Aggressive Nutrition Therapy in a Rehabilitation Hospital for Severe Tachypnoea and Profound Weight Loss With Interstitial Lung Disease: A Case Report

ABSTRACT

A 67‐year‐old male suffering from polymyositis‐associated interstitial lung disease (ILD) was transferred to a rehabilitation hospital. Upon admission, the patient presented with severe malnutrition (weight of 32.0 kg; BMI of 12.10 kg/m²; skeletal muscle index of 3.8 kg/m²) and rapid shallow breathing with pronounced exercise‐induced tachypnoea. The patient underwent physiotherapy, which included belt electrode skeletal muscle electrical stimulation and progressively titrated aerobic/resistance training. Following the initial stepwise optimisation for transient poor intake, an aggressive nutrition therapy was started. At discharge, the patient gained 4.6 kg in weight, with an increase in skeletal muscle mass from 13.9 to 15.5 kg. The skeletal muscle index had increased to 4.4 kg/m², representing an increase of 0.6 kg/m². Furthermore, the duration of continuous aerobic exercise had increased to 30 min, representing a 27‐min increase. This case may present a pragmatic strategy for the implementation of aggressive nutrition therapy during rehabilitation for tachypnoeic ILD.

For an ILD patient at a rehabilitation hospital presenting with marked low body weight and tachypnoea, aggressive nutrition therapy was combined with electrical stimulation therapy using belt electrode‐skeletal muscle electrical stimulation and aerobic exercise. The results are shown during the period indicated by the red frame, suggesting that alongside increased energy intake, the continuous exercise duration progressively lengthened, while the trends towards increased body weight and skeletal muscle mass persisted. Furthermore, rehabilitation strategies that maximise the effects of physiotherapy and achieve marked improvements by ensuring adequate energy intake should be more readily implemented.

1. Introduction

As modern acute and critical care improves survival, more patients reach rehabilitation settings with profound weakness after severe illness [1]. Interstitial lung disease (ILD) is a progressive condition, it is a common occurrence wherein survivors enter the post‐acute phase with persistent tachypnoea, dyspnoea, and severe deconditioning. The most extensive research has been conducted on the relationship between malnutrition and muscle wasting in chronic obstructive pulmonary disease (COPD). Conversely, the field of ILD has received comparatively less attention with regard to nutrition and body composition, despite the existence of plausible mechanisms for hypermetabolism [2]. This case was transferred to a rehabilitation hospital, presenting with significant weight loss and severe tachypnoea due to a complicated acute phase. Furthermore, following combined nutrition therapy and physiotherapy, marked recovery was observed in weight, skeletal muscle mass, and exercise tolerance.

2. Case Report

A 67‐year‐old Asian man (weight of 65.3 kg, BMI of 24.48 kg/m²) was independent in activities of daily living prior to illness. His medical history included dyslipidaemia, drug‐related renal dysfunction, dysphagia, which required gastrostomy placement. Following the outpatient management of polymyositis and interstitial lung disease (ILD), he was admitted due to acute respiratory deterioration/disease progression of polymyositis‐associated ILD following corticosteroid non‐adherence. Although he did not require admission to the ICU or mechanical ventilation, he underwent methylprednisolone pulse therapy (Day 1). Axial chest computed tomography (CT) on admission at acute‐care hospital shows bilateral, basal and subpleural ground‐glass/reticular opacities with fibrotic change, greater in the left lower lobe (Figure 1A). His course was complicated by severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) infection, bacteraemia, and dysphagia with poor intake requiring nasogastric tube feeding until Day 65. The patient received a systemic corticosteroid dosage of 2935 mg during their admission to the acute‐care hospital. This dosage was administered in two doses of 500 mg, followed by a gradual reduction from 40 mg to 10 mg. He was transferred for rehabilitation on Day 71.

FIGURE 1.

Physical examination and chest CT images. (A) Axial chest CT on admission at acute‐care hospital shows bilateral, basal and subpleural ground‐glass/reticular opacities with fibrotic change, greater in the left lower lobe. (B) The physical examination of the patient upon admission to the rehabilitation hospital revealed severe malnutrition (BMI of 12), indicating extreme underweight. This finding is particularly significant given that the patient had experienced marked weight loss during their stay in the acute‐care hospital. (C) On admission at the rehabilitation hospital, the bilateral basal ground‐glass opacities have decreased, while underlying fibrotic change persists. (D) After a period of 45 days spent at the rehabilitation hospital, no observable changes have been noted.

At admission to the rehabilitation hospital, the patient had an oxygen saturation (SpO₂) 97% on room air and presented with rapid shallow breathing (respiratory rate (RR) 40/min at rest). Nutritional status met severe malnutrition based on Global Leadership Initiative on Malnutrition criteria: weight 32.0 kg, BMI 12.10 kg/m², skeletal muscle mass 13.9 kg, fat mass 3.4 kg, and skeletal muscle mass (SMI) 3.8 kg/m² (Figure 1B). There had been a decrease in the bilateral basal ground‐glass opacities, whilst the underlying fibrotic changes remained persistent on chest CT (Figure 1C). It is noteworthy that the patient had transferred to our facility with a weight reduction of 33.3 kg (50.9%). The estimated energy requirement was 1600 kcal/day by registered dietitian, while the achieved energy intake was approximately 1200 kcal/day (75% of the provided meals). With regard to basic mobility, he was able to ambulate 15 m independently. An exercise tolerance test using a recumbent ergometer at 10 W for 3 min × 3 sets (total 9 min) showed maximal heart rate (HR) of 144 bpm, SpO₂ of 97%, RR of 60/min, and BORG rating of perceived exertion (RPE) scale of 13. Based on clinical reasoning, a strategy combining nutrition and physiotherapy was developed (Figure 2A).

FIGURE 2.

Clinical reasoning and progress. (A) Clinical reasoning identified reduced exercise tolerance as the primary issue, which was considered to be caused by excessive energy expenditure and low skeletal muscle mass. (B–E) The progression of key indicators is shown. During Phase 3, as indicated by the red box, the patient underwent aggressive nutrition therapy. Concurrently, an increased energy intake and improved exercise tolerance were observed, while a tendency towards weight gain was also noted.

Subsequent developments can be divided into three phases, marked by two turning points (Figure 2B–E).

• Phase 1: In a period of approximately the 25 days, the patient's condition remained stable. Nutrition therapy achieved full dietary intake. In physiotherapy, aerobic exercise duration was gradually extended while maintaining RPE scale intensity of ≤ 13. Moreover, belt electrode‐skeletal muscle electrical stimulation (B‐SES) (G‐TES; Homer Ion Corp., Tokyo, Japan) was initiated to induce widespread skeletal muscle contraction, aiming to increase skeletal muscle mass. Furthermore, considering that ILD patients with tachypnoea, and aiming an increase in skeletal muscle mass, the energy requirement was reset to 2170 kcal.

• Phase 2: At Day 30, gastric discomfort resulted in a significant reduction in oral intake after discontinuing mosapride due to polypharmacy concerns. The respiratory rate remained persistently high at 60 breaths per minute even at rest (PaCO₂ 36 Torr). Consequently, nutritional support was initiated via gastrostomy as part of nutrition therapy, while oral intake was switched to an easily digestible food form. Mosapride was restarted. Furthermore, aerobic exercise was discontinued and physiotherapy was suspended during the days when tachypnoea symptoms were severe. Following a 45‐day period at the rehabilitation facility, no discernible alterations have been observed on chest CT (Figure 1D).

• Phase 3: At Day 50, the symptoms of gastric discomfort were resolved, allowing the patient to resume full dietary (1800 kcal/day) intake and to perform aerobic exercise at levels equivalent to phase 1.

In order to extend the duration of aerobic exercise and increase the skeletal muscle mass, aggressive nutrition therapy was started, which entailed the patient's transfer by wheelchair to an external retail outlet. In this setting, the patient regularly procured, at their own expense, calorie‐rich oral nutritional supplements (ONS) corresponding to an additional 400 kcal/day and 8.7 g/day of protein (Calorie Mate BLOCK, Otsuka Pharmaceutical Co. Ltd., Japan) and milk for whey protein intake. The patient was able to exceed their target calorie intake (maximum energy intake 2740 kcal/day). In the absence of routine blood testing, we monitored for clinical signs of refeeding syndrome and metabolic complications; none were observed. In physiotherapy, as the energy intake increased, the duration of aerobic exercise and the intensity of B‐SES were gradually increased. Resistance trainings were also incorporated into the programme. The duration of aerobic exercise was increased to 30 min incrementally, although the RR of 40/min threshold was seldom exceeded. The talk test [3] was found to be satisfactory, and no decrease in SpO₂ level was observed. At 75 days (total hospitalisation of 146 days), his physical functions recovered and he was discharged from the rehabilitation hospital: Weight of 36.6 kg (+4.6 kg), skeletal muscle mass of 15.5 kg (+1.6 kg), SMI of 4.4 kg/m² (+0.6 kg/m²), continuous aerobic exercise time of 30 min (+27 min), 6‐min walk distance of 306 m.

3. Discussion

In the present case, persistent tachypnoea following an acute respiratory deterioration with progression of ILD, restricted exercise tolerance via poor nutritional intake and marked muscle wasting. This suggests that even under the dietary constraints of a rehabilitation hospital, gradual supplemental nutrition and physiotherapy adjustments tailored to respiratory status may still yield potential recovery of muscle mass and exercise tolerance.

It is hypothesised that the patient's clinical course in the acute care hospital can be attributed to the following factors: firstly, inflammation caused by worsening ILD, SARS‐CoV‐2 infection and bacteraemia; secondly, steroid administration; thirdly, prolonged nutritional deficiency; and fourthly, prolonged bed rest associated with this complex clinical course. It is conceivable that these complex factors resulted to excessive weight loss, reduced skeletal muscle mass, and the diminished exercise tolerance. As clinical reasoning was derived from the assessment results at the time of transfer to our rehabilitation hospital, we suggested that hyperventilation caused by ILD leads to energy deficiency, resulting in malnutrition and a reduction in skeletal muscle mass, which in turn exacerbates tachyponea. This reduction in skeletal muscle mass is, known to enhanced ventilatory response by increasing CO2 production through the early mobilisation of anaerobic metabolism, may induces to severe tachypnoea [4]. The key issues requiring improvement to achieve a return to home living was identified as reduced exercise tolerance. Consequently, a series of rehabilitation strategies were devised to address these issues.

The resting energy expenditure of ILD patients is approximately 120% of the predicted basal metabolic rate [2]. The maximum respiratory rate in cardiopulmonary exercise testing for ILD patients averaged 50.4 breaths per minute [5], indicating that the patient's exercise respiratory rate of 60 breaths per minute represents a high level of tachypnoea. Consequently, it was determined that this patient required a minimum of 120% of the aforementioned amount, which equates to a minimum of 1920 kcal. Subsequently, we planned an aggressive nutrition therapy aiming for an estimated daily energy surplus of 250 kcal, which is a pragmatic target of ~1 kg/month of weight gain [6, 7]. In this case, it was defined as a full meal intake plus a minimum of one daily serving of ONS (400 kcal/serving), which by itself achieved the intended additional energy intake. The results of the implementation of aggressive nutrition therapy in Phase 3 in an increased energy intake and extended continuous aerobic exercise time. It may have contributed to increased skeletal muscle mass and improved exercise tolerance through synergistic effects with physiotherapy. However, the presence of significant fluctuations in dietary intake complicates the setting of optimal weight targets, and the merits of exceeding the target calorie intake require further thorough research.

The aetiology of low skeletal muscle mass was hypothesised to be a combination of two factors added to malnutrition: slow‐twitch muscle atrophy due to disuse syndrome [8] and fast‐twitch muscle atrophy resulting from long‐term oral steroid use and pulse therapy, as glucocorticoid‐induced myopathy [9]. The approach to slow‐twitch muscle involved aerobic exercise and low‐load resistance training. However, due to the patient's severe tachypnoea, high‐intensity resistance training could not be performed, making it difficult to target fast‐twitch muscle. Therefore, we focused on electrical stimulation, which differs from voluntary contraction in that it mobilises fast‐twitch muscle fibre early. Among these methods, we adopted electrical stimulation [10]. It involves wrapping belts around one abdominal site and two lower limb sites, applying electrical current from the abdomen to the entire lower limb, thereby achieving widespread skeletal muscle contraction. The patient's clinical condition and B‐SES characteristics were to be well‐matched. However, ILD is a highly heterogeneous group of diseases, and the clinical course, reversibility and prognosis vary significantly depending on the subtype. Although it is considered appropriate to increase energy intake in ILD patients presenting with severe tachypnoea due to their high energy expenditure, this strategy should not be generalised to all ILD patients, particularly those who do not have malnutrition or sarcopenia, or those with ILD subtypes associated with a poor overall prognosis (as treatment goals may differ in these cases).

Since the exercise tolerance in this case tended to depend on energy intake, a combination of physical and aggressive nutrition therapy is essential. This is not a rare case, but rather an example of a growing trend that requires immediate action. However, there are barriers to providing aggressive nutrition therapy. In Japan, ONS cannot be provided as part of insurance‐covered treatments, much like medication, and patients must purchase them themselves. This remains a future challenge, particularly in rehabilitation hospitals that have limited treatment strategies.

Author Contributions

Y.M. contributed to the planning of the case report. Y.M., T.M., K.T., A.S., K.M. and S.K. contributed to the management of the case and the conceptualization. Y.M., T.Y. and T.O. contributed to its analysis and the preparation of the manuscript. All authors read and approved the final manuscript.

Funding

This work was supported by JSPS KAKENHI (Grant number: JP25K14498).

Consent

The authors declare that written informed consent was obtained for the publication of this manuscript and accompanying images and attest that the form used to obtain consent from the patient complies with the Journal requirements as outlined in the author guidelines.

Conflicts of Interest

The authors declare no conflicts of interest.

Morimoto Y., Yanase T., Matsuo T., et al., “Aggressive Nutrition Therapy in a Rehabilitation Hospital for Severe Tachypnoea and Profound Weight Loss With Interstitial Lung Disease: A Case Report,” Respirology Case Reports 14, no. 5 (2026): e70623, 10.1002/rcr2.70623.

Data Availability Statement

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.