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What caused an elevated diaphragm in this woman with cough and dyspnea?
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What caused an elevated diaphragm in this woman with cough
and dyspnea?
September 01, 2007
By Daniel B. Horton [1], Malcolm M. DeCamp [2], Benjamin J. Marano Jr, MD [3], Eamon Kato, MD [4],
Phillip M. Boiselle, MD [5], and David H. Roberts, MD [6]
A 52-year-old woman presented to her primary care physician complaining of a nonproductive
cough and dyspnea on exertion. These symptoms had a subacute onset over 4 weeks before her
initial visit. She denied fever, sputum production, hemoptysis, chest pain, palpitations, abdominal
pain, nausea, vomiting, and diarrhea. She did not have any known sick contacts.
A 52-year-old woman presented to her primary care physician complaining of a nonproductive cough
and dyspnea on exertion. These symptoms had a subacute onset over 4 weeks before her initial
visit. She denied fever, sputum production, hemoptysis, chest pain, palpitations, abdominal pain,
nausea, vomiting, and diarrhea. She did not have any known sick contacts.
Her past medical history was significant for obesity, hypertension, and recurrent bronchitis. Her
surgical history was notable only for bilateral knee arthroscopies. Colonoscopy performed several
months earlier was limited because of a redundant colon.
Her medications included lisinopril, 10 mg daily; a daily multivitamin; and a calcium supple- ment.
She reported allergies to codeine and penicillin, both of which caused hives. Her family history was
notable for breast cancer, lung cancer, and type 2 diabetes mellitus. She was a lifetime nonsmoker
and reported rare alcohol consumption. She worked as a teacher and denied any occupational
exposures. She was single and lived alone.
Physical examination revealed an afebrile, obese woman with normal heart rate, blood pressure, and
respiratory rate. She was in no acute distress. Examination of the chest was notable for decreased
breath sounds at the left lung base. She was referred for outpatient posteroanterior and lateral chest
radiographs, which are shown below (Figure 1).
Making the diagnosis
The patient's posteroanterior and lateral chest radiographs showed apparent marked elevation of
the left hemidiaphragm with associated shift of the mediastinal structures to the right. Prominent
bowel loops are identified in the area of apparent diaphragm elevation. The lungs were remarkable
for a focal wedge-shaped opacity in the left perihilar region. There were no pleural effusions. Cardiac
size was difficult to assess because of marked displacement and partial obscuration by the apparent
diaphragmatic elevation.
The most striking radiographic finding was the apparent elevation of the left hemidiaphragm. In
general, unilateral diaphragmatic elevation may occur secondary to conditions of the lung,
intra-abdominal processes, disorders of or trauma to the nerves that control the diaphragm, or
directly as a result of a diaphragmatic abnormality. For example, the diaphragm may be pulled
upward by a primary pulmonary process causing loss of volume or decreased compliance, such as a
lobectomy or pulmonary fibrosis. However, the diaphragm may be displaced superiorly by abdominal
organ enlargement (such as splenomegaly or a distended stomach) or by intra-abdominal infectious
or inflammatory processes (such as subphrenic or splenic abscess).
Paralysis of the diaphragm may result from a variety of conditions, most commonly, invasion of the
phrenic nerve by lung cancer. Other causes of diaphragmatic paralysis include phrenic nerve injury,
neuritis, CNS or spinal abnormalities, neural compression, and various neurological conditions. Focal
eventration of the diaphragm, a muscular defect that causes weakness, also may cause unilateral
elevation. Other conditions may mimic the appearance of an elevated hemidiaphragm, including a
subpulmonic effusion or a diaphragmatic hernia.
Our patient had no definitive clinical or radiographic findings to elicit a clue to the cause of apparent
diaphragmatic elevation, and a fluoroscopic study was initially recommended to assess for possible
diaphragmatic paralysis. However, careful review of her radiological history revealed that previous
CT colonography had demonstrated a left-sided diaphragmatic hernia, with displacement of
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What caused an elevated diaphragm in this woman with cough and dyspnea?
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omentum and 2 loops of colon into the thoracic cavity. Thus, the apparent elevation of the left
hemidiaphragm on the radiograph was the result of a diaphragmatic hernia rather than a true
diaphragmatic elevation.
The second major radiographic finding was the left perihilar opacity, which could have been caused
by focal lung compression by the hernia and/or an infectious process, such as a postobstructive
pneumonia. The patient was given a presumptive clinical diagnosis of community-acquired
pneumonia and was treated with azithromycin. However, her symptoms did not improve and, on
returning to her doctor, she was given levofloxacin, prednisone, and an albuterol inhaler for resistant
pneumonia and concomitant exacerbation of presumed reactive airway disease.
Nonetheless, her dyspnea and cough continued to worsen, accompanied by new production of green
sputum and intermittent fevers. She still denied hemoptysis, chest pain, palpitations, nausea,
vomiting, abdominal pain, melena, and bright red blood from the rectum.
Because of the patient's worsening clinical course, she was referred for additional imaging with CT. A
chest CT scan demonstrated the herniated abdominal contents in the left side of the chest, with
adjacent atelectasis and necrotizing pneumonia in the left lung (Figure 2). Additional CT findings
included a left upper lobe abscess and a loculated left-sided pleural effusion, which represented an
empyema. She was admitted to the hospital for further workup and management.
On admission, the patient's vital signs showed a temperature of 38.4°C (101.1°F), pulse of 118 beats
per minute, blood pressure of 154/93 mm Hg, respiration rate of 15 breaths per minute, and an
oxygen saturation of 95% on room air. Physical examination demonstrated diminished breath sounds
in the left lower lung field along with new left-sided scattered crackles and tachycardia, but findings
were otherwise normal and unchanged from the patient's previous examination.
Laboratory testing was notable for a red blood cell count of 3640/µL; hematocrit of 29.7%; mean
corpuscular volume of 82 fL; and white blood cell (WBC) count of 12,500/µL, with 74% neutrophils,
4% bands, and 18% lymphocytes. Chemistries were remarkable for normal levels of blood urea
nitrogen (9 mg/dL) and creatinine (0.6 mg/dL).
Blood was drawn for cultures, and the patient was given vancomycin, levofloxacin, and clindamycin
for broad coverage. She underwent CT-guided abscess drainage, which produced approximately 70
mL of purulent material that grew Streptococcus milleri in culture. Her antibiotic regimen was
simplified to ceftriaxone, 2 g intravenously every 24 hours. She responded favorably to the drainage
procedure and antibiotics, with declining fever and WBC count. All blood cultures were negative.
Her anemia was attributed to chronic inflammation. After her hematocrit level dropped to 23%, she
was given a transfusion of 2 units of packed red blood cells. After transfusion, her hematocrit level
remained stable.
A postprocedural CT scan of the chest demonstrated minimal abscess fluid, a virtually unchanged
empyema, and the herniated abdominal contents. The hernia consisted of 2 loops of large bowel,
including the splenic flexure and part of the descending colon, and omental fat, as well as the upper
pole of the left kidney, a new finding suggesting either an enlarging hernia or shifting hernial
contents. The CT scan also showed a posterior defect in the diaphragm of less than 10 cm, and a
diaphragmatic hernia of the Bochdalek type was diagnosed. Urgent herniorrhaphy was deferred
given the acute, purulent pleural infection and the possible need for a prosthetic repair.
Discussion
The Bochdalek hernia is most commonly encountered as a congeni- tal anomaly of the posterolateral
diaphragm in children. As Wells1 described in 1954, congenital Bochdalek hernias usually result from
the failure of the pleuroperitoneal canals to close during the first trimester of gestation, before the
twisting fetal intestines return from the yolk sac to the abdominal cavity.
Because this embryological defect in the pleuroperitoneal membrane allows for persistent
communication between the pleural and peritoneal cavities, these congenital hernias typically
present without a hernial sac. However, a small fraction of congenital Bochdalek hernias occur later
in gestation because of poor muscular development around the foramen of Bochdalek; these hernias
do possess a sac. Bochdalek hernias may occur on either or (rarely) both sides of the diaphragm, but
they have a left-sided predominance, which is attributed to the greater size of the left
pleuroperitoneal canal early in development,1 as well as a presumed protective effect of the liver on
the right, preventing herniation.2
There are other types of congenital diaphragmatic hernias.1 The rarer congenital Morgagni hernia
results from defects in the developing diaphragm anteromedially behind the sternum. Esophageal
hiatus hernias, most frequently seen in association with gastroesophageal reflux in adults, may occur
as a congenital anomaly of the diaphragm.
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What caused an elevated diaphragm in this woman with cough and dyspnea?
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Regardless of type, larger congenital diaphragmatic defects may permit the herniated abdominal
contents to compress nascent fetal lungs and compromise their development. Such hernias are
typically detected by prenatal ultrasonography and tend to present acutely with life-threatening
respiratory distress in the first days of life. Treatment of neonates with these hernias requires clinical
stabilization to manage and prevent pulmonary complications, especially pulmonary hypertension,
followed by surgical correction of the hernia.3
In contrast to the congenital diaphragmatic hernias that present in infants, adults are more likely to
present with hernias of the diaphragm that are acquired secondarily. Most commonly, such hernias
result from traumatic injury (blunt or penetrating) to the patient's chest or abdomen or from a
postoperative complication of thoracoabdominal surgery, such as that for esophageal cancer.4 Other
proposed causes of Bochdalek hernias acquired later in life include various activities or conditions
that increase intra-abdominal pressure, such as pregnancy, labor, and delivery; exercise; sexual
intercourse; sneezing; coughing; and consuming a large meal.5
Nevertheless, small Bochdalek (or Morgagni) hernias of congenital origin may evade early detection
and persist asymptomatically for months to years until incidental diagnosis or symptomatic
presentation,2,6-8 as in our case. A large review of adults who were undergoing abdominal CT
scanning identified incidental Bochdalek hernias in 0.17% of patients.9 Most of the hernias
discovered in this adult population contained only abdominal fat or omentum, but about one quarter
of these asymptomatic hernias involved solid or enteric organs, including the large intestine,
stomach, liver, spleen, pancreas,and kidney.
Unlike neonates who present with respiratory distress, adults who have Bochdalek hernias are more
likely to present with GI symptoms, such as abdominal pain, vomiting, and constipation, or with
nonspecific chest pain.2,7 Such complaints may be chronic and recurrent in some persons, but
numerous case reports exist of adults with undetected diaphragmatic hernias who presented acutely
with life-threatening GI complications, such as obstruction, strangulation, and rupture.10-12
Adults may also present with respiratory complaints, such as chronic dyspnea and cough,2,7 acute
cough with fever,13 or acute cardiopulmonary compromise.5,14,15 Recurrent respiratory infections are
another clinical presentation of late-presenting diaphragmatic hernias, although this has been
reported mostly among children presenting after infancy.7
Our patient had a history of recurring upper respiratory tract infections and was given a diagnosis of
a complicated pneumonia. It is merely speculative that the patient's hernia may have contributed to
her recurring respiratory infections. However, one might reasonably hypothesize that
hernia-associated airway obstruction and atelectasis, suggested by her initial chest radiograph and
confirmed by later imaging studies, could have caused reduced airway clearance and perhaps
resulted in a postobstructive pneumonia. The presentation of an extensive ipsilateral pneumonia
with abscess and multiloculated empyema, without resolution after standard regimens of adequate
antibiotics, in an otherwise healthy middle-aged woman, clinically supports the presence of an
anatomic abnormality.
Physical examination of patients with Bochdalek hernias may demonstrate diminished breath sounds
at the lung base and, depending on the anatomy of the hernia, bowel sounds in the thorax. Most
commonly, small Bochdalek hernias present radiographically as a focal bulge in the posterior left
hemidiaphragm contour and are thus readily distinguishable from true diaphragmatic elevation, in
which the entire diaphragm contour is elevated. However, in cases (such as in this patient) in which
the hernia is large, the radiographic appearance may mimic an elevated diaphragm.
Definitive diagnosis is established by cross-sectional imaging with CT or MRI, which can clearly
identify the diaphragmatic defect and involved abdominal structures as well as associated
complications, such as volvulus, bowel strangulation, or pulmonary infection. Multiplanar images in
the coronal and sagittal planes help characterize the precise location and extent of the herniation.
Small, incidental diaphragmatic hernias in adults may be managed expectantly and monitored with
symptom assessment and serial cross-sectional imaging. However, surgery is the definitive
treatment for symptomatic, and especially complicated, diaphragmatic hernias in adults. In general,
corrective surgery entails reduction of abdominal structures followed by repair of the defective
diaphragm, either through an open abdominal or thoracic incision or by using minimally invasive
techniques, such as laparoscopy16 or thoracoscopy.17
Outcome in this case
The patient was discharged afebrile without leukocytosis on a regimen of intravenous ceftriaxone,
which was switched to oral levofloxacin and clindamycin (500 mg and 450 mg daily, respectively)
because of the development of a pruritic rash while she was taking ceftriaxone. Her skin symptoms
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What caused an elevated diaphragm in this woman with cough and dyspnea?
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quickly resolved, and antibiotic treatment continued for a total of 19 weeks with resolution of the
empyema and without diarrhea or other complications. The patient subsequently underwent surgical
correction of her diaphragmatic hernia using a polytetrafluoroethylene prosthesis through a left
thoracotomy. Surgical exploration demonstrated a large hernial sac containing stomach, transverse
colon, and omentum herniating through a left-sided posterolateral diaphragmatic defect, consistent
with a congenital Bochdalek hernia. Her postoperative course was unremarkable, notable only for a
transient, small ipsilateral pneumothorax.
References:
REFERENCES
1. Wells LJ. Development of the human diaphragm and pleural sacs. Contrib Embryol.
1954;35:109-134.2. Kirkland JA. Congenital posterolateral diaphragmatic hernia in the adult. Br J
Surg. 1959; 47:16-22.3. Frenckner B, Ehren H, Granholm T, et al. Improved results in patients who
have congenital diaphragmatic hernia using preoperative stabilization, extracorporeal membrane
oxygenation, and delayed surgery. J Pediatr Surg. 1997;32: 1185-1189.4. Eren S, Kantarci M, Okur A.
Imaging of diaphragmatic rupture after trauma. Clin Radiol. 2006;61:467-477.5. Salacin S, Alper B,
Cekin N, Gulmen MK. Bochdalek hernia in adulthood: a review and an autopsy case report. J Forensic
Sci. 1994;39: 1112-1116.6. Sugg WL, Roper CL, Carlsson E. Incarcerated Bochdalek hernias in the
adult. Ann Surg. 1964;160:847-851.7. Osebold WR, Soper RT. Congenital posterolateral
diaphragmatic hernia past infancy. Am J Surg. 1976;131:748-754.8. Mei-Zahav M, Solomon M,
Trachsel D, Langer JC. Bochdalek diaphragmatic hernia: not only a neonatal disease. Arch Dis Child.
2003;88:532-535.9. Mullins ME, Stein J, Saini SS, Mueller PR. Prevalence of incidental Bochdalek's
hernia in a large adult population. AJR. 2001;177:363-366.10. Hines GL, Romero C. Congenital
diaphragmatic hernia in the adult. Int Surg. 1983;68: 349-351.11. Sinha M, Gibbons P, Kennedy SC,
Matthews HR. Colopleural fistula due to strangulated Bochdalek hernia in an adult. Thorax.
1989;44:762-763.12. Karanikas ID, Dendrinos SS, Liakakos TD, Koufopoulos IP. Complications of
congenital posterolateral diaphragmatic hernia in the adult. Report of two cases and literature
review. J Cardiovasc Surg (Torino). 1994;35:555-558. 13. Perhoniemi V, Helminen J, Luosto R.
Posterolateral diaphragmatic hernia in adults--acute symptoms, diagnosis and treatment. Case
report. Scand J Thorac Cardiovasc Surg. 1992;26:225-227.14. Kanazawa A, Yoshioka Y, Inoi O, et al.
Acute respiratory failure caused by an incarcerated right-sided adult Bochdalek hernia: report of a
case. Surg Today. 2002;32:812-815.15. Dalton AM, Hodgson RS, Crossley C. Bochdalek hernia
masquerading as a tension pneumothorax. Emerg Med J. 2004;21:393-394.16. Frantzides CT,
Carlson MA, Pappas C, Gatsoulis N. Laparoscopic repair of a congenital diaphragmatic hernia in an
adult. J Laparoendosc Adv Surg Tech A. 2000;10:287-290.17. Yamaguchi M, Kuwano H, Hashizume
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Links:
[1] http://www.physicianspractice.com/authors/daniel-b-horton
[2] http://www.physicianspractice.com/authors/malcolm-m-decamp
[3] http://www.physicianspractice.com/authors/benjamin-j-marano-jr-md
[4] http://www.physicianspractice.com/authors/eamon-kato-md
[5] http://www.physicianspractice.com/authors/phillip-m-boiselle-md
[6] http://www.physicianspractice.com/authors/david-h-roberts-md
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