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with an absolute eosinophil count of 0.57 to 0.9 9 109/L (reference range, 0.2–0.45 9 109/L) over the previous 5 years. Stool examination revealed the rhabditiform larvae of Strongyloides stercoralis (Figure 1). Serum IgE level was high at 1,120 IU/mL. She was treated with two doses of ivermectin (200 lg/kg daily), and the intravenous hydrocortisone was stopped. Over the next few days, her symptoms markedly improved, and the eosinophil count normalized. She was discharged after 11 days of admission, and her asthma became better controlled with a combined salmeterol and fluticasone inhaler. There was no further asthmatic exacerbation in the following 2 years, and her maintenance therapy was gradually tapered.
LETTERS TO THE EDITOR
1409
Yat-Fung Shea, MBBS Winnie Wing-Yee Mok, MBBS Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, China Jasper Fuk-Woo Chan, FRC Path Department of Microbiology, Carol Yu Centre for Infection, University of Hong Kong, Hong Kong, China Joseph Shiu-Kwong Kwan, FRCP Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, China
ACKNOWLEDGMENTS DISCUSSION Strongyloidiasis can present as asthma that may be refractory to the usual asthma treatment regime.1–4 The prevalence of S. stercoralis in individuals with asthma from endemic areas was reported to be as high as 13%.5 A high degree of clinical vigilance is needed to diagnose such cases of strongyloidiasis, because it may remain asymptomatic for years and manifest only as the individual ages and experiences immunosenescence. It is particularly relevant to older adults in endemic areas. The first clue to the diagnosis in the woman described above was the lack of clinical improvement despite the use of intravenous hydrocortisone during an asthma attack. The life cycle of the nematode starts with the filariform larvae inside soil penetrating the intact human skin. The larvae enter the venous circulation, reach the lungs, and penetrate the alveolar spaces. They then ascend through the bronchial tree, are swallowed, and reach the small bowel. The female worms embed in the submucosa of the duodenum and produce embryonated eggs. The eggs hatch and release the rhabditiform larvae in the intestinal wall. The larvae migrate into the bowel lumen and are passed into the feces or mature into filariform larvae. The filariform larvae can infect the intestinal mucosa or perianal skin to restart the parasitic cycle. Through this process of autoinfection, the parasite can persist for many years before its discovery.6 Corticosteroids are a well-known risk factor that can exacerbate the severity of strongyloidiasis, leading to hyperinfection syndrome or disseminated infection.3,7 The other clues in our patient’s case included her previous occupation as a farmer and the presence of on-andoff eosinophilia for years. Farmers and miners are two of the best known at-risk groups,8 others include nursing staff5 and conservancy services.9 It is important to consider repeating stool microbiological examinations in suspicious cases because a single stool sample may miss up to 70% of cases.4 A high level of awareness of possible underlying strongyloidiasis in individuals with asthma is important because initiation of antiparasitic treatment can improve asthmatic control and corticosteroids should also be avoided to prevent a hyperinfection syndrome or disseminated infection, which may be associated with a poor clinical outcome.10 Clinicians should have a strong clinical suspicion of strongyloidiasis in older adults with asthma living in endemic areas who have suboptimal response to asthma therapy.
Conflict of Interest: The authors have no financial or any other personal conflict to report. Author Contributions: Study concept and design: Shea, Mok. Acquisition of subject and data: Shea, Mok, Chan. Analysis and interpretation of data: all authors. Preparation of manuscript: all authors. Critical review and approval: all authors. Sponsor’s Role: None.
REFERENCES 1. Dunlap NE, Shin MS, Polt SS et al. Strongyloidiasis manifested as asthma. South Med J 1984;77:77–78. 2. Kabirdas D, Afonso B, Avella H et al. An elderly woman with asthma, eosinophilia, and septic shock. Cleve Clin J Med 2007;74(877–881):885– 886. 3. Altintop L, Cakar B, Hokelek M et al. Strongyloides stercoralis hyperinfection in a patient with rheumatoid arthritis and bronchial asthma: A case report. Ann Clin Microbiol Antimicrob 2010;9:27. 4. Khan WA, Santhanakrishnan K. Hypereosinophilic syndrome secondary to strongyloides infection: A case of recurrent asthma exacerbations. BMJ Case Rep 2013;2013:1–3. 5. Wehner JH, Kirsch CM, Kagawa FTJ et al. The prevalence and response to therapy of Strongyloides stercoralis in patients with asthma from endemic areas. Chest 1994;106:762–766. 6. Montes M, Sawhney C, Barros N. Strongyloides stercoralis: There but not seen. Curr Opin Infect Dis 2010;23:500–504. 7. Chan JF, Choy BY, Lai KN. Nephrotic syndrome secondary to strongyloidiasis: A common infection with an uncommon presentation. Hong Kong J Nephrol 2008;10:37–41. 8. Olsen A, van Lieshout L, Marti H et al. Strongyloidiasis—the most neglected of the neglected tropical diseases? Trans R Soc Trop Med Hyg 2009;103:967–972. 9. Shea YF, Chau KM, Hung IF et al. Strongyloidiasis in a nonagenarian who previously worked in conservancy services. Hong Kong Med J 2013;19:74–76. 10. Mokhlesi B, Shulzhenko O, Garimella PS et al. Pulmonary strongyloidiasis: The varied clinical presentations. Clin Pulm Med 2004;11:6–13.
UROLITHIASIS AS AN UNUSUAL CAUSE OF FAILURE TO THRIVE To the Editor: A 65-year-old woman presented to the emergency department (ED) from clinic for worsening failure to thrive, with a reported unintended weight loss of 175 pounds over the preceding year. She described experiencing early satiety, fatigue, dyspnea on exertion, and occasional bilious emesis over this time. She had been hospitalized in the intensive care unit 11 months earlier for
1410
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septic shock secondary to urinary tract infection (UTI) but had no dysuria or other urinary symptoms at that time. She required 4 months of posthospital rehabilitation, during which time she developed another UTI with associated dysuria that was treated effectively with outpatient antibiotics. Approximately 1 month after discharge from rehabilitation, she was hospitalized again for several days for sepsis secondary to UTI, noting only malodorous urine but no dysuria. Additional medical history included type 2 diabetes mellitus, obesity, hypertension, and bilateral lower extremity deep venous thromboses during rehabilitation with completion of 6 months of warfarin therapy. On admission, the patient’s blood pressure was 138/62 mmHg, pulse 72 beats per minute, respiration 18 breaths per minute, and temperature 35.8°C. Physical examination revealed a weak and ill-appearing obese woman with dry mucous membranes and dry, peeling lips. She exhibited marked alopecia, with dry, scaling skin on her back, arms, and legs. Cutaneous candidiasis was found under her breasts. Blood chemistry panel showed white blood cell count of 18.1 9 109 cells/L, hemoglobin 14.2 g/ dL, hematocrit 43.5%, platelets 527 9 109/L, sodium 142 mEq/L, potassium 3.2 mEq/L, creatinine 1.68 mg/dL, glycosylated hemoglobin 4.3%, albumin 2.5 g/dL, thyroidstimulating hormone 1.34 lIU/mL, cortisol 36.5 lg/dL, and total 25-OH vitamin D 10 ng/mL. Troponin I and creatine kinase-MB were negative. Urinalysis revealed more than 100 white blood cells per high-powered field, many bacteria, positive nitrites, 35 red blood cells per high-powered field, and no glucose or ketones. Urine culture grew more than 50,000 colony-forming units/mL of Escherichia coli; blood culture grew no organisms. She was started on empirical vancomycin and ceftriaxone and given 2 L of intravenous normal saline in the ED. Chest radiograph was negative. Colonoscopy and endogastroduodenoscopy did not reveal any masses or histopathological abnormalities. Computed tomography of the chest, abdomen, and pelvis showed no evidence of malignancy but revealed a 0.6-cm right proximal ureteral stone with moderate right hydronephrosis and hydroureter. On review of prior imaging, it was found that she had mild right hydronephrosis on an ultrasound obtained during her initial ICU stay 11 months earlier, although no stone was visualized on that ultrasound. She underwent successful placement of a 6 French 9 26 cm stent in her right ureter. Urology noted the stone to be impacted, and there was subsequent purulent drainage through her postoperative Foley catheter after stent placement. She remained afebrile after the procedure. A peripherally inserted central catheter was placed to allow for completion of a 14-day course of ceftriaxone. She improved clinically and was discharged to a rehabilitation facility in stable condition.
DISCUSSION Failure to thrive in older adults is defined as a lack of vitality and functional decline characterized by weight loss of greater than 5% of baseline, poor appetite, inactivity, and in this case, severe malnutrition.1,2 Although the differential diagnosis of failure to thrive includes infection, including infections of the urinary tract, infection from
JULY 2014–VOL. 62, NO. 7
JAGS
obstructive urolithiasis is not a common cause and was not initially considered in this woman. Common etiologies of failure to thrive in elderly adults include malignancy; cardiac or pulmonary disease; recurrent infection; inflammatory disorders such as inflammatory bowel disease or rheumatological disease; and anorexia due to psychiatric disease, dementia, or medication effect.2 Polypharmacy puts older adults at risk of failure to thrive, as do many individual classes of pharmaceuticals such as anticholinergic medications, benzodiazepines, opioids, diuretics, and beta-blockers.2 An atypical presentation of ureteral urolithiasis, which generally presents with symptoms of renal colic, complicated this case. This woman did not exhibit typical symptoms of renal colic, and did not complain of the flank pain, abdominal pain, or groin pain that would be expected in someone with a 6-mm3 impacted ureteral stone. Older adults often present with atypical or nonspecific symptoms of disease or may not have symptoms at all.1 It is congruent with this that older adults tend to present with atypical pain or no pain at all with urolithiasis and are more likely to have larger stones and a higher risk of developing bacteremia.4 It is important to consider urolithiasis with possible indolent infection in an older adult presenting with failure to thrive with no other obvious etiology. Michael C. Bond, MA Department of Medicine, University of North Carolina, Chapel Hill, North Carolina Dorothea H. Ellis, MD, MS Department of Physical Medicine and Rehabilitation, University of North Carolina, Chapel Hill, North Carolina Charles C. Sims, MD Department of Medicine, University of North Carolina, Chapel Hill, North Carolina Lindsay A. Wilson, MD, MPH Division of Geriatric Medicine, Department of Medicine, University of North Carolina, Chapel Hill, North Carolina
ACKNOWLEDGMENTS Conflict of Interest: The authors have no financial or any other personal conflict to report. Author Contributions: Study concept and design: Bond, Ellis, Wilson. Patient care, acquisition of subjects, analysis and interpretation of data, preparation of manuscript: all authors. Sponsor’s Role: None.
REFERENCES 1. Rocchiccioli J, Sanford J. Revisiting geriatric failure to thrive: A complex and compelling clinical condition. J Gerontol Nurs 2009;35:18–24. 2. Robertson RG, Montagnini M. Geriatric failure to thrive. Am Fam Physician 2004;70:343–350. 3. Portis AJ, Sundaram CP. Diagnosis and initial management of kidney stones. Am Fam Physician 2001;63:1329–1338. 4. Krambeck AE, Lieske JC, Li X et al. Effect of age on the clinical presentation of incident symptomatic urolithiasis in the general population. J Urol 2013;189:155–164.
JULY 2014–VOL. 62, NO. 7
with an absolute eosinophil count of 0.57 to 0.9 9 109/L (reference range, 0.2–0.45 9 109/L) over the previous 5 years. Stool examination revealed the rhabditiform larvae of Strongyloides stercoralis (Figure 1). Serum IgE level was high at 1,120 IU/mL. She was treated with two doses of ivermectin (200 lg/kg daily), and the intravenous hydrocortisone was stopped. Over the next few days, her symptoms markedly improved, and the eosinophil count normalized. She was discharged after 11 days of admission, and her asthma became better controlled with a combined salmeterol and fluticasone inhaler. There was no further asthmatic exacerbation in the following 2 years, and her maintenance therapy was gradually tapered.
LETTERS TO THE EDITOR
1409
Yat-Fung Shea, MBBS Winnie Wing-Yee Mok, MBBS Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, China Jasper Fuk-Woo Chan, FRC Path Department of Microbiology, Carol Yu Centre for Infection, University of Hong Kong, Hong Kong, China Joseph Shiu-Kwong Kwan, FRCP Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, China
ACKNOWLEDGMENTS DISCUSSION Strongyloidiasis can present as asthma that may be refractory to the usual asthma treatment regime.1–4 The prevalence of S. stercoralis in individuals with asthma from endemic areas was reported to be as high as 13%.5 A high degree of clinical vigilance is needed to diagnose such cases of strongyloidiasis, because it may remain asymptomatic for years and manifest only as the individual ages and experiences immunosenescence. It is particularly relevant to older adults in endemic areas. The first clue to the diagnosis in the woman described above was the lack of clinical improvement despite the use of intravenous hydrocortisone during an asthma attack. The life cycle of the nematode starts with the filariform larvae inside soil penetrating the intact human skin. The larvae enter the venous circulation, reach the lungs, and penetrate the alveolar spaces. They then ascend through the bronchial tree, are swallowed, and reach the small bowel. The female worms embed in the submucosa of the duodenum and produce embryonated eggs. The eggs hatch and release the rhabditiform larvae in the intestinal wall. The larvae migrate into the bowel lumen and are passed into the feces or mature into filariform larvae. The filariform larvae can infect the intestinal mucosa or perianal skin to restart the parasitic cycle. Through this process of autoinfection, the parasite can persist for many years before its discovery.6 Corticosteroids are a well-known risk factor that can exacerbate the severity of strongyloidiasis, leading to hyperinfection syndrome or disseminated infection.3,7 The other clues in our patient’s case included her previous occupation as a farmer and the presence of on-andoff eosinophilia for years. Farmers and miners are two of the best known at-risk groups,8 others include nursing staff5 and conservancy services.9 It is important to consider repeating stool microbiological examinations in suspicious cases because a single stool sample may miss up to 70% of cases.4 A high level of awareness of possible underlying strongyloidiasis in individuals with asthma is important because initiation of antiparasitic treatment can improve asthmatic control and corticosteroids should also be avoided to prevent a hyperinfection syndrome or disseminated infection, which may be associated with a poor clinical outcome.10 Clinicians should have a strong clinical suspicion of strongyloidiasis in older adults with asthma living in endemic areas who have suboptimal response to asthma therapy.
Conflict of Interest: The authors have no financial or any other personal conflict to report. Author Contributions: Study concept and design: Shea, Mok. Acquisition of subject and data: Shea, Mok, Chan. Analysis and interpretation of data: all authors. Preparation of manuscript: all authors. Critical review and approval: all authors. Sponsor’s Role: None.
REFERENCES 1. Dunlap NE, Shin MS, Polt SS et al. Strongyloidiasis manifested as asthma. South Med J 1984;77:77–78. 2. Kabirdas D, Afonso B, Avella H et al. An elderly woman with asthma, eosinophilia, and septic shock. Cleve Clin J Med 2007;74(877–881):885– 886. 3. Altintop L, Cakar B, Hokelek M et al. Strongyloides stercoralis hyperinfection in a patient with rheumatoid arthritis and bronchial asthma: A case report. Ann Clin Microbiol Antimicrob 2010;9:27. 4. Khan WA, Santhanakrishnan K. Hypereosinophilic syndrome secondary to strongyloides infection: A case of recurrent asthma exacerbations. BMJ Case Rep 2013;2013:1–3. 5. Wehner JH, Kirsch CM, Kagawa FTJ et al. The prevalence and response to therapy of Strongyloides stercoralis in patients with asthma from endemic areas. Chest 1994;106:762–766. 6. Montes M, Sawhney C, Barros N. Strongyloides stercoralis: There but not seen. Curr Opin Infect Dis 2010;23:500–504. 7. Chan JF, Choy BY, Lai KN. Nephrotic syndrome secondary to strongyloidiasis: A common infection with an uncommon presentation. Hong Kong J Nephrol 2008;10:37–41. 8. Olsen A, van Lieshout L, Marti H et al. Strongyloidiasis—the most neglected of the neglected tropical diseases? Trans R Soc Trop Med Hyg 2009;103:967–972. 9. Shea YF, Chau KM, Hung IF et al. Strongyloidiasis in a nonagenarian who previously worked in conservancy services. Hong Kong Med J 2013;19:74–76. 10. Mokhlesi B, Shulzhenko O, Garimella PS et al. Pulmonary strongyloidiasis: The varied clinical presentations. Clin Pulm Med 2004;11:6–13.
UROLITHIASIS AS AN UNUSUAL CAUSE OF FAILURE TO THRIVE To the Editor: A 65-year-old woman presented to the emergency department (ED) from clinic for worsening failure to thrive, with a reported unintended weight loss of 175 pounds over the preceding year. She described experiencing early satiety, fatigue, dyspnea on exertion, and occasional bilious emesis over this time. She had been hospitalized in the intensive care unit 11 months earlier for
1410
LETTERS TO THE EDITOR
septic shock secondary to urinary tract infection (UTI) but had no dysuria or other urinary symptoms at that time. She required 4 months of posthospital rehabilitation, during which time she developed another UTI with associated dysuria that was treated effectively with outpatient antibiotics. Approximately 1 month after discharge from rehabilitation, she was hospitalized again for several days for sepsis secondary to UTI, noting only malodorous urine but no dysuria. Additional medical history included type 2 diabetes mellitus, obesity, hypertension, and bilateral lower extremity deep venous thromboses during rehabilitation with completion of 6 months of warfarin therapy. On admission, the patient’s blood pressure was 138/62 mmHg, pulse 72 beats per minute, respiration 18 breaths per minute, and temperature 35.8°C. Physical examination revealed a weak and ill-appearing obese woman with dry mucous membranes and dry, peeling lips. She exhibited marked alopecia, with dry, scaling skin on her back, arms, and legs. Cutaneous candidiasis was found under her breasts. Blood chemistry panel showed white blood cell count of 18.1 9 109 cells/L, hemoglobin 14.2 g/ dL, hematocrit 43.5%, platelets 527 9 109/L, sodium 142 mEq/L, potassium 3.2 mEq/L, creatinine 1.68 mg/dL, glycosylated hemoglobin 4.3%, albumin 2.5 g/dL, thyroidstimulating hormone 1.34 lIU/mL, cortisol 36.5 lg/dL, and total 25-OH vitamin D 10 ng/mL. Troponin I and creatine kinase-MB were negative. Urinalysis revealed more than 100 white blood cells per high-powered field, many bacteria, positive nitrites, 35 red blood cells per high-powered field, and no glucose or ketones. Urine culture grew more than 50,000 colony-forming units/mL of Escherichia coli; blood culture grew no organisms. She was started on empirical vancomycin and ceftriaxone and given 2 L of intravenous normal saline in the ED. Chest radiograph was negative. Colonoscopy and endogastroduodenoscopy did not reveal any masses or histopathological abnormalities. Computed tomography of the chest, abdomen, and pelvis showed no evidence of malignancy but revealed a 0.6-cm right proximal ureteral stone with moderate right hydronephrosis and hydroureter. On review of prior imaging, it was found that she had mild right hydronephrosis on an ultrasound obtained during her initial ICU stay 11 months earlier, although no stone was visualized on that ultrasound. She underwent successful placement of a 6 French 9 26 cm stent in her right ureter. Urology noted the stone to be impacted, and there was subsequent purulent drainage through her postoperative Foley catheter after stent placement. She remained afebrile after the procedure. A peripherally inserted central catheter was placed to allow for completion of a 14-day course of ceftriaxone. She improved clinically and was discharged to a rehabilitation facility in stable condition.
DISCUSSION Failure to thrive in older adults is defined as a lack of vitality and functional decline characterized by weight loss of greater than 5% of baseline, poor appetite, inactivity, and in this case, severe malnutrition.1,2 Although the differential diagnosis of failure to thrive includes infection, including infections of the urinary tract, infection from
JULY 2014–VOL. 62, NO. 7
JAGS
obstructive urolithiasis is not a common cause and was not initially considered in this woman. Common etiologies of failure to thrive in elderly adults include malignancy; cardiac or pulmonary disease; recurrent infection; inflammatory disorders such as inflammatory bowel disease or rheumatological disease; and anorexia due to psychiatric disease, dementia, or medication effect.2 Polypharmacy puts older adults at risk of failure to thrive, as do many individual classes of pharmaceuticals such as anticholinergic medications, benzodiazepines, opioids, diuretics, and beta-blockers.2 An atypical presentation of ureteral urolithiasis, which generally presents with symptoms of renal colic, complicated this case. This woman did not exhibit typical symptoms of renal colic, and did not complain of the flank pain, abdominal pain, or groin pain that would be expected in someone with a 6-mm3 impacted ureteral stone. Older adults often present with atypical or nonspecific symptoms of disease or may not have symptoms at all.1 It is congruent with this that older adults tend to present with atypical pain or no pain at all with urolithiasis and are more likely to have larger stones and a higher risk of developing bacteremia.4 It is important to consider urolithiasis with possible indolent infection in an older adult presenting with failure to thrive with no other obvious etiology. Michael C. Bond, MA Department of Medicine, University of North Carolina, Chapel Hill, North Carolina Dorothea H. Ellis, MD, MS Department of Physical Medicine and Rehabilitation, University of North Carolina, Chapel Hill, North Carolina Charles C. Sims, MD Department of Medicine, University of North Carolina, Chapel Hill, North Carolina Lindsay A. Wilson, MD, MPH Division of Geriatric Medicine, Department of Medicine, University of North Carolina, Chapel Hill, North Carolina
ACKNOWLEDGMENTS Conflict of Interest: The authors have no financial or any other personal conflict to report. Author Contributions: Study concept and design: Bond, Ellis, Wilson. Patient care, acquisition of subjects, analysis and interpretation of data, preparation of manuscript: all authors. Sponsor’s Role: None.
REFERENCES 1. Rocchiccioli J, Sanford J. Revisiting geriatric failure to thrive: A complex and compelling clinical condition. J Gerontol Nurs 2009;35:18–24. 2. Robertson RG, Montagnini M. Geriatric failure to thrive. Am Fam Physician 2004;70:343–350. 3. Portis AJ, Sundaram CP. Diagnosis and initial management of kidney stones. Am Fam Physician 2001;63:1329–1338. 4. Krambeck AE, Lieske JC, Li X et al. Effect of age on the clinical presentation of incident symptomatic urolithiasis in the general population. J Urol 2013;189:155–164.
