Management of Septic Shock Secondary to Submandibular Phlegmon and Ventilator-Associated Pneumonia in the Intensive Care Unit

INTRODUCTION

Sepsis, defined as life-threatening organ dysfunction caused by a dysregulated host response to infection, remains a significant global health challenge, contributing to approximately 20% of all-cause mortality worldwide [1]. With an estimated 31.5 million cases of sepsis annually, including 19.4 million severe cases and 5.3 million deaths, sepsis is a leading cause of mortality in hospitals and intensive care units (ICUs), despite advances in early diagnosis, surgical interventions, and antimicrobial therapy [1]. Septic shock, the most severe form of sepsis, is characterised by persistent hypotension and hyperlactatemia despite adequate fluid resuscitation, necessitating urgent and multifaceted management to improve patient outcomes [2].

Infections triggering sepsis can originate from various sources, including odontogenic, respiratory, intra-abdominal, soft tissue, urinary tract, intracranial, and bacteraemic foci [2]. Submandibular phlegmon, an odontogenic deep neck infection, typically arises from dental pathology, particularly the second or third mandibular molars, and can rapidly progress to diffuse cellulitis or abscess formation in the submandibular, submental, or sublingual spaces, as seen in Ludwig’s angina [3]. This condition is associated with significant complications, including airway obstruction requiring tracheostomy, mediastinitis, and pulmonary complications such as ventilator-associated pneumonia (VAP), empyema, acute respiratory distress syndrome (ARDS), and multiorgan failure [4,5]. Jankowska et al. reported that 59% of neck infections in 24 patients were odontogenic, with all cases yielding positive bacterial cultures, often exacerbated by immunological deficiencies [3]. Effective management of septic shock due to submandibular phlegmon and associated VAP requires rapid source control, intravenous antibiotics, fluid resuscitation, and comprehensive supportive care, including lung-protective mechanical ventilation, analgesia, nutritional support, and thromboprophylaxis, to optimise patient outcomes [2]. This case report examines the diagnosis and management of a patient with septic shock secondary to submandibular phlegmon complicated by VAP in the ICU, highlighting the evidence-based strategies to address these critical conditions.

CASE DESCRIPTION

A 22-year-old male patient, weighing 55 kg and 160 cm tall, presented to the emergency department with progressive submandibular swelling, pain, dysphagia, and dyspnoea. These symptoms were preceded by untreated bilateral lower dental pain. The patient had no comorbidities or allergies. The vital signs were as follows: Glasgow Coma Scale E4M6V5, blood pressure 110/80 mmHg (mean arterial pressure 90 mmHg), heart rate 82 bpm, respiratory rate 22/min, oxygen saturation 97%, and temperature 38.2°C. Physical examination revealed bilateral submandibular oedema extending to the neck region. Laboratory tests indicated leukocytosis (24,220/mm³), normal haemoglobin and platelet levels, mild hyponatraemia, and a lactate level of 2.1 mmol/L. Imaging confirmed the presence of a submandibular abscess and tracheal narrowing. The diagnosis was septic shock secondary to submandibular phlegmon resulting from gangrenous dental pathology (teeth 36-38, 46-48).

Table 1. Patient Case Summary

Section	Details
Patient Profile	22-year-old male, 55 kg, 160 cm. Presented with progressive submandibular swelling, pain, dysphagia, and dyspnea. No known comorbidities/allergies.
Initial Symptoms	Bilateral lower dental pain (untreated), submandibular swelling, dysphagia, dyspnea.
Vital Signs (ED)	GCS: E4M6V5, BP: 110/80 mmHg (MAP 90), HR: 82 bpm, RR: 22/min, SpO₂: 97%, Temp: 38.2°C
Laboratory Findings	WBC: 24,220/mm³ (leukocytosis), Hb/platelets: normal, Na: mild hyponatremia, Lactate: 2.1 mmol/L
Imaging Findings	Submandibular abscess, tracheal narrowing
Diagnosis	Septic shock due to submandibular phlegmon (dental origin: teeth 36–38, 46–48)

Preoperative antibiotics, specifically metronidazole and ceftriaxone, were administered. Surgical intervention included incision and drainage, as well as dental extractions; postoperative instability necessitated norepinephrine administration and transfer to the intensive care unit (ICU). ICU management over 35 days involved mechanical ventilation, sedation, nutritional support, and serial debridements. Complications included ventilator-associated pneumonia (diagnosed on day 18), resistant infections (Acinetobacter, carbapenem-resistant Klebsiella pneumoniae, Pseudomonas), pericarditis (day 2), pleural effusions (requiring thoracostomy on day 9), and multiple reintubations (days 6, 11, 17, 25). Antibiotic therapy was escalated to meropenem and amikacin, followed by levofloxacin and cotrimoxazole. Rehabilitation commenced on day 13, leading to extubation on day 33 and transfer to a semi-ICU setting on day 35. Scoring assessments included an APACHE II score of 11, with the SOFA score peaking at 8 and declining to 5, and a RASS score ranging from -4 to 0. The patient experienced resolution of shock, improved oxygenation (P/F ratio increased from 157 to 282 by day 35), and mobilization. Persistent leukocytosis prompted an immunocompromise workup, which returned negative results. A dermatology consultation was sought for a rash. To enhance readability, original daily data tables have been condensed into key time points (days 1, 10, 20, 30, 35) with trends. For interactivity in digital manuscripts, consider hyperlinked expansions or dashboards; here, summaries focus on means/ranges and graphical trends.

Table 2. Interventions and Clinical Course

Aspect	Details
Pre-op Treatment	IV Metronidazole + Ceftriaxone
Surgical Interventions	Day 0: Incision, drainage, dental extractionDays 6, 20, 31: Necrotomy/debridementDay 20: Skin grafting
ICU Admission	Required due to postoperative instability and septic shock
ICU Duration	35 days; ventilatory support, sedation, nutritional support, physiotherapy
Complications	VAP (Day 18), multidrug-resistant infections (Acinetobacter, CR-Kp, Pseudomonas), pericarditis (Day 2), pleural effusion (Day 9), multiple reintubations
Rehabilitation	Started Day 13; extubated Day 33; moved to semi-ICU Day 35

Table 3. Severity Scores and Outcomes

Score / Parameter	Value / Trend
APACHE II	11
SOFA Score	Peaked at 8, declined to 5 by Day 35 (Mean: 5.4 ± 1.6)
RASS	-4 initially, improved to 0 (Mean: -1.2 ± 1.3)
P/F Ratio	Improved from 157 to 282 by Day 35
Leukocytes	Persistent leukocytosis; peak ~43,920/mm³ (Day 9); immunocompromise ruled out
Final Outcome	Resolution of shock, improved respiratory function, mobilized by Day 35

Table 4. Summary of Vital Signs and Laboratory Parameters at Key Intervals

Parameter	Day 1	Day 10	Day 20	Day 30	Day 35	Trend / Notes
BP (mmHg)	105/75	154/100	131/79	140/70	120/78	Systolic: 132 ± 17; Diastolic: 82 ± 12
MAP (mmHg)	85	118	97	93	92	Mean: 98 ± 13
Heart Rate (bpm)	138	112	86	104	82	Mean: 102 ± 15 (tachycardia early)
Respiratory Rate (/min)	12	33	20	20	20	Mean: 25 ± 6 (peaks mid-course)
Temperature (°C)	38.2	36.9	36.7	36.7	36.5	Mean: 37.1 ± 0.6 (febrile early)
SOFA Score	8	–	4	5	5	Mean: 5.4 ± 1.6 (decreasing trend)
RASS	-4	–	–	–	–	Mean: -1.2 ± 1.3 (improving alertness)
Hemoglobin (g/dL)	9.8	10.3	10.5	11.7	12.4	Range: 7.6 – 12.8 (anemia resolving)
Leukocytes (/mm³)	11,130	35,800	10,680	11,920	19,280	Peak: 43,920 (Day 9); persistent elevation
Platelets (/mm³)	148,000	695,000	381,000	508,000	422,000	Thrombocytosis mid-course
Sodium (mEq/L)	138	133	135	135	–	Range: 131 – 144 (mild hyponatremia episodes)
Lactate (mmol/L)	3.6	1.6	–	–	–	Range: 0.9 – 3.6 (early normalization)

Figure 1. P/F Ratio Over Time: Respiratory function improves.

Table 5. Ventilator Settings and ABG

Parameter	Day 1	Day 10	Day 20	Day 30	Day 35	Trend
Mode	VC-CMV	NRM	PSV	CPAP	NRM	Shift from controlled to spontaneous
FiO₂	0.5	0.44–0.80	0.4	0.4	0.44	0.4 – 0.8 (decreasing)
P/F Ratio	307	168	395	247	282	157 – 445 (improving)
pH	7.374	7.473	7.448	–	–	7.259 – 7.497 (stable)

Table 6. Summary of Therapies and Procedures

Category	Interventions	Details
Antibiotics	Metronidazole/Ceftriaxone → Meropenem/Amikacin → Ampicillin-sulbactam → Levofloxacin/Cotrimoxazole	Culture-based escalation, ~30 days
Surgery	I&D + extractions (Day 0), Debridements (Days 6, 20, 31), Grafting (Day 20)	4 procedures
Ventilation	Multiple intubations/extubations; CPAP/T-piece weaning from Day 13	35 days of support
Supportive	Norepinephrine, electrolyte correction, physiotherapy (from Day 13), nutrition advancement (Day 21)	Ongoing throughout ICU stay

Table 7. Fluid Balance and FASTHUG Summary

Parameter	Early (Days 1–10)	Mid (Days 11–20)	Late (Days 21–35)
Fluid Balance	+100 to –500 cc	+50 to –583 cc	+50 to +558 cc
Feeding	Fasting to liquid diet	Liquid diet	Liquid → Oral diet
Analgesia/Sedation	Fentanyl, Midazolam, Propofol	Fentanyl, Paracetamol	Paracetamol only

Table 8. Complications Overview

Complication	Onset Day	Resolution / Status
Hemodynamic Instability	Day 1	Resolved by Day 5
Pericarditis	Day 2	Treated with colchicine
VAP / Pneumonia	Day 18	Improved by Day 35
Resistant Infections	Days 4–25	Cleared with adjusted antibiotics
Pleural Effusion	Day 9	Drained; partial resolution

The PaO₂/FiO₂ ratio declined sharply to 157 on day 11, indicating severe oxygenation impairment compatible with acute respiratory distress syndrome (ARDS). Following optimization of mechanical ventilation, aggressive respiratory physiotherapy, and infection control, the ratio gradually improved, reaching 395, which signified significant recovery of pulmonary function (Fig. 1).

DISCUSSION

The management of the 22-year-old male patient with septic shock secondary to submandibular phlegmon and ventilator-associated pneumonia (VAP) illustrates the complexity of treating severe odontogenic infections and their nosocomial complications in the ICU setting. Submandibular phlegmon, progressing to Ludwig’s angina, represents a rapidly spreading cellulitis of the sublingual and submandibular spaces, often initiated by odontogenic infections such as gangrenous radiculitis and chronic apical periodontitis, as observed in this case [4,6]. The patient’s presentation with submandibular swelling, dysphagia, and trismus aligns with the clinical hallmarks of Ludwig’s angina, where infection from mandibular molars (teeth 36, 38, 46, 47, and 48) spreads percontinuitatum to adjacent soft tissues, risking airway obstruction [6].

The pathophysiology involves bacterial invasion from necrotic pulp or periodontal pockets, penetrating cortical bone and soft tissues, leading to abscess formation within 5–7 days if untreated [4]. Delayed intervention, as noted in this patient with a one-week history of untreated dental pain, increased the risk of complications such as septic shock and airway compromise, necessitating urgent surgical and medical management [4,5]. The initial chest X-ray revealing tracheal narrowing underscores the critical need for airway protection, achieved through intubation and surgical drainage, consistent with recommendations for early source control to mitigate life-threatening complications like mediastinitis or acute respiratory distress syndrome [4-7].

The development of VAP on day eight, confirmed by a Clinical Pulmonary Infection Score (CPIS) of 7, positive sputum cultures (Klebsiella pneumoniae and Pseudomonas aeruginosa), and bilateral bronchopneumonia with pleural effusion, highlights the challenges of managing healthcare-associated infections (HAIs) in mechanically ventilated patients [8-10]. VAP, a common HAI with a mortality rate of 24–50%, is driven by risk factors such as prolonged ventilation (>48 hours), reintubations, and oropharyngeal colonization, all present in this case [10]. The patient’s CPIS, incorporating leukocytosis (34,970/mm³), reduced P/F ratio (210), and microbiological findings, supported the VAP diagnosis on day 17 following bronchoalveolar lavage [11,12]. Despite adherence to VAP prevention bundles, including chlorhexidine oral hygiene and head elevation (30°–45°), as per Indonesian Ministry of Health guidelines (Permenkes 27/2017), the patient developed VAP, likely exacerbated by multiple reintubations and persistent immunosuppression from sepsis [10,11]. The identification of multidrug-resistant (MDR) pathogens, including carbapenem-resistant K. pneumoniae (CR-Kp) and P. aeruginosa, necessitated antibiotic escalation to meropenem and amikacin, followed by levofloxacin and cotrimoxazole based on sensitivity profiles. However, delays in culture-guided therapy and antibiotic shortages (days 22–25) underscore the challenges of managing MDR infections in resource-limited settings, potentially contributing to prolonged ICU stay and recurrent respiratory distress [13-15].

Septic shock, diagnosed based on persistent hypotension requiring norepinephrine (0.05–0.25 mcg/kg/min) and hyperlactatemia (post-operative lactate 3.6 mmol/L), was managed per Surviving Sepsis Campaign (SSC) 2021 guidelines, emphasizing early fluid resuscitation (30 mL/kg crystalloid), vasopressor support, and source control [15,16]. The patient’s initial lactate of 2.1 mmol/L pre-operatively, rising to 3.6 mmol/L post-operatively, and subsequent decline to 2.4 mmol/L by day two, reflects effective resuscitation and improved tissue perfusion, aligning with SSC recommendations to monitor lactate as a marker of hypoperfusion [16-20]. Surgical interventions, including incision and drainage, necrotomy, and skin grafting, were critical for source control, reducing the infectious burden and preventing further systemic spread [21,22]. However, the initial use of ceftriaxone and metronidazole without prior culture, followed by delayed culture on ICU day two, deviated from SSC guidelines advocating for pre-antibiotic cultures to guide de-escalation [15]. This likely contributed to the prolonged use of broad-spectrum antibiotics (meropenem, amikacin) and challenges in transitioning to targeted therapy, particularly with MDR pathogens like Acinetobacter baumannii and CR-Kp [15].

The FASTHUG mnemonic guided comprehensive ICU care, addressing feeding, analgesia, sedation, thromboprophylaxis, head elevation, ulcer prophylaxis, and glycemic control. Enteral nutrition, initiated on day three and escalated to 2,000 kcal by day 21, aligned with ASPEN/SCCM guidelines for early enteral nutrition (EEN) in patients on low-dose vasopressors (<0.14 mcg/kg/min), supporting recovery despite initial gastric residue issues [23]. The patient’s low nutritional risk (NRS 2002 = 3, NUTRIC = 2) justified standard feeding without specialized intervention, with caloric targets (25–35 kcal/kg/day) met to prevent muscle atrophy [24,25]. Analgesia with paracetamol (1 g/6 h IV) and fentanyl (25 mcg/h) maintained pain scores (BPS 3–4, CPOT 0–1) below significant thresholds, ensuring comfort without respiratory depression [22]. Sedation transitioned from propofol to dexmedetomidine to minimize delirium risk, adhering to 2013 Pain, Agitation, and Delirium guidelines [26-28]. Thromboprophylaxis was withheld due to a low Padua score (1) and bleeding risk post-surgery, consistent with ACCP and ASH guidelines prioritizing mechanical prophylaxis in high-bleeding-risk patients [29,30]. Omeprazole (40 mg/12 h IV) effectively prevented stress ulcers, and glycemic control was maintained without insulin, as glucose levels remained within 110–180 mg/dL, reducing the risk of hyperglycemia-related complications [31-33].

The patient’s prolonged ICU course, marked by recurrent reintubations, MDR infections, and surgical interventions, underscores the multifaceted challenges of managing odontogenic sepsis and VAP. The SOFA score of 8 on day one, predicting a mortality risk <33.3%, improved to 3 by discharge, reflecting effective multidisciplinary management despite complications [3]. However, antibiotic stewardship gaps, including delayed cultures and therapy interruptions, highlight the need for robust microbiological surveillance and resource availability to optimize outcomes in resource-constrained settings [15]. The successful extubation on day 33 and transfer to the semi-intensive unit on day 35 demonstrate the efficacy of combined surgical, antimicrobial, and supportive care in achieving clinical stability, emphasizing the importance of early source control, guideline-directed therapy, and comprehensive ICU protocols like FASTHUG in managing complex septic shock cases [15,22].

CONCLUSION

The management of a 22-year-old male patient with submandibular phlegmon complicated by septic shock and ventilator-associated pneumonia (VAP) highlights the critical need for swift, multidisciplinary intervention to address the rapid progression of odontogenic infections and their complications. Immediate airway management, initiated within one hour of diagnosing sepsis and septic shock, combined with early surgical source control through incision, drainage, and necrotomy, played a vital role in improving patient outcomes and preventing severe complications such as mediastinitis or acute respiratory distress syndrome. The complexity of managing VAP, driven by multidrug-resistant pathogens like Klebsiella pneumoniae, Pseudomonas aeruginosa, and carbapenem-resistant Acinetobacter baumannii, required tailored antibiotic therapy with levofloxacin and cotrimoxazole, lung-protective ventilation, and supportive measures including fluid resuscitation guided by fluid responsiveness, enteral nutrition, and analgesia/sedation using paracetamol, fentanyl, and dexmedetomidine. Progressive mobilization, incorporating physiotherapy and physical activity such as sitting, standing, and breathing exercises for 30–60 minutes daily, facilitated weaning despite multiple reintubations, underscoring its importance in recovery. Despite challenges like delayed culture results (5–7 days) and antibiotic shortages, effective interprofessional collaboration, early diagnosis, and adherence to comprehensive ICU protocols like FASTHUG were instrumental in achieving clinical stability, enabling extubation on day 33 and transfer to the semi-intensive unit by day 35, ultimately reducing morbidity and mortality risks.

DECLARATIONS

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CONSENT FOR PUBLICATION

The Authors agree to be published in the Journal of Society Medicine.

FUNDING

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COMPETING INTERESTS

The authors declare no conflicts of interest in this case report.

AUTHORS’ CONTRIBUTIONS

All authors made substantial contributions to the case report. AFH was responsible for patient management, data collection, and initial drafting of the manuscript. All authors reviewed and approved the final version of the manuscript, ensuring its accuracy and integrity, and are accountable for all aspects of the work.

ACKNOWLEDGMENTS

None