Shinshu Med J, 67⑵：113～119, 2019

Cardiac Arrest Due to Tension Pneumoperitoneum Caused by
Esophagogastric Perforation and Pyloric Stenosis : A Case Report
Hiroshi Miyama1）＊, Mayumi Okada1）, Hiroshi Takayama1）
Hiroshi Imamura1） and Futoshi Muranaka2）
1） Department of Emergency and Critical Care Medicine, Shinshu University School of Medicine
2） Department of Surgery, Shinshu University School of Medicine

Tension pneumothorax is one of the causes of sudden cardiac arrest with evidence of obstructive shock andsubcutaneous emphysema. Emergency chest decompression is a treatment of choice in such a situation. Herein,
we report a case of an out-of-hospital cardiac arrest due to tension pneumoperitoneum caused by esophagogastric perforation. A 40-year-old man with a history of duodenal ulcer and pyloric stenosis complained of suddenonset abdominal pain and developed cardiac arrest during transportation to our hospital. He had jugular venous
distention ; subcutaneous emphysema in the upper body trunk, arms, and neck ; and a markedly distended
abdomen. Immediate needle-chest decompression was not effective, but after volume resuscitation, adrenaline
administration, and abdominal decompression by nasogastric tube, spontaneous circulation was resumed.
Radiological findings revealed tension pneumoperitoneum due to esophagogastric perforation. Emergency
laparotomy was performed, and the perforation of the esophagogastric junction was detected. The patient wasdischarged from the hospital without any disability. Notably, in the treatment of a patient with cardiac arrest
having subcutaneous emphysema, the cause of obstructive shock could exist not only in the chest, but also in
the abdomen. Shinshu Med J 67 : 113―119, 2019
(Received for publication November 12, 2018 ; accepted in revised January 4, 2019)
Key words : cardiac arrest, esophagogastric perforation, tension pneumoperitoneumⅠ Introduction
Tension pneumothorax is one of the causes ofdecompression, successfully improved his circulation.
Ⅱ

Case Reportsudden cardiac arrest with evidence of obstructive

A 40-year-old man in shock was transferred toshock and subcutaneous emphysema. Emergency

the emergency department of our hospital. He had achest decompression is a treatment of choice in suchhistory of duodenal ulcer and Helicobacter pylori

a situation.

infection. Endoscopic examination more than 1 year

Herein, we report a patient with esophagogastricago revealed stenosis of the duodenal bulb from theperforation due to pyloric stenosis and who had

stomach pylorus and stomach distension. He had

obstructive shock, subcutaneous emphysema, andbeen taking proton-pump inhibitors orally for thetension pneumoperitoneum. The patient developed

previous 5 months. On the day of admission, he sud-cardiac arrest during transfer to the emergency de-

denly complained of abdominal pain and collapsed atpartment. Nasogastric tube insertion, but not chest

home. At the time of contact with emergency medical services, he was found to have Japan coma scale＊

Corresponding author : Hiroshi Miyama
Department of Emergency and Critical Care Medicine,
Shinshu University School of Medicine, 3-1-1 Asahi,
Matsumoto, Nagano 390-8621, Japan
E-mail : hiromiya@shinshu-u.ac.jp

No. 2, 2019of 20, heart rate of 120 beats/min, respiratory rate of
60 breaths/min, and 85 ％ oxygen saturation of arterial blood measured by pulse oximeter at room air.
His blood pressure could not be measured, but the113Miyama・Okada・Takayama et al.
Table 1
ALB

5.4

g/dl

CK

164

Laboratory data upon admission
U/l

WBC

6.23 ×103/ul
4

venous blood gas

UN

15.1

mg/dl

AMY

123

U/l

RBC

555 ×10 /ul

pH

7.019

Cre

1.23

mg/dl

Na

156

mEq/l

Hb

17.3

g/dl

pCO2

120 mmHg

AST

44

U/l

K

4.2

mEq/l

HCT

54.9

％

ALT

12

U/l

Cl

104

mEq/l

γGT

27

U/l

Na/Cl

1.5

T-bil

1.01

mg/dl

CRP

0.32

ALP

257

U/l

eGFRcre54 ml/min/1.73m2

LDH

299

U/l

Procalcitonin 0.17

mg/dl

ng/ml

pO2

8.7 mmHg

4

PLT37.7 ×10 /ul

HCO3

29.6 mmol/l

PT

12.6

sec

BE

-7.9 mmol/l

APTT

19.8

sec

SAT

5.6

％

PT-INR

1.03

G-Lac

113

mg/dl

D-dimer

7.5

μg/ml

ALB : albumin, UN : Urea nitrogen, Cre : creatinine, AST : aspartate aminotransferase, ALT : alanine aminotransferase
γGT : gamma glutamyl transpeptitase, T-bil : Total bilirubin, ALP : alkaline phosphatase, LD : lactate dehydrogenase,
CK : creatinine kinase,
AMY : amylase, Na : serum sodium, K serum potassium, Cl : serum chloride, eGFR : estimated glomerular filtration rate,
CRP : c-reactive protein
WBC : white blood cell, RBC : red blood cell, Hb : hemoglobin, Hct : hematocrit, PLT : platelet
PT : Prothrombin time, APTT : activated partial thromboplastin time
BE : Base excess, SAT : saturation, G-Lac : Lactate in blood gas, P/F : pO2/FiO2

radial pulse was palpable. His abdomen was distend-

Immediate blood examination after arrival at theed. During transportation to our hospital, ventilation

hospital showed marked elevation of the partial

was assisted with a bag valve mask. However, thepressure of carbon dioxide and lactic acid (Table 1).

patient developed cardiac arrest.

Chest X-ray images at the time of admission

On arrival at the hospital, electrocardiography

showed subcutaneous emphysema on both sides ofshowed pulseless electrical activity. Physical exam-

the chest. X-ray image of the abdomen showed freeination showed jugular venous distention, subcutane-

air and dilatation of the intestinal tract (Fig. 1). Chest

ous emphysema in the upper body trunk, arms, andcomputed tomography (CT) scan showed subcutane-neck, and markedly distended abdomen. Immediate

ous and mediastinal emphysema (Fig. 2). Abdominal

decompression of the bilateral chest with needle was

CT scan showed wall irregularities, wall thickening

tried considering the possibility of obstructive shockand stenosis of the pylorus, marked dilatation of thedue to tension pneumothorax. However, there wasstomach, and dilatation of the small intestine (Fig. 3).

no rush of air, and the patient did not recover after

Emergency laparotomy was performed for gastro-the procedure. Tracheal intubation, volume resusci-

intestinal perforation. The operation demonstrated

tation, and intravenous administration of adrenaline

perforation of the abdominal esophagus on the small

were simultaneously performed. Spontaneous circu-

curvature side (Fig. 4) and necrosis due to strangula-lation was resumed 10 min after arrival at the emer-tion at two sites in the small intestine. The leakage

gency room. However, his blood pressure was stillof a large amount of stomach contents like coffee

low. Tympanic sound was heard by percussion ofresidue was observed from the perforation site to

the abdomen. When the 14 Fr nasogastric tube was

the peritoneal cavity. Proximal gastrectomy and re-inserted after return of spontaneous circulation, mas-construction with double tract using the jejunum

sive air and approximately 3 l of stomach content

were performed. In addition, the ileum was partiallywere aspirated. Subsequently, the tightness of theexcised in two places and the stump end, and end-

abdominal wall was improved, and his blood pres-to-end anastomosis was performed.

sure increased.
114

Meropenem and noradrenaline were administered,
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Cardiac arrest due to tension pneumoperitoneum

Fig. 1 Chest and abdominal X-ray images on admission (supine position)a : Chest radiograph showing subcutaneous emphysema on both sides (arrows).
b : Abdominal X-ray image before placing the nasogastric tube showing free air under thediaphragm (arrow) and dilation of the intestinal tract.

Fig. 2 Computed tomography (CT) images from neck to chest after emergency transporta : Prominent subcutaneous emphysema in the posterior cervical region (arrows).
b, c : Chest CT images showing subcutaneous emphysema from the bilateral anterior thorax tothe lateral thorax around the trachea (arrows).

Fig. 3 Abdominal computed tomography confirmed wall irregularity (arrow) on the dilated
stomachʼs minor curvature, pyloric thickening (arrowhead), and dilated small intestine.
No. 2, 2019115

Miyama・Okada・Takayama et al.

Fig. 4 Macroscopic finding of the resected specimen. The large perforation of the abdominal
esophagus on the small curvature side was detected (arrow).

and endotoxin adsorption therapy was done for sep-

First, as a predisposition to esophagogastric perfo-

tic shock after the operation. Recombinant thrombo-

ration, there was severe stenosis of the pyloric partmodulin was administered for disseminated intravas-of the stomach due to chronic and recurrent duode-cular coagulation. The trachea was extubated on the

nal ulcer. As a result, chronic increase in luminal

day after surgery. Noradrenaline administration waspressure and dilatation of the stomach had oc-

completed on the second day after surgery. The pa-

curred1）2）. Previous studies reported that a portion oftient could drink water about a week after surgery.

the stomach wall became ischemic due to chronic

He had ileus after starting oral ingestion, but recov-

gastric distension or became perforated due to par-ered with fasting. Pathological examination showed

tial necrosis3）4）. For this reason, the esophagogastric

the black color change which is thought to be necro-junction was possibly easily perforated by a stronger

sis in the full-thickness layer of the stomach wall,

stimulus, as a continuous pressure load was applied

but did not show any malignant lesion and severe

to the stomach wall in our patient. Moreover, gastro-

inflammation around the perforation area. He wasintestinal perforation is triggered by alcohol, over-discharged on the 35th day after surgery, and pro-eating, vomiting, convulsions, and labored breath-

ton-pump inhibitor has been prescribed (Fig. 5). He

ing2）. Esophageal perforation that spreads into thehas had no recurrence and has returned to daily life.

thoracic cavity is called Boerhaave syndrome5）. Oc-

Ⅲ Discussion

casionally, the perforation spreads into both the thoracic and abdominal cavities3）4）6）7）. In a previous re-This is a rare case of an out-of-hospital cardiac

port, preventive gastrojejunostomy was performedarrest due to tension pneumoperitoneum. Several

on duodenal stenosis accompanied by high gastricfactors should be considered in the presented case,dilatation to prevent rupture1）.

such as predisposing factors of esophagogastric per-The second point is the cause of tension pneumo-

foration, the cause of tension pneumoperitoneum, theperitoneum. Generally, free air found in the gastriccause of the cardiac arrest, and the decision-making

or duodenal perforation is often small. However, inin the emergency department.

our patient, as a result of pyloric stenosis, there was

116

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Cardiac arrest due to tension pneumoperitoneum

Fig. 5 Hospital course
CRP, C-reactive protein ; Plt, platelet ; WBC, white blood cella chronic increase in the luminal pressure and dila-increase in intraperitoneal pressure because of thetation of the stomach. It was thought that the pres-assisted ventilation with a bag valve mask. Thus, thesure in the abdominal cavity suddenly increased

pre-hospital-assisted ventilation exacerbated the

because a large amount of stomach contents and air

shock state in this case.

entered into the abdominal cavity at high pressureThis patient had jugular venous dilatation andjust after the esophagogastric perforation. The in-subcutaneous emphysema in the neck, upper arm,crease in intraperitoneal pressure likely caused theand anterior chest just after arrival at the hospital.

decrease in the venous return from the inferior vena

Thus, tension pneumothorax was suspected. Needle7）-9）. In the re-decompression of the chest was tried, but it was notported cases of tension pneumoperitoneum, perfora-

effective. Spontaneous circulation was achieved aftertion of the hollow organ has been the most frequent

volume resuscitation and intravenous administration

cava, resulting in an obstructive shock

10）. Moreover, tensionof adrenaline. Ideally, the most effective treatment

pneumoperitoneum was reported as a complicationfor obstructive shock in this situation might be per-of medical procedures such as endoscopic examina-

cutaneous needle decompression of the abdominal

cause at about 80 ％ to 90 ％

8）
11）
-14）

tion

15）

, laparoscopic mass feeding , and inappro-

priate cardiopulmonary resuscitation7）16）-18）.

cavity12）15）. Puncture from the front side of the abdominal wall is not difficult because internal organs

In some cases, patients with tension pneumoperi-

are pushed to the dorsal side in the abdominal cavi-

toneum develop cardiac arrest. When the cardiacty11）14）. Furthermore, there have been case reports in

output severely decreases due to the decrease inwhich tension pneumoperitoneum was improved byvenous return and increase in afterload by severe

insertion of a nasogastric tube and reduction of in-pneumoperitoneum, cardiac arrest can occur. In the

traperitoneal pressure via a stomach tube similarlypresent case, it appears that a large amount of air

to our case8）. Usually when we treat a patient withentered into the peritoneal cavity and caused further

subcutaneous and mediastinal emphysema with ob-

No. 2, 2019117

Miyama・Okada・Takayama et al.

structive shock, we first suspect tension pneumotho-

confirmation of X-ray images. In this case, theserax. In previous reports, subcutaneous and mediasti-

methods were carried out for safe and accurate in-nal emphysema were detected in lower intestinal

dwelling of the nasogastric tube.

19）
-21）

.

In conclusion, this patient with chronic severe gas-

Therefore, we should consider that the cause of ob-

tric distension due to pyloric stenosis had tension

structive shock exists occasionally not only in thepneumoperitoneum and cardiac arrest after perfora-

chest, but also in the abdomen.

tion of the esophagogastric junction. The patienttract perforation into the retroperitoneal space

Generally, there is a risk of incorrect insertion into

successfully recovered after appropriate volume

the trachea, with esophageal perforation occurring

resuscitation, decompression of intraperitoneal pres-during placement of the nasogastric tube. With thesure by nasogastric tube, and laparotomy. Physicians

perforation of the upper gastrointestinal tract, an in-should note that in case of obstructive shock andcreased risk of expansion of the perforation is sus-

subcutaneous emphysema in the chest, the cause

pected and misdirected insertion into the abdominal

can exist even in the abdomen.

cavity will occur. To confirm accurate indwelling of
the nasogastric tube, several methods have been

Conflict interest : The authors declare no conflict ofperformed, such as considering the inserted lengthinterest.

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