Key Clinical Message
Portal vein gas detected by point-of-care ultrasound in critical care
medicine, in situations of unidentified shock and hypoxemia indicates a
high likelihood of underlying intestinal ischemia.
Abstract
Background:
Portal venous gas is a rare finding in adults and is typically
associated with underlying intestinal ischemia. Portal venous gas can be
detected by a bedside point of care ultrasound examination in adult
patients in critical care units(CCU). Findings include echogenic bubbles
flowing centrifugally throughout the portal venous system.
We present the case of a 73-year-old female with advanced ischemic
cardiomyopathy and cardiorenal syndrome who was managed in the CCU. She
developed vague abdominal pain and respiratory depression requiring
intubation and dialysis during her course of treatment in the CCU. Her
findings were consistent with portal venous gas upon point-of-care
ultrasound, prompting computed tomography of her abdomen and surgical
consultation. She was ultimately found to have nonobstructive mesenteric
ischemia.
Introduction
Nonocclusive mesenteric ischemia (NOMI) is a rare complication in
critically ill patients with multiple comorbidities and dialysis
patients, with potentially fatal consequences if not recognized early
(1). Usually, it presents with nonspecific symptoms in critically ill
patients who might be intubated, leading to a delay in diagnosis (1).
POCUS has an evolving role in establishing a diagnosis of unexplained
shock and deterioration of critically ill patients at the bedside (2).
We present a critically ill patient who initially improved and then
deteriorated acutely and was found to have intestinal ischemia after
detecting portal vein gas by POCUS.
Case report
A 73-year-old female presents with a medical history significant for
hypertension, diabetes mellitus type 2, diabetic nephropathy with
chronic renal impairment, dual pacemaker due to sick sinus syndrome, and
an ST elevation myocardial infarction 10 months earlier managed with
three drug-eluting stents (one in the left main coronary artery, one in
the proximal right coronary artery, and another in the proximal
circumflex artery). She was fed by PEG 6 months ago because of refusal
to eat and the possibility of true bulbar palsy and early signs of
Alzheimer’s disease. Her medications prior to admission were furosemide
80 mg twice daily, carvedilol 6.25 mg twice daily, spironolactone 50 mg
once daily, and clopidogrel 75 mg once daily.
The patient was admitted with hypotension and pulmonary edema and
received ventilator support after tracheal intubation. She was initially
managed with inotropes and renal replacement therapy with improvement,
and on hospital day 3, she was extubated. This event was followed by
acute on chronic renal failure, requiring a restart of renal replacement
therapy.
Echocardiogram showed severe global hypokinesia of the left ventricle
with a low ejection fraction (EF) (< 20%), bilateral lung
ultrasonic B lines, bilateral mild pleural effusions, and low cardiac
output. There was generalized edema.
She improved initially and infusions of noradrenaline and dobutamine
were discontinued.
On day 7 after extubation, the patient underwent hemodialysis 9 hours
before her acute deterioration with an episode of hypotension (blood
pressure, 85/42 mm Hg) during hemofiltration that resolved with
temporary use of a noradrenaline infusion during the procedure. The
patient developed tachypnea (33 breaths/min) and vague abdominal pain.
Physical examination showed a blood pressure of 105/45 mm Hg and a heart
rate of 93 beats/min. Her abdomen was slightly distended but nontender,
with hypoactive bowel sounds throughout. Blood work showed elevations of
alanine aminotransferase (360.1 U/L), aspartate aminotransferase (577.3
U/L), lactate dehydrogenase (381 U/L), white blood cell count (16.00 x
103/L [12.45 x 109/L]), and
C-reactive protein (83.4 mg/L) levels. Anion gap metabolic acidosis with
lactate rising from 1.8 to 8.6 mmol/L (0.5 to 1.5 mmol/L), and pH 7.00
constituting lactic acidosis was also observed.
The above episode necessitated the restart of the noradrenaline and
dobutamine infusions. Due to tachypnea and hypoxemia, she was
reintubated. POCUS to the abdomen showed sluggish movement of the
intestines. Initially, bedside echocardiography was performed and showed
severely impaired systolic function. While assessing the inferior vena
cava, hyperechoic dot artifacts were observed throughout the left upper
lobe of the liver, which were consistent with air extending to the
periphery of the liver and hilum (Videos 1 and 2, Figure 1).
Furthermore, discrete echogenic bubbles flowed centrifugally throughout
the portal vein with disruption of the normal Doppler pulse because of
air in the hepatic portal vein. These findings were consistent with
portal venous gas (PVG), raising the possibility for bowel ischemia. CT
of the abdomen with intravenous and oral contrast showed portal venous
gas (Figure 4) in its tributaries, as well as in the superior mesenteric
vein, which is a feature highly suggestive of bowel ischemia. Foci of
gas were observed in the walls of the stomach, right side of the colon
and some segments of small bowel loops (pneumatosis intestinalis), which
also raises the possibility of ischemic bowel. Marked atherosclerotic
changes in the aorta and its great branches were noted, with an
attenuated hepatic artery, superior mesenteric artery and celiac trunk
with nonvisualized inferior mesenteric artery. Minimal fluid was found
in the pelvis. Despite extensive calcification of the superior
mesenteric artery and its branches, neither occlusive thrombosis nor
significant luminal narrowing was detected.
The surgeon evaluated her and diagnosed nonocclusive diffuse intestinal
ischemia. The family was counselled, and no further interventions were
recommended. She passed away 3 days later.
Discussion
PVG is an ominous radiological sign and reflects an abdominal surgical
emergency. Intestinal ischemia is the typical pathology and cause of
PVG, occurring in up to 72% of cases (3). PVG has been reported in
cases with underlying inflammatory bowel disease when there was mucosal
damage and infection with gas-producing organisms (4). However,
infection with gas-forming organisms, especially Clostridium, and
anaerobic streptococci can lead to gas in the portal vein and intestinal
walls (5). Complicated diverticular disease of the colon and infection
with gas-forming organisms has also been demonstrated in a case study
(6). Other causes of PVG include intestinal perforation, enterovenous
fistula following surgical procedures, and malignant bowel obstruction
complicated by ischemia (5).
Our case report showed both PVG and pneumatosis intestinalis. Both signs
occurred together in 41.7% of the cases. PVG occurred separately in
33.3% of the cases, while PI occurred separately in 25% of the cases
(7). Many studies have claimed that, when accompanied by PVG, PI is
often associated with bowel ischemia (7,8). The combination of
pneumatosis intestinalis, portal venous gas, and acidosis typically
portends bowel ischemia and inevitable necrosis (9). Furthermore, in
cases with bowel ischemia, the presence of PVG and pneumatosis
intestinalis is highly suggestive of transmural bowel ischemia (91%)
and is associated with higher mortality (72%), whereas each sign cannot
independently differentiate between transmural and partial thickness
bowel ischemia. It was associated with lower mortality rates, 44% and
56% for PI and PVG, respectively (10).
Acute mesenteric ischemia and hypoperfusion of the small bowel could be
due to occlusive or nonocclusive obstruction of the arterial blood
supply or obstruction of venous outflow. The superior mesenteric artery
(SMA) is commonly occluded by emboli or thrombosis, while venous
thrombosis commonly affects the superior and inferior mesenteric veins.
NOMI accounts for 5% to 15% of patients with acute mesenteric ischemia
(11). The mechanism behind hypoperfusion of the bowels in NOMI is
related to the maintenance of cerebral and cardiac blood flow at the
expense of the bowels (12). Neurohormonal mediators (vasopressin and
angiotensin), along with other vasoactive and chronotropic drugs, can
trigger spasms and decrease blood flow to the intestines(12).
Classically, NOMI occurs in critically ill patients with severe
cardiovascular disease; has life-threatening complications (sepsis,
myocardial infarction, and congestive heart failure), with chronic renal
impairment/hemodialysis; and patients are often receiving multiple
drugs, including vasopressors and inotropes (13).
Usually, the early symptoms of NOMI are mild and nonspecific, and
abdominal pain is absent in 25% of patients. In addition, the presence
of precipitating factors and comorbidities in the majority of cases,
such as congestive heart failure and renal failure requiring
hemodialysis that are usually complicated with hypotension, intubation
and sedation, can hide the early signs of NOMI [14]. Necrosis and
perforation can occur, and in many cases, the diagnosis can be
confirmed. The patient typically develops hypotension and shock of
underdetermined cause. POCUS plays an important role in detecting the
sources of surgical emergencies and detecting serious surgical
conditions.
With the increasing practice of and need for point-of-care ultrasound in
critical care and emergency medicine, especially in situations of
unidentified shock and hypoxemia, and the limited knowledge about portal
venous gas in the point-of-care setting, intensive care physicians
should be aware of findings of concern related to air in the portal
system as a bedside test indicating a potential need for more advanced
imaging or surgical consultation, given the high likelihood of
underlying intestinal ischemia.
Acknowledgements
We thank Ahmadi Hospital Management, Kuwait Oil Company for their
unlimited support.
CONFLICT OF
INTEREST
The authors declare no conflicts of interest.