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What did you do for a living? The importance of a Comprehensive Geriatric Assessment
European Geriatric Medicine 6 (2015) 462–464
Available online at
ScienceDirect www.sciencedirect.com
EGM clinical case
What did you do for a living? The importance of a Comprehensive Geriatric Assessment K. Hasmukharay a, N. Saedon b, Y.K. Pang c, C.K. Liam c, K.M. Tan b,* a
Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia Division of Geriatric Medicine, Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia c Division of Respiratory Medicine, Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia b
A R T I C L E I N F O
Article history: Received 20 April 2015 Accepted 28 June 2015 Available online 7 August 2015
We present the case of an 80-year-old woman who had a 12-month history of progressive exertional dyspnoea, nonproductive cough, generalised weakness, and weight loss. Of note, she had worked until her fifties in many different jobs including 15 years of farming, managing paddy fields and vegetable farms, followed by five years in a wood factory. She was admitted to our hospital in September 2014 with a dense ischaemic stroke. Her medical history included hypertension and ischaemic heart disease. She had multiple admissions to different cardiology units in other hospitals with the symptoms described above. She was treated for congestive cardiac failure, after which, standard treatment of frusemide failed to improve her symptoms. On examination, she was alert, afebrile, tachypnoiec with a respiratory rate of 28 breaths/minute, blood pressure of 135/ 75 mmHg and oxygen saturation of 88% by pulse oximetry on room air. Pulmonary auscultation revealed course crepitations bibasally up to the level of midzones of both lung fields. She did not have the usual signs of heart failure such as raised jugular venous pressure and peripheral oedema. She had dysphasia and complete paralysis of her right side in keeping with her stroke. Her chest radiograph revealed bilateral diffuse lung fibrosis (Fig. 1a) and high resolution computed tomography (HRCT) (Fig. 1b–d) revealed dense fibrosis as well as traction bronchiolectasis at right upper lobe and both lower lobes, whereas the right middle lobe and left upper lobe showed reticulonodular opacities and ground-glass changes.
* Corresponding author at: Department of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia. Tel.: +60 3 79492299. E-mail address: [email protected] (K.M. Tan).
She was seen by a respiratory physician who diagnosed hypersensitivity pneumonitis (HP). She was prescribed intravenous methylprednisolone 250 mg once daily. Her arterial blood gases improved (Table 1) and she felt better and was less tachypnoeic. Although her respiratory parameters were improving, one day after completing the 3-day course of pulse methylprednisolone therapy, she became breathless again with pyrexia and leucocytosis requiring non-invasive ventilation and antibiotics. She unfortunately succumbed to a hospital-acquired infection 11 days after admission.
Discussion The first cases of HP, also known as extrinsic allergic alveolitis were described at the beginning of the twentieth century, in farmers exposed to hay or straw. HP was also reported among metal machining workers [1,2]. This is a syndrome caused by repeated inhalation of specific antigens from occupational or environmental exposure in sensitised individuals causing an exaggerated immune response, leading to the onset of symptoms similar to acute or progressive lung damage, sometimes irreversible [3], as with our patient. HP is considered a granulomatous interstitial disease of the lung [4]. A history of exposure to potential agents or changes in the environment or both is essential for the diagnosis. The interval between exposure to the antigen and clinical manifestations of lung disease is unknown, although symptoms can occur as soon as 4–12 h after exposure. In chronic and low-level exposures, the onset is insidious, without episodes of acute illness. In these situations, pulmonary fibrosis becomes prominent and only in advanced stages [5] do respiratory symptoms appear. Our case
http://dx.doi.org/10.1016/j.eurger.2015.06.006 1878-7649/ß 2015 Elsevier Masson SAS and European Union Geriatric Medicine Society. All rights reserved.
K. Hasmukharay et al. / European Geriatric Medicine 6 (2015) 462–464
463
Fig. 1. (a) Chest radiograph showing bilateral diffuse lung fibrosis with greater upper lobe involvement. (b–d) HRCT showing fibrosis and traction bronchiolectasis in both upper lobes and lower lobes.
represents the lack of specificity of the complaints and the long evolution of symptoms. Many older adults may have been heavily involved in farming and other agricultural sectors as their occupation. They are most at
risk of undiagnosed HP. These patients may present to the emergency department with exertional dyspnoea and are commonly diagnosed with congestive cardiac failure, but unfortunately fail to respond to the usual, standard heart failure treatment. We
Table 1 The patient’s blood investigation results.
Methylprednisolone started 4 .9 . 2 0 1 4
5 .9 .2 0 1 4
6 .9 . 2 0 1 4
7 . 9 .2 0 1 4
Haemoglobin (g/dL)
11.8
11.8
-
11.8
White blood cell count
8.3
11.5
-
12.9
3 L/minute
3 L/minute
3 L/minute
via nasal
via nasal
via nasal
prongs
prongs
prongs
9
( x 10 /L ) Oxygen supplementation
Non-invasive ventilation with: FiO2: 0.8 IPAP: 18 cmH2O PEEP: 8 cmH2O PS: 16 cmH2O
Arterial blood gases pH
7 .4 3 0
7.378
90
112
77.5
45
41.6
39.8
7 .4 8 8
7 .4 1 1
PO2 (mmHg)
63
PCO2 (mmHg)
41
Oxygen saturation (%)
92
96.4
98
94
Bicarbonate (mmol/L)
31
27.7
27.2
23
FiO2, inspired oxygen fraction; IPAP, inspiratory positive airway pressure; EPAP, expiratory positive airway pressure; PS, pressure support.
464
K. Hasmukharay et al. / European Geriatric Medicine 6 (2015) 462–464
would like to highlight the importance of revisiting the diagnosis and considering previous occupational history in the Comprehensive Geriatric Assessment. This can lead to a revelation of an underlying disease in an older person who may have atypical presentation of the illness.
Disclosure of interest The authors declare that they have no conflicts of interest concerning this article.
References [1] Gupta A, Rosenman KD. Hypersensitivity pneumonitis due to metal working fluids: Sporadic or under reported? Am J Ind Med 2006;49(6):423–33. [2] Hodgson MJ, Bracker A, Yang C, Storey E, Jarvis BJ, Milton D, et al. Hypersensitivity pneumonitis in a metal-working environment. Am J Ind Med 2001;39(6): 616–28. [3] Girard M, Lacasse Y, Cormier Y. Hypersensitivity pneumonitis. Allergy 2009;64(3):322–34. [4] De Vuyst P, Dalphin JC. Occupational interstitial lung diseases]. Rev Prat 2007; 57(20):2266–76. [5] Vourlekis JS, Schwarz MI, Cherniack RM, Curran-Everett D, Cool CD, Tuder RM, et al. The effect of pulmonary fibrosis on survival in patients with hypersensitivity pneumonitis. Am J Med 2004;116(10):662–8.
Available online at
ScienceDirect www.sciencedirect.com
EGM clinical case
What did you do for a living? The importance of a Comprehensive Geriatric Assessment K. Hasmukharay a, N. Saedon b, Y.K. Pang c, C.K. Liam c, K.M. Tan b,* a
Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia Division of Geriatric Medicine, Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia c Division of Respiratory Medicine, Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia b
A R T I C L E I N F O
Article history: Received 20 April 2015 Accepted 28 June 2015 Available online 7 August 2015
We present the case of an 80-year-old woman who had a 12-month history of progressive exertional dyspnoea, nonproductive cough, generalised weakness, and weight loss. Of note, she had worked until her fifties in many different jobs including 15 years of farming, managing paddy fields and vegetable farms, followed by five years in a wood factory. She was admitted to our hospital in September 2014 with a dense ischaemic stroke. Her medical history included hypertension and ischaemic heart disease. She had multiple admissions to different cardiology units in other hospitals with the symptoms described above. She was treated for congestive cardiac failure, after which, standard treatment of frusemide failed to improve her symptoms. On examination, she was alert, afebrile, tachypnoiec with a respiratory rate of 28 breaths/minute, blood pressure of 135/ 75 mmHg and oxygen saturation of 88% by pulse oximetry on room air. Pulmonary auscultation revealed course crepitations bibasally up to the level of midzones of both lung fields. She did not have the usual signs of heart failure such as raised jugular venous pressure and peripheral oedema. She had dysphasia and complete paralysis of her right side in keeping with her stroke. Her chest radiograph revealed bilateral diffuse lung fibrosis (Fig. 1a) and high resolution computed tomography (HRCT) (Fig. 1b–d) revealed dense fibrosis as well as traction bronchiolectasis at right upper lobe and both lower lobes, whereas the right middle lobe and left upper lobe showed reticulonodular opacities and ground-glass changes.
* Corresponding author at: Department of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia. Tel.: +60 3 79492299. E-mail address: [email protected] (K.M. Tan).
She was seen by a respiratory physician who diagnosed hypersensitivity pneumonitis (HP). She was prescribed intravenous methylprednisolone 250 mg once daily. Her arterial blood gases improved (Table 1) and she felt better and was less tachypnoeic. Although her respiratory parameters were improving, one day after completing the 3-day course of pulse methylprednisolone therapy, she became breathless again with pyrexia and leucocytosis requiring non-invasive ventilation and antibiotics. She unfortunately succumbed to a hospital-acquired infection 11 days after admission.
Discussion The first cases of HP, also known as extrinsic allergic alveolitis were described at the beginning of the twentieth century, in farmers exposed to hay or straw. HP was also reported among metal machining workers [1,2]. This is a syndrome caused by repeated inhalation of specific antigens from occupational or environmental exposure in sensitised individuals causing an exaggerated immune response, leading to the onset of symptoms similar to acute or progressive lung damage, sometimes irreversible [3], as with our patient. HP is considered a granulomatous interstitial disease of the lung [4]. A history of exposure to potential agents or changes in the environment or both is essential for the diagnosis. The interval between exposure to the antigen and clinical manifestations of lung disease is unknown, although symptoms can occur as soon as 4–12 h after exposure. In chronic and low-level exposures, the onset is insidious, without episodes of acute illness. In these situations, pulmonary fibrosis becomes prominent and only in advanced stages [5] do respiratory symptoms appear. Our case
http://dx.doi.org/10.1016/j.eurger.2015.06.006 1878-7649/ß 2015 Elsevier Masson SAS and European Union Geriatric Medicine Society. All rights reserved.
K. Hasmukharay et al. / European Geriatric Medicine 6 (2015) 462–464
463
Fig. 1. (a) Chest radiograph showing bilateral diffuse lung fibrosis with greater upper lobe involvement. (b–d) HRCT showing fibrosis and traction bronchiolectasis in both upper lobes and lower lobes.
represents the lack of specificity of the complaints and the long evolution of symptoms. Many older adults may have been heavily involved in farming and other agricultural sectors as their occupation. They are most at
risk of undiagnosed HP. These patients may present to the emergency department with exertional dyspnoea and are commonly diagnosed with congestive cardiac failure, but unfortunately fail to respond to the usual, standard heart failure treatment. We
Table 1 The patient’s blood investigation results.
Methylprednisolone started 4 .9 . 2 0 1 4
5 .9 .2 0 1 4
6 .9 . 2 0 1 4
7 . 9 .2 0 1 4
Haemoglobin (g/dL)
11.8
11.8
-
11.8
White blood cell count
8.3
11.5
-
12.9
3 L/minute
3 L/minute
3 L/minute
via nasal
via nasal
via nasal
prongs
prongs
prongs
9
( x 10 /L ) Oxygen supplementation
Non-invasive ventilation with: FiO2: 0.8 IPAP: 18 cmH2O PEEP: 8 cmH2O PS: 16 cmH2O
Arterial blood gases pH
7 .4 3 0
7.378
90
112
77.5
45
41.6
39.8
7 .4 8 8
7 .4 1 1
PO2 (mmHg)
63
PCO2 (mmHg)
41
Oxygen saturation (%)
92
96.4
98
94
Bicarbonate (mmol/L)
31
27.7
27.2
23
FiO2, inspired oxygen fraction; IPAP, inspiratory positive airway pressure; EPAP, expiratory positive airway pressure; PS, pressure support.
464
K. Hasmukharay et al. / European Geriatric Medicine 6 (2015) 462–464
would like to highlight the importance of revisiting the diagnosis and considering previous occupational history in the Comprehensive Geriatric Assessment. This can lead to a revelation of an underlying disease in an older person who may have atypical presentation of the illness.
Disclosure of interest The authors declare that they have no conflicts of interest concerning this article.
References [1] Gupta A, Rosenman KD. Hypersensitivity pneumonitis due to metal working fluids: Sporadic or under reported? Am J Ind Med 2006;49(6):423–33. [2] Hodgson MJ, Bracker A, Yang C, Storey E, Jarvis BJ, Milton D, et al. Hypersensitivity pneumonitis in a metal-working environment. Am J Ind Med 2001;39(6): 616–28. [3] Girard M, Lacasse Y, Cormier Y. Hypersensitivity pneumonitis. Allergy 2009;64(3):322–34. [4] De Vuyst P, Dalphin JC. Occupational interstitial lung diseases]. Rev Prat 2007; 57(20):2266–76. [5] Vourlekis JS, Schwarz MI, Cherniack RM, Curran-Everett D, Cool CD, Tuder RM, et al. The effect of pulmonary fibrosis on survival in patients with hypersensitivity pneumonitis. Am J Med 2004;116(10):662–8.