acute respiratory distress syndrome

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Related to acute respiratory distress syndrome: Acute Respiratory Failure


1. sharp.
2. having severe symptoms and a short course. Some serious illnesses that were formerly considered acute (such as myocardial infarction) are now recognized to be acute episodes of chronic conditions.
acute care the level of care in the health care system that consists of emergency treatment and critical care. Called also secondary care.
acute coronary syndrome a classification encompassing clinical presentations ranging from unstable angina through myocardial infarctions not characterized by alterations in Q waves; the classification sometimes also includes myocardial infarctions characterized by altered Q waves.
acute respiratory distress syndrome (ARDS) a group of symptoms accompanying fulminant pulmonary edema and resulting in acute respiratory failure; called also shock lung, wet lung, and many other names descriptive of etiology or clinical manifestations. Many etiologic factors have been associated with ARDS, including shock, fat embolism, fluid overload, oxygen toxicity, fluid aspiration, narcotic overdose, disseminated intravascular coagulation, multiple transfusions, inhalation of toxic gases, diffuse pulmonary infection, and systemic reactions to sepsis, pancreatitis, and massive trauma or burns.

ARDS is characterized clinically by dyspnea, tachypnea, tachycardia, cyanosis, and hypoxemia. PaO2/FIO2 remains low (below 2 cc) even with oxygen therapy at high oxygen concentrations. The lung compliance is decreased so that the lung is stiffer and more difficult to ventilate. Chest radiographs show signs of bilateral interstitial and alveolar edema. Cardiac filling pressures are normal, and the pulmonary capillary wedge pressure is below 18 torr.

Most authorities consider that the syndrome has three phases or stages that characterize its progression: the exudative stage, the fibroproliferative or proliferative stage, and the resolution or recovery stage. The exudative stage comes first, two to four days after onset of lung injury, and is distinguished by the accumulation of excessive fluid in the alveoli with entrance of protein and inflammatory cells from the alveolar capillaries into the air spaces. The fibroproliferative stage comes second and is characterized by an increase in connective tissue and other structural elements in the lungs in response to the initial injury. It begins between the first and third weeks after the initial injury and may last up to ten weeks. Microscopic examination reveals lung tissue that appears densely cellular. The patient is at risk for pneumonia, sepsis, and pneumothorax at this time. The third stage is the resolution or recovery stage. During this stage the lung reorganizes and recovers, although it continues to show signs of fibrosis. Lung function may continue to improve for as long as six to twelve months or even longer, depending on the precipitating condition and severity of the injury. It is important to remember that there are often different levels of pulmonary recovery in patients with ARDS.

Some authorities refer to a fourth phase or stage of ARDS, the period after the resolution or recovery stage. Some patients continue to experience health problems caused by the acute illness, such as coughing, limited exercise tolerance, and fatigue. Anxiety, depression, and flashback memories of the critical illness may also occur and be similar to posttraumatic stress disorder.
Treatment and Patient Care. Mechanical ventilation must be begun at the first signs of hyperventilation and hypoxemia, before obvious signs of respiratory distress develop. A cuffed endotracheal tube or tracheostomy tube is used to maintain an airway. The patient is ventilated at the lowest oxygen concentration that maintains the arterial oxygen saturation (SaO2) at 90 per cent. positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) may be used to increase the number of alveoli that remain open at the end of exhalation and thus decrease pulmonary shunt. hemodynamic monitoring, using a swan-ganz catheter, is done to measure cardiac output, pulmonary capillary wedge pressure, and right atrial wedge pressure. An arterial line is placed to continuously monitor blood pressure and measure arterial blood gases. A diuretic such as furosemide (Lasix) may be administered to reduce fluid volume overload and pulmonary edema. If infection develops, antibiotics are administered. Hemodynamic parameters, arterial blood gas levels, intake and output, breath sounds, vital signs, inspiratory pressure, tidal volume, inspired oxygen concentration, and end-expiratory pressure are all continuously monitored.
acute situational reaction a transient, self-limiting acute emotional reaction to severe psychological stress. See acute stress disorder, adjustment disorder, posttraumatic stress disorder, and brief reactive psychosis.
acute stress disorder an anxiety disorder characterized by development of anxiety, dissociation, and other symptoms within one month following exposure to an extremely traumatic event, the symptoms including reexperiencing the event, avoidance of trauma-related stimuli, anxiety or increased arousal, and some or all of the following: a subjective sense of diminished emotional responsiveness, numbing, or detachment, derealization, depersonalization, and amnesia for aspects of the event. If persistent, it may become posttraumatic stress disorder.
acute stress reaction acute situational reaction.


pertaining to respiration.
acute respiratory distress syndrome (adult respiratory distress syndrome) a group of symptoms accompanying fulminant pulmonary edema and resulting in acute respiratory failure; see also acute respiratory distress syndrome.
respiratory care
1. the health care profession providing, under qualified supervision, diagnostic evaluation, therapy, monitoring, and rehabilitation of patients with cardiopulmonary disorders; it also employs educational activities to support patients and their families and to promote cardiovascular health among the general public.
2. the care provided by members of this profession.
3. the diagnostic and therapeutic use of medical gases and their administering apparatus, environmental control systems, humidification, aerosols, medications, ventilatory support, bronchopulmonary drainage, pulmonary rehabilitation, cardiopulmonary resuscitation, and airway management.
respiratory distress syndrome, neonatal (respiratory distress syndrome of the newborn (RDS)) a condition of the newborn marked by dyspnea with cyanosis, heralded by such prodromal signs as dilatation of the nares, grunting on exhalation, and retraction of the suprasternal notch or costal margins. It usually occurs in newborns who are preterm, have diabetic mothers, or were delivered by cesarean section; sometimes there is no apparent predisposing cause.

This is the major cause of death in neonates and survivors have a high risk for chronic neurologic complications. No one factor is known to cause the condition; however, prematurity and interrupted development of the surfactant system is thought to be the major causative factor. Surfactant is secreted by the epithelial cells of the alveoli. It acts as a detergent, decreasing the surface tension of fluids that line the alveoli and bronchioles and allowing for uniform expansion of the lung and maintenance of lung expansion. When there is an inadequate amount of surfactant, a great deal of effort is required to re-expand the alveoli with air; thus the newborn must struggle for each breath. Insufficient expansion of the alveoli results in partial or complete collapse of the lung (atelectasis). This in turn produces hypoxemia and elevated serum carbon dioxide levels.

The hypoxemia causes metabolic acidosis from increased production of lactic acid and respiratory acidosis due to the hypercapnia. The lowered pH constricts pulmonary blood vessels and inhibits intake of oxygen, thus producing more hypoxemia and interfering with the transport of substances necessary for the production of the sorely needed surfactant.
Patient Care. In order to minimize the hazards of oxygen toxicity and retinopathy of prematurity, the blood gases of the newborn with respiratory distress syndrome must be carefully monitored to assess response to therapy. The goal is to administer only as much oxygen as is necessary to maintain an optimal level of oxygenation.

To improve respiratory function, intubation, suctioning of the air passages, and continuous positive airway pressure via nasal prongs are commonly used, as well as instillation of artificial surfactant. Monitoring is conducted using transcutaneous oxygen monitoring or a pulse oximeter. To optimize breathing effort and facilitate air exchange, the newborn is positioned on the back with a shoulder support to keep the neck slightly extended, or on the side with the head supported. Because of the drying effect of oxygen therapy and the prohibition of oral fluids, mouth care must be given frequently to prevent drying and cracking of the lips and oral mucosa.
respiratory failure a life-threatening condition in which respiratory function is inadequate to maintain the body's need for oxygen supply and carbon dioxide removal while at rest; it usually occurs when a patient with chronic airflow limitation develops an infection or otherwise suffers an additional strain on already seriously impaired respiratory functions. Inadequate or unsuccessful treatment of respiratory insufficiency from a variety of causes can lead to respiratory failure. Called also ventilatory failure.

Early symptoms include dyspnea, wheezing, and apprehension; cyanosis is rarely present. As the condition worsens the patient becomes drowsy and mentally confused and may slip into a coma. blood gas analysis is an important tool in diagnosing respiratory failure and assessing effectiveness of treatment. The condition is a medical emergency that can rapidly progress to irreversible cardiopulmonary failure and death. Treatment is concerned with improving ventilation and oxygenation of tissues, restoring and maintaining fluid balance and acid-base balance, and stabilizing cardiac function.
respiratory insufficiency a condition in which respiratory function is inadequate to meet the body's needs when increased physical activity places extra demands on it. Insufficiency occurs as a result of progressive degenerative changes in the alveolar structure and the capillary tissues in the pulmonary bed, as, for example, in chronic airflow limitation and pulmonary fibrosis. Treatment is essentially supportive and symptomatic. If the condition is not successfully managed it may progress to respiratory failure.
respiratory therapist a health care professional skilled in the treatment and management of patients with respiratory problems, who administers respiratory care. The minimum educational requirement is an associate degree, providing knowledge of anatomy, physiology, pharmacology, and medicine sufficient to serve as a supervisor and consultant. Those registered by the National Board for Respiratory Therapy are designated Registered Respiratory Therapist (RRT).
respiratory therapy respiratory care.
respiratory therapy technician a health care professional who has completed a specialized one- or two-year educational program and who performs routine care, management, and treatment of patients with respiratory problems under the supervision of a respiratory therapist. Such programs are usually found in community colleges and are accredited by the Joint Review Committee for Respiratory Therapy Education.
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

a·dult res·pi·ra·to·ry dis·tress syn·drome (ARDS),

acute lung injury from a variety of causes, characterized by interstitial or alveolar edema and hemorrhage as well as perivascular pulmonary edema associated with hyaline membrane formation, proliferation of collagen fibers, and swollen epithelium with increased pinocytosis.
Farlex Partner Medical Dictionary © Farlex 2012

a·dult res·pi·ra·to·ry dis·tress syn·drome

(ARDS) (ă-dŭlt' res'pir-ă-tōr-ē dis-tres' sin'drōm)
Disorder with rapid onset of progressive malfunction of the lungs usually associated with malfunction of other organs attributable to inability to take in oxygen. Condition is associated with extensive injury to the alveolar capillary membrane, lung inflammation, and small blood vessel injury in affected organs.
Synonym(s): acute respiratory distress syndrome, wet lung (2) , white lung.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012

Acute Respiratory Distress Syndrome

DRG Category:189
Mean LOS:5.2 days
Description:MEDICAL: Pulmonary Edema and Respiratory Failure
DRG Category:207
Mean LOS:14.6 days
Description:MEDICAL: Respiratory System Diagnosis with Ventilator Support 96+ Hours
DRG Category:208
Mean LOS:7 days
Description:MEDICAL: Respiratory System Diagnosis with Ventilator Support < 96 Hours
DRG Category:3
Mean LOS:34.5 days
Description:SURGICAL: Tracheostomy with MV 96+ Hours or Primary Diagnosis Except for Face, Mouth, and Neck with Major Operating Room

The term adult respiratory distress syndrome (ARDS) was first coined by Ashbaugh and Petty in 1971. Previously, terms such as stiff lung, wet lung, shock lung, adult hyaline-membrane disease, and others were used to describe this syndrome that occurs after catastrophic events such as major surgical procedures, serious injuries, or other critical illnesses. In 1992, the American-European Consensus Conference on ARDS recommended changing the name back to what Ashbaugh and Petty originally named it in 1967, acute respiratory distress syndrome, because this condition affects children, teenagers, and adults.

ARDS, the most severe form of acute lung injury, is defined as noncardiogenic pulmonary edema that occurs despite low to normal pressures in the pulmonary capillaries. Many theories and hypotheses are currently under investigation. Patients with ARDS are characterized as having high-permeability pulmonary edema (HPPE) in contrast to cardiogenic pulmonary edema. In ARDS, the alveolar-capillary membrane is damaged, and both fluid and protein leak into the interstitial space and alveoli. Recent research has focused on possible mediators of the membrane damage, such as neutrophils, tumor necrosis factor (TNF), bacterial toxins, and oxygen free radicals, among others. The onset of symptoms generally occurs within 24 to 72 hours of the original injury or illness.

As ARDS progresses, patients exhibit decreased lung volumes and markedly decreased lung compliance. Type II pneumocytes, the cells responsible for surfactant production, are damaged. This deficiency is thought to be partly responsible for the alveolar collapse and the decrease in lung volumes that occur. In addition, fibroblasts proliferate in the alveolar wall, migrate into the intra-alveolar fluid, and ultimately convert the exudate (fluid with high concentration of protein and cellular debris) into fibrous tissue. Refractory hypoxemia occurs as the lungs are perfused but not ventilated (a condition called capillary shunting) owing to the damage to the alveoli and developing fibrosis. As ARDS progresses, respiratory failure and cardiopulmonary arrest can develop.


Various conditions can predispose a patient to ARDS, but they usually represent a sudden catastrophic situation. These conditions can be classified into two categories: direct lung injury and indirect lung injury. Direct injury occurs from situations such as gastric aspiration, near drowning, chemical inhalation, and oxygen toxicity. Indirect injury occurs from mediators released during sepsis, multiple trauma, thermal injury, hypoperfusion or hemorrhagic shock, disseminated intravascular coagulation, drug overdose, and massive blood transfusions. The most common risk factor for ARDS is sepsis from an abdominal source. Approximately 150,000 new cases of ARDS occur each year. Mortality rates vary and have been estimated to be between 40% and 50%, but older patients and patients with severe infections have a higher rate. Survivors generally have almost normal lung function a year after the acute illness.

Genetic considerations

There may be genetic factors that influence both susceptibility and progression of ARDS. Survivors are more likely than nonsurvivors to have certain alleles of the genes that code for angiotensin-converting enzyme (ACE) and interleukin (IL)-6.

Gender, ethnic/racial, and life span considerations

ARDS can occur equally across genders and at any age, including during childhood, to those who have been subjected to severe physiological stresses such as sepsis, burns, or trauma. Ethnicity and race have no known effects on the risk for ARDS.

Global health considerations

People who live in developing nations without well-developed emergency medical systems may not survive the initial insult, and therefore ARDS may not occur. If critical care is not available to manage ARDS, mortality will be very high. In Europe, investigators have reported an incidence of 17.9 cases per 100,000 individuals for acute lung injury and 13.5 cases per 100,000 individuals for ARDS.



The patient with ARDS appears in acute respiratory distress with a marked increase in the work of breathing that may lead to nasal flaring, the use of accessory muscles to breathe, and profound diaphoresis. The respiratory rate may be more than 30 to 40 breaths per minute. If ARDS has progressed, the patient may have a dusky appearance with cyanosis around the lips and nailbeds, or the patient may be very pale. Hypoxemia usually leads to restlessness, confusion, agitation, and even combative behavior.

Physical examination

Palpation of the peripheral pulses reveals rapid, sometimes thready, pulses. Blood pressure may be normal or elevated initially and then decreased in the later stages. Auscultation of the lungs differs depending on the stage of ARDS. In the early stage, the lungs have decreased breath sounds. In the middle stages of ARDS, the patient may have basilar crackles or even coarse crackles. In the late stage of ARDS, if the disease has been left untreated, the patient may have bronchial breath sounds or little gas exchange with no breath sounds. If airway and breathing are not maintained, the patient becomes fatigued and apneic. When the patient is intubated and mechanically ventilated, the lungs may sound extremely congested, with wheezes and coarse crackles throughout.

Diagnosis involves excluding other causes of acute respiratory failure. A consensus conference has defined ARDS as having the following features: acute bilateral lung infiltrates, a ratio of Pao2 to inspired oxygen concentration (Fio2) of less than 200, and no evidence of heart failure or volume overload.


Patients may exhibit anxiety and fear because of hypoxemia and the real threat of death. Feelings of social isolation and powerlessness can occur as the patient is placed on mechanical ventilation and is unable to verbalize.

Diagnostic highlights

General Comments: The diagnosis of ARDS can be controversial and is one of exclusion. There are no specific markers that identify alveolar-capillary membrane damage. Early in ARDS, the pH is elevated and the Paco2 is decreased because of hyperventilation. In the later stages, the Paco2 is elevated and the pH is decreased. Other supporting tests include pulmonary function tests, pulse oximetry, and pulmonary capillary wedge pressure.

TestNormal ResultAbnormality With ConditionExplanation
Chest x-rayClear lung fieldsDiffuse bilateral infiltrates without cardiomegaly or pulmonary vascular redistributionFindings reflect noncardiogenic pulmonary edema
Arterial blood gases (ABGs)Pao2 80–100 mm Hg; Paco2 35–45 mm Hg; SaO2 > 95%Pao2 < 80 mm Hg; Paco2 varies; SaO2 < 95%Poor gas exchange leads to hypoxemia and, as respiratory failure progresses, to hypercapnea

Primary nursing diagnosis


Impaired gas exchange related to increased alveolar-capillary permeability, interstitial edema, and decreased lung compliance


Respiratory status: Gas exchange; Respiratory status: Ventilation; Comfort level; Anxiety control


Airway insertion and stabilization; Airway management; Respiratory monitoring; Oxygen therapy; Mechanical ventilation; Anxiety reduction

Planning and implementation


mechanical ventilation.
The treatment for ARDS is directed toward the underlying cause and maintaining gas exchange. To this end, almost all patients with ARDS require endotracheal intubation and mechanical ventilation with a variety of positive-pressure modes. Common methods for mechanical ventilation include pressure-controlled ventilation with an inverse inspiratory-expiratory ratio. This mode alters the standard inspiratory-expiratory ratio of 1:2 to 1:3 by prolonging the inspiratory rate and changing the ratio to 1:1. It also controls the amount of pressure in each breath to stabilize the alveoli and to reestablish the functional residual capacity (FRC) to normal levels. If possible, the physician attempts to limit the fraction of inspired oxygen (Fio) to less than 0.50 (50%) to reduce complications from oxygen toxicity. Positive end-expiratory pressure (PEEP) is often added to the ventilator settings to increase the FRC and to augment gas exchange. Lung-protective, pressure-targeted ventilation, a method whereby controlled hypoventilation is allowed to occur, minimizes the detrimental effects of excessive airway pressures and has also been used in ARDS with positive outcomes.

Pharmacologic highlights

General Comments: Use of genetically engineered surfactant has been studied in ARDS but has not demonstrated the success that has occurred in premature infants with surfactant deficiency. Although high- and low-dose corticosteroids have been used in ARDS, studies have not demonstrated improvement in patient outcomes and their use remains controversial. Simvastatin, a hydroxymethylglutaryl-coenzyme A reductase inhibitor, may improve oxygenation and respiratory mechanics in some patients. If the patient is difficult to ventilate, she or he may receive skeletal muscle relaxants such as cisatracurium (Nimbex) or vecuronium (Norcuron), which are neuromuscular-blocking agents that paralyze the patient’s skeletal muscles. These medications are used only when the patient’s gas exchange is so poor as to threaten his or her life. Neuromuscular-blocking agents paralyze the patient without affecting mental status, so the patient requires sedation to counteract the accompanying fear and anxiety that occur when the patient is unable to move.

Medication or Drug ClassDosageDescriptionRationale
Nitric oxideInhalation route; dosage variedPulmonary vascular vasodilatorDecreases pulmonary vascular resistance with increased perfusion to ventilated areas; no long-term outcome benefit has been observed, but it may improve oxygenation temporarily


To augment gas exchange, the patient needs endotracheal suctioning periodically. Prior to suctioning, hyperventilate and hyperoxygenate the patient to prevent the ill effects of suctioning, such as cardiac dysrhythmias or hypotension. Turn the patient as often as possible, even every hour, to increase ventilation and perfusion to all areas of the lung. If the patient has particularly poor gas exchange, consider a rocking bed that constantly changes the patient’s position. Prone position may improve oxygenation in selected patients. If the patient’s condition allows, get the patient out of bed for brief periods, even if he or she is intubated and on a ventilator. Evaluate the patient’s condition to determine if soft restraints are appropriate. Although restraints are frustrating for the patient, they may be necessary to reduce the risk of self-extubation.

If the patient requires medications for skeletal muscle paralysis, provide complete care and make sure the medical management includes sedation. Use artificial tears to moisten the patient’s eyes because the patient loses the blink reflex. Provide passive range-of-motion exercises every 8 hours to prevent contractures. Reposition the patient at least every 2 hours for comfort and adequate gas exchange and to prevent skin breakdown. Provide complete hygiene, including mouth care, as needed. Assist the patient to conserve oxygen and limit oxygen consumption by spacing all activities, limiting interruptions to enhance rest, and providing a quiet environment.

The patient and family are likely to be fearful and anxious. Acknowledge their fear without providing false reassurance. Explain the critical care environment and technology but emphasize the importance of the patient’s humanness over and above the technology. Maintain open communication among all involved. Answer all questions and provide methods for the patient and family to communicate, such as a magic slate or point board.

Evidence-Based Practice and Health Policy

Schmidt, M., Zogheib, E., Roze, H., Repesse, X., Lebreton, G., Luyt, C., …Combes, A. (2013). The PRESERVE mortality risk score and analysis of long-term outcomes after extracorporeal membrane oxygenation for severe acute respiratory distress syndrome. Intensive Care Medicine, 39(10), 1704–1713.

  • Mortality rates for ARDS exceed 50%, and those who survive experience persistent physical, functional, and psychological impairments.
  • Mechanical ventilation with extracorporeal membrane oxygenation (ECMO) has been proposed as protective against ventilator-induced lung injury; however, identifying patients who would most benefit in the long term from this highly specialized and costly intervention is encouraged.
  • Investigators of one study among 140 ARDS patients who received ECMO developed an algorithm to predict death for severe ARDS posttreatment with ECMO (PRESERVE) using eight pre-ECMO parameters including age, body mass index, immunocompromised status, prone positioning, days of mechanical ventilation, sepsis-related organ failure assessment, plateau pressure, and positive end-expiratory pressure.
  • The PRESERVE algorithm predicted survival probabilities of 97%, 79%, 54%, and 16% for score ranges from 0 to 2, 3 to 4, 5 to 6, and ≥ 7, respectively (p < 0.001) for ARDS patients who received ECMO.

Documentation guidelines

  • Respiratory status of the patient: respiratory rate, breath sounds, and the use of accessory muscles; ABG levels; pulse oximeter and chest x-ray results
  • Response to treatment, mechanical ventilation, immobility, and bedrest
  • Presence of any complications (depends on the precipitating condition leading to ARDS)

Discharge and home healthcare guidelines

Prompt attention for any infections may decrease the incidence of sepsis, which can lead to ARDS.

If patients survive ARDS, few residual effects are seen. Complications are directed to any other conditions the patient may have.

Diseases and Disorders, © 2011 Farlex and Partners
References in periodicals archive ?
ARDS Berlin definition The Berlin definition of acute respiratory distress syndrome Timing Within I week of a known clinical insult or new or worsening respiratory symptoms Chest imaging (a) Bilateral opacities-not fully explained by efusions, lobar/lung collapse, or nodules Origin of edema Respiratory failure not fully explained by cardiac failure or fluid overload.
Increased levels ofsoluble receptor for advanced glycation end products (sRAGE) and high mobility group box 1 (HMGB1) are associated with death in patients with acute respiratory distress syndrome. Clin Biochem 2011; 4: 601-604, doi: 10.1016/j.clinbiochem.2010.12.014.
Mass Spectrometry-based Proteomics in Acute Respiratory Distress Syndrome: A Powerful Modality for Pulmonary Precision Medicine.
Early predictive factors of survival in the acute respiratory distress syndrome. A multivariate analysis.
Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med.
Tatum, "Acute respiratory distress syndrome incidence, but not mortality, has decreased nationwide: a National Trauma Data Bank study," The American Surgeon, vol.
(28.) Parsons PE, Matthay MA, Ware LB, Eisner MD; National Heart, Lung, Blood Institute Acute Respiratory Distress Syndrome Clinical Trials Network.
Acute respiratory distress syndrome (ARDS) is an inflammatory condition characterized by pulmonary edema, hypoxia, and massive influx of inflammatory cells as per the American Thoracic Society (ATS) guidelines.
Morais, "Noninvasive ventilation for acute respiratory distress syndrome: the importance of ventilator settings," Journal of Thoracic Disease, vol.
Emergent severe acute respiratory distress syndrome caused by adenovirus type 55 in immunocompetent adults in 2013: a prospective observational study.
These complications include shock, severe anaemia secondary to haemolysis, acute renal and hepatic failure, seizures and very rarely the acute respiratory distress syndrome (ARDS).4 It has been hypothesized that ARDS is secondary to an exacerbated inflammatory response after commencement of anti-malarial therapy.5 Extremely rarely, however, ARDS may develop prior to initiation of treatment.6 Very few cases of the latter category have been reported and our case belongs to it.

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