MARIA REYNA- XAVIER UNIVERSITY HOSPITAL

DEPARTMENT OF INTERNAL MEDICINE

February 24, 2016
8:00 AM
Take My Breath Away
A case report on survival of 39-year old male with Hospital-Acquired Pneumonia
from Acute Respiratory Distress Syndrome
Ababon, Antoniette * Barba, Aila * Cacho, Nicanor Jr. * Eppie, Settie Jamalia * Oliveros, Francis

ABSTRACT
Background: Acute respiratory distress syndrome (ARDS) is a clinical syndrome of severe dyspnea of
rapid onset, hypoxemia, and diffuse pulmonary infiltrates leading to respiratory failure.
Objective: This report aims to discuss an important cause of respiratory failure, to discuss the etiology,
epidemiology, pathophysiology, clinical manifestations, treatment and management, and prognosis of
acute respiratory distress syndrome (ARDS), and to determine the effect on quality of life and return to
work in survivors of ARDS.
Case Summary: This is a case of a thirty nine year old male with a history of respiratory tract infection
with recent hospitalization for 3 days due to community-acquired pneumonia - moderate risk (CAP-MR)
and was subsequently referred in this institution
due to respiratory distress. Patient has unstable vital
signs and crackles on all lung fields. Laboratory results revealed leukocytosis with predominance of
neutrophils, compensated respiratory alkalosis and ETA culture of an isolate of S. hemolyticus. Chest xray revealed diffuse alveolar infiltrates and echocardiogram showed moderate hypertension. Patient was
treated with low tidal volume ventilation (LTTV), inotropics, broad- spectrum IV antibiotics and diuretics.
Patient was discharged after 13 days.
Conclusion: Current mortality from ARDS is 41-65%, with most deaths due to sepsis and non pulmonary
organ failure. However, it has declined with improvements in general critical care treatment and with the
introduction of low tidal volume ventilation. Survivors of ARDS are at risk of cognitive, psychologic and
physical morbidity. In most patients, lung volumes and spirometry will normalize by six months, and
diffusion capacity should normalize by five years. A small percentage of patients are left with residual
deficits and supplemental oxygen is rarely required.
Recommendation: We suggest that studies be done in the local setting as to determine the prevalence
of ARDS and the most common risk factors that predispose them to having ARDS.

INTRODUCTION
Acute respiratory distress syndrome is an important cause of acute respiratory failure that is often
associated with multiple organ failure. The likelihood of survival is determined by the severity of lung
injury, the extent of non pulmonary organ dysfunction, pre-existing medical conditions, and the quality of
supportive care.
This report aims to discuss a case of 39 year old male who came in due to dyspnea and to
discuss the etiology, epidemiology, pathophysiology, clinical manifestations, treatment and management,
and prognosis of acute respiratory distress syndrome.
CLINICAL PRESENTATION
This is a case of E.R. 39 years old, male, separated, Roman Catholic, school principal, born on
July 5, 1976 and currently residing at Casisang, Malaybalay, Bukidnon. The source of information was the
patients sister, cousin and himself with 98% reliability.
1 week prior to admission, patient had onset of intermittent undocumented fever associated with
nonproductive cough and bilateral frontal headache, throbbing, non-radiating with pain score of 9/10. It
was not associated with colds, vomiting and dyspnea. Patient took Paracetamol 500mg every 4 hours
and Naproxen sodium 500mg which afforded temporary relief. Still no consult was done.
4 days prior to admission, condition persisted, this time associated with dyspnea prompting
consult to a Local Hospital at Malaybalay City where he was subsequently admitted. Diagnostics done
were CBC which showed WBC of 5.9, hemoglobin 15.0, hematocrit 45.6, lymphocytes 17, neutrophils 77,
monocytes 4 and eosinophils 2, basophils 0 and chest xray which showed mild pulmonary congestive
changes and mild cardiomegaly. Patient was initially managed as Community Acquired PneumoniaModerate Risk. Patient was started with Ceftriaxone 1gram IVTT every 8 hours, Levofloxacin 500mg once
a day per orem and Salbutamol nebulization which offered no improvement.
3 days prior to admission, while admitted in Malaybalay, patient was still febrile, dyspneic with
severe headache, pain score of 9-10/10 so the attending physician requested for Typhidot revealing IgM
positive. Urinalysis done which showed yellow, hazy urine with specific gravity: of 1.025, pH of 6.0, no
protein and glucose, WBC of 1-3/hpf, RBC of 10-15/hpf, epithelial cells rare,. Patient was now treated as
a case of Community Acquired Pneumonia- Moderate Risk and Typhoid Fever. Medications were
continued. Other diagnostics showed FBS 101.24 mg/dl, creatinine 0.9mg/dl, and creatinine clearance
112.22ml/min.
8 hours prior to admission, patient was persistently febrile with worsening of dyspnea. Patient had
oxygen saturation of 50% at room air and oxygen inhalation at 10 lpm via face mask was given which
raised the oxygen saturation to 72%. Persistence of condition prompted referral to MRXUH for further
management and subsequently admitted.
Patient is non-hypertensive, non-diabetic and non-asthmatic. No history of tuberculosis treatment.
He was hospitalized when he was 8 years old due fall sustaining fracture in his left arm where close
reduction and casting was done. He has no previous surgical operation. Patient has no known food and
drug allergies.
There is a history of hypertension, bronchial asthma and diabetes mellitus on the maternal side.
No other heredofamilial disease.
Patient is a graduate of BS in Animal Science and BS in Education and currently working as an
elementary school principal in Malaybalay City for 8 years. He is a smoker for 28 pack years and quit
smoking for 5 years already. He is a chronic alcoholic beverage drinker and denies illicit drug use. Patient
was separated from his wife and they had 2 children. After the separation, he with other woman and had
3 children. Patient denied history of men-to-men sexual contact.

Patient was examined awake, oriented, can speak in phrases and in respiratory distress. Vital
signs: BP: 80/50 mmHg, HR: 105 bpm, tachycardic, RR: 52 cpm, tachypneic, T: febrile at 38.9 C, SaO2:
67%, Weight: 72kg, Height: 170 cm and BMI: 24, normal. Skin was cyanotic, with good skin turgor,
anicteric sclerae, pinkish palpebral conjunctivae, non-hyperemic posterior pharyngeal wall, no tonsillar
axudates or congestion, neck was supple, trachea at midline, no neck vein distension no cervical
lymphadenopathies. In the chest and lungs examination, intercostals, subcostal and supraclavicular
retractions, increased fremitus, dullness on mid-basal lung field and diffuse crackles on all lung fields with
occasional wheeze. PMI was noted at 5th intercostal space, midclavicular, distinct heart sounds,
tachycardic with no murmurs. Abdomen was flat, abdominal breathing, normoactive bowel sounds, soft,
tympanitic, no tenderness, no organomegaly. Extremities was cold, strong pulses, no edema on upper
and right lower extremity, CRT<2 seconds. Neurologic exam was within normal limits.
IMPRESSION: Acute Respiratory Distress Syndrome; Septic shock secondary to Hospital Acquired
Pneumonia; R/O Typhoid Fever
PROBLEMS IDENTIFIED
1. ARDS and Septic shock secondary to HOSPITAL ACQUIRED PNEUMONIA
Upon admission, patient complained cough and dyspnea. Upon physical examination, patient
was awake, restless and in respiratory distress. He was hypotensive (BP-80/50mmHg), tachycardic
(HR-105bpm), tachypneic (52cpm) and febrile (T-38.9C) with desaturation of 67% at room air and 81%
even with O2 inhalation at 10 LPM. Supraclavicular retractions, abdominal breathing and dullness on midbasal lung field noted. Crackles on all lung fields and occasional wheeze was auscultated. Arterial blood
gas was done and revealed compensated respiratory alkalosis. He was then intubated and hooked to
mechanical ventilator, subsequently admitted at ICU. Repeat ABG post-intubation revealed partially
compensated metabolic acidosis. Impression was Acute respiratory distress syndrome and septic shock
secondary to hospital acquired pneumonia. Diagnostic exams were ordered: CBC revealed leukocytosis
with neutrophil predominance. ECG showed Sinus Tachycardia. Chest X-ray revealed Cardiomegaly LV
form, Pulmonary edema vs Pneumonia. ETA Gram staining showed pus cells 1-2/OIF, EC 0-1/OIF, G(-)
cocco-bacilli/rods occasional; ETA cultured Staphylococcus hemolyticus with MRSA, Beta-lactamase
producing staphylococci. Blood culture showed No growth after 5 days of incubation. ESR was high at
72mm/hr. BNP was 16.9pg/mL, hence we rule out cardiogenic cause of pulmonary edema. D-Dimer was
elevated at 3.1, with elevated Trop I of 0.062I but normal CKMB of 2.1 ng/dL. Protime was 14.4sec,
Control 12.2, % Act 65.3, INR 1.23, Ratio 1.18. Tubex test revealed IgM and IgG negative hence Typhoid
fever was ruled out. Venoclysis was started with PNSS 1L @10cc/hr. Levophed 2amp + D5W 42cc at
27cc/hr was infused. Meropenem 1gm IV q8h, Vancomycin 4g IV drip q12h, Azithromycin 500mg tab OD
PO, Salbutamol+Ipratropium 1 neb q6h, N-acetylcysteine 600mg 1 tab in 3cc of water OD and
Paracetamol 500mg/tab q4h prn for fever were started.
On the 1st hospital day, there was less frequent dyspnea and cough with no episode of
hypotension. Vital signs were the following: BP-90/60mmHg, HR-106, Temp- 38.6C and O2 sat -95-99%.
Physical examination revealed no retractions, but still with abdominal breathing. Rales was auscultated
on mid-basal lung field, with no wheezing. Repeat ABG revealed compensated metabolic acidosis.
Repeat Chest x-ray revealed significant clearing of the alveolar densities in both lungs due to resolving
pulmonary edema. Intercurrent pneumonia is considered. There is complete resolution of the bilateral
pleural effusion. Levophed was discontinued. Other medications were continued.
On the 2nd hospital day, patient was comfortable with occasional cough. Vital signs were the
following: BP-110/70mmHg, HR-84, Temp- 38C, and O2 sat of 95-99%. Physical examination revealed
decreasing rales on mid-basal lung field. Repeat CBC showed leukocytosis with predominance of

neutrophils, anemia and thrombocytosis. Repeat Chest x-ray revealed no significant change in the
reticular and patchy densities in both lungs which maybe due to pulmonary edema or pneumonia.
Medications were continued.
On the 3rd hospital day, patient still complained occasional cough. Vital signs were the following:
BP-100/60mmHg, HR-82, Temp- 38.6C and O2 sat -95-99%. Physical examination revealed rales on
basal lung field. Repeat CBC showed leukocytosis with neutrophils predominance. Medications were
continued.
On the 4th hospital day, patient still has occasional cough. Vital signs were the following:
BP-100/70mmHg, HR-79, Temp- 37.1C and O2 sat -97-99%. Physical examination revealed decreasing
basal rales. Weaning from mechanical ventilator was started. Medications were continued.
On the 5th hospital day, patient has no subjective complaints. Vital signs were the following:
BP-110/70mmHg, HR-86, Temp- 37C and O2 sat -98-100%. Physical examination revealed decreasing
basal rales. Repeat CBC revealed leukocytosis with neutrophil predominance. Same medications were
given.
On the 6th hospital day, patients condition was improving. Vital signs were stable. Decreasing
rales was auscultated. Weaning from mechanical ventilator was continued. Medications were continued.
On the 7th hospital day, improving condition noted. Patient tolerated weaning hence continued.
Same medications were continued.
On the 8th hospital day, weaning was tolerated with 98% O2 saturation. Patient was then
extubated and hooked to O2 support at 5-6lpm via nasal cannula. Meropenem was decreased to 1gram
IV drip to run in 2 hours every 12 hours. Hydrocortisone 100mg IV every 8 hours for 4 doses was given.
Other medications were continued.
On the 9th hospital day, there was clinical improvement noted, however patient still complained
with occasional cough. Vital signs were stable and decrease in bibasal rales noted. Trial of feeding and
bladder training was started. O2 inhalation was decreased to 2-4 lpm.
On the 10th hospital day, condition was improving. Decreasing bibasal rales auscultated. O2
inhalation was decreased to 1 lpm. Patient was put to diet as tolerated. Step-down antibiotics with oral
Trimethoprim-sulfamethoxazole 165/800mg BID was started.
On the 11th hospital day, patient was transferred to private room. Moreover, on the 12th hospital
day, patient still complained infrequent cough and had episode of shortness of breath upon walking
~3meters. Physical examination findings revealed decreased rales on both basal lung fields. Patient was
given bathroom privileges. Lastly, on the 13th hospital day, patient was discharged to home with improved
condition.
2. ACUTE KIDNEY INJURY secondary to SEPSIS
Upon admission, there was noted decrease in the urine output as confirmed with the increasing
Creatinine of 0.6 (Crea Cl = 169mL/min) to 1.02 (Crea Cl = 99mL/min). Other laboratories revealed Na
139.2, K 4.36, BUN 16.6, and Urinalysis: amber, hazy, SG 1.030, pH 6.0, sugar (-), protein trace, WBC 5/
hpf, RBC plenty, EC 3/hpf. Impression was Acute kidney injury secondary to sepsis. Fluid hydration with
PNSS was regulated to 40cc/hr. Appropriate antibiotics were given. Furosemide 40mg IV was started.
On the 2nd HD, patients input was 1988cc, while output was 2950cc with negative fluid balance
of 1272cc. On the 3rd HD, input was 2148cc and output was 2030cc, still with negative fluid balance of
1390cc. Then on the 4th HD, input was 3054cc and output was 2800cc, with negative balance of 1136cc.
On the 5th HD, with appropriate antibiotics and adequate hydration, Crea went down to 0.82 (Crea Cl =
123mL/min), with positive balance of 200cc noted (input-3206cc and output-1870cc). Furosemide IV was
continued to maintain POSITIVE Fluid Balance.
However, on the 5th hospital day, input of 2734cc and output of 3200cc with a negative balance
of 266cc was noted. Repeat Creatinine revealed 0.7mg/dL, with Crea Cl of 145mL/min. Same

medications were continue and furosemide dose was decreased. On the succeeding days, adequate
urine output and positive fluid balance was achieved.
3. CARDIOMEGALY
Upon admission, patient was denied chest pain, however dyspenic. On physical examination,
patient was tachycardic, tachypneic and hypotensive. Jugular venous pressure was normal. Adynamic
precordium, distinct heart sounds and no murmurs were noted. ECG showed Sinus Tachycardia with no
signs of hypertrophy. Chest x-ray however revealed an enlarged heart with a CTR of 0.66 and the
presence of pulmonary edema. Cardiogenic pulmonary edema was an initial consideration.
On the 1st HD, patient still has no complaints of chest pain. Repeat ECG revealed sinus
tachycardia.CK-MB levels were at 2.1 ng/mL, BNP of 16.9 pg/mL, and slight elevation of troponin I at
0.062 ng/mL was noted.
On the 2nd HD day 2D echo was done and showed concentric left ventricular remodeling with
adequate contractility and systolic function, normal left atrium, and moderate pulmonary hypertension. A
repeat chest x-ray was done revealing a CTR ratio of 0.57.
Cardiogenic cause of Pulmonary edema was ruled out since BNP and CK-MB were normal
despite the elevated Troponin I which may be due to existing infection that is further supported by 2D
echo findings.
FINAL DIAGNOSIS:

ACUTE RESPIRATORY DISTRESS SYNDROME resolved

SEPSIS secondary to HOSPITAL ACQUIRED PNEUMONIA resolved

AKI secondary to SEPSIS - resolved

DISCUSSION
Presented here is a male 39 year old with a history of progressive dyspnea with hypoxemia
previously managed as a Community Acquired Pneumonia- Moderate Risk and Typhoid Fever and was
referred in this institution for intensive care unit (ICU) admission. Among the conditions may be
considered are acute respiratory distress syndrome (ARDS), congestive heart failure (CHF) and
pulmonary embolism.
According to American Thoracic Society, dyspnea is a "subjective experience of breathing
discomfort that consists of qualitatively distinct sensations that vary in intensity. The experience derives
from interactions among multiple physiological, psychological, social, and environmental factors and may
induce secondary physiological and behavioral responses. Patient arrived dyspneic and can speak only
in phrases while on high back rest in tripod position. Patient appeared cyanotic and when it is associated
with dyspnea it is considered an ominous sign, hence, emergent treatment was required. The approach to
dyspnea is based on the algorithm provided by Harrisons. Common clinical indicators in the history
includes orthopnea seen in CHF, mechanical impairment of the diaphragm in obesity, or asthma triggered
by esophageal reflux; nocturnal dyspnea seen in CHF or asthma; acute, intermittent episodes of dyspnea
seen in myocardial infarct (MI), bronchospasm, or PE; chronic persistent dyspnea seen in chronic
obstructive pulmonary disease (COPD), interstitial lung disease, & chronic thromboembolic disease; and,
platypnea defined as dyspnea in the upright position with relief in the supine position. This is seen in
patients with left atrial myxoma or hepatopulmonary syndrome. In the physical examination, inability of
the patient to speak in full sentences an impairment of the ventilatory pump with reduced vital capacity.
Increased work of breathing was seen in our patient. This is evidenced by supraclavicular retractions, use

of accessory muscles of ventilation, and the tripod position which are indicative of increased airway
resistance or stiff lungs and chest wall. During the general examination, cyanosis was noted which is
indicative of hypoxemia. During examination of the chest movement was symmetric; on percussion,there
was dullness which is indicative of pleural effusion; and on auscultation (rales, diminished breath sounds,
which are clues to disorders of the airways, and interstitial edema or fibrosis). On cardiac examination,
there were no signs of elevated right heart pressures (jugular venous distention, edema, accentuated
pulmonic component to the second heart sound); left ventricular dysfunction (S3 and S4 gallops); and
valvular disease (murmurs). Upon examining the abdomen there was no paradoxical movement of the
abdomen (inward motion during inspiration), a sign of diaphragmatic weakness; rounding of the abdomen
during exhalation is suggestive of pulmonary edema. Clubbing of the digits and the presence of joint
swelling or deformation were not present that may indicate interstitial pulmonary fibrosis and collagenvascular process, respectively.
After history and PE, a chest radiograph was obtained. There was no indication of hyperinflation
seen in obstructive lung disease nor low lung volumes seen in interstitial edema or fibrosis, diaphragmatic
dysfunction, or impaired chest wall motion. The pulmonary parenchyma was not suggestive of interstitial
disease and emphysema. It did not show prominent pulmonary vasculature in the upper zones indicating
pulmonary venous hypertension, nor enlarged central pulmonary arteries suggesting pulmonary artery
hypertension. The cardiac silhouette was not enlarged unlike in a dilated cardiomyopathy or valvular
disease. Bilateral pleural effusions were present typically CHF and some forms of collagen vascular
disease. On the other hand, unilateral effusions raise the specter of carcinoma and pulmonary embolism
but may also occur in heart failure which are our considerations initially. Computed tomography (CT) of
the chest was not necessary and this is generally reserved for further evaluation of the lung parenchyma
(interstitial lung disease) and possible pulmonary embolism. Electrocardiogram showed sinus tachycardia
and there was no evidence of ventricular hypertrophy and prior myocardial infarction. Echocardiography
is indicated in patients in whom systolic dysfunction, pulmonary hypertension, or valvular heart disease is
suspected. This was done on the 2nd hospital day in our patient revealing concentric left ventricular
remodeling with adequate contractility and systolic function, normal left atrium and moderate pulmonary
hypertension. If a patient has evidence of both pulmonary and cardiac disease, a cardiopulmonary
exercise test should be carried out to determine which system is responsible for the exercise
limitation.The first goal is to correct the underlying problem responsible for the symptom. If this is not
possible, lessening the intensity of the symptom and its effect on the patients quality of life may be
attempted.
It is useful to categorize the causes of noncardiogenic pulmonary edema in terms of whether the
injury to the lung is likely to result from direct, indirect, or pulmonary vascular causes. Direct injuries
include chest trauma (e.g. pulmonary contusion), aspiration, smoke inhalation, pneumonia, oxygen
toxicity, pulmonary embolism, and reperfusion. Indirect injury is the consequence of mediators that reach
the lung via the blood stream. This includes sepsis, pancreatitis, nonthoracic trauma, leukoagglutination
reactions, multiple transfusions, intravenous drug use, (e.g., heroin) and cardiopulmonary bypass. The
third category includes conditions that may be the consequence of acute changes in pulmonary vascular
pressures, possibly the result of sudden autonomic discharge in the case of neurogenic and high altitude
pulmonary edema, or sudden swings of pleural pressure, as well as transient damage to the pulmonary
capillaries in the case of reexpansion pulmonary edema.
The history is essential for assessing the likelihood of underlying cardiac disease as well as for
identification of one of the conditions associated with noncardiogenic pulmonary edema. Pneumonia was
identified as the direct cause. This consequently spread hematogenously resulting into sepsis, The
physical examination in cardiogenic pulmonary edema is notable for evidence of increased intracardiac
pressures (S3 gallop, elevated jugular venous pulse, peripheral edema), in which these are absent in our
patient, and rales and/or wheezes on auscultation of the chest. In contrast, the physical examination in
noncardiogenic pulmonary edema is dominated by the findings of the precipitating condition; pulmonary

findings may be relatively normal in the early stages. The diagnostic evaluation is aimed at identifying
specific causes of ARDS that are amenable to treatment and excluding other conditions that also present
with acute hypoxemia, bilateral alveolar infiltrates, and respiratory distress. The chest radiograph in
cardiogenic pulmonary edema typically shows an enlarged cardiac silhouette, peribronchial thickening,
prominent vascular markings in the upper lung zones, and Kerley B lines; pleural effusions are common.
In noncardiogenic pulmonary edema, heart size is normal, alveolar infiltrates are distributed more
uniformly throughout the lungs, and pleural effusions are uncommon. Initial chest radiograph showed
patchy densities in both lungs, more at the right upper lobe and heart magnified and enlarged with CTR of
0.66. Chest x-ray in ARDS rarely shows cardiomegaly. Further work-up was done by obtaining basic
natriuretic peptide (BNP) revealing 16.9 pg/mL. The study found that a plasma BNP level less than 100
pg/mL identified ARDS with a sensitivity, specificity, positive predictive value, and negative predictive
value of 27, 95, 90, and 44 percent, respectively. Finally, the hypoxemia of cardiogenic pulmonary edema
is due largely to V/Q mismatch and responds to the administration of supplemental oxygen. In contrast,
hypoxemia in noncardiogenic pulmonary edema is due primarily to intrapulmonary shunting and typically
persists despite high concentrations of inhaled O2. This was evident with SpO2 of 81% when patient was
administered with O2 therapy via face mask.
Pneumonia is an infection of the pulmonary parenchyma and is the most common cause of direct
lung injury approximately 40-50%. It is classified as a community-acquired (CAP) or health careassociated (HCAP).
Pneumonia results from the proliferation of microbial pathogens at the alveolar level and the
host's response to those pathogens. Microorganisms gain access to the lower respiratory tract via micro
aspiration from the oropharynx, which is the most common route, inhalation of contaminated droplets,
hematogenous spread, or contiguous extension from an infected pleural or mediastinal space. Classic
pneumonia (typified by that due to Streptococcus pneumoniae) presents as a lobar pattern and evolves
through four phases. The initial phase is edema with the presence of proteinaceous exudate (often
bacteria) in the alveoli. This is followed by red hepatization in which erythrocytes and neutrophils are
present in the alveolar exudate. In the third phase, gray hepatization, neutrophils predominate, with
abundant fibrin deposition and bacteria are absent. In the final phase, resolution, macrophages are the
dominant cell type in the alveolar space and there is clearing of debris and inflammation. Typical
symptoms of pneumonia are fever, chills, sweats, cough (either nonproductive or productive of mucoid,
purulent or blood-tinged sputum), pleuritic chest pain and dyspnea. Chest x-ray is usually adequate for
diagnostics. Other diagnostics include sputum stains and culture, blood cultures and serology. Common
complications of sever CAP include respiratory failure, shock and multi organ failure, bleeding diatheses,
and exacerbation of comorbid disease.
HCAP is associated with hospitalization for 48 hours, hospitalization for 2 days in the prior 3
months, nursing home or extended-care facility residence, antibiotic therapy in the preceding 3 months,
chronic dialysis, home infusion therapy, home wound care, and contact with a family member who has a
multidrug-resistant (MDR) infection.The HCAP category is subdivided into hospital-acquired pneumonia
(HAP), which is defined as pneumonia occurring 48 hours or more after admission that was not incubating at the time of admission, and ventilator-associated pneumonia (VAP), which is defined as
pneumonia appearing more than 48 to 72 hours after endotracheal intubation. In a Philippine study,
overall incidence of HAP is 6 per 1000 admission and mortality rates of 42.4%. Data regarding the
etiology of HAP, including VAP, P. aeruginosa was the most common pathogen causing HAP (42.1%).In
patients with HAP excluding VAP, the panel noted that the etiologic scenario has not changed much over
time. P. aeruginosa was reported to be the most common pathogen (19% of isolates), followed by E. coli.
Earlier studies also identified P. aeruginosa (31.1% of isolates) and E. coli (15.5%) as highly prevalent
organisms. The time of onset of pneumonia is an important epidemiologic factor for specific pathogens
and clinical outcomes in HAP. Early-onset HAP or VAP occurs within the first 5 days of hospitalization and
carries a better prognosis. Late-onset HAP or VAP occurs after 5 days or more of hospitalization and is

more likely associated with multidrug-resistant pathogens and increased morbidity and mortality. (Chawla,
2008).
Sepsis is the most common cause of ARDS approximately 80%. Fever or hypothermia,
leukocytosis or leukopenia, tachypnea, and tachycardia are the cardinal signs of the systemic response,
that is often called the systemic inflammatory response syndrome (SIRS). Sepsis is defined as SIRS with
known/identifiable source of infection, on the other hand, septic shock is defined as sepsis with
cardiovascular collapse. Upon admission, patient was noted to be hypotensive, febrile, tachycardic and
tachypneic. Patient was then managed as a case of septic shock secondary to hospital-acquired
pneumonia.
The goals during the first 6 hrs of resuscitation for patients with sepsis- induced tissue
hypoperfusion are the ff: Central venous pressure 812 mm Hg; Mean arterial pressure (MAP) 65 mm
Hg; Urine output 0.5 mL/kg/hr; Central venous (superior vena cava) or mixed venous oxygen saturation
70% or 65%, respectively; and to normalize lactate. Cultures should be done as clinically appropriate
before antimicrobial therapy if no significant delay (> 45 mins) in the start of antimicrobial(s). At least 2
sets of blood cultures (both aerobic and anaerobic bottles) should be obtained before antimicrobial
therapy. Imaging studies should be performed promptly to confirm a potential source of infection.
Crystalloid is recommended as the initial fluid of choice in the resuscitation of severe sepsis and septic
shock. Vasopressor therapy is given to target a mean arterial pressure (MAP) of 65 mm Hg, and
Norepinephrine is the first choice vasopressor. Dopamine is recommended as an alternative vasopressor
agent to norepinephrine only in highly selected patients (eg, patients with low risk of tachyarrhythmias
and absolute or relative bradycardia).
Effective intravenous antimicrobials should be administered within the first hour of recognition of
septic shock and severe sepsis. Initial empiric anti-infective therapy of one or more drugs that have
activity against all likely pathogens (bacterial and/or fungal or viral) and that penetrate in adequate
concentrations into tissues presumed to be the source of sepsis should be started. For neutropenic
patients with severe sepsis and for patients with difficult-to-treat, multidrugresistant bacterial pathogens
such as Acinetobacter and Pseudomonas spp.,combination empirical therapy is recommended. For
patients with severe infections associated with respiratory failure and septic shock, combination therapy
with an extended spectrum beta-lactam and either an aminoglycoside or a fluoroquinolone is for P.
aeruginosa bacteremia. Moreover, a combination of beta-lactam and macrolide is recommended for
patients with septic shock from bacteremic Streptococcus pneumoniae infections.
Empiric combination therapy should not be administered for more than 35 days. De-escalation
to the most appropriate single therapy should be performed as soon as the susceptibility profile is known.
The duration of therapy is typically 710 days; longer courses may be appropriate in patients who have a
slow clinical response, undrainable foci of infection, bacteremia with S. aureus; some fungal and viral
infections or immunologic deficiencies, including neutropenia.
The SSC Executive Committee has revised the improvement bundles for the management of
sepsis a follows: TO BE COMPLETED WITHIN 3 HOURS, measure lactate level, obtain blood cultures
prior to administration of antibiotics, administer broad spectrum antibiotics, and administer 30ml/kg
crystalloid for hypotension or lactate 4mmol/L; TO BE COMPLETED WITHIN 6 HOURS: apply
vasopressors (for hypotension that does not respond to initial fluid resuscitation) to maintain a mean
arterial pressure (MAP) 65mmHg; un the event of persistent hypotension after initial fluid administration
(MAP < 65 mm Hg) or if initial lactate was 4 mmol/L, re-assess volume status and tissue perfusion and
document; and lastly re-measure lactate if initial lactate elevated.
As with the case of our patient, fluid resuscitation was initiated with crystalloid PNSS IL at 40cc/
hr. He was given with Levophed, a norepinephrine. After resuscitation, BP was normalized to
100/60mmHg; MAP was 70mmHg, and urine output was 1cc/kg/hr. In the course of hospitalization, ETA
cultured Staphylococcus hemolyticus and chest x-ray revealed pulmonary edema vs pneumonia.
Combination of Meropenem (beta-lactam, Azithromycin (macrolide) and Vancomycin (glycopeptides)

was initiated. These two antibiotic have coverage to Gram-positive bacteria. After 10 days of antibiotic
therapy, step-down antibiotic therapy was done. Meropenem, Vancomycin and Azithromycin were
discontinued, and shifted to Trimethoprim-Sulfamethoxazole, which showed to be sensitive against
Staphylococcus haemolyticus.
In the setting of the ICU, acute decompensated heart failure(cardiogenic shock phenotype) is the
most common alternative diagnosis for ARDS. A chest radiograph by itself often cannot distinguish
cardiogenic from non cardiogenic pulmonary edema. Clinical evaluation suggesting CHF may include the
presence of cough, dyspnea, fatigue, tachycardia, hypotension, desaturation, supraclavicular retractions,
and crackles. However, patientt did not present with edema, ascites, JVP elevation, and displacement of
point of maximal impulse (PMI) Although these were manifested in our patient, however, this was ruled
out after the 2D echocardiogram.
Pulmonary embolism (PE) results from deep-vein thrombosis that have broken off and traveled to
the pulmonary arterial circulation. Tachypnea and tachycardia are common in PE. Low grade fever, neck
vein distention and a loud P2 on cardiac examination can be seen. Hypotension and cyanosis suggest
massive PE. Patient had elevated D-dimer level (3.1 mg/L), however, hospitalized patients often presents
with this due to other disease processes . Normal d-dimer level (<5 mg/mL by ELISA) essentially rules out
PE. Patient had elevated troponin (0.353 ng/mL) level which is associated with increased risk of
complications in PE. The ECG can show S1Q3T3 sign in PE, but that finding was not observed in this
patient. A normal chest x-ray is common. Chest CT with IV contrast has become the primary diagnostic
test for PE. Based on history, the patient did not have prolonged immobilization, long bone trauma nor
surgical operations and there were no clinical signs of thrombophlebitis, hence, PE is ruled out.
Patients condition can also be attributed to asthma in acute exacerbation due to cough, dyspnea,
family history of asthma, tachycardia, cyanosis, desaturation, retractions and wheezing, however, patient
had no history of atopy, hence, this was our least consideration.
Acute respiratory distress syndrome (ARDS) is a clinical syndrome of severe dyspnea of rapid
onset, hypoxemia, and diffuse pulmonary infiltrates leading to respiratory failure. The development of the
new definition aimed to try and improve feasibility, reliability, face and predictive validity. ARDS can be
diagnosed once cardiogenic pulmonary edema and alternative causes of acute hypoxemic respiratory
failure and bilateral infiltrates have been excluded. The Berlin Definition of ARDS requires that all of the
following criteria be present to diagnose ARDS: First, respiratory symptoms must have begun within one
week of a known clinical insult, or the patient must have new or worsening symptoms during the past
week. Second, bilateral opacities consistent with pulmonary edema must be present on a chest
radiograph or computed tomographic (CT) scan. These opacities must not be fully explained by pleural
effusions, lobar collapse, lung collapse, or pulmonary nodules. Third, the patients respiratory failure must
not be fully explained by cardiac failure or fluid overload. An objective assessment (eg, echocardiography)
to exclude hydrostatic pulmonary edema is required if no risk factors for ARDS are present. Fourth,
moderate to severe impairment of oxygenation must be present, as defined by the ratio of arterial oxygen
tension to fraction of inspired oxygen (PaO2/FiO2). The severity of the hypoxemia defines the severity of
the ARDS: Mild ARDS The PaO2/FiO2 is >200 mmHg, but 300 mmHg, on ventilator settings that
include positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) 5 cm
H2O; Moderate ARDS The PaO2/FiO2 is >100 mmHg, but 200 mmHg, on ventilator settings that
include PEEP 5 cm H2O; and, severe ARDS The PaO2/FiO2 is 100 mmHg on ventilators setting that
include PEEP 5 cm H2O. In the case of our patient, PaO2/FiO2 (53.2mmHg/0.6) is 88 mmHg which is in
the severe category.
Common triggers of ARDS include sepsis, pneumonia, aspiration, multiple blood transfusions,
inhaled/ ingested toxins, and trauma. The clinical disorders associated with ARDS may be caused by
direct lung injury and indirect lung injury. Direct lung injury is due to pneumonia, aspiration of gastric
contents, pulmonary contusion, near-drowning and toxic inhalation injury. On the other hand, indirect lung
injury is caused by sepsis, severe trauma (e.g. multiple bone fractures, flail chest, head trauma, burns,

multiple transfusions, drug overdose, pancreatitis and post cardiopulmonary bypass. In comparison with
acute lung injury (ALI), they only differ on Pao2/Fio2 ratio 200 - 300 with the same above parameters.
The risk of developing ARDS may be particularly high among septic patients with a history of
alcoholism, which was present in the patient. This was illustrated by a prospective cohort study that
determined the incidence of ARDS in 220 patients with septic shock (43 vs 22%) (Siegel, 2014). The
incidence of ARDS among patients who chronically abuse alcohol was 70 percent, compared to 31
percent among patients who did not chronically abuse alcohol. A possible explanation for these findings is
that alcoholism may decrease the concentration of glutathione in the epithelial lining fluid, predisposing
the lung to oxidative injury. Alternatively, chronic alcohol abuse may increase the risk of ARDS by
enhancing inappropriate leukocyte adhesion to endothelial cells.
The annual incidences of ALI and ARDS are estimated to be up to 80/100,000 and 60/100,000,
respectively. Approximately 10% of all intensive care unit (ICU) admissions suffer from acute respiratory
failure, with ~20% of these patients meeting criteria for ALI or ARDS.. Worldwide, the incidence of ARDS
varies widely due to controversies regarding the clinical definition and its distinguishing characteristics.
The pathogenesis is thought to be dependent on endothelial injury. There are three phases in the
natural history of ARDS. First is the exudative phase is due to the activation of chemical mediators
characterized by alveolar edema and leukocytic inflammation, with subsequent development of hyaline
membranes from diffuse alveolar damage. The alveolar edema is most prominent in the dependent
portions of the lungs; this causes atelectasis and reduced compliance. Clinical manifestations are
hypoxemia, tachypnea, and progressive dyspnea develop, and increased pulmonary dead space can also
lead to hypercarbia. Chest x-ray reveals bilateral diffuse alveolar and interstitial opacities. The duration of
this phase is typically up to 7 days in length and usually begins within 12-36 hours after the inciting insult.
Proliferative phase is the second phase that can last from approximately days 7 to 21 days after an
inciting insult. Although most patients recover, some will develop progressive lung injury and evidence of
pulmonary fibrosis. Even among patients who show improvement, dyspnea and hypoxemia often press
during this phase. Fibrotic phase is the last phase in which majority of patients recover within 3-4 weeks
of the initial pulmonary injury, some experience progressive fibrosis, necessitating prolonged ventilatory
support and/or supplemental oxygen.
In the setting of the ICU, congestive heart failure (CHF) is the most common alternative diagnosis
for ARDS. A chest radiograph by itself often cannot distinguish cariogenic from non cariogenic pulmonary
edema. Clinical evaluation suggesting CHF may include the presence of elevated neck veins, displaced
apical pulse, lower extremity edema, bibasilar rales, an enlarged cardiac silhouette and/or prior
myocardial infarction evidenced on and electrocardiogram (ECG). Although these were manifested in our
patient, however, this was ruled out after the 2D echocardiogram.
Pulmonary embolism (PE) results from deep-vein thrombosis that have broken off and traveled to
the pulmonary arterial circulation. Tachypnea and tachycardia are common in PE. Low grade fever, neck
vein distention and a loud P2 on cardiac examination can be seen. Hypotension and cyanosis suggest
massive PE. Patient had elevated D-dimer level (3.1 mg/L), however, hospitalized patients often presents
with this due to other disease processes . Normal d-dimer level (<5 mg/mL by ELISA) essentially rules out
PE. Patient had elevated troponin (0.353 ng/mL) level which is associated with increased risk of
complications in PE. The ECG can show S1Q3T3 sign in PE, but that finding was not observed in this
patient. A normal chest x-ray is common. Chest CT with IV contrast has become the primary diagnostic
test for PE. Based on history, the patient did not have prolonged immobilization, long bone trauma nor
surgical operations and there were no clinical signs of thrombophlebitis, hence, PE is ruled out.
Patients with ARDS are at high risk for complications. Patients with ARDS are predisposed to
pulmonary barotrauma due to the physical stress of positive pressure mechanical ventilation on acutely
damaged alveolar membranes. It was previously common for patients with ARDS to develop single or
multiple, sequential, loculated pneumothoraces. Clinical experience suggests that such complications are
less common now that low tidal volume ventilation has become widespread. This is supported by the

observations that (a) low tidal volume ventilation reduces the plateau airway pressure and (b) a lower
plateau airway pressure is associated with a lower incidence of pulmonary barotrauma Nosocomial
pneumonia is an important cause of morbidity and mortality in patients who have ARDS. Other
complications are related to critical illness and being in the intensive care unit (eg, delirium, deep venous
thrombosis, gastrointestinal bleeding due to stress ulceration, and catheter-related infections) (HansenFlaschen & Siegel, 2015).
Pulmonary hypertension (PH), an abnormal elevation in pulmonary artery pressure, may be the
result of left heart failure, pulmonary parenchymal or vascular disease, thromboembolism, or a
combination of these factors. Whether the pulmonary hypertension arises from cardiac, pulmonary, or
intrinsic vascular disease, it generally is a feature of advanced disease. The right ventricle responds to an
increase in pulmonary vascular resistance by increasing right ventricular (RV) systolic pressure to
preserve cardiac output. Exertional dyspnea is the most common symptom attributable to pulmonary
hypertension. Other common symptoms are fatigue, angina pectoris, syncope, near syncope, and
peripheral edema. The physical examination typically reveals increased jugular venous pressure, a
reduced carotid pulse, and a palpable RV impulse. Most patients have an increased pulmonic component
of the second heart sound, a right-sided fourth heart sound, and tricuspid regurgitation. Peripheral
cyanosis and/or edema tend to occur in later stages of the disease. On chest x-ray, it shows an enlarged
central pulmonary artery. On ECG, it may demonstrate RV hypertrophy and RA enlargement.
Echocardiogram shows RV and RA enlargement; RV systolic pressure can be estimated from Doppler
recording of tricuspid regurgitation. A color flow doppler was done in our patient revealing increased
relative wall thickness of 0.5 with adequate contractility and systolic function, this translates to concentric
left ventricular remodeling. The course of ARDS and pulmonary vasoconstriction, which are potentially
reversible, act together to elevate pulmonary vascular resistance (PVR). These contribute to the structural
changes of the heart that is a sequelae of endothelial injury and repair (Ryan, 2014). In some patients,
chronic changes occur in the pulmonary circulation, resulting in progressive remodeling of the
vasculature, which can sustain or promote pulmonary hypertension even if the initiating factor is removed.
In addition to the findings of the color flow doppler, main pulmonary artery pressure by pulmonary
acceleration time was 35 mmHg. Severity of PH is based on these values: mean pulmonary artery
pressure (mPAP) >25 mmHg, moderate PH is mPAP between 30 and 45 mmHg and severe PH is mPAP
>45 mmHg. In the case of our patient, he has moderate pulmonary hypertension. Sepsis is a major risk
factor for ARDS development. It can also lead to severe acute arterial pulmonary hypertension, which
was manifested in our patient. The therapy of acute pulmonary hypertension in patients with sepsis and
ARDS is generally aimed at optimizing gas exchange and minimizing ventilator induced lung injury.
Inhaled pulmonary vasodilators are sometimes used in order to prevent or relieve acute cor pulmonale,
however this was not done in our patient.
Treatment
General care requires treatment of the underlying medical or surgical problem that caused lung
injury, minimizing iatrogenic complications, prophylaxis to prevent venous thromboembolism and
gastrointestinal hemorrhage, prompt treatment of infections, and adequate nutritional support. The patient
was in respiratory distress and was addressed with intubation. He was placed on mechanical ventilator on
volume control mode, TV of 430 mL (approximately 5.7 mL/PDW), FiO2 of 60% and PEEP of 6 cmH2O
with SpO2 range of 92-99%, where in the goal of oxygenation is achieved. It has been shown that
mechanical ventilation with low tidal volumes ( 6 mL/kg predicted body weight) provide reduced mortality
compared with higher today volumes (12 mL/kg predicted body weight) minimizing ventilator-induced lung
injury. In ARDs, alveolar collapse can occur due to alveolar/interstitial fluid accumulation and loss of
surfactant, thus worsening hypoxemia. This has been reduced by combining low tidal volume and use
positive end-expiratory pressure (PEEP) at levels that strive to minimize alveolar collapse and achieve
adequate oxygenation with the lower FIO2. Other techniques that may prove oxygenation while limiting

alveolar distention include extending the time of inspiration on the ventilator (inverse ratio ventilation) and
placing the patient in the prone position. However, these approaches are not of proven benefit in reading
mortality from ARDs. Patients are slowly weaned from ventilation, and follow with extubation trials. The
patient met the criteria: normothermic, hemodynamically stable, demonstrated satisfactory ventilation on
CPAP or T-piece, pH 7.35 ( no respiratory acidosis) and PaO2 > 80 mmHg with FiO2 50%, hence. the
patient was extubated on 8th day of hospitalization without complications.
Patients with ARDS have increased pulmonary vascular permeability leading to interstitial and
alveolar edema. Therefore, they should receive IV fluids only as needed to achieve adequate cardiac
output and tissue oxygen delivery as assed by urine output, acid-base status and arterial pressure. There
is no convincing evidence currently to support the use of glucocorticoids or nitric oxide in ARDS.
Mortality from ARDS has declined with improvements in general critical care treatment and with
the introduction of low tidal volume ventilation. Current mortality from ARDS is 41-65%, with most deaths
due to sepsis and non pulmonary organ failure. Increase risk of mortality from ARDS is associated with
advanced age, preexisting organ dysfunction (e.g. chronic liver disease, chronic immunosuppression,
chronic renal disease) and direct lung injury compared with indirect lung injury. Most surviving ARDS
patients do not have significant long-term pulmonary disability. Randomized trials showed reduction in the
mortality from 35 to 26 percent between 1996 and 2005. Many studies have showed factors during the
acute illness that predict mortality. Such factors can be categorized as patient-, disease-, or treatmentrelated. No single factor has proven to be superior to the others. Patient related factors includes age in
which older patients appear to be increased risk for death, illustrated in a multicenter cohort study
revealing a 24% among patients 15 to 19 years to 60% among 85 years of age or older. This compels the
patient having a slight increase in mortality being a 39 year old. Secondly, disease-related predictors of
mortality include severe hypoxemia present in the patient, failure of oxygenation to improve, pulmonary
vascular dysfunction, increased dead space, infection, a high severity of illness score, a non-traumatic
cause of the ARDS, and certain biomarkers and gene polymorphisms. Lastly, treatment-related predictors
of mortality include a positive fluid balance, glucocorticoid therapy prior to the onset of ARDS, packed red
blood cell transfusions, and being in an ICU that does not mandate care by an intensivist.
Survivors have are at risk of cognitive, psychologic, and physical morbidity. Cognitive dysfunction
following ARDS varies among studies, ranging from 30 to 55 percent. Psychiatric illnesses also appear to
be common among survivors of ARDS, with depression, anxiety, and post traumatic stress disorder as the
most common disorders reported. Survivors of ARDS frequently have persistent, abnormal exercise
endurance and physical disabilities. Furthermore, lung function following ARDS is commonly
compromised for as long as five years. However, it is uncertain whether decreased lung function results in
physical impairment. Upon discharge, approximately 80 percent of patients will have a reduction in
diffusing capacity and a smaller percentage will have airflow obstruction (20 percent) or restriction (20
percent) on spirometry and lung volumes. In most patients, lung volumes and spirometry will normalize
(ie, measure within 80 percent of predicted values) by six months, and diffusion capacity should normalize
by five years. A small percentage of patients are left with residual deficits and supplemental oxygen is
rarely required. Additional sequelae of ARDS include minor imaging abnormalities, as well as increased
risk of death, poor quality of life, and family stress (also known as post-intensive care syndrome-family).
Although most patients experience excellent radiologic recovery, at 180 days post diagnosis,
abnormalities persist in a significant minority and correlate with worse pulmonary function and quality of
life. Important predictors of death were the presence of comorbidities and discharge to another facility
(eg, hospital, long term acute care facility, nursing home, hospice). Despite these abnormalities, some
survivors are able to return to work (Siegel, 2014).

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