https://doi.org/10.53453/ms.2026.5.10
Septic shock and multiple organ dysfunction syndrome following
ammonia-induced caustic injury: case report and literature review
Ieva Naravaitė
1
, Donatas Cibulskis
2
1
Faculty of Medicine, Academy of Medicine, Lithuanian University of Health Sciences, Kaunas, Lithuania
2
Clinic of Nephrology, Department of Clinical Toxicology and Therapeutic Apheresis, Hospital of Lithuanian
University of Health Sciences Kaunas Clinics, Kaunas, Lithuania
Abstract
Introduction. Ammonia solution is an aqueous alkali with a pungent odor and is widely used in different settings.
This clinical case reports a 75-year-old male who ingested 10 milliliters of 10% ammonia solution. The patient
suffered from chemical pneumonitis by inhalation exposure and aspiration which led to secondary bacterial
infection, progressing to sepsis, septic shock and multiple organ dysfunction syndrome (MODS).
Case presentation. A 75-year-old male was admitted to Hospital of Lithuanian University of Health Sciences
Kaunas Clinics following accidental ingestion of 10 ml of 10% ammonia solution. He initially complained of
odynophagia, dysphagia, hypersalivation and dyspnea. Esophagogastroduodenoscopy revealed caustic esophageal
injury, while imaging findings were consistent with chemical pneumonitis. Initial laboratory evaluation
demonstrated impaired renal function with a need for hemodialysis later on. The patient’s clinical condition
deteriorated, with the development of acute hypoxemic respiratory failure, worsening acute kidney injury and
systemic inflammatory response. He was transferred to the intensive care unit, where endotracheal intubation,
mechanical ventilation and vasopressor support were started. The clinical course ultimately led to septic shock
and multiple organ dysfunction syndrome, resulting in a fatal outcome.
Conclusions. Ammonia ingestion in elderly patients with significant comorbidities carries a high risk of deep
alkali-induced gastrointestinal injury, aspiration-related pneumonia and rapid progression to sepsis and
multiorgan failure. Early airway assessment, urgent evaluation and close monitoring are essential to improve
prognosis in this high-risk population.
Keywords: ammonia poisoning, aspiration pneumonia, sepsis, septic shock, multiple organ dysfunction
syndrome.
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Medical Sciences 2026 Vol. 14 (3), p. 80-87, https://doi.org/10.53453/ms.2026.5.10
80
1. Introduction
Ammonia is a colorless, volatile gas soluble in
water, forming ammonium hydroxide. Ammonium
hydroxide is used in various environments, from
industrial settings handling anhydrous ammonia to
household use of ammonia-containing cleaning or
medical solutions. Routes of exposure include
inhalation, which may cause respiratory tract
irritation, inflammation, edema, burns, severe pain
and potentially respiratory distress or failure.
Ingestion may lead to nausea, vomiting, chest or
epigastric pain, caustic burns, ulceration, perforation
or mediastinitis, while direct skin or eye contact
causes mucosal irritation and injury [1]. As a strong
alkali, ammonium hydroxide causes liquefactive
necrosis with deep tissue penetration; the severity of
injury is determined by concentration, ingested
volume and contact time [2]. Complications vary by
severity: mild cases may resolve within 2–3 weeks,
whereas moderate cases may progress to
hemorrhagic gastrointestinal ulceration, shock,
esophageal perforation with mediastinitis, airway
edema with stridor dyspnea, fever, secondary
bacterial or fungal infection and sepsis [2]. Adult
cohorts demonstrate high morbidity and non-trivial
mortality after caustic ingestion, emphasizing the
need for guideline-directed triage, early evaluation
and selective endoscopy [3].
2. Case presentation
A 75-year-old male with a history of multiple
strokes and myocardial infarction presented to the
Emergency Department in Hospital of Lithuanian
University of Health Sciences Kaunas Clinics after
accidental ingestion of approximately 10 milliliters
of 10% ammonia solution. Baseline post-stroke
hemiplegia limited reliable communication which
was magnified by the swallowing of the ammonia.
He reported throat pain, dysphagia, drooling and
dyspnea.
Nasopharyngolaryngoscopy showed oral mucosal
burns with inflammation of the soft palate and
pharynx, laryngeal and epiglottic oedema with
copious secretions. Esophagogastroduodenoscopy
demonstrated caustic esophageal injury (Zargar
grade IIB), erosive gastropathy and hyperemic
duodenitis. Early labs showed increased creatinine
(148 μmol/L) and low GFR (39.3 mL/min/1.73 m
2
)
that may have resulted not only from acute kidney
injury secondary to toxic exposure, but also from a
possible exacerbation or progression of a previously
unrecognized chronic kidney disease, potentially
aggravated by comorbid cardiovascular conditions
(previous myocardial infarctions or strokes leading
to systemic hypoperfusion) or age-related renal
structural changes. Patient was conscious, stable but
needing additional oxygen therapy. Initial chest X-
ray showed reactive changes in lungs and chest
computed tomography (CT) showed ground-glass
opacities and parabronchial thickening which
suggested infiltration or chemical pneumonitis.
Later, the patient’s condition worsened by acute
respiratory distress with rising oxygen demand,
growing inflammatory markers, rising creatinine
levels and uremic markers. The increase in
leukocyte count and CRP while on broad-spectrum
antibiotics raised concern for chemical pneumonitis
(rather than primary bacterial pneumonia), likely
triggered by inhalation and subsequent aspiration of
the ammonia solution.
Moreover, hypernatremia emerged (serum sodium
149 mmol/L, later progressing to 160 mmol/L)
alongside declining kidney function and acute
hypoxemic respiratory failure (oxygen saturation
remaining 85% on 10 L/min supplemental oxygen
with tachypnea). At the same time, blood pressure
fell to 74/51 mmHg (MAP 59 mmHg) and mental
status worsened. With an escalating
immunocompetent cells number, this multitude of
symptoms supported a diagnosis of sepsis despite
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81
ongoing broad-spectrum antibiotic treatment. He
was transferred to the ICU, where he was intubated
for airway protection and oxygenation, sedated and
a central venous catheter was inserted to permit
vasoactive infusions and hemodynamic monitoring.
The patient was febrile, and despite fluid
resuscitation required a vasopressor (noradrenaline)
for persistent hypotension, consistent with septic
shock in the context of aspiration-associated sepsis.
For the acute respiratory failure, the patient was
placed on synchronized intermittent mandatory
ventilation (SIMV) to support respiratory function.
The positive-end expiratory pressure (PEEP)
increased from 5 to 10 cmH
2
O, indicating worsening
pulmonary compliance and progression of
pneumonia. Concomitant with the deteriorating
respiratory status, the patient became anuric with
progressively rising creatinine and uremic markers
(317 to 399 to 539 μmol/L and 26.7 to 31 to 35.5
mmol/L accordingly). Although diuresis was
initially achieved with furosemide, the patient then
required hemodialysis. The development of
complete renal failure and increasing demand for
vasopressors, combined with a history of ammonia
poisoning, chemical pneumonitis and pneumonia –
accompanied by persistently elevated inflammatory
markers despite broad-spectrum antibiotic treatment
– was consistent with multiple organ dysfunction
syndrome (MODS). Arterial blood gas analysis
demonstrated a mixed metabolic and respiratory
acidosis (pH 7.21, pCO
2
46.5 mmHg, pO
2
83.6
mmHg, HCO
-
3
17.2 mmol/L with base excess of -
9.2 mmol/L).
Despite maximal supportive therapy, including
sedation, mechanical ventilation and high-dose
vasopressor support, the patient’s condition was
critically severe and continued to deteriorate. He
developed sinus tachycardia of 145 beats per minute
(BPM) and hypotension (BP 80/35 mmHg). Despite
continuous administration of two high-dose
vasopressors and fluids, the patient‘s heart rhythm
progressed from sinus bradycardia to asystole, with
unsuccessful adult guideline cardiopulmonary
resuscitation.
3. Discussion
Accidental ingestion of concentrated ammonia
solution leads to liquefactive necrosis, where
enzymes from microbes and lysosomes dissolve
cellular components and surrounding tissue,
resulting in rapid tissue softening and breakdown
[4]. Necrosis of the affected organ wall and overall
tissue typically last for about three to four days.
Damage consists of inflammation, thrombosis and
ulcer formation. Stricture risk depends on injury
depth and collagen deposition [5].
Following ingestion, the extent of injury may
progress rapidly through the mucosa into
submucosal and muscular layers, independent of
symptom severity, emphasizing that clinical
presentation does not reliably predict injury grade.
Liquid alkalis like ammonia hydroxide primarily
damage the esophagus due to adherence to its
mucosa, rarely reaching the stomach. Aspiration
may also cause laryngeal and tracheobronchial
injury, as observed in this case [5].
Early endoscopic evaluation within 12 to 24 hours
remains the gold standard for staging and
management. Endoscopy after 48 hours is
discouraged because of increased perforation risk
due to tissue friability, so it is advised to do an
endoscopy right away after initial patient evaluation
with the Zargar classification being the most widely
accepted tool for stratification of mucosal damage
[2, 6–8]. Computed tomography (CT) can
complement endoscopy by identifying transmural or
extraluminal injury or perforation and helping to
guide surgical decision-making [9].
A similar association between ammonia exposure
and kidney injury was reported in a young,
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82
previously healthy adult who developed reversible
acute tubular necrosis (ATN) requiring short-term
dialysis after accidental ammonia poisoning. In that
case, renal recovery occurred once the direct toxic
and ischemic event resolved. In contrast, our
patient’s kidney injury developed in the context of
concentrated ammonia ingestion, severe caustic
injury, aspiration and evolving systemic
inflammation – the kidney injury was likely
multifactorial, driven by hemodynamic instability,
systemic inflammatory response and probable
exacerbation of a previous kidney disease.
Additionally, advanced age and pre-existing
neurologic impairment significantly reduced renal
reserve, making the kidney injury more severe.
Thus, while both cases demonstrate the nephrotoxic
potential of ammonia, the pattern in our patient
reflects a broader MODS-related kidney injury,
rather than the isolated, fully reversible ATN seen in
the younger individual [10].
Prospective research in France containing data of
3544 adult cases with ingestion of substances
causing caustic trauma showed that in up to 24% of
all observed corrosive ingestion cases, patients
suffered from pulmonary complications. Overall, in-
hospital mortality rate was 8%. Importantly, older
age, comorbidities and proper care administration
were the most important factors in general patient
mortality and morbidity [11]. Ultimately, another
literature review of ingestion of caustic agents
described complications across a broad spectrum.
The most common complication of GI tract were
strictures, hemorrhage and perforation, while
systemic complications included disseminated
intravascular coagulation (DIC), multi-organ system
failure and sepsis [12].
Another study included a total of 176 patients who
had ingested various caustic agents, including
alkalis, acids and other corrosive substances. Among
them, 61 were elderly (over 60 years). The elderly
group demonstrated considerably poorer clinical
outcomes across multiple parameters. Respiratory
involvement occurred in 19 of 61 elderly patients
(31.1%), compared with 20 of 115 non-elderly
patients (17.4%), making it a leading cause of
morbidity in older individuals. Respiratory failure
requiring mechanical ventilation was particularly
frequent among the elderly, affecting 17 patients
(27.9%), nearly twice the rate seen in younger
adults. Although the overall occurrence of
gastrointestinal complications was similar between
the two age groups, older patients experienced a
higher proportion of peritonitis or mediastinitis,
which developed in 8 elderly patients (13.1%)
versus 6 younger patients (5.2%). Antibiotic therapy
was required more often among the elderly (39
patients, 63.9%). In addition, mortality was higher,
with 14 deaths (23.0%) among the elderly versus 13
(11.3%) in the younger group. Overall, these results
highlight that elderly patients are significantly more
vulnerable to severe respiratory and systemic
complications, prolonged hospitalization, and
higher mortality following ingestion of any type of
caustic agent [13].
Chemical pneumonitis secondary to ammonia
exposure can result from aspiration or inhalation of
vapors during ingestion or emesis. Even though
aspiration can occur in otherwise healthy
individuals, certain comorbidities significantly
increase the risk. Post-stroke patients with
hemiplegia, as in the presented case, are particularly
vulnerable due to impaired bulbar function, weak or
absent cough and gag reflexes, and reduced
consciousness or coordination of swallowing
muscles. Aspiration in this particular population
often goes unnoticed. Additional risk factors include
advanced age and immobility; all of which were
presented in the case [14, 15]. Ammonia, as
mentioned before, is a strong tissue irritant soluble
in water and mainly damages the upper airways and
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can extend to the bronchi and alveoli, causing
irritation of respiratory tract, chemical burns,
bronchospasm, pneumonitis, edema and acute
respiratory distress syndrome (ARDS).
Management is mainly supportive and it contains
additional oxygen therapy, airway protection and
ventilation with small tidal volumes if ARDS occurs
[1, 16].
In animal (mice) model of ammonia poisoning by
inhalation, researchers demonstrated acute
respiratory and lung damage. Various inflammatory
mediators (such as IL-1β and IL-6) and neutrophils
rose in both bronchoalveolar fluid and blood. On day
7, the overall mice condition worsened, showing
macrophage infiltration, pulmonary hemorrhaging
and endothelial dysfunction with coagulation
deviation, while no respiratory collagen increase
was observed [17].
In humans, the pathophysiology involves alkaline
agents producing protein hydrolysis and
saponification of damaged mucosa through
interaction with tissue lipids and proteins minutes
after ingestion. This chemical reaction causes
liquefactive necrosis, allowing the alkali to penetrate
progressively through tissue layers and greatly
increasing the risk of full-thickness tissue wall
injury. Esophageal damage is mainly localized in the
middle and lower thirds of the organ, as well as the
stomach. The process generates heat and
hemorrhagic swelling regarding thrombosis of small
vessels, which provokes bacterial colonization to the
injured tissue site. Later on, inflammatory response
is initiated, further promoting bacterial infiltration.
Studies have shown that connective tissue formation
of damaged organ is seen only after a few weeks, to
which leads to a stricture [18]. The greater surface
tension of alkaline substances prolongs their
interaction with the esophageal lining, while the
stomach’s acidic environment partially neutralizes
their effect. This difference accounts for the
esophagus sustaining more extensive injury than the
stomach. For these first two to three weeks, the
injured organs’ walls are the weakest, so while
ulcerations penetrate beyond the muscular layer of
the organ, the structural integrity of the wall is
compromised, making tissues completely delicate
and susceptible to perforation [19].
Management of ammonia poisoning is restricted due
to extended inner tissue damage. A few keys to
maintain patient‘s stable condition is managing the
airway, especially when upper airway is severely
damaged on nasopharyngoscopy. If the injured
expresses stridor, voice changes, respiratory distress
and the saturation is dropping, intubation needs to be
performed before airway swelling or collapse. In this
case, videolaryngoscopy should be considered to
minimize further mucosal injury. Once the airway is
secured, persistent hypoxia and a rising alveolar–
arterial oxygen gradient should prompt early
bronchoscopy to assess lower airway injury. Fluid
resuscitation is essential, as oropharyngeal and
gastrointestinal burns from caustic ingestion can
lead to hypotension due to fluid shifts from the
intravascular to the interstitial compartment.
Intravenous access must be established, and an
initial bolus of isotonic crystalloid solution should
be administered. Hemodynamic status should be
monitored using standard indicators. Patients who
are conscious and can safely swallow, small
amounts of water may be given after ingestion to
mildly dilute the corrosive substance but, since
tissue injury occurs almost immediately, later
dilution offers no benefit. Chemical neutralization
using weak acids or alkalis should never be
attempted, as it can trigger exothermic reactions that
exacerbate tissue damage. Use of corticosteroids is
clinically inconsistent [20].
In otherwise severe clinical cases, sepsis or multiple
organ dysfunction syndrome (MODS) may develop
as a consequence of extensive mucosal necrosis,
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84
translocation of bacteria or superinfection of
pulmonary injury. According to Sepsis-3 definitions
and World Health Organization (WHO), sepsis is
defined as a life-threatening organ dysfunction
caused by a dysregulated host immune response to
infection [21, 22]. As per Sepsis-3 and Surviving
Sepsis Campaign (SSC) 2021, Sequential Organ
Failure Assessment (SOFA) clinically optimizes
organ dysfunction, and sepsis is suspected when a
suspected or confirmed infection leads to new organ
dysfunction (SOFA ≥ 2) [23].
Current SSC 2021 guidelines emphasize the
importance of time and within 1 hour, specialists
should measure lactate, do early blood cultures,
prompt broad-spectrum antibiotic therapy,
administrate crystalloids, and point early
vasopressor use (preferably norepinephrine) to
maintain MAP ≥65 mmHg [24].
In contrast to the clinical case, a case report of a 19-
year-old woman who ingested hydrochloric acid
(Harpic) and developed a reversible episode of
chemical pneumonitis with short-term ventilatory
support. The difference of both cases lies both in the
type of caustic agent and the patient’s
vulnerabilities. Hydrochloric acid typically causes
superficial coagulative necrosis, and despite
presenting with Zargar IIIA injury and transient
respiratory failure, the young patient recovered fully
without long-term consequences. In our case,
ingestion of concentrated ammonia, a potent alkali,
resulted in liquefactive necrosis, deeper tissue
penetration, and a higher risk of transmural injury,
perforation and secondary infection. Moreover, the
elderly age, post-stroke bulbar dysfunction, and
impaired protective airway reflexes significantly
increased the likelihood and severity of aspiration,
leading to rapid respiratory deterioration and
systemic complications. This comparison highlights
how agent chemistry and host factors – especially
advanced age and neurologic impairment –
profoundly influence the progression, severity and
outcomes in caustic ingestion [25].
4. Conclusions
Ammonia ingestion in elderly patients with
significant comorbidities and reduced physiological
reserve carries a high risk of rapid clinical
deterioration. Due to the alkali nature of ammonia
and its ability to cause liquefactive necrosis, these
patients are particularly vulnerable to deep
gastrointestinal injury, aspiration-related chemical
pneumonia and progression to sepsis, septic shock
and multiple organ dysfunction syndrome. Age-
related factors, such as impaired airway reflexes,
post-stroke bulbar dysfunction and diminished
organ resilience further amplify the severity of
complications. Therefore, such patients
require urgent evaluation, early airway assessment,
and close inpatient or ICU monitoring. Awareness
of the pathophysiology and potential outcomes of
caustic alkali exposures is crucial for timely
intervention and improving the prognosis of this
high-risk population.
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