Guidelines for the Management of Pulmonary Oedema in Patient

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Pulmonary edema is the accumulation of excess fluid in the extravascular space of the lungs. This accumulation might occur slowly, as in a affected individual with occult renal failure, or with dramatic suddenness, as in a patient with left ventricular failure after an acute myocardial infarction. Pulmonary edema most commonly presents with dyspnea.
Etiology:
Pulmonary edema is a common problem associated with a variety of medical problems. In light of these multiple brings about, it's helpful to think about pulmonary edema in terms of underlying physiologic principles.

Pathophysiology:
All blood vessels leak. In the adult human, leakage from the pulmonary circulation represents lower than 0.01% of pulmonary blood flow, or even a baseline filtration of around 15 mL/h. Two thirds of this flow occurs across the pulmonary capillary endothelium into the pericapillary interstitial room.

This really is 1 of two extravascular spaces in the lung-the interstitial room and also the airspaces-that contain the alveoli and connecting airways.


These two spaces are protected by different barriers. The pulmonary capillary endothelium limits extravasation to the interstitial space whilst the alveolar epithelium lines the airspaces and protects them towards the free motion of fluid.

Edema fluid doesn't readily key in the alveolar space simply because the alveolar epithelium is nearly impermeable towards the passage of protein. This protein barrier creates a powerful osmotic gradient that favors accumulation of fluid within the interstitium. The amount of fluid that crosses the pulmonary capillary endothelium is determined by the area area from the capillary bed, the permeability of the vessel wall, and the net pressure driving it throughout that wall (transmural or driving stress).

The transmural pressure represents the balance in between websites hydrostatic forces that often move fluid out of the capillary and also the net colloid osmotic forces that often maintain it in. The Starling equation Jv ≈ ([Pc - Pi] - [ c - i]) illustrates this relationship mathematically, where Jv may be the net fluid motion in or out of the lungs, Pc is the capillary hydrostatic pressure, Pi is the interstitial hydrostatic stress, is the reflection coefficient, and c and i are the capillary and interstitial hydrostatic pressures. Acute Renal Failure Pathophysiology Diagram

An imbalance in 1 or a lot more of these four factors-capillary endothelial permeability, alveolar epithelial permeability, hydrostatic pressure, and colloid osmotic pressure-lies behind almost all clinical presentations of pulmonary edema. In the shorthand of clinical practice, these four elements are grouped into two types of pulmonary edema: cardiogenic, referring to edema resulting from a net increase in transmural stress (hydrostatic or osmotic); and noncardiogenic, referring to edema resulting from increased permeability.

The former is largely a mechanical procedure, the latter largely an inflammatory one. Nevertheless, these two types of pulmonary edema are not exclusive but closely linked: Pulmonary edema happens when the transmural stress is excessive for a given capillary permeability. For instance, within the presence of damaged capillary endothelium, small increases in otherwise normal transmural pressure might cause big raises in edema formation.

Similarly, when the alveolar epithelial barrier is broken, even the baseline filtration throughout an intact endothelium might trigger alveolar flooding. A number of mechanisms aid in the clearance of ultrafiltrate and guard against its accumulation as pulmonary edema. Although you will find no lymphatics in the alveolar septa, you will find "juxta-alveolar" lymphatics within the pericapillary space that normally clear all of the ultrafiltrate.

The pericapillary interstitium is contiguous using the perivascular and peribronchial interstitium. The interstitial pressure there's negative relative to the pericapillary interstitium, so edema fluid tracks centrally, away in the airspaces. In impact, the perivascular and peribronchiolar interstitium acts as a sump for edema fluid. It can accommodate approximately 500 mL with only a little rise in interstitial hydrostatic pressure.

Simply because this edema fluid is protein depleted relative to blood, there is an osmotic balance that favors resorption in the interstitium into the bloodstream. This is the main source of resorption of fluid from these collection locations. The perivascular and peribronchiolar interstitium is also contiguous using the interlobular septa and also the visceral pleura. In the event of pulmonary edema, there's increased interstitial flow to the pleural space exactly where parietal pleural lymphatics are very effective at clearance

[mo2008osman]

Guidelines for the Management of Pulmonary Oedema in Patients
with Kidney Failure
Pulmonary oedema is a life-threatening condition that can be particularly difficult to
manage in patients who have co-existing kidney failure. Failure to identify and manage
such patients appropriately and in a timely fashion can and will increase the risk to the
patient, including the risk of death
.ONLY IF A PATIENT HAS RENAL FAILURE (AS DEMONSTRATED BY SERUM UREA
AND CREATININE LEVELS) AND HAS SEVERE FLUID OVERLOAD OR PULMONARY
OEDEMA SHOULD THIS GUIDELINE BE FOLLOWED
Guidelines for the Management of Pulmonary Oedema in Patients with
Kidney Failure
YES
NO
YES NO
YES NO
YES NO
Patient has Renal Failure and evidence of
significant fluid overload and/or pulmonary oedema
Stop all iv fluids, restrict oral fluid intake, nurse in upright position, administer
100 % oxygen, use oxygen saturation monitor, monitor hourly urine output
Patient is anuric and/or in respiratory
distress and/or is a known dialysis patient?
Contact the on-call Nephrology Consultant
for advice, and consider discussing with
Intensive Care.
[100%O2, CPAP (if available), IV nitrate
infusion, IV diamorph or morphine and
loop diuretics (due to venodilatory effects)
can buy some time, but the definitive
Patient previously on loop diuretics? treatment is usually dialysis]
Patient responds to treatment: (reduced shortness of breath, and diuresis >30ml/hr)?
Give iv furosemide 100mg. Double dose every 60
minutes to a maximum of 400mg as per clinical
response and as allowed by cardiovascular status
Give iv furosemide 40mg. Double dose
every 60 minutes to a maximum of 320mg
as per clinical response and as allowed by
cardiovascular status
Discuss case with Medical SpR and/or
Nephrologist on-call to establish most
appropriate ward for ongoing care
1. Review hourly to consider further iv diuretics.
2. Discuss case with Medical SpR and/or Nephrologist oncall
to establish most appropriate ward for ongoing care
1. Give iv nitrates (isoket 0.05% starting at
1ml/hr) if cardiovascular status allows
(avoid if systolic BP<100mmHg, and/or
HR>120/min)
2. If BP>100mmHg, then give iv diamorphine
or morphine
Patient responds to treatment: (reduced shortness of breath, and diuresis >30ml/hr)?
Contact on-call Nephrology
Consultant and/or Intensive Care
for further advice
Beware of ototoxicity with rapid infusions of large doses of loop diuretics: give at
a maximum rate recommended in BNF (4mg/min for furosemide)
Duties and responsibilities
The attending doctor must either implement the management plan themselves and review
the patient regularly (at least every 15 minutes for the first hour), or ensure that the
appropriate handover has taken place to provide safe continuity of care for the patient.
The attending doctor must ensure that the nursing staff are aware of the management
plan, and any trigger factors that they must make someone aware of (e.g. what level of
blood pressure should be a cause of concern for any specific patient).
The attending doctor should seek advice from the Medical SpR on-call, who in turn should
consider discussing the case with the on-call Consultant Nephrologist. The attending
doctor may contact the on-call Consultant Nephrologist directly if they are unable to
contact the SpR. All anuric patients with renal failure must be discussed with the
Consultant Nephrologist on-call.
The Nursing staff must ensure that they are aware of the management plan for the patient,
frequency of relevant observations, and escalation plan for management.
Monitoring effectiveness
Episodes of pulmonary oedema/severe fluid overload are inevitable in some patients with
Acute Kidney Injury. This guideline will not prevent such episodes, but should facilitate
timely management of such episodes.
Annual audits of the management of AKI will be undertaken as part of the response to the
NCEPOD report on AKI. We will include in these audits the details of the acute
management of the fluid balance in patients with Renal Failure.
References
Rose D. Diuretics. Kidney Int 1991;39:336
Brater DC. et al. Use of diuretics in patients with renal disease. Contemporary issues in
Nephrology. Phamacotherapy of Renal Disease and Hypertension and Hypertension, vol
17, Bennett WM, McCarron DA (eds), Churchill Livingstone, New York 1987
Agostoni P. et al. Sustained improvement in functional capacity after removal of body fluid
with isolated ultrafiltration in chronic cardiac insufficiency: failure of furosemide to provide
the same result.