Introduction
Many cancer therapeutic drugs are known to induce pulmonary damage that can result in a variety of clinicopathologic changes. These can result in severe consequences. Drug-induced pulmonary toxicity leads to hypersensitivity lung disease, pneumonitis, non-cardiogenic pulmonary edema, and acute respiratory distress syndrome. These conditions are similar in regard to time to time to cancer treatment. Non-specific symptoms like progressive dyspnea, cough, and often a low-grade fever can challenge the recognition of subclinical syndromes. Non-cardiogenic pulmonary edema is a rarely cited and less recognized pulmonary toxic syndrome of anticancer therapy.
What Is Non-Cardiogenic Pulmonary Edema?
Non-cardiogenic pulmonary edema is a rare disease condition that results in acute hypoxia (low oxygen level) secondary to rapid deterioration in respiratory status. This condition results due to multiple etiologies. The main cause is increased capillary permeability, and changes in pressure gradients within the pulmonary capillaries and vasculature are mechanisms due to which non-cardiogenic pulmonary edema occurs. Non-cardiogenic pulmonary edema is a classification of pulmonary edema in which the underlying cause is not due to left ventricular dysfunction. Various mechanisms are responsible for noncardiogenic edema to develop. The various pathophysiology is low alveolar pressure post obstructive edema (complication due to upper airway obstruction), neurogenic edema (a clinical complication that occurs due to onset of pulmonary edema along with an insult to the central nervous system), vasculitis (inflammation of blood vessels), high altitude pulmonary edema (pulmonary edema that occurs in low landers who ascend to a high altitude greater than 2500 to 3000 m). Decreased alveolar pressure after fast removal of pleural effusion, pneumothorax, and lung lobes is called reexpansion edema. Mortality for this condition is 20%.
What Are the Causes of Non-Cardiogenic Pulmonary Edema?
The causes of non-cardiogenic pulmonary edema are:
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Pulmonary edema in pulmonary thromboembolism (obstruction of blood vessels by a blood clot).
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Pulmonary edema due to air embolism.
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ARDS (acute respiratory distress syndrome occurs when fluid builds up in elastic tiny air sacs) is pulmonary edema with diffuse alveolar damage.
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Fluid overload.
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Pulmonary edema with acute asthma.
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Post obstructive pulmonary edema.
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Pulmonary venous-occlusive disease.
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Near drowning pulmonary edema.
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Heroin-induced pulmonary edema.
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High-altitude pulmonary edema.
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Neurogenic pulmonary edema (an increase in the pulmonary interstitial and alveolar fluid that occurs due to acute central nervous system injury and develops rapidly after injury).
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Reperfusion pulmonary edema.
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Postpneumonectomy pulmonary edema (a rare complication that occurs after pneumonectomy).
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Re-expansion pulmonary edema (a rare condition that occurs when collapsed lung is allowed to expand).
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Post lung volume reduction pulmonary edema.
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Transfusion-related to acute lung injury.
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Opioid overdose.
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Salicylate toxicity (a fatal condition, also known as Aspirin poisoning).
What Is the Difference Between Cardiogenic and Noncardiogenic Pulmonary Edema?
Cardiogenic pulmonary edema is caused by high pulmonary capillary pressure, estimated by pulmonary artery occlusion pressures, and is responsible for abnormal excess fluid movement in the alveoli. Cardiogenic pulmonary edema is frequently caused by acute, decompensated heart failure. Individuals diagnosed with cardiogenic pulmonary edema represent decreased arterial oxygen saturation, dyspnea, and alveolar infiltrates while imaging the chest. The fluid accumulation results from elevated cardiac filling pressures. Decompensated heart failure is attributed to left ventricular diastolic and systolic dysfunction, with or without cardiac pathology. This includes valve abnormalities and coronary artery disease. In the absence of underlying heart conditions, causes of cardiogenic pulmonary edema include severe hypertension, fluid overload, severe renal disease, and renal artery stenosis.
In contrast, non-cardiogenic pulmonary edema is recognized by the presence of alveolar fluid accumulation in chest imaging without hemodynamic evidence. Non-cardiogenic pulmonary edema occurs due to excessive pulmonary capillary permeability. The causes include excessive renin-angiotensin-aldosterone system activity, increased endothelin levels, excessive circulating catecholamines, and impaired nitric oxide synthesis.
What Is the Differential Diagnosis of Non-cardiogenic Pulmonary Edema?
The differential diagnosis includes cardiogenic pulmonary edema as a cause of pulmonary edema that needs to be ruled out. Appropriate evaluation for ARDS is important, HAPE is an option that reveals a quick ascent in attitude. Medication and drugs are used to assess for salicylate toxicity and opioid overdose, as they overlook etiologies of pulmonary edema. The differential diagnosis of this condition are:
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Drug overdose from salicylates and opioids.
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Pulmonary embolism.
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High altitude pulmonary edema (HAPE is a life-threatening form of noncardiogenic pulmonary edema that occurs in individuals at high altitudes).
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Acute respiratory distress syndrome (ARDS).
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Transfusion-related acute lung injury (TRALI is a serious and potentially fatal complication of blood product transfusion in individuals and develops rapid onset of lung injury)
How Is Non-cardiogenic Pulmonary Edema Managed?
The treatment of non-cardiogenic pulmonary edema mainly depends on treating the underlying cause. Currently, there is no treatment that addresses vascular permeability in ARDS. Management involves supportive care and treatment of underlying disease until the acute lung injury is resolved. Inhaled nitric oxide, high-frequency ventilation, anti-inflammatory therapy, and prostacyclin fail to show consistent benefits. Other causes of noncardiogenic pulmonary edema are managed along with supportive care, mechanical ventilation, and supplemental oxygen if required based on the inciting cause.
What Is the Prognosis of Non-cardiogenic Pulmonary Edema?
The prognosis of non-cardiogenic edema depends on the cause. Severe ARDS usually carried 40 % of the mortality rate. HAPE recurs in 60 % of individuals. The prognosis is poor in neurogenic pulmonary edema, a condition associated with the insult to the central nervous system, with intracranial hemorrhage. Non-cardiogenic pulmonary edema in context with other neurologic conditions like epilepsy. Ischemia-reperfusion injury consists of 25 % of the mortality rate after lung transplantation. Mortality in cases of TRALI can reach up to 47 % in individuals with non-cardiogenic pulmonary edema.
What Are the Complications of Non-Cardiogenic Pulmonary Edema?
The main complications of non-cardiogenic pulmonary edema are ventilator-dependent respiratory failure requiring intubation and possibly prolonged requirement of the ventilator; this necessitates prompt diagnosis to prevent the severity of the complications. Chronic use of opioids can also lead to salicylate toxicity and related complications. Opioid users must be educated about these harmful effects and the possible sequelae of pulmonary edema.
Conclusion
The accurate diagnosis of non-cardiogenic pulmonary edema is important. Recognizing reactions during blood transfusions can prevent TRALI. Prescribed opioids and salicylates can recognize rare adverse effects such as the development of pulmonary edema. ARDS can promptly be managed by intensive care providers and respiratory therapy. Individuals with pulmonary edema are successfully managed with diuretics, high-dose corticosteroids, and oxygen supplementation. Immediate discontinuation of chemotherapy is recommended on lung toxicity suspicion and in rare cases, lung biopsy should be taken into consideration.
