First manifestation of acute exacerbation of idiopathic interstitial pneumonia during emergency maxillary drainage: a case report

Abstract

Acute exacerbation of idiopathic interstitial pneumonia (AE-IIP) can be triggered by invasive procedures and carries a mortality rate of approximately 50%. We report a case of a 73-year-old man who presented to a dental emergency room with maxillary swelling and a fever of 39.0℃. Initially, the patient was prescribed analgesics and antibiotics. The following day, because of an elevated C-reactive protein (CRP) level (18.0 mg/dL), emergency incision and drainage were performed. During the procedure, he developed tachypnea, dry cough, and hypoxia (SpO2, 85–90%). The patient was immediately transferred to a medical emergency hospital, where chest computed tomography confirmed the diagnosis of IIP. The patient was admitted to the respiratory care unit and was treated with corticosteroid pulse therapy and antibiotics. The patient was discharged on day 39 with ambulatory oxygen therapy. High CRP levels and acute hypoxia may be critical early indicators of AE-IIP. Dental anesthesiologists must recognize that oral infections can trigger severe and potentially fatal systemic inflammatory responses, including AE-IIP.

INTRODUCTION

Idiopathic interstitial pneumonia (IIP) is a chronic condition; however, its acute exacerbation (AE-IIP) is a severe complication with a high mortality rate of approximately 50% [1,2]. AE-IIP is often associated with invasive surgery, general anesthesia, and respiratory infections. Symptoms typically include tachypnea, palpitations, and dry cough resulting from rapid clinical and radiological deterioration triggered by surgical stress and elevated circulating inflammatory cytokines [3]. Herein, we present a case of AE-IIP in a 73-year-old man who developed acute hypoxia and elevated C-reactive protein (CRP) levels during emergency subgingival debridement and drainage of a maxillary abscess.

CASE REPORT

A 73-year-old man (height, 173 cm; weight, 72 kg) presented to our dental emergency room (ER) with complaints of localized maxillary swelling and a sensation of warmth that had persisted for 3 days. His medical history included bronchial asthma. Upon examination, his temperature was 39.0℃, blood pressure (BP) was 141/90 mmHg, and heart rate (HR) was 120 beats/min. The dental anesthesiologist suspected a systemic infection and prescribed loxoprofen (180 mg) and amoxicillin (750 mg). The patient was referred to his primary care physician for evaluation the following day.

The physician ruled out influenza and COVID-19 but noted a CRP level of 18.0 mg/dl, white blood cell count of 7100/µL, BP was 100/70 and HR was 100 beats/min. Consequently, the patient returned to our hospital for immediate treatment of the maxillary swelling because the physician considered the maxillary infection to be the source of the systemic inflammation. Cone-beam computed tomography (CBCT) and dental radiography revealed a cyst-like lesion at the apex of the left maxillary lateral incisor with perforation of the palatal cortical bone, indicating abscess formation secondary to apical periodontitis (Fig. 1-A and B). Under local anesthesia (3.6 mL of 2% lidocaine), a 10 mm incision was made, followed by subgingival debridement to remove bacterial deposits and drain a small amount of purulent exudate (Fig. 1-C). The patient was diagnosed with left maxillary periostitis secondary to acute suppurative apical periodontitis originating from the left maxillary lateral incisor. Purulent discharge was obtained through the incision. After thorough irrigation of the abscess cavity, a film drain was placed to complete the procedure.

Fig. 1. Patient’s oral findings and radiographic images at the second visit. (A) Dental radiograph demonstrating a radiolucent lesion associated with apical periodontitis. (B) Cone-beam computed tomography (CBCT) image revealing a cyst-like lesion at the apex of the left maxillary lateral incisor with perforation of the palatal cortical bone. (C) Intraoral photograph showing palatal swelling and subgingival bacterial deposits.

During the procedure, the patient developed tachypnea and dry cough. His peripheral capillary oxygen saturation dropped to 85~90% on room air, and repeat blood work showed a CRP of 20.1 mg/dl, and white blood cell count of 9700/µl. Because the severe systemic inflammation and hypoxia could not be explained solely by the dental infection, the patient was transferred to a medical emergency hospital. Chest radiography and CT revealed superimposed ground-glass opacities and consolidation on the left side, raising suspicion of IIP (Fig. 2-A and B).

Fig. 2. Chest radiograph and computed tomography (CT) images. (A) Chest radiograph showing diffuse reticular opacity in the left lung. (B) Chest computed tomography (CT) showing superimposed ground-glass opacities and consolidation of the left lung.

After AE-IIP was confirmed, he was admitted to the respiratory care unit and underwent endotracheal aspiration and bronchoalveolar lavage on hospital day 1. He developed respiratory failure requiring nasal high-flow ventilation but refused invasive mechanical ventilation. The treatment included corticosteroid pulse therapy (methylprednisolone, 1 g/day for 3 days) and intravenous piperacillin/tazobactam (4.5 g every 8 h). Bronchoalveolar lavage (BAL) showed a neutrophildominant inflammation with no bacterial growth (Table 1). After successful treatment, the patient was discharged on day 39 and required oxygen therapy at a flow rate of 1 L/min during ambulation. One month after discharge, the patient recovered sufficiently and visited his primary dentist for routine therapy without supplemental oxygen. He was followed-up every 2 months at a regular hospital.

Table 1. Clinical timeline from initial dental presentation to the development of acute exacerbation of idiopathic interstitial pneumonia (AE-IIP).

	Day 1	Day 2 (9:00)	Day 2 (11:30)	Day 2 (18:00)	Day 4
Healthcare facility	This institution (dental ER)	Private clinic	This institution (dental clinic)	Medical ER	General hospital (RCU)
CRP (mg/dL)	(-)	18.0	20.1	19.75	12.94
Imaging findings	(-)	(-)	CBCT	CXR; Chest CT	Chest CT
Imaging diagnosis	(-)	(-)	Maxillary abscess	IIP	AE-IIP
Management	Amoxicillin	Influenza (-); COVID-19 (-); Refer to dental clinic	Incision and drainage; CTRX 2 g; Refer to medical ER	Refer to medical RCU	BAL; steroid pulse; TAZ/PIPC 4.5 g

AE-IIP, acute exacerbation-IIP; BAL, bronchoalveolar lavage; CBCT, Cone-beam computed tomography; CTRX, Ceftriaxone; CXR, Chest X-ray; ER, emergency room; IIP, idiopathic interstitial pneumonia; TAZ/PIPC, tazobactam/piperacillin.

DISCUSSION

This case demonstrates that a localized maxillary infection and subsequent minor surgical intervention can trigger AE-IIP in susceptible individuals. AE-IIP progresses rapidly and has a 50% mortality rate [1], highlighting the importance of early diagnosis and intervention [2].

Initial medical interviews and examinations were insufficient. Preparation is possible if the IPP is identified in advance. A retrospective review revealed that the patient had been diagnosed with IIP 10 years prior. Although annual CT follow-up showed no progression as recently as four months earlier, his recent persistent cough continued for over a month following the COVID-19 infection. This suggests the presence of an underlying inflammatory lung condition before the emergency room visit [4]. High fever and the palatal abscess were likely acute triggers of AE-IIP. Upon presentation, the patient met the criteria for a quick Sepsis-related Organ Failure Assessment (qSOFA) score of 2 (respiratory rate ≥ 22/min, systolic blood pressure ≤ 100 mmHg) [5]. High-dose glucocorticoid therapy is effective for AE-IIP [6,7]. Usui et al. showed that systemic inflammatory response syndrome and elevated serum procalcitonin levels were independent predictors of mortality in AE-IIP [8].

Although we did not culture the microbiota from the abscess, evidence links oral dysbiosis to lung diseases such as asthma and pulmonary fibrosis [9]. Pathogens, such as Porphyromonas gingivalis, can induce excessive inflammatory mediators, aggravating tissue destruction [10]. Even at low concentrations, oral pathogens can cause chronic inflammation in distant sites.

The incidence of acute exacerbation of interstitial lung disease after non-pulmonary surgery was 6.3%, with a mortality rate of 80% [11]. High preoperative CRP level is a key risk factor. Therefore, the risk of acute exacerbation of interstitial lung disease (ILD) must be considered in patients with underlying ILD and elevated CRP levels prior to dental procedures.

In conclusion, dental anesthesiologists should be vigilant regarding the systemic impact of oral infections. Continuous monitoring of respiratory status (including peripheral capillary oxygen saturation) and inflammatory biomarkers is vital in patients with a history of IIP. The early detection of impaired respiratory function can accelerate interventions and prevent fatal outcomes.