History

Fact Explanation
Introduction Adult respiratory distress syndrome(ARDS) is a condition characterized by acute inflammation of the lungs triggered by a pulmonary or an extrapulmonary insult. This cause bilateral and diffuse damage to the lung vascular endothelium and alveolar epithelium, causing a protein rich pulmonary edema, hyaline membrane formation, reduced lung compliance, difficult air exchange and acute respiratory failure. These occur in the absence of cardiac failure.[1][2][3][5]
History of a predisposing event The conditions that could predispose to (or associated with development of ARDS) could be either by direct lung injury or by indirect or extra pulmonary injury. Direct injury may result from pneumonia, inhalation injury, aspiration, pulmonary vasculitis, pulmonary contusion and drugs(e.g. bleomycin, opiates, salicylates) or oxygen toxicity. Indirect injury could occur by septic shock,amniotic/eat embolism, massive hemorrhage, massive burns, major trauma, acute pancreatitis etc.[1][2][3][4][5]
Progressive shortness of breath Acute onset rapidly progressive dyspnea associated with significant hypoxemia are diagnostic features of ARDS.[1][2][3]
Multi-organ failure ARDS is often associated with multi-organ failure.[1][2][3]
References
  1. SAGUIL A, FARGO M. Acute Respiratory Distress Syndrome: Diagnosis and Management. Am Fam Physician.[online] 2012 Feb 15;85(4):352-358.[viewed on 20 Oct 2014] Available from; http://www.aafp.org/afp/2012/0215/p352.html
  2. UDOBI KF, TOUIJER K. Acute Respiratory Distress Syndrome. Am Fam Physician. [online]2003 Jan 15;67(2):315-322.[viewed on 20 Oct 2014] Available from; http://www.aafp.org/afp/2003/0115/p315.html#sec-8
  3. SUMMERS C, SINGH NR, WHITE JF, MACKENZIE IM, JOHNSTON A, SOLANKI C, BALAN KK, PETERS AM, CHILVERS ER. Pulmonary retention of primed neutrophils: a novel protective host response, which is impaired in the acute respiratory distress syndrome. Thorax [online] 2014 Jul, 69(7):623-9 [viewed 20 October 2014] Available from: doi:10.1136/thoraxjnl-2013-204742
  4. WITCZAK A, PRYSTUPA A, KURYS-DENIS E, BORYS M, CZUCZWAR M, NIEMCEWICZ M, KOCIK J, MICHALAK A, PIETRZAK A, CHODOROWSKA G, KRUPSKI W, MOSIEWICZ J, TOMASIEWICZ K. Acute respiratory distress syndrome (ARDS) complicating influenza A/H1N1v infection--a clinical approach. Ann Agric Environ Med [online] 2013, 20(4):820-2 [viewed 20 October 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/24364461
  5. MATTHAY MA, WARE LB, ZIMMERMAN GA. The acute respiratory distress syndrome. J Clin Invest [online] 2012 Aug 1, 122(8):2731-40 [viewed 20 October 2014] Available from: doi:10.1172/JCI60331

Examination

Fact Explanation
General examination Patient will appear dyspnoeic. Can have elevated or reduced body temperature. Cyanosis may be seen in the lips, tongue and nail beds. Look for features of a predisposing cause. For e.g. Features of sepsis such as hypotension (refractory to resuscitation), warm peripheries, bounding peripheral pulse etc. and a site of infection, intravascular lines, drain sites, surgical wounds, signs of lung consolidation, features of suggestive of acute abdomen. [1][2]
Examination of respiratory system Patient will have tachypnea. Auscultation of lungs will elicit bilateral lung crackles due to pulmonary edema. If there is decreased breath sounds over one lung in a ventilated patient, look for pneumothorax or wrong placement of the endotracheal tube in the right main bronchus. Presence of subcutaneous air may suggest barotrauma.[1][2]
Examination of cardiovascular system Patient will have tachycardia. SIgns of congestive heart failure or that of intravascular volume overload, such as elevated jugular venous pressure, cardiac murmurs and gallops, peripheral edema etc. because these should be excluded as the cause for pulmonary edema.[1][2]
Examination of abdomen Look for features of acute abdomen such as abdominal distension,tenderness, guarding or rigidity etc. which may lead to the diagnosis of an intra-abdominal pathology which may have lead to the development of ARDS.[1][2]
References
  1. SAGUIL A, FARGO M. Acute Respiratory Distress Syndrome: Diagnosis and Management. Am Fam Physician.[online] 2012 Feb 15;85(4):352-358.[viewed on 20 Sep 2014] Available from; http://www.aafp.org/afp/2012/0215/p352.html
  2. UDOBI KF, TOUIJER K. Acute Respiratory Distress Syndrome. Am Fam Physician. [online]2003 Jan 15;67(2):315-322.[viewed on 20 Oct 2014] Available from; http://www.aafp.org/afp/2003/0115/p315.html#sec-8

Differential Diagnoses

Fact Explanation
Infectious Pneumonia These patients will have features such as productive cough, fever, pleuritic chest pain and sputum culture will be positive.[1][2]
Ventilator-Associated Pneumonia Patients who are provided with invasive ventilatory support are at risk of developing ventilator associated pneumonia. This can both predispose to and worsen ARDS.[1][2]
Hypersensitivity Pneumonitis Also called extrinsic allergic alveolitis. There is usually acute onset dyspnea, cough, chest tightness, wheeze etc following exposure to a trigger agent such as dust, bird feathers, molds etc.[1][2]
Congestive cardiac failure These patients also develop dyspnea due to pulmonary edema, but there will be additional findings such as elevated jugular venous pressure, peripheral edema, third heart sound, cardiomegaly and elevated plasma BNP level.[1][2]
Acute exacerbation of asthma There will be additional clinical signs such as presence of cough, wheeze, ronchi and response to bronchodilators.[1][2]
Septic Shock These patients will have fever or hypothermia, tachypnea, tachycardia, hypotension refractory to fluid resuscitation, warm peripheries, bounding peripheral pulse, oliguria, a positive septic screen with elevated or depressed white blood cell count.[1][2]
Drug toxicity History of suicide attempt, mental illness, drug abuse and clinical features of poisoning may direct towards this diagnosis.[1][2][3]
Acute lung injury This is characterized by presence of radiographic finding of acute diffuse bilateral lung infiltrates, hypoxemia with PaO2:FiO2 ratio<300 with no evidence of left atrial hypertension. The pathophysiology and etiology are similar to ARDS.[4]
References
  1. SAGUIL A, FARGO M. Acute Respiratory Distress Syndrome: Diagnosis and Management. Am Fam Physician.[online] 2012 Feb 15;85(4):352-358.[viewed on 20 Sep 2014] Available from; http://www.aafp.org/afp/2012/0215/p352.html
  2. UDOBI KF, TOUIJER K. Acute Respiratory Distress Syndrome. Am Fam Physician. [online]2003 Jan 15;67(2):315-322.[viewed on 20 Oct 2014] Available from; http://www.aafp.org/afp/2003/0115/p315.html#sec-8
  3. WENG CH, HU CC, LIN JL, LIN-TAN DT, HSU CW, YEN TH. Predictors of acute respiratory distress syndrome in patients with paraquat intoxication. PLoS One [online] 2013, 8(12):e82695 [viewed 20 October 2014] Available from: doi:10.1371/journal.pone.0082695
  4. JOHNSON ER, MATTHAY MA. Acute Lung Injury: Epidemiology, Pathogenesis, and Treatment J Aerosol Med Pulm Drug Deliv [online] 2010 Aug, 23(4):243-252 [viewed 20 October 2014] Available from: doi:10.1089/jamp.2009.0775

Investigations - for Diagnosis

Fact Explanation
Arterial blood gas analysis(ABG) Placement of an arterial line will be needed as regular ABG analysis should be done. ABG provides level of PaO2, FiO2, PaCO2, blood pH etc. which helps in the diagnosis, assessment for the need of ventilation and for monitoring progression of ARDS. A ratio of PaO2:FiO2 <200 is one of the diagnostic features of ARDS. Patients ABG analysis will show hypoxemia with respiratory alkalosis initially but with the rise of carbondioxide, the patient develops respiratory acidosis. If the ARDS is associated with sepsis there will be metabolic acidosis with or without partial respiratory compensation. [1][2][3][6]
Complete blood count Leukopenia or leukocytosis may be seen in patients with sepsis.[1][2][5]
Liver function tests Done to assess presence of any liver function abnormality which may worsen the clinical state of the patient.[1][2]
Plasma B-natriuretic peptide (BNP) Done to differentiate presence of cardiogenic pulmonary edema. BNP will be elevated in cardiogenic pulmonary edema.[1][2]
Chest X-ray(CXR) Will show bilateral diffuse lung infiltrates with ground glass appearance. CXR will also help to diagnose presence of pneumothorax and pneumomediastinum which can be complications of positive pressure ventilation.[1][2]
Computed tomography (CT) of chest Is indicated in some patients as it is more sensitive in detecting emphysema, pleural effusions, pneumomediastinum, lung cysts and pneumothoraces.[1][2][4]
2D-echocardiography Done when there is suspicion of cardiac failure.[1][2]
Pulmonary artery catheter monitoring Pulmonary artery catheter enables to measure pulmonary capillary wedge pressure(PCWP). PCWP <19mmHg with normal capillary oncotic pressure is seen in ARDS. [1][2]
Brochoscopy Helps to detect infection, alveolar hemorrhage, acute eosinophilic pneumonia etc. Culture material can be obtained by bronchoalveolar lavage (BAL) that can be analyzed for for for cell differential count, cytology, Gram stain, culture etc.[1][2][5]
Septic screen with blood/urine/sputum culture Done when there is suspicion of sepsis.[1][2]
References
  1. SAGUIL A, FARGO M. Acute Respiratory Distress Syndrome: Diagnosis and Management. Am Fam Physician.[online] 2012 Feb 15;85(4):352-358.[viewed on 20 Sep 2014] Available from; http://www.aafp.org/afp/2012/0215/p352.html
  2. UDOBI KF, TOUIJER K. Acute Respiratory Distress Syndrome. Am Fam Physician. [online]2003 Jan 15;67(2):315-322.[viewed on 20 Oct 2014] Available from; http://www.aafp.org/afp/2003/0115/p315.html#sec-8
  3. WITCZAK A, PRYSTUPA A, KURYS-DENIS E, BORYS M, CZUCZWAR M, NIEMCEWICZ M, KOCIK J, MICHALAK A, PIETRZAK A, CHODOROWSKA G, KRUPSKI W, MOSIEWICZ J, TOMASIEWICZ K. Acute respiratory distress syndrome (ARDS) complicating influenza A/H1N1v infection--a clinical approach. Ann Agric Environ Med [online] 2013, 20(4):820-2 [viewed 20 October 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/24364461
  4. OBADINA ET, TORREALBA JM, KANNE JP. Acute pulmonary injury: high-resolution CT and histopathological spectrum. Br J Radiol [online] 2013 Jul, 86(1027):20120614 [viewed 20 October 2014] Available from: doi:10.1259/bjr.20120614
  5. MCGUIRE WW, SPRAGG RG, COHEN AB, COCHRANE CG. Studies on the pathogenesis of the adult respiratory distress syndrome. J Clin Invest [online] 1982 Mar, 69(3):543-53 [viewed 20 October 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/7037851
  6. DICKSON RP. Mechanical ventilation of patients with and without ARDS: how far have we come? Respir Care [online] 2013 Apr, 58(4):712-4 [viewed 20 October 2014] Available from: doi:10.4187/respcare.02384

Investigations - Fitness for Management

Fact Explanation
Serum creatinine Done to assess renal function because these patients may develop acute renal failure most commonly due to acute tubular necrosis which requires renal replacement therapy. [1][2]
Electrocardiogram Done to detect arrhythmia, myocardial infarction etc. which cause sudden deterioration of a patient with ARDS.[1][2]
References
  1. UDOBI KF, TOUIJER K. Acute Respiratory Distress Syndrome. Am Fam Physician. [online]2003 Jan 15;67(2):315-322.[viewed on 20 Oct 2014] Available from; http://www.aafp.org/afp/2003/0115/p315.html#sec-8
  2. SAGUIL A, FARGO M. Acute Respiratory Distress Syndrome: Diagnosis and Management. Am Fam Physician.[online] 2012 Feb 15;85(4):352-358.[viewed on 20 Sep 2014] Available from; http://www.aafp.org/afp/2012/0215/p352.html

Investigations - Followup

Fact Explanation
APACHE II score This is a system devised to assess the severity of disease in patients admitted to the ICU as result of any disease. It takes a number of clinical signs and laboratory values in to count. This system can be used to assess the severity of ARDS patients admitted to the ICU. [1][2]
References
  1. SAGUIL A, FARGO M. Acute Respiratory Distress Syndrome: Diagnosis and Management. Am Fam Physician.[online] 2012 Feb 15;85(4):352-358.[viewed on 20 Sep 2014] Available from; http://www.aafp.org/afp/2012/0215/p352.html
  2. CAMPBELL NN, TOOLEY MA, WILLATTS SM. APACHE II scoring system on a general intensive care unit: audit of daily APACHE II scores and 6-month survival of 691 patients admitted to a general intensive care unit between May 1990 and December 1991. J R Soc Med [online] 1994 Feb, 87(2):73-77 [viewed 20 October 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1294319

Management - General Measures

Fact Explanation
Education of the patient/family Education regarding the nature of the disease, prognosis, available treatment options, importance of physiotherapy and pulmonary rehabilitation etc. should be done.[1][3]
Fluid Management/Cardiovascular support This is important in order to optimize oxygen delivery to tissues. Most patients with ARDS wil be hemodynamically compromised due to underlying causes. These patients benefit from fluid resuscitation. The aim should be to maintain a low normal intravascular volume whilst maintaining the mean arterial pressure and cardiac index. This is done to prevent worsening of capillary leakage due to over resuscitation which will further compromise oxygenation. Inotrope/ vasopressor treatment may be required depending on the patient's condition.[1][3][6]
Nutrition support Enteral feeding should be encouraged always. This is because when compared to parenteral feeding, it helps to maintain the integrity of the gut mucosa and is associated with lower risk of systemic sepsis. If the patient has been on prolonged ventilation or has multi-organ failure gastric stress ulcer prophylaxis with H2 receptor blockers should be considered. Delayed gastric emptying and reduced gut motility will respond to prokinetic drugs or may require nasojejunal feeding. Nutritional supplementation with initial total parenteral nutrition will be needed in severe cases of ARDS. [1][3][4]
Prophylaxis for venous thromboembolism Prolong immobilization leads to deep vein thrombosis and pulmonary thromboembolism. These patients may require prophylactic treatment to prevent these complications. There are methods of mechanical prophylaxis such as anti-embolism stockings , foot impulse devices, intermittent pneumatic compression devices or pharmacological prophylaxis with fondaparinux sodium, low molecular weight heparin(LMWH), unfractionated heparin (UFH) can be employed. These should be continue until the patient is no longer at increased risk of venous thromboembolism. [1][3][9]
Physiotherapy and lung function improvement Survivors of ARDS may have persistent functional disability after discharge from ICU. These may be of limitation to lung function and also extrapulmonary such as muscle wasting and weakness. Follow up of these patients with physiotherapy and pulmonary rehabilitation will help to improve their quality of life and also to recover with minimal residual limitations. [1][3][10]
Intubation/Tracheostomy Will be required if the patient needs prolonged mechanical ventilation. Both methods allow to establish a more stable airway which allows mobilization. If patient requires ventilation for a longer period or has difficulty weaning from the ventilator, tracheostomy can be considered.[8]
Treat underlying cause The main goal of treatment is to identify and treat the underlying cause while providing optimal support for organ failure. [1][3][5][6][7]
Corticosteroid treatment Treatment with low dose steroids has shown benefit for some patients in the acute stage. This is particularly seen in patients with ARDS due to sepsis. The value of this treatment is still under study. [1][2][3][6]
References
  1. SAGUIL A, FARGO M. Acute Respiratory Distress Syndrome: Diagnosis and Management. Am Fam Physician.[online] 2012 Feb 15;85(4):352-358.[viewed on 20 Sep 2014] Available from; http://www.aafp.org/afp/2012/0215/p352.html
  2. TAREK ALDABBAGH T, MILBRANDT EB, LINDEN A. Steroids in early ARDS? Critical Care. BioMed central Ltd.[online] 2007, 11: 308 (DOI 101186/cc5908) [viewed on 20 Oct 2014] Available from; http://www.biomedcentral.com/content/pdf/cc5908.pdf
  3. UDOBI KF, TOUIJER K. Acute Respiratory Distress Syndrome. Am Fam Physician. [online]2003 Jan 15;67(2):315-322.[viewed on 20 Oct 2014] Available from; http://www.aafp.org/afp/2003/0115/p315.html#sec-8
  4. KULICK D,DEEN D, Specialized Nutrition Support. Am Fam Physician.[online] 2011 Jan 15;83(2):173-183.[viewed on 20 Oct 2014] Available from; http://www.aafp.org/afp/2011/0115/p173.html
  5. DíAZ-ALERSI R, NAVARRO-RAMíREZ C. High or conventional positive end-expiratory pressure in adult respiratory distress syndrome. Med Intensiva [online] 2014 Jun-Jul, 38(5):311-4 [viewed 20 October 2014] Available from: doi:10.1016/j.medin.2013.09.007
  6. BOYLE AJ, MAC SWEENEY R, MCAULEY DF. Pharmacological treatments in ARDS; a state-of-the-art update. BMC Med [online] 2013 Aug 20:166 [viewed 20 October 2014] Available from: doi:10.1186/1741-7015-11-166
  7. DICKSON RP. Mechanical ventilation of patients with and without ARDS: how far have we come? Respir Care [online] 2013 Apr, 58(4):712-4 [viewed 20 October 2014] Available from: doi:10.4187/respcare.02384
  8. ALHAJHUSAIN A, ALI AW, NAJMUDDIN A, HUSSAIN K, AQEEL M, EL-SOLH AA. Timing of tracheotomy in mechanically ventilated critically ill morbidly obese patients. Crit Care Res Pract [online] 2014:840638 [viewed 20 October 2014] Available from: doi:10.1155/2014/840638
  9. National Clinical Guideline Centre – Acute and Chronic Conditions (UK). Venous Thromboembolism: Reducing the Risk of Venous Thromboembolism (Deep Vein Thrombosis and Pulmonary Embolism) in Patients Admitted to Hospital. London: Royal College of Physicians (UK); 2010. (NICE Clinical Guidelines, No. 92.) 2, Summary of recommendations. Available from: http://www.ncbi.nlm.nih.gov/books/NBK116536/
  10. One-Year Outcomes in Survivors of the Acute Respiratory Distress Syndrome. HERRIDGE M, CHEUNG AM, TANSEY CM, MARTYN AM, GRANADOS ND, SAIDI FA, COOPER AB, GUEST CB, MAZER CD, MEHTA SM, STEWART TE, BARR A, COOK D, SLUTSKY AS. N Engl J Med [online]2003; 348:683-693 February 20, 2003DOI: 10.1056/NEJMoa022450 [viewed on 23 Oct 2014] Available from; http://www.nejm.org/doi/full/10.1056/NEJMoa022450#t=articleDiscussion

Management - Specific Treatments

Fact Explanation
Intensive care unit(ICU)/ High dependency unit(HDU) care Almost all patients with ARDS will require admission to ICU/HDU. Make arrangement for this early. [1][2][4][5]
Ventilation These patients require respiratory support to improve gas exchange and correct hypoxia. Patients with ARDS will require a high oxygen concentration (provided with non-rebreather mask) and with reservoir FiO2 of 60-80% or continuous positive airway pressure. Non invasive Positive Pressure Ventilation (NIPPV) is prefered than mechanical ventilation due to the complications owing to intubation & other related procedures. NIPPV employs usage of different interfaces such as mouth piece or nasal, face, or helmet mask and different ventilatory modes such as volume support pressure support, bilevel positive airway pressure [BiPAP] , proportional-assist ventilation [PAV], continuous positive airway pressure [CPAP]. The patient with ARDS will require high FiO2, Low Vte (Tidal Volume) and high PEEP, which can be achived by CPAP. CPAP provides constant positive pressure through out the respiratory cycle and allows a higher FiO2, approaching 80-100%. It acts by opening the collapsing alveoli filled with fluid, increases the functional residual capacity and compliance so that the work of breathing is reduced and gas exchange is increased. Depending on the severity, mechanical or invasive ventilation methods will be adopted. Indications for mechanical ventilation include inadequate oxygenation with PaO2< 8kPa or FiO2> 0.6, PaCO2 level>6kPa, clinical signs of incipient respiratory/cardiovascular failure. Prolong high FiO2 (>65%) can cause further damage to lungs due to O2 radicals. Other preventable complication of mechanical ventilation include volutrauma and barotrauma. Volutrauma is damage caused to alveoli by the overdistention during mechanical ventilation with a ventilator set for an excessively high tidal volume. Barotrauma as the mane implies, refers to alveolar injury caused by increased alveolar pressure. These can be prevented in ARDS patients by using a low Vte and moderate/high PEEP during mechanical ventilation. [1][2][3][5][6][7][8][9][10]
References
  1. SAGUIL A, FARGO M. Acute Respiratory Distress Syndrome: Diagnosis and Management. Am Fam Physician.[online] 2012 Feb 15;85(4):352-358.[viewed on 20 Sep 2014] Available from; http://www.aafp.org/afp/2012/0215/p352.html
  2. UDOBI KF, TOUIJER K. Acute Respiratory Distress Syndrome. Am Fam Physician. [online]2003 Jan 15;67(2):315-322.[viewed on 20 Oct 2014] Available from; http://www.aafp.org/afp/2003/0115/p315.html#sec-8
  3. DíAZ-ALERSI R, NAVARRO-RAMíREZ C. High or conventional positive end-expiratory pressure in adult respiratory distress syndrome. Med Intensiva [online] 2014 Jun-Jul, 38(5):311-4 [viewed 20 October 2014] Available from: doi:10.1016/j.medin.2013.09.007
  4. BOYLE AJ, MAC SWEENEY R, MCAULEY DF. Pharmacological treatments in ARDS; a state-of-the-art update. BMC Med [online] 2013 Aug 20:166 [viewed 20 October 2014] Available from: doi:10.1186/1741-7015-11-166
  5. DICKSON RP. Mechanical ventilation of patients with and without ARDS: how far have we come? Respir Care [online] 2013 Apr, 58(4):712-4 [viewed 20 October 2014] Available from: doi:10.4187/respcare.02384
  6. KUCHNICKA K, MACIEJEWSKI D. Ventilator-associated lung injury. Anaesthesiol Intensive Ther [online] 2013 Jul-Sep, 45(3):164-70 [viewed 20 October 2014] Available from: doi:10.5603/AIT.2013.0034
  7. David C. CHAO DC, SCHEINHORN DJ. Barotrauma vs Volutrauma. Chest.[online] 1996;109(4):1127-1128.[viewed on 20 Oct 2014] doi:10.1378/chest.109.4.112. Available from; http://journal.publications.chestnet.org/article.aspx?articleid=1069640
  8. SLUTSKY AS. Ventilator-induced lung injury: from barotrauma to biotrauma. Respir Care [online] 2005 May, 50(5):646-59 [viewed 14 October 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/15912625
  9. ALBAICETA GM, BLANCH L. Beyond volutrauma in ARDS: the critical role of lung tissue deformation. Critical Care[online] 2011, 15:304 [viewed on 20 Oct 2014] Available from; http://ccforum.com/content/15/2/304
  10. KEOGH BF, RANIERI VM. Ventilatory support in the acute respiratory distress syndrome. Br Med Bull [online] 1999, 55(1):140-64 [viewed 20 October 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/10695084