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Year : 2017  |  Volume : 18  |  Issue : 2  |  Page : 32-38

Acute respiratory distress syndrome: A case presentation

Junior Lecturer, College of Nursing, CMC, Vellore, India

Date of Web Publication9-Jun-2020

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Acute Respiratory Distress Syndrome (ARDS) is a major condition in an Intensive Care Unit. It was previously known as non-cardiogenic pulmonary edema. It is caused by various conditions due to damage to the lung, but the main reason is sepsis. It damages the alveolar capillary membrane that leads to interstitial and alveolar edema, diffuse alveolar damage, refractory hypoxemia, and ventilation perfusion mismatch. The common clinical manifestation is dyspnea with diffuse infiltration in chest X-ray. The management of ARDS includes setting low tidal volume, high Positive End Expiratory Pressure (PEEP) and low plateau pressure. Prone positioning will improve perfusion to the patient and thereby increase PaO2/FiO2 ratio. The recent trend of High Frequency Oscillation Ventilation (HFOV) is used to manage ARDS.

Keywords: Acute Respiratory Distress Syndrome, Acute Lung Injury, dyspnea, ventilation

How to cite this article:
Rajakumari A. Acute respiratory distress syndrome: A case presentation. Indian J Cont Nsg Edn 2017;18:32-8

How to cite this URL:
Rajakumari A. Acute respiratory distress syndrome: A case presentation. Indian J Cont Nsg Edn [serial online] 2017 [cited 2022 Dec 6];18:32-8. Available from: https://www.ijcne.org/text.asp?2017/18/2/32/286267

  Introduction Top

Acute Respiratory Distress Syndrome (ARDS) is a common condition that occurs among critically ill patients. It is a major condition where many patients do not survive due to refractory hypoxemia. The incidence and prevalence of ARDS varies widely. In United States the incidence is 64 to 78 cases per 1,00,000 population (Goss, Brower, Hudson, & Rubenfeld, 2003; Rubenfeld et al., 2005). The incidence in Northern Europe & Spain were 17 and 7.2 cases per 1, 00, 000 population (Luhr et al., 1999; Villar et al., 2011). The incidence of ARDS in Surgical ICU of a tertiary care centre in South India is 11.4% (Singh, Gladdy, Chandy, & Sen, 2014).

  Definition Top

ARDS was first defined by American-European Consensus Conference (AECC) in 1994. The Berlin definition in 2011 was established by European Society of Intensive Care Medicine, American Thoracic Society, and the Society of the Critical Care to enable physicians to effectively diagnose ARDS.

ARDS is defined by the onset of respiratory symptoms, radiographic changes such as bilateral opacities not fully explained by effusions, consolidation, or atelectasis, and origin of edema not fully explained by cardiac failure or fluid overload within one week of clinical insult (Force, 2012 ; Pneumatikos & Papaioannou, 2012).

  Severity of ARDS Top

The severity of ARDS is assessed based on the PaO2/FiO2 (P/F) ratio (Force, 2012). The normal PaO2/FiO2 ratio is 500. A higher ratio indicates better gas exchange. The P/F ratio reflects how well the lungs absorb oxygen from expired air (Helwick, 2009).

  • MildARDS - P/F ratio is between 200 to 300
  • Moderate ARDS - P/F ratio is between 100 to 200
  • Severe ARDS - P/F ratio is less than 100

  Etiology Top

The causes of ARDS include direct lung injury and indirect lung injury as given in [Table 1] (Pneumatikos, & Papaioannou, 2012; Urden, Stacy, & Lough, 2012).
Table 1: Causes of ARDS

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  Pathophysiology Top

There are four stages in the development of ARDS. The first stage is known as inflammatory stage. It occurs within first 12 hours of an insult/injury. Any direct or indirect injury to the lung stimulates the immune system to produce neutrophils, macrophages and platelets. These cells accumulate at the site of an injury in the lungs. Further, these cellular mediators initiate the humoral mediators Cytokines, Interleukin -1 Beta, Interleukin -6, Interleukin -10, Platelet Activating Factor (PAF), Granulocyte Macrophage-colony Stimulating Factor, Intercellular Adhesion Molecule-1, Substance P, Chemokines, Vasular Endothelial Growth Factor, Reactive Oxygen Species And Reactive Nitrogen Species causing damage to the alveolar capillary membrane (Bhatia & Moochhala, 2004). The second stage is called exudative stage. It occurs within 24 hours. The alveolar capillary membrane is formed by the micro-vascular endothelium and the epithelial lining of the alveoli. Injury to the micro-vascular endothelium and Type I alveoli cells leads to increased capillary permeability and influx of protein rich fluid into the alveolar space further leading to interstitial and alveolar edema. Injury to the Type II alveoli cells causes decreased production of surfactant. Surfactant plays a major role in maintaining compliance of the lung. Hence, decreased production of surfactant can cause decreased compliance of the lung leading to alveolar collapse. Further it worsens hypoxemia and leads to ventilation-perfusion mismatch (Harman, 2017).

The third stage is called fibro-proliferative stage. It starts from 2-10 days of the insult. The healing process takes place in this stage. The cellular granulation and collagen deposition takes place in the lung. The alveloli become large and irregular in shape and pulmonary capillaries are scarred and obliterated. The last stage is called remodelling/resolution stage. The intra-alveolar fluid is transported out of the alveolus into the interstitium and Type II alvelolar cells multiply and produce surfactant (Bellingan, 2002; Tomashefski, 1990; Urden et al, 2012).

  Clinical Manifestations Top

There are no specific clinical manifestations seen in ARDS, but the most common clinical manifestations are dyspnea, tachypnea, restlessness, apprehension, use of accessory muscles while breathing. On auscultation, decreased air entry and crackles will be heard (Morton, Fontaine, & Hudak, 2009). The patient suffers with general respiratory distress. If undetected and untreated this condition can progress to respiratory failure and death.

  Diagnostic Tests Top

Various investigations are done to confirm ARDS (Harman, 2017).

• History Collection

History will indicate that the patient has worsening dyspnea and will also reveal any direct or indirect lung injury.

• Physical Examination

There is no specific physical examination finding for ARDS. The patient will have tachypnea and tachycardia. If ARDS developed as a result of sepsis, the patient will be febrile and hypotensive. Auscultation of the lungs will reveal bilateral crackles and decreased air entry.
Figure 1: Pathophysiology of ARDS

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• Arterial Blood Gas (ABG)

Blood gas findings will show a decreased PaO2 and P/F ratio.

• Chest X-ray

Diffuse, patchy interstitial and alveolar infiltrates can be visualised in the chest X-ray

• Broncho-Alveolar Lavage (BAL)

It helps to differentiate from pulmonary eosinophilia. Presence ofneutrophils indicates ARDS.

• Echo Cardiography

Echo-cardiography will be generally normal. Left Ventricular Ejection Fraction is normal. It is done to make sure that the patient does not have any cardiac cause.

  Medical Management Top

The medical management includes general management, mechanical ventilation, prone positioning, and management with Extracorporeal and Intracorporeal Gas exchange.

General Management

The main medical management includes identifying and treating the cause such as sepsis due to intravascular lines, urinary catheters, draining abscess, debridement of necrotic tissue. If it is because of blood transfusions, the transfusion needs to be stopped. Vital signs such as temperature, pulse rate, respiratory rate, Arterial Blood Pressure (ABP), and Central Venous Pressure (CVP) or Pulse Pressure Variation (PPV) should be monitored closely. Antibiotics should be started based on culture and sensitivity report. Measures to prevent Deep Vein Thrombosis (DVT), Hospital Acquired Infections (HAI), and pressure ulcers should be put in place (Harman, 2017).

Mechanical Ventilation

The next important management in ARDS is mechanical ventilation. Many studies indicate that protective lung ventilation strategies will decrease the patient’s mortality. In mechanical ventilation, usually the tidal volume is set between 6 to 8 ml/kg, but for these patients the tidal volume should be less than 6 ml/kg to prevent Ventilator Associated Lung Injury (VALI) or Ventilator Induced Lung Injury (VILI) (The Acute Respiratory Distress Syndrome Network, 2000). The tidal volume is calculated based on predicted weight of the patient. The predicted weight depends on height and sex of the patient. The formula to calculate predicted weight for men is 50 + 0.91 (height -152.4cm) and for women is 45.5 + 0.91 (height - 152.4 cm) (John, Subramani, Peter, Pichamuthu, & Chacko, 2011). Permissive hypercapnia will help to maintain low tidal volume and prevent atelectrauma and biotrauma. Positive End Expiratory Pressure (PEEP) should be 10 to 15 cm of HO to prevent alveolar collapse, to stabilise alveoli and increase Functional Residual Capacity (FRC). Inspiratory Plateau Pressure (IPP) should be less than 30cm of H2O (Cordingley & Keogh, 2002; Walkey, Summer, Ho, & Alkana, 2012). Inverse Ratio Ventilation (IRV) is followed to prevent alveolar collapse and increase FRC, the ratio can be set as 2:1 or 3:1 depending on patients’ condition, but, it requires sedation with neuro muscular blockade to prevent from fighting against ventilator.

The other modes of ventilation such as Bi-level Positive Airway Pressure (BiPAP) and Airway Pressure Release Ventilation (APRV) can be used. In APRV mode, the upper and lower pressure can be set at pre-set time intervals; this improves ventilation perfusion matching. In BiPAP mode, inspiratory and expiratory pressure can be set to prevent alveolar collapse (Cordingley & Keogh, 2002). Pressure Control Ventilation (PCV) can be set to maintain inspiratory plateau pressure. The new trend is to have High Frequency Oscillatory Ventilation (HFOV) if patient does not improve on regular ventilation. HFOV uses a piston pump to deliver the lower tidal volumes at very high respiratory rates (Sud et al., 2010). HFOV also decreases mortality in these patients (Derdak et al., 2002)

Prone Positioning

Prone positioning will help in increasing perfusion to the non-consolidated regions of the lung. It also facilitates removal of secretions. The patient needs to be sedated and paralysed before proning, which can last from 30 minutes to 40 hours (John et al., 2011).

Extracorporeal and Intracorporeal Gas exchange

This is the last method used if the all other measures fail.

It is otherwise called as artificial lung or membrane/fiber oxygenator. There are three techniques involved in this method. They are Extra Corporeal Membrane Oxygenation (ECMO), Extra Corporeal Carbon dioxide Removal (ECCO2R) and Intra Vascular Oxygenation (IVOX) (Urden et al., 2012).

  Complications Top

Following are the complications due to high pressure and volume ventilation and some might be due to immobility and hospital acquired infections (Harman, 2017; Urden et al., 2012).

  • Barotrauma
  • Pneumomediastinum
  • Pneumothorax
  • Biotrauma
  • Atelectrauma
  • Cardiac dysrhythmias
  • Venous thromboembolism
  • Ventilator Associated Pneumonia
  • Pressure ulcer
  • Encephalopathy
  • Oxygen toxicity

  Nursing Management Top

The nursing management of a patient with ARDS is discussed using a case report.

Mrs. A, a 35 year old female came with the complaints of severe abdominal pain and vomiting for the past one year, was treated symptomatically and diagnosed to have choledocholithiasis and cholecystitis which progressed to acute pancreatitis. She had been admitted in her own town on numerous occasions. She became pregnant and after she delivered a girl baby, her condition worsened. She developed postpartum hemorrhage which worsened to Disseminated Intravascular Coagulation (DIC). She had been referred to a tertiary care centre for further management. In the Intensive Care Unit (ICU), she was transfused blood and blood products such as Packed Red Blood Cells (PRC), cryoprecipitate and Fresh Frozen Plasma (FFP) for deranged coagulation parameters. Her Glasgow Coma Scale (GCS) score was 2T/15. She was on Endotracheal Tube (ET) connected to mechanical ventilator under Synchronised Intermittent Mandatory Ventilation (P-SIMV) with the PEEP of10 cm ofH2O with FiO2 0.5. Her blood pressure was 90/60 mm Hg. Her weight was 60 kg and height was 160 cm. Serum amylase was 350U/L and serum lipase was 400 U/L. Once her condition stabilised, she underwent cholecystectomy.

Postoperatively her ABG revealed metabolic acidosis and P/F ratio was 146. She was started on Inj. Soda Bicarbonate infusion at 10ml/hr. Her hemoglobin level dropped to 6.5gm%. Whole blood was transfused. She was ventilated and was on SIMV mode and PEEP was increased to 12 cm of H2O, respiratory rate was set as 20 breaths/mt and the inspiratory time was 1:2. The WBC count was 25,000 /ccmm and BAL revealed presence of neutrophils. Her blood pressure dropped to 70 mm Hg systolic, so she was started on Inj. Nor-adrenaline at 5 mcg/min. In spite of mechanical ventilation, her P/F ratio did not improve. She was positioned in prone for 24 hours. She received Inj. Midazolam at 2mg/hr, Inj. Atracurium at 20 mg/hr. Intravenous infusion was maintained with 0.9% Normal Saline at 40 ml/hr and Total Parenteral Nutrition (TPN) at 20 ml/hr. These measures increased the BP to 100/60 mm of Hg and Hb to 8 gm%. With prone positioning, her P/F ratio also improved from 192 to 300 and later it increased to 400. She was weaned off from ventilator gradually such that she was on Adaptive Support Ventilation (ASV). She tolerated T-piece trial and was extubated from the ventilator. Once she was stabilised, she was transferred to the surgical ward and from there she was discharged home.

Nursing care of Mrs. A is discussed using the nursing process approach.

1. Nursing Diagnosis: Ineffective airway clearance related to pooling of trachea-bronchial secretions

Expected Outcome: She maintains patent airway as evidenced by equal air entry bilaterally and absence of secretions


Assessed the colour, amount and consistency of secretions. Found thick, copious and white colour sputum. On auscultation, bilateral equal air entry and bi-basilar crackles were heard. Performed chest physiotherapy and administered nebulization with Salbutamol 5mg over 6 hours to loosen secretions. Performed closed suctioning two hourly or whenever needed to remove secretions. Changed position every 2 hours to mobilise the secretions. Administered 0.9% Normal Saline infusion at 40ml/hr for adequate hydration.

Evaluation: She maintained a patent airway as evidenced by bilateral equal air entry during auscultation and absence of thick copious secretions.

2. Nursing Diagnosis: Impaired breathing pattern related to decreased energy and respiratory muscle fatigue

Expected Outcome: She maintains effective breathing pattern as evidenced by normal respiratory rate and breath sounds during auscultation


Assessed Respiratory Rate (RR), rhythm, depth and use of accessory muscles for breathing, and also the breath sounds for abnormal lung sounds. Initially, the RR was 32/mt, and she was using the sternocleidomastoid muscle and trapezus muscle for breathing. Crackles were heard on auscultation. ABG revealed metabolic acidosis. Her SpO2 was 90%. Maintained and adjusted the ventilator settings according to ABG values. Initially, she was on endotracheal tube connected to mechanical ventilator. She was on pressure support- SIMV mode with 50% FiO2 with pressure support of 22 cm of H O and PEEP of 10 cm of H O. Later, she was weaned from ventilator and maintained an effective breathing pattern. Administered TPN at 20ml/hr and later it was increased to 80 ml/hr to meet her energy requirements.

Evaluation: She maintained effective breathing pattern as evidenced by normal breath sounds, respiratory rate of 24/mt, SpO2 of 100% without mechanical ventilation.

3. Nursing Diagnosis: Impaired gas exchange related to ventilation perfusion mismatch

Expected Outcome: She maintains effective gas exchange as evidenced by P/F ratio more than 300, SpO2 more than 90%


Assessed her SpO2, SaO2, PaO2 levels and P/F ratio, SpO2 was 90%, SaO2 was 88%, PaO2 was 73 mm of Hg and P/F ratio was 146 initially. Maintained ET cuff pressure of 25 cm of Hg to prevent air leak. Maintained PEEP at 10 cm of H2O to open the alveoli to promote gas exchange. Positioned her prone for 24 hours to promote gas exchange. After prone positioning her P/F ratio improved to 192 which later improved to 400.

Evaluation: She maintained effective gas exchange as evidenced by a P/F ratio of400 and SpO2of 98%.

4. Nursing Diagnosis: Decreased cardiac output related to alterations in preload

Expected Outcome: She maintains optimal cardiac output as evidenced by blood pressure between 90 to 120 mm Hg systolic, heart rate of 60 to 100/mt, urine output 30 ml/hr


Assessed HR, BP, peripheral pulses, colour and temperature of the extremities, capillary refill time, blood loss during surgery and the hemoglobin level. Initially, HR was 166/mt, BP was 90/60 mm of Hg, peripheral pulses were weak and thready. Extremities were pale but warm to touch, capillary refill time was more than 3 seconds and the Hb was 6.5gm%. Assessed her general overall intake and output especially the wound drain. The wound drain was 500ml in the first 24 hrs post operatively. Crystalloids - 0.9% Normal Saline at 40 ml/hr and colloids namely blood and blood products were administered to maintain fluid balance. Inj. Noradrenaline 5mcg/mt was administered to increase the contractility of the heart. After these measures, the BP increased to 100/60 mm of Hg and the Hb increased to 8 gm%.

Evaluation: She maintained optimal cardiac output as evidenced by BP which increased to 100 /60 mm of Hg and with ionotropic support her HR was 90/mt and urine output was about 1900 ml in 24 hours.

5. Nursing Diagnosis: Altered nutrition less than body requirements related to lack of exogenous nutrients and increased metabolic demand

Expected Outcome: Her nutritional status is improved as evidenced by her tolerance to TPN


Assessed body weight, height, serum albumin levels and lymphocytes counts. Her weight was 60 kg, height was 160 cm and the serum albumin was 1.5 gm%. Her random blood sugar, was above 200gm/dl. So she was on continuous Insulin infusion and her blood sugar was monitored every two hours. As her albumin was low and energy requirements were high she was administered TPN. Administered TPN at 20 ml/hr and the rate was increased to 40 ml/hr and 80 ml/hr subsequently. Administered antiemetic Inj. Emeset 8mg every 8 hours to avoid vomiting.

Evaluation: Her nutritional status marginally improved as evidenced by tolerance to TPN and absence of hyperglycemia. She was transferred from ICU to the surgical ward.

  Conclusion Top

Protective lung ventilation will decrease the inflammatory response of the immune system and decrease mortality related to ARDS. Prone positioning enhances perfusion to the lung. Caring for a patient with ARDS is challenging yet rewarding for critical care nurses.

Conflicts of Interest: The author has declared no conflicts of interest.

  References Top

Bellingan, G. J. (2002). The pulmonary physician in critical care 6: The pathogenesis of ALI/ARDS. Thorax, 57(6), 540-546.  Back to cited text no. 1
Bhatia, M., & Moochhala, S. (2004). Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome. The Journal of Pathology, 202(2), 145-156.  Back to cited text no. 2
Cordingley, J. J., & Keogh, B. F. (2002). The pulmonary physician in critical care· 8: Ventilatory management of ALI/ARDS. Thorax, 57(8), 729-734.  Back to cited text no. 3
Derdak, S., Mehta, S., Stewart, T. E., Smith, T., Rogers, M., Buchman, T. G., … & Multicenter Oscillatory  Back to cited text no. 4
Ventilation for Acute Respiratory Distress Syndrome Trial (MOAT) Study Investigators. (2002). High- frequency oscillatory ventilation for acute respiratory distress syndrome in adults: A randomized, controlled trial. American Journal of Respiratory and Critical Care Medicine, 166(6), 801-808. doi.org/ 10.1164 /rccm.2108052  Back to cited text no. 5
Force, A. D. T. (2012). Acute respiratory distress syndrome. Jama, 307(23), 2526-2533. doi.org /10.1001/ jama.2012.5669  Back to cited text no. 6
Goss, C. H., Brower, R. G., Hudson, L. D., & Rubenfeld, G. D. (2003). Incidence of acute lung injury in the United States. Critical Care Medicine, 31(6), 1607-1611.  Back to cited text no. 7
Harman, M. E. (2017). Acute Respiratory Distress Syndrome: Background, pathophysiology, etiology. Medscape. Retrieved from http ://emedicine. medscape.com/article/165139-overview#showall  Back to cited text no. 8
Helwick, C. (2009). P/F Ratio may be a marker of potential intraoperative Ventilator-Induced Lung Injury. Retrieved from http://en. citizendium.org /wiki/P:F_ratio  Back to cited text no. 9
John, G., Subramani, K., Peter, J.V., Pichamuthu, K., & Chacko, B. (2011). Essentials of critical care. Vellore: Chummy Printers.  Back to cited text no. 10
Luhr, O. R., Antonsen, K., Karlsson, M., Aardal, S., Thorsteinsson, A., Frostell, C. G., … & ARF Study Group. (1999). Incidence and mortality after acute respiratory failure and acute respiratory distress syndrome in Sweden, Denmark, and Iceland. American Journal of Respiratory and Critical Care Medicine, 159(6), 1849-1861.  Back to cited text no. 11
Morton, P. G., Fontaine, D. K., & Hudak, C. M. (2009). Critical Care Nursing. A Holistic approach. China: Lippincott Williams & Wilkins.  Back to cited text no. 12
Pneumatikos, I., & Papaioannou, V. E. (2012). The new Berlin definition: What is, finally, the ARDS. Pneumon, 25(4), 365-368.  Back to cited text no. 13
Rubenfeld, G. D., Caldwell, E., Peabody, E., Weaver, J., Martin, D. P., Neff, M., … & Hudson, L. D. (2005). Incidence and outcomes of acute lung injury. New England Journal of Medicine, 353(16), 1685-1693.  Back to cited text no. 14
Singh, G., Gladdy, G., Chandy, T. T., & Sen, N. (2014). Incidence and outcome of acute lung injury and acute respiratory distress syndrome in the surgical intensive care unit. Indian Journal of Critical Care Medicine: Peer-Reviewed, Official Publication of Indian Society Of Critical Care Medicine, 15(10), 659  Back to cited text no. 15
Sud, S., Sud, M., Friedrich, J. O., Meade, M. O., Ferguson, N. D., Wunsch, H., & Adhikari, N. K. (2010). High frequency oscillation in patients with acute lung injury and acute respiratory distress syndrome (ARDS): Systematic review and meta-analysis. British Medical Journal, 340, c2327.  Back to cited text no. 16
The Acute Respiratory Distress Syndrome Network. (2000). Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. New England Journal of Medicine, 342(18), 1301-1308. doi.org/ 10.1056/NEJM200005043421801  Back to cited text no. 17
Tomashefski Jr, J. F. (1990). Pulmonary pathology of the adult respiratory distress syndrome. Clinics in Chest Medicine, 11(4), 593-619.1  Back to cited text no. 18
Urden, D.L., Stacy, M.K., & Lough, E.M. (2012). Critical Care Nursing: Diagnosis and Management. Missouri: Elsevier Publications.  Back to cited text no. 19
Villar, J., Blanco, J., Añón, J. M., Santos-Bouza, A., Blanch, L., Ambrós, A., … & Fernández, R. L. (2011). The ALIEN study: Incidence and outcome of acute respiratory distress syndrome in the era of lung protective ventilation. Intensive Care Medicine, 37(12), 1932-1941.  Back to cited text no. 20
Walkey, A. J., Summer, R., Ho, V., & Alkana, P. (2012). Acute respiratory distress syndrome: Epidemiology and management approaches. Clinical Epidemiology, 4, 159. doi.org/10.2147/CLEP.S28800  Back to cited text no. 21


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  [Table 1]


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