Long post. PART 1
Trying to treat ARDS in the field seems futile.
My summary drawn from:
https://emedicine.medscape.com/article/165139-overview
Acute Respiratory Distress Syndrome
Updated: Oct 17, 2018
*****
Early use Corticosteriods seem NOT to improve mortality, but I have not necessary seen the latest study data on that.
FLUIDS: "Type one reflects primarily acute lung injury without antecedent systemic processes like sepsis or pancreatitis. Type two is acute lung injury with an overwhelming systemic insult like sepsis.
Important to note, type one patients benefit from a fluid-restrictive management strategy (infra vide)"
VENTILATION: One item is that those positive-pressure breathing masks (CPAP) so many people have can, so some extent, substitute for a real ventilator. Lots of technical issues in the pressure curves and oxygen saturation, but in the field helping respiration might be the best you can do.
"The use of positive end-expiratory pressure (PEEP) to diminish alveolar collapse and the use of low tidal volumes and limited levels of inspiratory filling pressures appear to be beneficial in diminishing the observed VALI.
"Generally, oxygen concentrations higher than 65% for prolonged periods (days) can result in DAD, hyaline membrane formation, and, eventually, fibrosis.
ARDS is uniformly associated with pulmonary hypertension"
MORBIDITY PREDICTORS:
"Indices of oxygenation and ventilation, including the PaO2/FiO2 ratio, do not predict the outcome or risk of death. The severity of hypoxemia at the time of diagnosis does not correlate well with survival rates. However, the failure of pulmonary function to improve in the first week of treatment is a poor prognostic factor.
Peripheral blood levels of decoy receptor 3 (DcR3), a soluble protein with immunomodulatory effects, independently predict 28-day mortality in ARDS patients.
In a study comparing DcR3, soluble triggering receptor expressed on myeloid cells (sTREM)-1, TNF-alpha, and IL-6 in ARDS patients, plasma DcR3 levels were the only biomarker to distinguish survivors from nonsurvivors at all time points in week 1 of ARDS. [11] Nonsurvivors had higher DcR3 levels than survivors, regardless of APACHE II scores, and mortality was higher in patients with higher DcR3 levels."
PRESENTATION:
"With the onset of lung injury, patients initially note dyspnea with exertion. This rapidly progresses to severe dyspnea at rest, tachypnea, anxiety, agitation, and the need for increasingly high concentrations of inspired oxygen.
Physical Examination
Physical findings often are nonspecific and include tachypnea, tachycardia, and the need for a high fraction of inspired oxygen (FiO2) to maintain oxygen saturation. The patient may be febrile or hypothermic. Because ARDS often occurs in the context of sepsis, associated hypotension and peripheral vasoconstriction with cold extremities may be present. Cyanosis of the lips and nail beds may occur.
Examination of the lungs may reveal bilateral rales. Rales may not be present despite widespread involvement."
"Because cardiogenic pulmonary edema must be distinguished from ARDS, carefully look for signs of congestive heart failure or intravascular volume overload, including jugular venous distention, cardiac murmurs and gallops, hepatomegaly, and edema."
COMPLICATIONS:
"ventilator-associated pneumonia (VAP) and line sepsis. The incidence of VAP in ARDS patients may be as high as 55% and appears to be higher than that in other populations requiring mechanical ventilation. Preventive strategies including elevation of head of the bed, use of subglottic suction endotracheal tubes, and oral decontamination."
"Renal failure is a frequent complication of ARDS, particularly in the context of sepsis. Renal failure may be related to hypotension, nephrotoxic drugs, or underlying illness. Fluid management is complicated in this context, especially if the patient is oliguric. Multisystem organ failure, rather than respiratory failure alone, is usually the cause of death in ARDS.
Other potential complications include ileus, stress gastritis, and anemia. Stress ulcer prophylaxis is indicated for these patients. Anemia may be prevented by the use of growth factors (erythropoietin)."
FIELD EXPEDIENT WORKUP ITEMS:
"Approach Considerations
Acute respiratory distress syndrome (ARDS) is defined by the acute onset of bilateral pulmonary infiltrates and severe hypoxemia in the absence of evidence of cardiogenic pulmonary edema. Workup includes selected laboratory tests, diagnostic imaging, hemodynamic monitoring, and bronchoscopy. ARDS is a clinical diagnosis, and no specific laboratory abnormalities are noted beyond the expected disturbances in gas exchange and radiographic findings.
Laboratory Tests
In ARDS, if the partial pressure of oxygen in the patient’s arterial blood (PaO2) is divided by the fraction of oxygen in the inspired air (FiO2), the result is 300 or less. For patients breathing 100% oxygen, this means that the PaO2 is less than 300.
In addition to hypoxemia, arterial blood gases often initially show a respiratory alkalosis. However, in ARDS occurring in the context of sepsis, a metabolic acidosis with or without respiratory compensation may be present.
As the condition progresses and the work of breathing increases, the partial pressure of carbon dioxide (PCO2) begins to rise and respiratory alkalosis gives way to respiratory acidosis. Patients on mechanical ventilation for ARDS may be allowed to remain hypercapnic (permissive hypercapnia) to achieve the goals of low tidal volume and limited plateau pressure ventilator strategies aimed at limiting ventilator-associated lung injury."
MANAGEMENT:
" A study by Martin-Loeches et al concluded that the early use of corticosteroids was also ineffective in patients with the pandemic H1N1 influenza A infection, resulting in an increased risk of superinfections. [23] This finding was also echoed in a study by Brun-Buisson et al, who found no evidence of benefit associated with corticosteroids in patients with ARDS secondary to influenza pneumonia but did find that early corticosteroid therapy may be harmful. [24]
Numerous pharmacologic therapies, including the use of inhaled synthetic surfactant, intravenous (IV) antibody to endotoxin, ketoconazole, simvastatin, and ibuprofen, have been tried and are not effective. [25]
A study that examined the use and outcomes associated with rescue therapies in patients with ARDS determined that these therapies offered no survival benefit. [26] The study also determined that rescue therapies are most often used in younger patients with more severe oxygenation deficits.
Inhaled nitric oxide (NO), a potent pulmonary vasodilator, seemed promising in early trials, but in larger controlled trials, it did not change mortality rates in adults with ARDS. [27, 28] A systematic review, meta-analysis, and trial sequential analysis of 14 randomized controlled trials, including 1303 patients, found that inhaled nitric oxide did not reduce mortality and results in only a transient improvement in oxygenation. [29]
Although no specific therapy exists for ARDS, treatment of the underlying condition is essential, along with supportive care, noninvasive ventilation or mechanical ventilation using low tidal volumes, and conservative fluid management.
Because infection is often the underlying cause of ARDS, early administration of appropriate antibiotic therapy broad enough to cover suspected pathogens is essential," ...
...
"With the development of the National Institutes of Health (NIH)–sponsored ARDS Clinical Trials Network, several large well-controlled trials of ARDS therapies have been completed. Thus far, the only treatment found to improve survival in ARDS is a mechanical ventilation strategy using low tidal volumes (6 mL/kg based upon ideal body weight).
The main concerns are missing a potentially treatable underlying cause or complication of ARDS. In these critically ill patients, pay careful attention to early recognition of potential complications in the intensive care unit (ICU), including pneumothorax, IV line infections, skin breakdown, inadequate nutrition, arterial occlusion at the site of intra-arterial monitoring devices, DVT and pulmonary embolism (PE), retroperitoneal hemorrhage, gastrointestinal (GI) hemorrhage, erroneous placement of lines and tubes, and the development of muscle weakness."