolute increase.2 The most important clinical management in thyroid storm is early recognition and treatment. The diagnosis of thyroid storm remains a clinical one, aided by abnormal thyroid hormone levels. In the patient presented herein, no history of thyroid disease existed, and the expected clinical clues, such as goiter or ocular findings, were absent. Instead, the patient presented with abdominal pain and rapidly proceeded to cardiovascular collapse. The rare presentation and serious complications resulted in a diagnostic challenge. Thyroid storm is a systemic disease and many of the clinical features associated with this disorder result from over activity of the sympathetic nervous system. Gastrointestinal presentations (commonly limited to an enhanced intestinal transport in simple thyrotoxicosis) can dominate the clinical picture 400
in patients with thyroid storm. Nausea, vomiting, diarrhea, and even acute abdomen are typical findings.3 Cardiac decompensation is also frequently noted in thyroid storm and may occur in the absence of underlying heart disease. Congestive heart failure or cardiac arrhythmias such as atrial fibrillation are commonly observed. Excessive thyroid hormone levels, via direct and indirect mechanisms, alter cardiovascular physiology. A decline in systemic vascular resistance and increased heart rate, myocardial contractility, and cardiac mass have been reported.4 As noted in the patient presented herein, peripheral vasodilation (as the early manifestation of excess thyroid hormone levels), coupled with volume depletion due to vomiting and/or diarrhea may have contributed to the subsequent vascular collapse. The patient described herein presented for evaluation of abdominal pain. Diagnosing thyroid storm may be difficult because of the nonspecific and overlapping manifestations of the thyrotoxic state (ie, tachycardia, fever, vomiting, diarrhea, and abdominal pain) compared with those of intra-abdominal disease processes, such as acute pancreatitis or gastrointestinal (GI) tract sepsis. In addition, although there are a multitude of systemic medical disorders that can present with abdominal pain, thyroid storm, one of the potential life-threatening conditions, is not always in the differential diagnosis. In this patient, a normal serum lipase level and an unremarkable CT of the pancreas had ruled out the diagnosis of acute pancreatitis.5 The patient’s history suggests that GI tract sepsis may have occurred concurrently with thyroid storm and may have been the precipitating factor. However, all cultures of blood, urine, sputum, and stool demonstrated no November 2007 Volume 334 Number 5
Hsiao et al
Table 1. Diagnostic Point Scale for Thyroid Storm System
Parameters
Thermoregulatory (body temperature, °C)
37.2–37.7 37.8–38.2 38.3–38.8 38.9–39.4 39.5–39.9 ⬎39.9
Central nervous system
Gastrointestinalhepatic Cardiovascular Tachycardia (beats/min) Congestive heart failure Atrial fibrillation Precipitating event Final score 45 or greater 25–44 ⬍25
Absent Mild (agitation) Moderate (delirium, psychosis, extreme lethargy) Severe (seizure, coma) Absent Moderate (diarrhea, nausea/ vomiting, abdominal Severe (unexplained jaundice) 99–109 110–119 120–129 130–139 ⬎139 Absent Mild (pedal edema) Severe (pulmonary edema) Absent Present Absent Present
Scoring Points 5 10 15 20 25 30 0 10 20 30 0 10 20 5 10 15 20 25 0 5 10 0 10 0 10
Highly suggestive of thyroid storm Suggestive of impending thyroid storm Unlikely to represent thyroid storm
Adapted from Burch HB, Wartofsky L.3
growth of bacteria. Her rapid recovery after the institution of definitive therapy suggests that thyroid storm was the primary etiology that accounted for her critical illness. Indeed, we cannot conclusively exclude the possibility of a viral GI tract infection or superimposed culture-negative sepsis that responded to concurrent and empirical administration of antibiotics. In this previously healthy, young patient, the presence of new-onset and persistent atrial fibrillation may have been the most significant key to her diagnosis. Although in fewer than 1% of patients, new-onset atrial fibrillation results from thyrotoxicosis, Klein and Ojamaa6 recommended that serum thyrotropin should be measured in all patients to rule out thyroid disease. Because the manifestations of thyroid storm are variable, Burch and Wartofsky3 proposed a quantitative diagnostic scale (Table 1), where a score exceeding 45 points is highly suggestive of thyroid storm. Even though the scale was designed to aid in the prompt recognition of impending thyroid storm and provide an aggressive therapeutic approach, it should not be substituted for sound clinical judg-
THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
ment.3 According to the scale, our patient scored 105 points, which is greater than 2 times that required to be highly suggestive of thyroid storm. Flasar and Goldberg5 reported that a CT of the abdomen is more sensitive and specific for nearly all etiologies of acute abdominal pain, and it is recommend as the initial imaging modality of choice for evaluation of most presentations of acute abdominal pain. However, it should be kept in mind that since a CT scan with iodinated contrast medium can lead to enhanced thyroid hormone synthesis and aggravate hyperthyroidism, iodinated contrast media should be avoided in patients suspected of hyperthyroidism or thyroid storm.7 In the case presented herein, it was more of a lucky coincidence that our patient underwent non– contrast-enhanced abdominal CT rather than diagnostic forethought. Our patient’s blood gas analysis and laboratory findings revealed lactic acidosis, a feature rarely reported in patients with thyroid storm. We speculate that several factors could have contributed to lactic acidosis: (1) increased lactate production caused by tissue hypoxia after congestive heart failure, pulmonary edema, and intravascular volume depletion and (2) decreased lactate clearance in the liver caused by sepsis or thyroid storm itself. Once a diagnosis of thyroid storm is established, treatment should be initiated immediately. Clinical improvement is generally expected within 12 to 24 hours, but full recovery may take 7 to 8 days.2 The experience with the patient described throughout highlights that even in the absence of an antecedent history of thyroid disease or clinical clues, such as goiter, exophthalmos, lid lag, or lid retraction, it is important to keep thyroid storm in the differential diagnosis of abdominal pain complicated by multiorgan dysfunction syndrome. Early recognition and prompt therapies probably attenuated organ dysfunction from peaking in our patient, thus allowing her full recovery. References 1. Singer PA, Cooper DS, Levy EG, et al. Treatment guidelines for patients with hyperthyroidism and hypothyroidism: Standards of Care Committee, American Thyroid Association. JAMA 1995;273:808–12. 2. Tietgens ST, Leinung MC. Thyroid storm. Med Clin North Am 1995;79:169–84. 3. Burch HB, Wartofsky L. Life-threatening thyrotoxicosis: thyroid storm. Endocrinol Metab Clin North Am 1993;22: 263–77. 4. Kahaly GJ, Dillmann WH. Thyroid hormone action in the heart. Endocr Rev 2005;26:704–28. 5. Flasar MH, Goldberg E. Acute abdominal pain. Med Clin North Am 2006;90:481–503. 6. Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system. N Engl J Med 2001;344:501–9. 7. van der Molen AJ, Thomsen HS, Morcos SK, et al. Effect of iodinated contrast media on thyroid function in adults. Eur Radiol 2004;14:902–7.
401
ABSTRACT: Thyroid storm is a rare but life-threatening condition caused by exaggerated thyrotoxic manifestations. Untreated thyroid storm is fatal, and the case fatality rate is 21% to 30%. The most important clinical management in thyroid storm is early recognition and treatment. We present the case of a previously healthy young woman in whom suspected gastrointestinal tract sepsis complicated by multi-organ dysfunction syn-
drome masked the major symptomatology of thyroid storm. This patient highlights the importance of a high clinical suspicion for potentially life-threatening conditions, such as thyroid storm, even in the absence of clinical clues (exophthalmos, lid lag, and goiter) or a history of thyrotoxicosis. KEY INDEXING TERMS: Abdominal pain; Multi-organ dysfunction syndrome; Thyroid storm. [Am J Med Sci 2007;334(5):399–401.]
T
normochromic normocytic anemia (Hb, 11.6 g/dL), a prolonged prothrombin time of 16 seconds (international normalized ratio, 1.93), mildly deranged liver and renal profiles (aspartate aminotransferases, 104 U/L; alanine aminotransferases, 46 U/L; total bilirubin, 1.3 mg/dL; creatinine, 1.2 mg/dL), an elevated amylase concentration of 626 U/L, and a normal lipase concentration of 25 U/L. Serum electrolytes included a Na⫹ level of 144 mEq/L, K⫹ of 5.0 mEq/L, and Cl– of 109 mEq/L. Arterial blood gas analysis on room air included a pH of 7.13, a PCO2 of 43 mm Hg, a PO2 of 89 mm Hg, and a measured HCO3⫺ of 14.8 mEq/L; the anion gap was 20.2 mEq/L. The serum lactic acid was 10 mmol/L (normal: 0.8 to 2.2). The serum and urine ketones were negative. The serum toxicology results were entirely negative. All other parameters were within normal limits. An electrocardiogram was interpreted as atrial fibrillation with a rapid ventricular rate of 120 to 150 beats per minute. Chest radiography demonstrated bilateral pulmonary infiltrates and pleural effusion. One hour after admission, the patient had cardiovascular collapse and shock developed. The patient became increasingly obtunded and dyspneic and required endotracheal intubation as well as mechanical ventilation for respiratory failure. After the blood pressure was stabilized via fluid resuscitation and administration of inotropic agents, emergent computed tomography (CT) of the abdomen (non– contrast-enhanced instead of contrast-enhanced due to the deteriorated renal function by hypotension) was performed and was unremarkable. On gastroscopy, only a mild esophagitis was identified. A transthoracic echocardiogram revealed four mildly dilated cardiac chambers in the absence of valvular defects or regional wall motion abnormalities. In the following 2 days of the patient’s admission, she remained febrile and tachycardic with alternating lethargy and agitation despite appropriate fluid resuscitation and empiric antibiotics administration. A diagnosis of thyroid storm was not achieved until the third day of admission, when the results of the thyroid function tests (ordered because of persistent atrial fibrillation) were available (Figure 1). The most stunning components of the panel included a thyroid-stimulating hormone level of 0.05 mU/L (normal: 0.3 to 5.0) and a free thyroxin level of 5.4 ng/dL (normal: 0.8 to 2.0). The standard treatment for thyroid storm was immediately administered and included oral propranolol (40 mg every 8 hours), intravenous hydrocortisone (100 mg every 8 hours), and oral propylthiouracil (200 mg every 4 hours) followed by Lugol’s solution (8 drops every 6 hours) 1 hour later. Within 24 hours, a
hyroid storm refers to the sudden onset of lifethreatening manifestations of thyrotoxicosis accompanied by systemic organ decompensation. Prompt recognition is the key to successful management. We discuss a patient in thyroid storm who lacked the tell-tale clinical signs (exophthalmos, lid lag, and goiter) at the time of initial assessment and did not give a medical history of thyroid disease. This case serves to illustrate the variable presentation of thyroid storm that may delay its diagnosis and initiation of life-saving treatment. Case Report
In September 2005, a 38-year-old woman presented to our hospital with a 1-week history of insomnia, dyspnea on exertion, and nonbloody diarrhea. Approximately 12 hours before admission, the patient’s dyspnea had worsened. Nausea, vomiting, and severe abdominal pain rapidly ensued. On physical examination, the patient was alert, irritable, febrile (38.3°C), tachypneic (28 breaths/min), and tachycardic (135 beats/min) but normotensive (125/70 mm Hg). The patient had prominent jugular venous distention. No exophthalmos, goiter, lid lag, or lid retraction was noted. No heart murmur was identified on auscultation, but rales were noted bilaterally. Tender distension with no rebounding pain in the epigastric region was identified, and bowel sounds were sluggish. Laboratory test results revealed a leukocytosis of 12.1⫻109/L (neutrophils, 43.7%),
From the Division of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. Submitted December 28, 2006; accepted in revised form April 27, 2007. Correspondence: Dr. Chih-Tsueng He, Division of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Sec. 2, Chenggong Road, Neihu District, Taipei City 114, Taiwan (E-mail: [email protected]). THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
399
Abdominal Pain Complicated by Multi-Organ Dysfunction Syndrome
Figure 1. Twelve-lead ECG demonstrating atrial fibrillation with a rapid ventricular rate of 150 to 200 beats/min.
dramatic clinical improvement was identified, particularly with reference to the patient’s level of the agitation, hyperthermia, and tachycardia. Within 1 week, mechanical ventilation was successfully weaned and the patient recovered uneventfully. All blood, urine, sputum, and stool cultures were negative for bacterial organisms. When last seen in October 2006, the patient was clinically and biochemically euthyroid and was continuing to take propranolol and propylthiouracil as directed.
Discussion Thyroid storm is a rare but life-threatening condition caused by exaggerated thyrotoxic manifestations, including advanced fever, marked tachycardia, gastrointestinal dysfunction, and central nervous system involvement, varying from confusion to coma.1 The pathogenesis of thyroid storm has not been determined. It has been suggested that the rate of the elevation of thyroid hormone levels is more important than the absolute increase.2 The most important clinical management in thyroid storm is early recognition and treatment. The diagnosis of thyroid storm remains a clinical one, aided by abnormal thyroid hormone levels. In the patient presented herein, no history of thyroid disease existed, and the expected clinical clues, such as goiter or ocular findings, were absent. Instead, the patient presented with abdominal pain and rapidly proceeded to cardiovascular collapse. The rare presentation and serious complications resulted in a diagnostic challenge. Thyroid storm is a systemic disease and many of the clinical features associated with this disorder result from over activity of the sympathetic nervous system. Gastrointestinal presentations (commonly limited to an enhanced intestinal transport in simple thyrotoxicosis) can dominate the clinical picture 400
in patients with thyroid storm. Nausea, vomiting, diarrhea, and even acute abdomen are typical findings.3 Cardiac decompensation is also frequently noted in thyroid storm and may occur in the absence of underlying heart disease. Congestive heart failure or cardiac arrhythmias such as atrial fibrillation are commonly observed. Excessive thyroid hormone levels, via direct and indirect mechanisms, alter cardiovascular physiology. A decline in systemic vascular resistance and increased heart rate, myocardial contractility, and cardiac mass have been reported.4 As noted in the patient presented herein, peripheral vasodilation (as the early manifestation of excess thyroid hormone levels), coupled with volume depletion due to vomiting and/or diarrhea may have contributed to the subsequent vascular collapse. The patient described herein presented for evaluation of abdominal pain. Diagnosing thyroid storm may be difficult because of the nonspecific and overlapping manifestations of the thyrotoxic state (ie, tachycardia, fever, vomiting, diarrhea, and abdominal pain) compared with those of intra-abdominal disease processes, such as acute pancreatitis or gastrointestinal (GI) tract sepsis. In addition, although there are a multitude of systemic medical disorders that can present with abdominal pain, thyroid storm, one of the potential life-threatening conditions, is not always in the differential diagnosis. In this patient, a normal serum lipase level and an unremarkable CT of the pancreas had ruled out the diagnosis of acute pancreatitis.5 The patient’s history suggests that GI tract sepsis may have occurred concurrently with thyroid storm and may have been the precipitating factor. However, all cultures of blood, urine, sputum, and stool demonstrated no November 2007 Volume 334 Number 5
Hsiao et al
Table 1. Diagnostic Point Scale for Thyroid Storm System
Parameters
Thermoregulatory (body temperature, °C)
37.2–37.7 37.8–38.2 38.3–38.8 38.9–39.4 39.5–39.9 ⬎39.9
Central nervous system
Gastrointestinalhepatic Cardiovascular Tachycardia (beats/min) Congestive heart failure Atrial fibrillation Precipitating event Final score 45 or greater 25–44 ⬍25
Absent Mild (agitation) Moderate (delirium, psychosis, extreme lethargy) Severe (seizure, coma) Absent Moderate (diarrhea, nausea/ vomiting, abdominal Severe (unexplained jaundice) 99–109 110–119 120–129 130–139 ⬎139 Absent Mild (pedal edema) Severe (pulmonary edema) Absent Present Absent Present
Scoring Points 5 10 15 20 25 30 0 10 20 30 0 10 20 5 10 15 20 25 0 5 10 0 10 0 10
Highly suggestive of thyroid storm Suggestive of impending thyroid storm Unlikely to represent thyroid storm
Adapted from Burch HB, Wartofsky L.3
growth of bacteria. Her rapid recovery after the institution of definitive therapy suggests that thyroid storm was the primary etiology that accounted for her critical illness. Indeed, we cannot conclusively exclude the possibility of a viral GI tract infection or superimposed culture-negative sepsis that responded to concurrent and empirical administration of antibiotics. In this previously healthy, young patient, the presence of new-onset and persistent atrial fibrillation may have been the most significant key to her diagnosis. Although in fewer than 1% of patients, new-onset atrial fibrillation results from thyrotoxicosis, Klein and Ojamaa6 recommended that serum thyrotropin should be measured in all patients to rule out thyroid disease. Because the manifestations of thyroid storm are variable, Burch and Wartofsky3 proposed a quantitative diagnostic scale (Table 1), where a score exceeding 45 points is highly suggestive of thyroid storm. Even though the scale was designed to aid in the prompt recognition of impending thyroid storm and provide an aggressive therapeutic approach, it should not be substituted for sound clinical judg-
THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
ment.3 According to the scale, our patient scored 105 points, which is greater than 2 times that required to be highly suggestive of thyroid storm. Flasar and Goldberg5 reported that a CT of the abdomen is more sensitive and specific for nearly all etiologies of acute abdominal pain, and it is recommend as the initial imaging modality of choice for evaluation of most presentations of acute abdominal pain. However, it should be kept in mind that since a CT scan with iodinated contrast medium can lead to enhanced thyroid hormone synthesis and aggravate hyperthyroidism, iodinated contrast media should be avoided in patients suspected of hyperthyroidism or thyroid storm.7 In the case presented herein, it was more of a lucky coincidence that our patient underwent non– contrast-enhanced abdominal CT rather than diagnostic forethought. Our patient’s blood gas analysis and laboratory findings revealed lactic acidosis, a feature rarely reported in patients with thyroid storm. We speculate that several factors could have contributed to lactic acidosis: (1) increased lactate production caused by tissue hypoxia after congestive heart failure, pulmonary edema, and intravascular volume depletion and (2) decreased lactate clearance in the liver caused by sepsis or thyroid storm itself. Once a diagnosis of thyroid storm is established, treatment should be initiated immediately. Clinical improvement is generally expected within 12 to 24 hours, but full recovery may take 7 to 8 days.2 The experience with the patient described throughout highlights that even in the absence of an antecedent history of thyroid disease or clinical clues, such as goiter, exophthalmos, lid lag, or lid retraction, it is important to keep thyroid storm in the differential diagnosis of abdominal pain complicated by multiorgan dysfunction syndrome. Early recognition and prompt therapies probably attenuated organ dysfunction from peaking in our patient, thus allowing her full recovery. References 1. Singer PA, Cooper DS, Levy EG, et al. Treatment guidelines for patients with hyperthyroidism and hypothyroidism: Standards of Care Committee, American Thyroid Association. JAMA 1995;273:808–12. 2. Tietgens ST, Leinung MC. Thyroid storm. Med Clin North Am 1995;79:169–84. 3. Burch HB, Wartofsky L. Life-threatening thyrotoxicosis: thyroid storm. Endocrinol Metab Clin North Am 1993;22: 263–77. 4. Kahaly GJ, Dillmann WH. Thyroid hormone action in the heart. Endocr Rev 2005;26:704–28. 5. Flasar MH, Goldberg E. Acute abdominal pain. Med Clin North Am 2006;90:481–503. 6. Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system. N Engl J Med 2001;344:501–9. 7. van der Molen AJ, Thomsen HS, Morcos SK, et al. Effect of iodinated contrast media on thyroid function in adults. Eur Radiol 2004;14:902–7.
401