J Intensive Care Med 2012 Sosa 55 7

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DOI: 10.1177/08850666103934682012 27: 55 originally published online 21 January 2011J Intensive Care Med

Andrs F. Sosa and Gisela BanauchA 24-Year-Old Man With Cough, Rhabdomyolysis, and Pneumomediastinum

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Case Reports

A 24-Year-Old Man With Cough,Rhabdomyolysis, andPneumomediastinum

Andres F. Sosa, MD1 and Gisela Banauch, MD1

Abstract

Background: Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) frequently causes severe necrotizingpneumonia in young patients. Case: We present the case of a 24-year-old male, who was brought to the emergency departmentwith persistent fevers, confusion, and severe cough. He was found to have necrotizing pneumonia, pneumomediastinum, and

rhabdomyolysis with renal failure. Cultures were positive for influenza A and CA-MRSA. After a prolonged intensive care unit(ICU) stay, he made a complete recovery. Conclusion: Community-acquired MRSA pneumonia is a growing health threat

that typically presents in young adults after, or in conjunction with, a flu-like illness. It is characterized by a rapidly progressive

deteriorating clinical course.

Keywords

community-acquired MRSA, pneumonia, pneumomediastinum, rhabdomyolysis

Received February 4, 2010. Submitted April 19, 2010.

Introduction

Community-acquired methicillin-resistant Staphylococcus

aureus (CA-MRSA) pneumonia is a growing threat that causes

severe necrotizing pneumonia in young adults. It is often

preceded by a flu-like illness and characterized by a stormy

disease course and high mortality.1 Community-acquired MRSA

very often carries the Panton-Valentine leukocydin (PVL), a

pore-forming toxin that significantly increases the microorgan-

isms virulence.2 Pneumomediastinum and rhabdomyolysis are

rare complications that have been described with staphylococcal

pneumonia3,4and may misguidethe clinicians initial impression.

Case

A 24-year-old man was brought to the emergency department

with a 1-week history of persistent high fevers, intense produc-

tive cough, and progressive confusion and lethargy. Initially hecomplained of sore throat, fevers, chills, headache, nausea,

myalgias, and fatigue; the cough was severe enough to trigger

vomiting. Two days before admission, he had been diagnosed

with community-acquired pneumonia and prescribed a 5-day

course of azithromycin by his primary care physician. Despite

the oral antibacterial therapy, his condition continued to dete-

riorate. On the day of admission, his family noticed him to

be lethargic and confused, prompting them to seek further

medical attention in the emergency room. The patient had no

prior medical history of note. He did not have known allergies

and had been taking azithromycin for the past 2 days. He was a

lifelong nonsmoker. The patient was from central Massachusetts

and had not traveled outside this area during his adult life.

His physical examination was remarkable for temperature,

39.5

C; heart rate, 149 beats/min; respiratory rate, 28 breaths/min;blood pressure, 70/58; oxygen saturation 95% on4Lofsupple-

mental oxygen delivered by nasal cannula. The patient was

well developed and appeared acutely ill and diaphoretic.

His breathing was labored, and he was using his accessory

musculature. He was aroused promptly to voice; there was

minimal confusion to current events. Oral mucosa was dry.

The findingson cardiac examinationwerenormal.His pulmonary

examination revealed dullness to percussion, decreased tactile

fremitus, diminished breath sounds, rales, ronchi, and wheezes

throughout the right hemithorax. The remainder of his physical

examination was unremarkable.

Laboratory findings were remarkable for leukocyte

count 9.8 thousand/mm3, hemoglobin 13.1 g/dL, platelets165 thousand/mm3, 46% bandemia. Serum chemistry showed

1 Pulmonary, Allergy & Critical Care Medicine, University of Massachusetts

Medical School, UMass-Memorial Medical Center, Worcester, MA, USA

Corresponding Author:

Andres F. Sosa, Umass Memorial MedicalCenter, 55 Lake Av. North,Worcester,

MA 01655, USA

Email: [email protected]

Journal of Intensive Care Medicine

27(1) 55-57

The Author(s) 2012

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sodium 124 mmol/L,potassium 3.7mmol/L,chloride93 mmol/L,urea nitrogen 47 mg/dL, creatinine 2.87 mg/dL, calcium 6.5 mg/

dL,magnesium 1.1 mg/dL; creatinekinase > 45 100U/L,creatine

kinase muscle brain subfraction 95.8 ng/mL, aspartate amino-

transferase 734 IU/L, alanine aminotransferase 173 IU/L, lactate

dehydrogenase 1145 IU/L. Microbiological analysis yielded

methicillin-resistant Staphylococcus aureus isolated from blood

and pulmonary secretions. Respiratory virus cultures were

positive for influenza A. Admission chest radiographs and

representative images from a chest computed tomography (CT)

on admission are shown in Figures 1 to 3. The patient was

intubated within 24 hours of arrival in the intensive care unit

(ICU). Bronchoscopy after intubation revealed copious amounts

of bloody, purulent secretions, and severe mucosal inflammation

with sloughing, more pronounced throughout the right tracheo-

bronchial tree.

The patient was treated with oseltamivir and rimantadine

for influenza A infection. In addition, he received linezolid,

vancomycin, and rifampin for severe MRSA pneumonia.

The presence of pneumomediastinum resolved shortly after

admission without further specific therapy. The patient

required a tube thoracostomy for drainage of an infected right

pleural space. His acute renal failure and rhabdomyolysis

resolved promptly with supportive therapy that included vol-

ume resuscitation and forced diuresis with urine alkalinization.

A percutaneous tracheotomy was inserted on hospital day#11

for prolonged mechanical ventilatory support. After a 30-day

ICU stay, he was discharged without further organ support to

a rehabilitation facility. He was seen 3 months later in the

pulmonary outpatient clinic and was doing remarkably well,

living at home and close to returning to work. His last chest

CT showed complete resolution of the large cavitating

infiltrates.

Discussion

In recent years, a new variant of CA-MRSA has emerged as a

serious threat, frequently affecting younger patients who have a

prior presentation of a flu-like illness and a violent disease

course with high mortality rates and prolonged admissions to

the ICU. Community-acquired MRSA pneumonia typically has

a different clinical course and epidemiologic incidence from

that of hospital-acquired MRSA pneumonia: hospital-acquired

MRSA pneumonia tends to affect older individuals with

Figure 1. Chest X-ray.

Figure 2. Chest computed tomography (CT).

Figure 3. Chest computed tomography (CT).

56 Journal of Intensive Care Medicine 27(1)



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significant comorbidities and has a more indolent course albeit

comparable mortality.1

During the 2006 to 2007 influenza season, 440 adults and

117 children were hospitalized due to community-acquired

pneumonia caused by S aureus; 386 (72%) were methicillin-

resistant, 49% required mechanical ventilation, and 13% died;

26%

of these patients had an associated influenza infection.

5

Other sources6 have reported mortality rates as high as 56%,

with a median survival of 10 days

Community-acquired MRSA was initially mostly isolated

from skin infections, typically of young athletes; the develop-

ment of severe pneumonia has been a growing problem of the

last decade. In 2002, the association with PVL was made. Up to

85% of CA-MRSA strains have PVL, a pore-forming toxin that

affects cells of the immune system and induces a strong inflam-

matory response that substantially enhances staphylococcal

virulence.2 PVL () strains have a higher binding affinity for

exposed basement membrane of damaged human airway

epithelium than PVL () strains7; this may play an important

role in their attachment to epithelium that has been previouslyinjured by a viral infection. Panton-Valentine leukocydin also

enhanced the transcription of secreted and cell wall-anchored

staphylococcal proteins.3

The classic clinical presentation of CA-MRSA pneumonia

is characterized by severe respiratory symptoms, hemoptysis,

hypotension, and high fever. Laboratory analyses often reveal

leukopenia and very high levels of C-reactive protein.

The chest radiograph may show necrotizing pneumonia with

multilobar cavitating infiltrates. In a series of 50 patients with

PVL MRSA pneumonia by Gillet et al,6 the median duration

of symptoms before hospitalization was 3 days, and 67.3% of

patients had a preceding flu-like illness. Virological studies

were done in 9 patients and 4 had influenza A infection.

Preexisting skin infections were found in only 24% of patients.

The clinical course during the first 48 hours was very severe,

and airway bleeding was often described (44%). Airway bleed-

ing, erythroderma, and leukopenia were associated with fatal

outcomes. Autopsy findings have shown that the entire respira-

tory tract may be affected. Extensive necrotic ulcerations of the

tracheal and bronchial mucosa and massive hemorrhagic

necrosis of the interalveolar septa in the presence of a large

concentration of microorganisms have been described.2

We found only 2 previous cases of pneumomediastinum in

the presence of methicillin-sensitive staphylococcal pneumonia,

both young patients with a rapidly progressive deteriorating

clinical course.4,8

Declaration of Conflicting Interests

The author(s) declared no conflicts of interest with respect to theauthorship and/or publication of this article.

Funding

The author(s) received no financial support for the research and/or

authorship of this article.

References

1. Rubinstein E, Kollef MH, Nathwani D. Pneumonia caused

by methicillin-resistant Staphylococcus aureus. Clin Infect Dis.

2008;46(suppl 5):S378-S385.

2. Gillet Y, Issartel B, Vanhems P, et al. Association between

Staphylococcus aureus strains carrying gene for Panton-Valentine

leukocidin and highly lethal necrotizing pneumonia in youngimmunocompetent patients. Lancet. 2002;359(9308):753-759.

3. Labandeira-Rey M, Couzon F, Boisset S, et al. Staphylococcus

aureus Panton-Valentine leukocidin causes necrotizing pneumo-

nia. Science. 2007;315(5815):1130-1133.

4. Roshan M, Venkatesha BM, Bhat EK, Nayak UA. Pneumome-

diastinum and pneumopericardium in staphylococcal bronchop-

neumonia. J Assoc Physicians India. 2003;51:884.

5. Kallen AJ, Hageman J, Gorwitz R, Beekmann SE, Polgreen PM.

Characteristics of Staphylococcus aureus community-acquired

pneumonia during the 20062007 influenza season. Clin Infect

Dis. 2007;45(12):1655.

6. Gillet Y, Vanhems P, Lina G, et al. Factors predicting mortality

in necrotizing community acquired pneumonia caused by

Staphylococcus aureus containing Panton-Valentine leukocidin.

Clin Infect Dis. 2007;45(3):315-321.

7. de Bentzmann S, Tristan A, Etienne J, Brousse N, Vandenesch F,

Lina G. Staphylococcus aureus isolates associated with necrotizing

pneumonia bind to basement membrane type I and IV collagens and

laminin. J Infect Dis. 2004;190(8):1506-1515.

8. Finnie IA, Jack CI, McKay JS. Pneumomediastinum and subcuta-

neous emphysema complicating staphylococcal pneumonia. Ulster

Med J. 1995;64(1):105-107.

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