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Near-Drowning: Epidemiology, Pathophysiology and Imaging Findings

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Journal of Trauma and Care
Review Article *Corresponding author
Bhagya Sannananja, Department of Radiology,

Near-Drowning: Epidemiology, University of Washington, 1959, NE Pacific St, Seattle, WA

98195, USA, Tel: 830-499-1446; Email:

Pathophysiology and Imaging

Submitted: 23 May 2017
Accepted: 19 June 2017
Published: 22 June 2017

Findings Copyright
© 2017 Sannananja et al.

Carlos S. Restrepo1, Carolina Ortiz2, Achint K. Singh1, and ISSN: 2573-1246

Bhagya Sannananja3* OPEN ACCESS

1
Department of Radiology, University of Texas Health Science Center at San Antonio,
USA Keywords
2
Department of Internal Medicine, University of Texas Health Science Center at San • Near-drowning
Antonio, USA • Immersion
3
Department of Radiology, University of Washington, USA\ • Imaging findings
• Lung/radiography
• Magnetic resonance imaging
Abstract • Tomography
Although occasionally preventable, drowning is a major cause of accidental death • X-Ray computed
worldwide, with the highest rates among children. A new definition by WHO classifies • Nonfatal drowning
drowning as the process of experiencing respiratory impairment from submersion/
immersion in liquid, which can lead to fatal or nonfatal drowning. Hypoxemia seems
to be the most severe pathophysiologic consequence of nonfatal drowning. Victims
may sustain severe organ damage, mainly to the brain. It is difficult to predict an
accurate neurological prognosis from the initial clinical presentation, laboratory and
radiological examinations. Imaging plays an important role in the diagnosis and
management of near-drowning victims. Chest radiograph is commonly obtained as the
first imaging modality, which usually shows perihilar bilateral pulmonary opacities; yet
20% to 30% of near-drowning patients may have normal initial chest radiographs.
Brain hypoxia manifest on CT by diffuse loss of gray-white matter differentiation, and
on MRI diffusion weighted sequence with high signal in the injured regions. This review
presents the epidemiology and pathophysiology of nonfatal drowning and a detail
description of the most common multisystem imaging findings.

INTRODUCTION
Worldwide, some half a million people die each year from
drowning, and for each death, there are one to four drowning
incidents serious enough to warrant hospitalization [1]. Organs
such as the brain, lungs and kidneys are mainly affected by
drowning accidents. However, the greatest permanent harm
in drowning accidents is to the brain, which has negligible
metabolic substrate reserves to subsist upon in the absence of
continuous delivery of oxygenated blood. Much of the literature
on near-drowning has concentrated on the respiratory effects
of aspiration and on the management of both early and late
respiratory complications such as aspiration pneumonia and
adult respiratory distress syndrome. Thoracic imaging findings
have been reported [2-4], but there is limited description of extra
thoracic imaging manifestations seen in affected individuals. The
aim of this article is to review the imaging findings and role of
the different imaging techniques in the evaluation of the victim
of nonfatal drowning.
EPIDEMIOLOGY
Drowning is a leading cause of unintentional injury death,
accounting for 0.7% of deaths worldwide [1]. CDC analyses from
National Vital Statistics System and National Electronic Injury
Surveillance System for 2005-2009, indicated that each year an
average of 3,880 persons were victims of fatal drowning and 34%
of all fatalities were persons under 20 years old and almost four
times more common in males. During the same period, there were
on average 5,789 persons treated annually in U.S. emergency
departments (ED) for nonfatal drowning cases, which included
those classified as having a precipitated or immediate cause of
“drowning/near-drowning,” and a diagnosis of “submersion”.
Children under 4 years old accounted for 52.8% of the ED visits,
and children aged 5–14 years accounted for 17.5%. Among
children aged ≤4 years, 50.1% of fatal incidents and 64.6% of
nonfatal incidents occurred in swimming pools. Drowning in
natural water settings increases with increasing age group [5].
Given the variety and inconsistency of definitions, particularly
with terms like dry drowning and near-drowning, the WHO
established in 2002 a new definition of drowning as, “the process
of experiencing respiratory impairment from submersion/
immersion in liquid”[6]. The drowning process begins with
respiratory impairment as the person’s airway goes below the

Cite this article: Restrepo CS, Ortiz C, Singh AK, Sannananja B (2017) Near-Drowning: Epidemiology, Pathophysiology and Imaging Findings. J Trauma Care
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surface of the liquid (submersion) or water splashes over the face involvement throughout the lung bilateral fields [4,20]. The most
(immersion). If the person is rescued at any time, the process of common radiographic finding is that of diffuse, hazy ground-glass
drowning is interrupted, which is termed a nonfatal drowning. If and alveolar opacities throughout the bilateral lungs. These tend
the person dies at any time because of drowning, this is termed to coalesce in the perihilar and medial lung zones with sparing
a fatal drowning. Any submersion or immersion incident without of the most lateral portions of the lung including the bases and
evidence of respiratory impairment should be considered a water the apices (Figure 1a). The distribution tends to be bilateral,
rescue and not a drowning [7]. but may also be asymmetrical with more extensive involvement
of the right or left lung (Figure 1b). This imaging presentation
PATHOPHYSIOLOGY is macro and microscopically indistinguishable from that of
The process of drowning begins with the airway under water, pulmonary edema, with alveolar hemorrhage, interstitial edema
leading to breath-holding; soon the person can no longer keep and dilation of alveolar spaces found on histopathological
his or her airway clear, water entering the mouth is voluntarily examination [21,22]. Air bronchogram is appreciated in those
spat out or swallowed. When the inspiratory drive is too high to areas with denser air-space disease. In the more severe cases,
resist, some amount of water is aspirated into the airways, and consolidation may extend to the entire parenchyma of both lungs,
coughing occurs as a reflex response. Sometimes laryngospasm with little or no areas of sparing. Parenchymal opacities tend to
occurs, but in such cases, it is rapidly terminated by the onset of worsen in the initial 24 to 48 hours before starting to resolve
brain hypoxia. (Figure 1c and 1d). In most cases there is complete clearing of
the lungs between 3-5 days. Persistent infiltrates after the first
As hypoxia, hypercapnia and acidosis ensue, the victim losses
week may represent superimposed bacterial pneumonia or adult
consciousness. This leads to larger fluid aspiration into the
respiratory distress syndrome [23].Diffuse areas of ground-
lungs, worsening respiratory and metabolic acidosis. The initial
glass attenuation characterize high resolution CT, which may
cardiovascular response to the process of drowning is tachycardia
be associated with interlobular septal thickening configuring a
and hypertension, though the worsening hypoxia and acidosis
crazy-paving appearance (Figure 2). Nodular and patchy areas of
leads to bradycardia, pulmonary hypertension and decreased
denser air-space consolidation can also be appreciated, randomly
cardiac output. Atrial fibrillation and other cardiac arrhythmias
distributed but predominantly in a central distribution [24]. In
may occur, progressing finally to a systole [8-11]. The process
a multidetector CT study of 28 drowned subjects, Levy et al.,
from submersion of the victim to cardiac arrest usually occurs in
reported ground-glass opacities with septal lines (89%), with
seconds to few minutes, although in very unusual cases reported
in ice water, this process can last up to one hour [12,13].
Hypoxia appears to be the single most important abnormality
in death resultant from submersion in water, while acidosis and
hypercarbia may contribute secondarily [11,13,14]. Hypoxemia is
initially due to apnea but once fluid aspiration occurs, acute lung
injury develops secondary to the effects of surfactant dysfunction
and washout, increased capillary permeability, alveolar collapse,
atelectasis, ventilation-perfusion mismatch and intrapulmonary
shunting [7,11,15-17].
A) B)
The greatest permanent harm in submersion accidents
is to the brain. The brain is sensitive to the timing, duration,
and intensity of hypoxia. Irreversible injury develops in the
hippocampus, basal ganglia, and cerebral cortex within 4–10 min.
Resuscitation at this stage may manifest in memory, movement,
and coordination disorders. Only a few additional minutes of
hypoxia may result in persistent coma or death [17-19] (Table 1).

IMAGING FINDINGS
Chest
Initial imaging evaluation of near-drowning victims is
typically performed with conventional chest radiograph. The
chest radiograph remains a rapid, simple and cost-effective
method of initial evaluation of these patients. From the
earliest reports on this subject the similarity between imaging
manifestations of near drowning and pulmonary edema have
been recognized. The classic papers by Rosenbaum et al and later
by Hunter et al., identify three basic imaging patterns: a) normal
radiograph with no obvious abnormality, b) perihilar pulmonary
edema, and c) generalized pulmonary edema with more diffuse
C) D)
Figure 1 Chest radiographs of three different patients with non-fatal
drowning. Figure 1a: 25-year-old female with non-fatal drowning
episode (swamp water). Bilateral airspace disease and consolidation
is noted, denser in the central and parahilar regions. Figure 1b:
4-year-old female with non-fatal drowning (swimming pool). AP view
of the chest demonstrates diffuse bilateral parenchymal opacities in
the bilateral lungs, more confluent in the right side. Figure 1c and
Figure 1d: 26-year-old male with non-fatal drowning. Initial chest
radiograph shows ground-glass opacities in the bilateral lungs.
Follow-up radiograph 24 hours later shows progressive bilateral
airspace consolidation.

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Drowning

Aspiration

Hypoxia, hypercapnia, acidosis

Acute lung injury Arrhythmia and cardiac failure Acute tubular necrosis

Multi-organ failure

Chest Abdomen Brain Paranasal sinus Spine

Pulmonary edema
Consolidation
Fluid in
tracheobronchial tree
sand bronchogram
Fluid and/or sand Cortical edema Air-fluid level Fractures
in bowel
Watershed infarcts
Periportal edema
Reversal sign
Periportal edema
White cerebellum

pneumothorax

pneumomediastinum

Takotsubo

Table 1 Pathophysiology and imaging findings of near drowning.

a predominant apical and parahilar distribution and severe
dense consolidation in one third of cases [25]. Pneumothorax,
pneumomediastinum and pneumopericardium are additional
findings seen in some patients (Figure 3). Kim et al., detected
interstitial pulmonary emphysema and pneumomediastinum
on thin-section CT in 2 of 6 patients, while Wunderlich et al.,
observed bilateral pneumothoraces in 1 of10 near-drowned
children [2,24,26]. Small bilateral pleural effusions have been
reported in 10% of drowned subjects, but are less common in
near-drowning patients [25].
Fluid from different types of aspirated content is commonly
seen within the trachea and main bronchi in drowned individuals
[27,28] (Figure 4).On post-mortem CT study in drowned
subjects, central airway fluid was highly prevalent (93%) which
in as much as 50% contained high attenuation sediment. This
high attenuation sediment may also affect second order bronchi
[25].Sand aspiration during drowning and near drowning may
occur; which can be identified on chest radiograph and chest
CT as radiodense material within the affected bronchi (“sand
bronchogram”) [3,26].
Between 20% and 30% of near-drowning patients may have
normal initial chest radiographs [2,27]. This generally represents
less severe cases, with good prognosis, but this is not always the
case, since abnormal parenchymal opacities may develop later.
Patients with obvious pulmonary symptoms with normal initial
radiographs have been documented.

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Brain
There are complex mechanisms involved in causing the
brain damage from drowning with hypoxia and ischemia being
A) B)
the primary contributory factors. Hypoxic-ischemic insult cause
different injury patterns in infants, older children and adults.
Imaging appearance also depends on the severity of the insult.
Severe asphyxia in infants causes involvement of basal
ganglia, thalami, brainstem and perirolandic cortex. Relative
sparing of thalami and perirolandic cortex is seen in children
between 1 and 2 years of age with severe asphyxia [36].
Figure 2 45-year-old female with ground-glass opacities and
interlobular septal thickening after non-fatal drowning. CT of the
chest, lung window image reveals “crazy paving” pattern in the
bilateral lungs.

Associations between “Takotsubo” or stress cardiomyopathy

and near-drowning syndrome have been suggested. A stressful
situation like a near-drowning episode may result in significant
sympathetic nerve activation and massive catecholamine release
that may induce left ventricular wall dysfunction and chest pain,
mimicking an acute myocardial infarction. Echocardiogram A) B)
in such patients reveals left ventricular enlargement and
abnormal wall motion, with an apical ballooning pattern as Figure 3 49-year-old female with bilateral pneumothoraces after
non-fatal drowning episode. Figure 3a: frontal chest radiograph
well as electrocardiogram changes typical for Takotsubo
shows dense consolidation throughout the bilateral lungs, in addition
cardiomyopathy [29-31]. Experimental animal models have to bilateral pneumothoraces. Figure 3b: CT of the chest at the level of
demonstrated massive release of catecholamine in drowning, the aortic arch show extensive pulmonary consolidation and bilateral
associated with severe myocardial necrosis [32]. pneumothoraces (arrows).

Paranasal sinuses and mastoid air cells

Fluid in the paranasal sinuses and bilateral mastoid cells is
reported in all fatal drowning subjects. In some of them high
attenuation material has been noted layering in the dependent
portion of the maxillary and sphenoid sinuses on CT, consistent
with inhaled high-density sediment [3,25] (Figure 5). In our
experience, this is also a common finding on CT of the head in
non-fatal drowning victims, with air-fluid levels detected within
the different paranasal cavities, particularly in the sphenoid and A) B)
maxillary sinuses.
Figure 4 12-year-old girl with tracheobronchial fluid after a non-
Abdomen fatal drowning episode. Figure 4a: CT image of the upper chest shows
an air-fluid level in the trachea (arrow) and patchy parenchymal
Probably the most common abdominal finding in drowning
opacities. Figure 4b: Mediastinal window, axial image at a lower level
and near-drowning victims is increased amount of gastric fluid shows right lower lobe atelectasis with endobronchial fluid (arrow).
with high attenuation content and distended stomach (89%
of cases) [25] (Figure 6a).Occasionally, high density within the
gastric lumen, reflecting aspirated sand or sediment can also
be appreciated on plain films [3]. In patients with extensive
pneumomediastinum and pneumothorax, free air may be seen
extending into the peritoneal cavity [26].
Abdominal visceral involvement in near drowning victims is
rare, but cases of acute kidney injury with acute tubular necrosis
and multisystem organ failure have been documented [33]. In a
series of 30adult patients with near-drowning episodes, Spicer
et al reported 50% developing acute kidney injury [34,35]. Fluid A) B)
overload during resuscitation, as well as acute heart failure and
acute kidney injury may be responsible mechanisms for the
Figure 5 23-year-old female with non-fatal drowning episode. CT
presence of periportal edema identified on the abdominal CT in shows air-fluid levels (arrows) within the sphenoid (Figure 5a) and
some patients (Figure 6b and 6c). bilateral maxillary sinuses (Figure 5b).

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Severe insult in older children and adults causes involvement Additional indicators of poor outcome (death or persistent
of basal ganglia, thalami, sensorimotor cortex, visual cortex, vegetative state) were high signal in the basal ganglia on T2-
cerebellum and hippocampi [37,38]. weighted images and abnormal signal intensity in the cortex
on T2-weighted images (69% sensitivity, 100% specificity) and
Mild to moderate insults cause involvement of the watershed
brainstem infarcts (25% sensitivity, 100% specificity).The best
zones (regions between the anterior cerebral and middle cerebral
correlation with patient outcome seems to be in days 3 to 4, when
arterial territory and between middle cerebral and posterior
an abnormal MR imaging exam has a positive predictive value of
cerebral arterial territory). Both cortex and white matter are
100% for persistent vegetative state or death [47].
involved [39].
CT shows diffuse loss of gray-white differentiation, effacement Cervical spine
of the cerebral sulci and decreased density of basal ganglia and Drowning and near-drowning victims may present associated
other structures (Figure 7). Up to 80% of initial CTs are normal traumatic injuries to the skull, facial bones, cervical spine, ribs,
[40] (Figure 8). Occasionally basal ganglia hemorrhagic infarction pelvis and extremities. In a series of 143 children involved in
may occur, but usually several days after the acute event. A submersion episodes, Hwang et al reported 4.9% prevalence of
“reversal sign” can be seen within 24 hours, which appears, as traumatic injuries, all in the cervical spine. This type of injury
increased attenuation of white matter in comparison to the gray
matter. The possible explanation of this sign is partial venous
outflow obstruction from increased intracranial pressure [41].
The “white cerebellum sign” is another imaging feature
described with severe hypoxic injury, which is seen as increased
attenuation of brainstem and cerebellum relative to the cerebral
hemispheres. Redistribution of blood to the posterior circulation
is a possible explanation for this appearance [42]. A)
In survivors, global parenchymal loss with ventriculomegaly B)
and widened subarachnoid spaces is noted, usually after the
second week [43]. CT has a strong predictive value for patient
outcome and residual neurologic injury. Patients with an abnormal
initial CT usually have worst prognosis, with higher mortality,
permanent neurological damage or persistent vegetative state.
Outcome is similarly poor for patients with a normal first CT who
developed abnormalities on a later CT examination. In a study
of 156 children with submersion injury, Rafaat et al., reported
C) D)
100% mortality amongst patients with an abnormal initial CT,
and 54% in those who developed abnormalities after a normal
initial CT, with 42% presenting persistent vegetative state [40]. Figure 6 Contrast enhanced CT of two different patients with near
drowning. Figure 6a: 6-year-old boy with gastric fluid, found
On MRI, diffusion weighted sequence shows the earliest in the bottom of a swimming pool by his sister who performed
findings with high signal in the injured regions and low signal cardiopulmonary resuscitation. CT of the abdomen shows fluid in
on the ADC map in the same locations suggestive of diffusion the gastric lumen and mild periportal edema. Figure 6b and 6c:
restriction. High signal on the diffusion-weighted images peak at 30-year-old male with periportal edema after a non-fatal drowning
episode. Contrast enhanced CT shows low-density fluid tracking the
3-5 days and then starts to become normal by the end of the first
intrahepatic portal veins (arrows). Low-density fluid is also noted in
week which is known as “pseudonormalization”. T2-weighted the stomach as well as bibasilar pulmonary opacities.
and FLAIR sequences become positive after 24-48 hours and
demonstrate increased signal. Cortical laminar necrosis is seen
in the chronic stage with increased signal intensity on the T1-
weighted images [44]. Imaging appearance of hypoxic-ischemic
encephalopathy is different in preterm and term neonates;
however drowning is a rare cause of hypoxic ischemic injury in
this age group (Figure 9) [45].
MR spectroscopy (MRS) is another imaging modality for
the detection of hypoxic-ischemic injury. MRS is more sensitive
for injury than other MR imaging sequences in the first 24
hours [45]. Most common MRS findings include a decrease of
N-Acetyl-Aspartate/Creatine ratio in 75.8% and presence of
A) B)
lactate in 65.5% [46]. In a series of 22 children with hypoxic
encephalopathy after a near-drowning episode, generalized / Figure 7 26-year-old female with non-fatal drowning episode. Non-
occipital edema had the strongest correlation with poor outcome. contrast CT of the head shows diffuse loss of gray-white differentiation
and cortical sulci consistent with cerebral edema.

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is particularly prevalent in near-drowning victims when the

predominant mechanism of injury was diving. When considered
across all ages the prevalence of cervical spine injury in drowning
and near-drowning victims is low (less than 0.5%), but the
incidence is significantly higher in adolescents (5%). This type of
injury more commonly affects the lower cervical spine between
C4 and C7 [48,49].In non-fatal drowning victims, a complete
work-up for the cervical spine injury should be obtained if there
is concern for a diving accident (Figure 10). Lavelle et al reported
a history or findings of abuse or neglect in 63% of pediatric
bathtub near-drowning victims, including bruising, fractures and
retinal hemorrhage [50]. A) B)
SUMMARY/CONCLUSION
Imaging plays a paramount role in the initial evaluation
as well as monitoring treatment response of near-drowning
victims. A chest radiograph is commonly obtained as the first
imaging modality, and typically reveals perihilar bilateral
pulmonary opacities that tend to resolve in the first week. Brain
hypoxia which more commonly affects the basal ganglia, thalami,
brainstem, perirolandic and sensorimotor cortex manifest on
CT by diffuse loss of gray-white matter differentiation, and
by high signal intensity in the injured region on T2 weighted D)
sequences, diffusion weighted MRI, and FLAIR, with some
C)
variation depending on patient’s age. In those cases, in which
the mechanism of injury includes diving, careful examination of
Figure 9 11-month-old male with anoxic brain injury after drowning.
the cervical spine should be part of the imaging protocol. Near Figure a: Axial FLAIR MR image shows hyperintensity in the bilateral
drowning can present with varied imaging findings involving basal ganglia, thalami and occipital lobes suggestive of anoxic brain
injury in a child who suffered a non-fatal drowning episode. Figures
b and c: Axial diffusion-weighted sequence and ADC map image
demonstrate diffusion restriction in the bilateral posterior parietal
regions suggestive of anoxic brain injury.

A) B)

D)
Figure 10 23-year-old male with diving accident and non-fatal
drowning episode. CT of the cervical spine shows oblique displaced
fracture through the C6 vertebral body with retropulsion of the
posterior fracture fragment into the spinal canal.

C) D) multiple organ systems, familiarity with imaging appearances is

Figure 8 30-year-old male with non-fatal drowning episode. Figures
a and b. Initial CT of the head at admission shows minimal loss of
gray-white matter differentiation. Figure c and d. Follow-up CT
obtained four days later shows progressive loss of differential density
between the gray and white matter both at the centrum semiovale and
gangliobasal regions.
important to ensure prompt diagnosis and management.
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Cite this article

Restrepo CS, Ortiz C, Singh AK, Sannananja B (2017) Near-Drowning: Epidemiology, Pathophysiology and Imaging Findings. J Trauma Care 3(3): 1026.

J Trauma Care 3(3): 1026 (2017)

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