Acute Respiratory Distress Syndrome PaperDiagnosisThe clinical features point to acute respiratory d

Acute Respiratory Distress Syndrome Paper

Diagnosis

The clinical features point to acute respiratory distress syndrome (ARDS). The clinical condition is characterized by severe hypoxemia resulting from failure in pulmonary gas exchange (Diamond et al., 2020). Other features are acute onset and presence pulmonary infiltrates, with potential life-threatening.

Reason for Diagnosis

The patient has tachypnea of 30 breaths per minute and is hypoxic with oxygen saturation of 89%, which is low. The temperature of 390 C points to a fever. Besides, the symptoms of worsening cough, fever and dyspnea have presented within 7 days, which marks the cut-off for acute respiratory distress syndrome (Diamond et al., 2020). The fact that the hypoxemia is severe and progressive in absence of cardiogenic pulmonary edema further reinforces the diagnosis of acute respiratory distress syndrome.

Whereas the cough, fever and tachypnea in the presence of leukocytosis of 20000 cells/mm3 point to infectious/inflammatory pulmonary pathology, the conditions would resolve on initiation of antibiotics in the case of pneumonia and ventilation. Thus, failure of resolving points to a non-infectious cause. Acute respiratory distress syndrome would form a more appropriate diagnosis since the symptoms result from capillary endothelial injury and diffuse alveolar damage (Diamond et al., 2020). The condition fails to resolve on antibiotics since the primary pathology in the patient has not been dealt with. Capillary endothelial injury and diffuse alveolar damage in ARDS result in progressive dyspnea and hypoxia.

The worsening symptoms are caused by the increasing damages to the pulmonary architecture, ending in sustained low arterial blood oxygen levels and increasing infiltrates bilaterally on chest x ray. The most current criteria for ARDS is the Berlin definition that characterizes ARDS as “respiratory failure within 1 week of a known insult or new/worsening respiratory symptoms, with evidence of non-cardiogenic pulmonary edema and progressive bilateral opacities on the radiograph plus a hypoxemia of PaO2/FiO2 less than 300 mmHg on at least Positive End-Expiratory Pressure (PEEP) or Continuous Positive Airway Pressure of greater than or equal to 5 cm H2O” (Diamond et al., 2020). The patient meets all the Berlin criteria.

The patient’s x ray exhibits infiltrates in both lower lobes. The film also shows progression of infiltrates throughout both lung fields. ARDS comprises bilateral opacities on chest radiograph or computed tomography that are unexplained by other conditions such as lobar or lung collapse, pleural effusions and pulmonary nodules.

Etiology of the Diagnosis

The cause for ARDS may be pulmonary or extra-pulmonary. Whereas both etiologies have similar incidence, pulmonary causes are more common than extra-pulmonary causes (Rawal, Yadav & Kumar, 2018). The suitable pulmonary cause in this patient would be pneumonia, as evidenced by cough and fever that point to an infective pathology. Pneumonia consists of inflammation of lung parenchyma, causing capillary vasodilatation at the level of the alveolar with subsequent exudation of material into the alveolar space. Persistence of the inflammation and the causative organism culminates in destruction of alveolocapillary membrane, interfering with the gaseous exchange mechanisms that underlie the pathophysiology of ARDS (Rawal, Yadav & Kumar, 2018).  The resultant effect is persistent hypoxia and dyspnea that is non-responsive to the management, with poor prognosis.

The condition progresses via various phases, commencing with alveolar-capillary damage, proliferative phase consisting of improved lung function and healing, and the last stage is the fibrotic phase that marks the end of the acute disease process. The pulmonary epithelial and endothelial cellular damage is marked inflammation, apoptosis, necrosis, and increased alveolar-capillary permeability, with resultant edema into alveolar spaces and proteinosis (Micheal et al., 2019). Alveolar edema limits gaseous exchange, resulting in hypoxemia. The lung bases may be more involved than the apices.

Histopathological lab features may include injury to vascular endothelium and pneumocyte type I. The mentioned factors cause leakage of proteinaceous fluid and blood into the alveolar airspace (Micheal et al., 2019). Other findings are pulmonary capillary congestion, alveolar hemorrhage, hyaline membrane formation and interstitial edema, which are all non-specific.

Common Causes of ARDS

The etiology of ARDS comprises both pulmonary and extrapulmonary causes. Within the lungs, ARDS follows pneumonia, particularly viral and bacterial pneumonia that are non-treated or under-treated (Curtis et al., 2017). For patients with altered levels of consciousness, aspiration of orogastric and esophageal contents has been implicated as causative of pneumonia, besides major trauma to the chest and inhalational burns. Other causes include transfusion associated acute lung injury (TRALI) and acute graft rejection following lung transplant.

Extrapulmonary causes of ARDS include systemic sepsis with foci from urinary, soft tissue or peritoneal sites. These factors culminate in a cytokine storm that negatively affects the functioning of exchange mechanisms in the lung by increasing the permeability of alveolocapillary membrane, with subsequent exudation and accumulation of pulmonary infiltrates (Curtis et al., 2017). The resultant effect is acute respiratory distress syndrome.

Acute pancreatitis is another known cause of ARDS. Pancreatic inflammation causes leakage of pancreatic enzymes into the bloodstream, which damage the alveoli wall and impede production of surfactant (Curtis et al., 2017). Alveoli damage and impaired surfactant production cause faulty alveoli functioning, disrupting the gaseous exchange process. Other proven causes of ARDS are drug overdose, drowning, hemorrhagic shock and inhalation of toxic fumes. Worth-noting, special risk factors to developing ARDS include alcohol consumption, smoking, advanced age, female gender, cardiovascular surgery and traumatic brain injury (Zayed & Askari, 2020). The pathophysiology of ARDS in the mentioned risk factors is varied, but in all cases, the lung function is altered.

A-a Gradient

The A-a gradient is the alveolar-arterial gradient that measures the difference between oxygen concentration in the alveoli and arterial system. Its significance is helping to narrow down differential diagnoses for hypoxemia. Its calculation follows the formula PAO2 – PaO2 where PAO2 is the oxygen concentration in the alveoli and PaO2 is oxygen concentration in the capillary (Handtzidiamantis & Amaro, 2020). The A-a gradient in this patient would increase, owing to dysfunction of the alveolar capillary unit.

Complications

Notwithstanding its life-threatening implications, no known drug is effective in preventing or managing ARDS. Thus, management is primarily supportive care, with focus on reducing shunt fraction, increasing oxygen delivery, decreasing oxygen consumption and preventing further injury. The patient is put on mechanical ventilation, given diuretics to protect against fluid overload and given nutritional support until the care provider observes evidence of improvement. Caution while ventilating is mandatory to prevent exacerbating alveolar damage and perpetuating lung injury in ARDS.  Other complications that must be avoided are barotraumas (damage due to extreme plateau pressures), volutrauma (damage due to large tidal volumes) and atelectrauma (damage due to atelectasis) (Diamond et al., 2020). The goals to reduce lung injury include the following: tidal volume of between 4 and 8 mL/kg of ideal body weight, respiratory rate of up to 35 bpm, plateau pressure of below 30 cm H20, SpO2 from 88 % to 95 %, pH of between 7.30 to 7.45, and inspiratory-to-expiratory time ratio of below 1 (Diamond et al., 2020).

Lung compliance may be improved by introducing neuromuscular blockade. Institution of neuromuscular blockers within the first 48 hours in ARDS improved the 90-day survival and increased the time off the ventilator. Alleviation of lung compliance should include assessing for other causes of reduced lung compliance, including hemothorax, pneumothorax, thoracic compartment syndrome and intraabdominal hypertension (Micheal et al., 2019). The prone position is proven to be beneficial in 50 to 70 % of patients in a recent study. The dangers of prone position include accidental dislodgment of tubes and lines. The benefits consist of recruitment of dependent lung zones, improved diaphragmatic excursion and increased functional residual capacity (Micheal et al., 2019). Maintenance in the prone position for a minimum of 8 hours daily would maximize the benefits. Additonal management strategies include conservative fluid management after resuscitation is attained and extracorporeal membrane oxygenation.

During hospitalization, frequent changes in position would prevent the development of bedsores and deep venous thrombosis (Micheal et al., 2019). The mentioned approach would be beneficial, considering ARDS patients are bed-ridden.

The patient’s prognosis is expected to be good. While ARDS had high mortality rates, recent advances in mechanical ventilation and early antibiotic administration and selection have resulted in a decline in mortality, particularly severe ARDS. The main causes of death were sepsis and multi-organ failure in the 1990s (Rawal, Yadav & Kumar, 2018). Notwithstanding, the effects of long hospitalization following ARDS include poor muscle function, weight loss and functional impairment. Hypoxia in the illness may culminate in diverse cognitive changes which may persist for several months after the patient is discharged (Rawal, Yadav & Kumar, 2018). Complete returning to normal life may be challenging post-treatment since the majority of patients report feelings of decreased exercise tolerance and feelings of dyspnea on exertion.

Postoperative Care and Rehabilitative Care

The majority of patients diagnosed with ARDS will require a tracheostomy and a percutaneous feeding tube during the recovery period. Tracheostomy improves the effectiveness of weaning from the ventilator, easing clearing of secretions and providing more comfort for the patient (Rawal, Yadav & Kumar, 2018). The tracheostomy would be recommendable at between 2 and 3 weeks after diagnosis, followed closely by the percutaneous feeding tube.

Worth-noting, a large proportion of ARDS patients experience difficulty eating, leading to muscle wasting. Parenteral or enteral feeding would be appropriate in their management plan, considering the gastrointestinal tract’s condition (Rawal, Yadav & Kumar, 2018). Starting the patients on low-carbohydrate diet may be beneficiary due to its anti-inflammatory and vasodilating effects.

References

• Cutts, S., Talboys, R., Papsula, C., Prempeh, E., Fanous, R. & Ail, D. (2017). Adult Respiratory Distress Syndrome. US National Library of Medicine National Institutes of Health, 99 (1): 12-16 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5392788/
• Diamond, M., Peniston F., Sanghavi, D.  & Sidharth, M. (2020). Acute Respiratory Distress Syndrome. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK436002/
• Hantzidiamantis, P. J., & Amaro, E. (2019). Physiology, Alveolar to Arterial Oxygen Gradient (Aa Gradient). StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK545153/#:~:text=The%20A%2Da%20gradient%2C%20or%20the,the%20differential%20diagnosis%20for%20hypoxemia.
• Micheal, A., Zemans, R., Zimmerman, G., Arabi., Y. Beitler, J., Mercat., Herridge, M., Randolph, G. & Calfee, C. (2019). Acute Respiratory Distress Syndrome. Nature Public Health Emergency Collection, 5(1), 18. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6709677/
• Rawal, G., Yadav, S., & Kumar, R. (2018). Acute respiratory distress syndrome: an update and review. Journal of Translational Internal Medicine, 6(2), 74-77. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6032183/
• Zayed, Y. and Askari, R. (2020). Respiratory Distress Syndrome. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK538311/

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