PROGRAMA DE MEDICINA Y ENFERMERIA

programa medicina y enfermeria UCEVA

Inestabilidad posterior de rodilla

prueba de lachman

maniobra de cajon posterior

examen fisico

falla renal cronica estadio IV

The Clinical Problem

Chronic kidney disease is characterized by a progressive decline in the GFR; the diagnosis is made on the basis of a reduced GFR for a minimum of 3 months, often accompanied by albuminuria. The Kidney Disease Outcomes Quality Initiative of the National Kidney Foundation has proposed a classification scheme for chronic kidney disease that has been widely adopted (Table 1Table 1Stages of Chronic Kidney Disease and Prevalence in Adults.). Stage IV chronic kidney disease denotes a severe decline in the GFR to 15 to 29 ml per minute per 1.73 m².1 Table 2Table 2Major Causes of Severe Chronic Kidney Disease. shows the major causes of severe chronic kidney disease among people in the United States.
Several studies have examined the incidence of chronic kidney disease overall, although less is known about the incidence of stage IV disease specifically. Chronic kidney disease (defined in the Framingham Study as a GFR that is <60% of the normal level) developed in about 9% of the subjects in the Framingham Study cohort during an 18-year follow-up period.5 In the Atherosclerosis Risk in Communities study, chronic kidney disease (defined as a persistent rise in the serum creatinine level) developed in 4.4 of 1000 white subjects and 8.8 of 1000 black subjects during a 14-year follow-up period.6 Data from the National Health and Nutrition Examination Surveys of 1988 to 1994 and 1999 to 2004 suggest that the prevalence of chronic kidney disease increased from 10 to 13% over the 10-year period from 1994 to 2004.2 This rise is probably attributable to a progressively aging population and the increased prevalence of obesity, diabetes, and hypertension.
Chronic kidney disease is a well-known risk factor for cardiovascular disease (Figure 1Figure 1Cardiovascular Disease in Patients with Chronic Kidney Disease.). Several conditions (e.g., diabetes and hypertension) may promote the development of chronic kidney disease and, together with proteinuria, are also risk factors for cardiovascular disease.7-9
Less than 2% of patients with chronic kidney disease ultimately require renal-replacement therapy.7 In part, this low rate is explained by the increased risk of death from cardiovascular causes before progression to end-stage renal disease can occur.7,8 Cardiovascular disease is the most frequent cause of death among patients with chronic kidney disease in longitudinal studies, but these studies involve primarily older patients and patients with diabetes and a history of cardiovascular disease.7,8 In a retrospective study of relatively young, well-nourished patients without diabetes and with a low prevalence of proteinuria, cardiovascular disease, and risk factors for cardiovascular disease, there was a higher incidence of kidney failure than of death during the course of the study.9
Cardiovascular complications associated with chronic kidney disease include angina pectoris, myocardial infarction, heart failure, stroke, peripheral vascular disease, arrhythmias, and sudden death (Figure 1).10 The risk of each of these conditions increases from early-stage to advanced chronic kidney disease.10 The increased risk of death and poor outcomes after myocardial infarction in patients with stage III or stage IV chronic kidney disease may be related to the frequent proximity of lesions to the coronary ostia.11 In laboratory animals, uremia is associated with cardiac fibrosis.12 In patients with advanced chronic kidney disease, uremic cardiomyopathy is characterized by diastolic dysfunction, heart failure, and left ventricular hypertrophy; these abnormalities, in combination with myocardial ischemia and electrolyte shifts, probably contribute to the high incidence of sudden death.10

Strategies and Evidence

Evaluation

An approach to the management of chronic kidney disease requires a correct diagnosis of the primary renal disease, attention to coexisting conditions, and an understanding of the systemic complications. Potentially reversible causes that may contribute to the decline in GFR in patients with chronic kidney disease should be identified. These include hypovolemia and hypotension; conditions associated with a decreased effective arterial-blood volume, such as cirrhosis and the nephrotic syndrome; obstructive uropathy, urinary tract infection, or occlusive renovascular disease; the use of nonsteroidal antiinflammatory drugs; and severe hypokalemia or hypercalcemia. A substantial loss of functioning nephrons is associated with functional, structural, and metabolic adaptations that contribute to the glomerular, vascular, and tubulointerstitial changes that are seen in patients with chronic kidney disease (Figure 2Figure 2Mechanisms Underlying the Progression from Early-Stage to Advanced Chronic Kidney Disease.). These maladaptive responses and associated complications are common mechanisms that are not specific to the primary cause of chronic kidney disease but that contribute to the progression of the disease. A comprehensive strategy to treat these complications is essential for slowing the progression to end-stage renal disease.

General Management

Renal function should be followed closely (every 1 to 3 months, depending on the rate of progression), by periodic estimation of the GFR4 (see the Supplementary Appendix, available with the full text of this article at NEJM.org). Although serum cystatin C has been proposed as a reliable marker for the estimation of the GFR, other factors besides the GFR may influence cystatin C levels, and this measurement is not used routinely in practice.13
The guidelines of the Kidney Disease Outcomes Quality Initiative recommend that patients with stage IV chronic kidney disease be referred to a nephrologist.1 However, this recommendation is not widely followed; in one study of U.S. veterans, less than 30% of the veterans with stage IV chronic kidney disease were seen by a nephrologist.14 Although there are no data from clinical trials to establish the optimal referral time, delayed referral of patients with late-stage chronic kidney disease is associated with suboptimal outcomes, including increased mortality.14,15 The practical challenges of providing adequate therapy for patients with chronic kidney disease include the large number of medicines that are often needed and the high rate of coexisting conditions16,17 that require meticulous follow-up at each visit. However, even among patients with chronic kidney disease who receive ongoing care from nephrologists, the management of the disease is not always optimal; the rates of use of ACE inhibitors, aspirin, statins, and beta-blockers that were reported in one study were only 41%, 65%, 24%, and 65%, respectively.17


http://www.nejm.org/doi/pdf/10.1056/NEJMcp0906797 

hipernatremia

The serum sodium concentration and thus serum osmolality are closely controlled by water homeostasis, which is mediated by thirst, arginine vasopressin, and the kidneys.1 A disruption in the water balance is manifested as an abnormality in the serum sodium concentration — hypernatremia or hyponatremia.2,3 Hypernatremia, defined as a rise in the serum sodium concentration to a value exceeding 145 mmol per liter, is a common electrolyte disorder. Because sodium is a functionally impermeable solute, it contributes to tonicity and induces the movement of water across cell membranes.4 Therefore, hypernatremia invariably denotes hypertonic hyperosmolality and always causes cellular dehydration, at least transiently (Figure 1Figure 1Extracellular-Fluid and Intracellular-Fluid Compartments under Normal Conditions and during States of Hypernatremia.). The resultant morbidity may be inconsequential, serious, or even life-threatening.5 Hypernatremia frequently develops in hospitalized patients as an iatrogenic condition, and some of its most serious complications result not from the disorder itself but from inappropriate treatment of it.6,7 In this article, we focus on the management of hypernatremia, emphasizing a quantitative approach to the correction of the fluid imbalance.8

Causes

Hypernatremia represents a deficit of water in relation to the body's sodium stores, which can result from a net water loss or a hypertonic sodium gain (Table 1Table 1Causes of Hypernatremia.). Net water loss accounts for the majority of cases of hypernatremia.9-11 It can occur in the absence of a sodium deficit (pure water loss) (Figure 1B) or in its presence (hypotonic fluid loss) (Figure 1C and Figure 1D). Hypertonic sodium gain usually results from clinical interventions or accidental sodium loading (Table 1 and Figure 1E).
Because sustained hypernatremia can occur only when thirst or access to water is impaired, the groups at highest risk are patients with altered mental status, intubated patients, infants, and elderly persons.12 Hypernatremia in infants usually results from diarrhea, whereas in elderly persons it is usually associated with infirmity or febrile illness.6,13,14 Thirst impairment also occurs in elderly patients.15,16 Frail nursing home residents and hospitalized patients are prone to hypernatremia because they depend on others for their water requirements.7

Clinical Manifestations

Signs and symptoms of hypernatremia largely reflect central nervous system dysfunction and are prominent when the increase in the serum sodium concentration is large or occurs rapidly (i.e., over a period of hours).1,6 Most outpatients with hypernatremia are either very young or very old.17 Common symptoms in infants include hyperpnea, muscle weakness, restlessness, a characteristic high-pitched cry, insomnia, lethargy, and even coma.5,13 Convulsions are typically absent except in cases of inadvertent sodium loading or aggressive rehydration.14,18,19 Unlike infants, elderly patients generally have few symptoms until the serum sodium concentration exceeds 160 mmol per liter.17,20 Intense thirst may be present initially, but it dissipates as the disorder progresses and is absent in patients with hypodipsia.5 The level of consciousness is correlated with the severity of the hypernatremia.6 Muscle weakness, confusion, and coma are sometimes manifestations of coexisting disorders rather than of the hypernatremia itself.
Unlike hypernatremia in outpatients, hospital-acquired hypernatremia affects patients of all ages.7 The clinical manifestations are even more elusive in hospitalized patients because they often have preexisting neurologic dysfunction. As in children, rapid sodium loading in adults can cause convulsions and coma.5,21 In patients of all ages, orthostatic hypotension and tachycardia reflect marked hypovolemia.
Brain shrinkage induced by hypernatremia can cause vascular rupture, with cerebral bleeding, subarachnoid hemorrhage, and permanent neurologic damage or death. Brain shrinkage is countered by an adaptive response that is initiated promptly and consists of solute gain by the brain that tends to restore lost water. This response leads to the normalization of brain volume and accounts for the milder symptoms of hypernatremia that develops slowly (Figure 2Figure 2Effects of Hypernatremia on the Brain and Adaptive Responses.).22-24 However, the normalization of brain volume does not correct hyperosmolality in the brain. In patients with prolonged hyperosmolality, aggressive treatment with hypotonic fluids may cause cerebral edema, which can lead to coma, convulsions, and death (Figure 2).14,18,19
The mortality rate associated with hypernatremia varies widely according to the severity of the condition and the rapidity of its onset. It is difficult, however, to separate the contribution of hypernatremia to mortality from the contribution of underlying illnesses.11,23


http://www.nejm.org/doi/pdf/10.1056/NEJM200005183422006 

Hiponatremia

Hyponatremia is defined as a decrease in the serum sodium concentration to a level below 136 mmol per liter. Whereas hypernatremia always denotes hypertonicity, hyponatremia can be associated with low, normal, or high tonicity.1,2 Effective osmolality or tonicity refers to the contribution to osmolality of solutes, such as sodium and glucose, that cannot move freely across cell membranes, thereby inducing transcellular shifts in water.3 Dilutional hyponatremia, by far the most common form of the disorder, is caused by water retention. If water intake exceeds the capacity of the kidneys to excrete water, dilution of body solutes results, causing hypo-osmolality and hypotonicity (Figure 1BFigure 1Extracellular-Fluid and Intracellular-Fluid Compartments under Normal Conditions and during States of Hyponatremia., 1E, 1F, and 1G). Hypotonicity, in turn, can lead to cerebral edema, a potentially life-threatening complication.4 Hypotonic hyponatremia can be associated, however, with normal or even high serum osmolality if sufficient amounts of solutes that can permeate cell membranes (e.g., urea and ethanol) have been retained (Figure 1C). Importantly, patients who have hypotonic hyponatremia but normal or high serum osmolality are as subject to the risks of hypotonicity as are patients with hypo-osmolar hyponatremia.
The nonhypotonic hyponatremias are hypertonic (or translocational) hyponatremia, isotonic hyponatremia, and pseudohyponatremia.1,2 Translocational hyponatremia results from a shift of water from cells to the extracellular fluid that is driven by solutes confined in the extracellular compartment (as occurs with hyperglycemia or retention of hypertonic mannitol); serum osmolality is increased, as is tonicity, the latter causing dehydration of cells (Figure 1D). Retention in the extracellular space of large volumes of isotonic fluids that do not contain sodium (e.g., mannitol) generates iso-osmolar and isotonic hyponatremia but no transcellular shifts of water. Pseudohyponatremia is a spurious form of iso-osmolar and isotonic hyponatremia identified when severe hypertriglyceridemia or paraproteinemia increases substantially the solid phase of plasma and the sodium concentration is measured by means of flame photometry.1,2 The increasing availability of direct measurement of serum sodium with the ion-specific electrode has all but eliminated this laboratory artifact.5
A common clinical problem, hyponatremia frequently develops in hospitalized patients.6 Although morbidity varies widely in severity, serious complications can arise from the disorder itself as well as from errors in management. In this article, we focus on the treatment of hyponatremia, emphasizing a quantitative approach to its correction.

Causes

Hypotonic (dilutional) hyponatremia represents an excess of water in relation to existing sodium stores, which can be decreased, essentially normal, or increased (Figure 1). Retention of water most commonly reflects the presence of conditions that impair renal excretion of water1,7,8; in a minority of cases, it is caused by excessive water intake, with a normal or nearly normal excretory capacity (Table 1Table 1Causes of Hypotonic Hyponatremia.).7
Conditions of impaired renal excretion of water are categorized according to the characteristics of the extracellular-fluid volume, as determined by clinical assessment (Table 1).9 With the exception of renal failure, these conditions are characterized by high plasma concentrations of arginine vasopressin despite the presence of hypotonicity.10,11 Depletion of potassium accompanies many of these disorders and contributes to hyponatremia, since the sodium concentration is determined by the ratio of the “exchangeable” (i.e., osmotically active) portions of the body's sodium and potassium content to total body water (Figure 1G).12-14 Patients with hyponatremia induced by thiazides can present with variable hypovolemia or apparent euvolemia, depending on the magnitude of the sodium loss and water retention.1,15-17
Excessive water intake can cause hyponatremia by overwhelming normal water excretory capacity (e.g., primary polydipsia) (Table 1). Frequently, however, psychiatric patients with excessive water intake have plasma arginine vasopressin concentrations that are not fully suppressed and urine that is not maximally dilute, thus contributing to water retention.18,19
Hyperglycemia is the most common cause of translocational hyponatremia (Figure 1D). An increase of 100 mg per deciliter (5.6 mmol per liter) in the serum glucose concentration decreases serum sodium by approximately 1.7 mmol per liter, with the end result a rise in serum osmolality of approximately 2.0 mOsm per kilogram of water.1 Retention of hypertonic mannitol, which occurs in patients with renal insufficiency, has the same effect. In both conditions, the resultant hypertonicity can be aggravated by osmotic diuresis; moderation of hyponatremia or frank hypernatremia can develop, since the total of the sodium and potassium concentrations in the urine falls short of that in serum.20
Massive absorption of irrigant solutions that do not contain sodium (e.g., those used during transurethral prostatectomy) can cause severe and symptomatic hyponatremia. Reflecting the composition of the irrigant, the resultant hyponatremia can be either hypotonic (with an irrigant containing 1.5 percent glycine or 3.3 percent sorbitol) or isotonic (with an irrigant containing 5 percent mannitol). Whether the symptoms derive from the presence of retained solutes, the metabolic products of such solutes, hypotonicity, or the low serum sodium concentration itself remains unclear.21,22
The most common causes of severe hyponatremia in adults are therapy with thiazides, the postoperative state and other causes of the syndrome of inappropriate secretion of antidiuretic hormone, polydipsia in psychiatric patients, and transurethral prostatectomy.1,17,23-25 Gastrointestinal fluid loss, ingestion of dilute formula, accidental ingestion of excessive water, and receipt of multiple tap-water enemas are the main causes of severe hyponatremia in infants and children.17,26

Clinical Manifestations

Just as in hypernatremia, the manifestations of hypotonic hyponatremia are largely related to dysfunction of the central nervous system, and they are more conspicuous when the decrease in the serum sodium concentration is large or rapid (i.e., occurring within a period of hours).27 Headache, nausea, vomiting, muscle cramps, lethargy, restlessness, disorientation, and depressed reflexes can be observed. Whereas most patients with a serum sodium concentration exceeding 125 mmol per liter are asymptomatic, those with lower values may have symptoms, especially if the disorder has developed rapidly.4 Complications of severe and rapidly evolving hyponatremia include seizures, coma, permanent brain damage, respiratory arrest, brain-stem herniation, and death. These complications often occur with excessive water retention in patients who are essentially euvolemic (e.g., those recovering from surgery or those with primary polydipsia); menstruating women appear to be at particular risk.23,28
Hypotonic hyponatremia causes entry of water into the brain, resulting in cerebral edema (Figure 2Figure 2Effects of Hyponatremia on the Brain and Adaptive Responses.). Because the surrounding cranium limits expansion of the brain, intracranial hypertension develops, with a risk of brain injury. Fortunately, solutes leave brain tissues within hours, thereby inducing water loss and ameliorating brain swelling.29,30 This process of adaptation by the brain accounts for the relatively asymptomatic nature of even severe hyponatremia if it develops slowly. Nevertheless, brain adaptation is also the source of the risk of osmotic demyelination.31-33 Although rare, osmotic demyelination is serious and can develop one to several days after aggressive treatment of hyponatremia by any method, including water restriction alone.34-36 Shrinkage of the brain triggers demyelination of pontine and extrapontine neurons that can cause neurologic dysfunction, including quadriplegia, pseudobulbar palsy, seizures, coma, and even death. Hepatic failure, potassium depletion, and malnutrition increase the risk of this complication.1,37

 http://www.nejm.org/doi/pdf/10.1056/NEJM200005183422006