Nephrotic syndrome (NS), a clinical syndrome rather than a disease, is characterized by renal glomerular injury and massive loss of protein in the urine. An accompanying loss of serum albumin, an increased level of serum lipids, and massive peripheral edema occur.
Pathophysiological changes are caused by a defect in the glomerular basement membrane, which results in increased membrane permeability to protein, particularly albumin. Loss of albumin through the glomerular membrane reduces serum albumin and decreases colloidal oncotic pressure in the capillary vascular beds. Subsequently, fluid leaks into the interstitial spaces, collects in body cavities, and creates massive generalized edema and ascites. Interstitial fluid shifts cause a decrease in the fluid volume within the vascular bed. The vascular fluid volume deficits stimulate the renin-angiotensin system and the release of aldosterone. These compensatory mechanisms cause renal tubular reabsorption of sodium and water, which further contributes to edema formation. Some patients become markedly immunosuppressed because of the loss of the immunoglobulin IgG in the urine. Enhanced urinary excretion of transferrin may lead to anemia, and loss of antithrombin III may lead to enhanced coagulation.
Complications occur because of the increased tendency for blood coagulation owing to increased blood viscosity. These changes may result in thromboembolic vascular occlusion in the kidneys, lungs, and lower extremities in particular. Other complications include accelerated atherosclerosis, acute renal failure, malnutrition, and a lowered resistance to infection.
Numerous factors contribute to the development of NS. These factors may be of idiopathic, secondary, or congenital origin. Idiopathic NS, the most common form, occurs in the absence of any systemic preexisting disease. One type, minimal change NS, is the most frequent form in children and, although the cause is unknown, is associated with autoimmune changes. Other causes of idiopathic NS are several forms of glomerulonephritis and focal sclerosis of the glomeruli. Secondary NS occurs during or following a known disease process, such as cancer, acquired immunodeficiency syndrome, or lupus erythematosus. It also follows drug toxicity, insect stings, and venomous animal bites. Congenital NS is transmitted by a recessive gene.
Nursing care plan assessment and physical examination
Patients may report no illness before the onset of symptoms; others have a history of systemic multisystem disease, such as lupus erythematosus, diabetes mellitus, amyloidosis, or multiple myeloma or have a history of an insect sting or venomous animal bite. Symptoms usually appear insidiously and may include lethargy, depression, and weight gain. The patient may describe gastrointestinal (GI) symptoms of nausea, anorexia, and diarrhea. Initially, patients report periorbital edema in the morning and abdominal or extremity edema in the evening.
In the early stages, inspect the patient’s appearance for periorbital edema, ascites, and peripheral edema. In later stages, inspect the patient for massive generalized edema of the scrotum, labia, and abdomen. Pitting edema is usually present in dependent areas. The patient’s skin appears extremely pale and fragile. You may note areas of skin erosion and breakdown. Often, urine output is decreased from normal and may appear characteristically dark, frothy, or opalescent. Some patients have hematuria as well. Patients with severe ascites may be in acute respiratory distress, with an increase in respiratory rate and effort. When you auscultate the patient’s lungs, you may hear adventitious breath sounds, such as crackles, or the breath sounds may be distant because of a pleural effusion. When you auscultate the patient’s blood pressure, you may find orthostatic changes.
During the acute phases of the illness, assess the patient’s fluid status by ongoing monitoring of the patient’s weight, fluid intake and output, and degree of pitting edema. Measure the patient’s abdominal girth daily and record changes. Monitor for signs of complications, particularly thromboembolic complications such as renal vein thrombosis (sudden flank pain, a tender costovertebral angle, macroscopic hematuria, and decreased urine output) and extremity arterial occlusion (decreased distal pulses, blanched and cold extremities, delayed capillary refill).
Patients and family members may express fear or display signs of anxiety related to changes in the patient’s appearance. The uncertain prognosis and the possibility of lifestyle changes add to their stress. Because of the insidious onset of symptoms, parents and significant others often verbalize guilt over not seeking medical attention sooner.
Nursing care plan primary nursing diagnosis: Fluid volume excess (total body) related to excessive serum protein loss and resultant volume shifts out of vascular bed.
Nursing care plan intervention and treatment plan
Edema is controlled by restricting salt to 2 to 3 g/day. Dietary alterations also include a highprotein diet with restrictions of cholesterol and saturated fat. If the patient has accompanying renal insufficiency, restriction of dietary protein may complicate the dietary plan. The amount of protein lost in the urine needs to be added to the calculated protein restriction to arrive at the total daily protein intake. Most patients need nutritional consultation with a dietitian to identify an appropriate diet within the restrictions. Involve the patient, parents, or significant others in the meal selection to ensure that the diet is appealing to the patient. Discuss the optimal fluid intake for the patient with the physician so that the patient is well hydrated and yet does not have continued fluid retention.
Other collaborative interventions are primarily pharmacologic. In spite of the excessive edema, patients need to be monitored for dehydration and hypokalemia, particularly when they are on diuretic therapy. Patients need to maintain an adequate fluid intake and a diet high in potassium (unless they have renal insufficiency).
Focus on maintaining the patient’s fluid balance, promoting skin care, preventing nosocomial infection, and providing supportive measures. To maintain the patient’s skin integrity, turn the patient every 2 hours. Observe the skin closely for areas of breakdown until the edema resolves. Use an egg-crate mattress or specialty bed to limit irritation to skin pressure points, and encourage the patient or parents to avoid tight-fitting clothing and diapers.
Note that both the medications and the disease process may lead to immunosuppression. Implement scrupulous infection control measures, such as hand washing, sterile technique with invasive procedures, and clean technique for all noninvasive procedures to reduce the chance of infection. Do not assign patients to rooms with other patients who have infectious processes. Encourage visitation, but ask visitors with infections to wait until they are infection free before visiting. To limit the risk of blood clotting, encourage the patient to be as mobile as possible considering his or her underlying condition. If the patient is bedridden, use active and passive range-of-motion exercises at least every 4 hours and have the patient wear compression boots when immobile in bed.
Note that some patients have a disturbed body image because of the side effects of steroid therapy (moon face, increased facial and body hair, abdominal distension, and mood swings). Encourage the patient to express these feelings and note that they are temporary until the condition resolves and the steroids are discontinued. If the patient desires, limit visitation to immediate family only until the patient resolves the anxiety over the body image disturbance.
Nursing care plan discharge and home health care guidelines
Teach the patient and family about the disease process, prognosis, and treatment plan. Explain that they need to monitor the urine daily for protein and keep a diary with the results of the tests. Have the patient or family demonstrate the testing techniques before discharge to demonstrate their ability to perform these monitoring tasks. Instruct the patient and family to avoid exposure to communicable diseases and to engage in scrupulous infection control measures such as frequent hand washing. Encourage patients with hypercoagulability to maintain hydration and mobility and to follow the medication regimen.
Teach the patient and family the purpose, dosage, route, desired effects, and side effects for all prescribed medications. Inform patients on anticoagulant therapy of the need for laboratory monitoring of activated partial thromboplastin time or prothrombin time. Caution patients who are receiving steroid therapy to take the dosages exactly as prescribed; explain that skipping doses could be harmful or life-threatening. In cases of long-term steroid therapy, explain the signs of complications, such as GI bleeding, stunted growth (children), bone fractures, and immunosuppression. Encourage patients to resume normal activities as soon as possible.