Intrinsic Renal Failure Diagnosis

Intrinsic Renal Failure Diagnosis

During acute intrinsic renal failure, three clinical phases can be distinguished. The initial phase of injury is the period between the onset of insult and established renal failure. This phase can last several hours or, rarely, days. The second phase is that of established renal failure or the maintenance phase, characterized by reduction of the GFR and azotemia. This phase usually lasts several days to weeks. Oliguria that lasts more than 90 days often indicates the possibility of residual structural impairment.

The third or recovery phase results in a gradual increase in GFR and diuresis. An increase in urine output will improve the fluid and electrolyte imbalance. Glomerular filtration recovers more rapidly than tubular function, and the patient may demonstrate a lengthy period of tubular dysfunction, such as an inability to concentrate urine and increased salt losses. Recovery may extend over several weeks to months; the usual time of renal recovery is about 30 days.

A history may help in establishing the etiology of intrinsic renal failure. Edema, skin infection, or smoky urine suggests postinfection glomerulonephritis; purpuric rash, abdominal pain, and diarrhea suggest vasculitis; and urticarial rash, use of drugs, fever, and arthralgia may indicate acute interstitial nephritis. Once the kidney has developed intrinsic renal failure, the signs and symptoms usually are independent of the etiology. Nonspecific generalized symptoms (lethargy, anorexia, vomiting, abdominal pain) can be present. Signs of fluid retention (peripheral and pulmonary edema, hypertension) and changes in urine pattern (oliguria, anuria, or polyuria) are prominent. The hallmark of intrinsic renal failure is the worsening of azotemia, with a daily rise in serum creatinine (0.5 to 1.5 mg/dL) and in BUN (10 to 20 mg/dL).

Hyponatremia frequently is dilutional, secondary to fluid retention and/or to the administration of hypotonic solutions. Hyperkalemia develops primarily as the result of decreased GFR and cellular catabolism. Metabolic acidosis results from the reduced capacity of the kidneys to regulate acid base homeostasis and lactic acid accumulation. Hyperphosphatemia develop secondary to decreased filtration as well as cell destruction. Low serum calcium is secondary to hyperphosphatemia, resistance to parathyroid hormone, and abnormalities in vitamin D metabolism. Usually, hypocalcemia is asymptomatic, but can lead to tetany, convulsions, or hypotension. The uric acid level may become markedly elevated during the oliguric phase.

Anemia is a result of the dilution, decreased erythropoiesis, hemolysis, and blood loss. Leukopenia or leukocytosis can be evident. Microangiopathic hemolytic anemia (Coombs negative) with fragmented erythrocytes on the peripheral smear and thrombocytopenia are characteristics of hemolytic-uremic syndrome. Coagulation abnormalities accompanied by an increase in bleeding time secondary to the platelet dysfunction are found in severe uremia.

Proteinuria of more than 1 g/d, numerous dysmorphic red blood cells, and red blood cell and granular casts are seen in glomerulonephritis and vasculitis. In the case of acute interstitial nephritis, pyuria, eosinophiluria, scant casts (mainly white blood cell casts), and tubular cells are present. Myoglobinuria or hemoglobinuria should be suspected whenever there exists a urine sample that has blood on the dipstick and only 1 to 2 red blood cells in the sediment. Urinary sediment with numerous coarse granular or pigmented casts and/or tubular cells are characteristic of ATN. Urinary indices will reflect tubular dysfunction and injury and will document the inability of the kidney to concentrate urine and conserve sodium (a urine osmolality <350 mOsm/kg H2O, urine Na >40 mEq/L, FENa >2.5%).

Renal ultrasonography usually shows enlarged kidneys with a uniform increased cortical echogenicity; a renal scan shows poor uptake and excretion of radioisotope.



image source: http://en.wikipedia.org/wiki/Acute_kidney_injury

Postrenal Failure Diagnosis

Postrenal Failure Diagnosis

The pediatrician must be alert to the possibility of renal obstruction. When a child presents with the signs of azotemia and a sudden decrease in urine output, the history and physical examination can help determine the location and cause of obstruction. The patient may have had frequent urinary tract infections, hematuria, trauma, underlying lesions, an alteration in the urinary pattern (decrease in urine stream, dribbling), and presence of lower abdominal or flank pain secondary to renal enlargement and dilatation of the collecting system. The physical examination may reveal a palpable suprapubic mass, such as in male newborns who have posterior urethral valves. This is the most common cause of postrenal failure in boys.

Rectal and gynecologic examinations should be done to exclude extrinsic causes of renal obstruction. The patency of the urinary tract must be established first in every patient who has Acute Renal Failure (ARF). Thus, in patients who have ARF, assessment by renal ultrasonography must include evaluation of the lower urinary tract and bladder.

Urinalysis can reveal microscopic or macroscopic hematuria with eumorphic (normal-appearing) red blood cells, pyuria in case of infection, crystals such as calcium oxalate in nephrolithiasis, or ethylene glycol intoxication. A plain abdominal radiograph can demonstrate radiopaque stones or an ileus secondary to colic, suggest abdominal masses, and provide data about bony structures. Renal ultrasonography can detect the pattern of hydronephrosis and sometimes the site of obstruction.



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Prerenal Failure Diagnosis

Prerenal Failure Diagnosis

The patient who has prerenal failure will evidence the signs and symptoms of decreased effective blood volume or perfusion. There may be a history of vomiting, diarrhea, recent febrile illness, surgery, imbalance between input and output, heart problems, thirst, weight loss, or decrease in urine output. Signs of moderate or severe dehydration (hypotension, tachycardia, decreased skin turgor, dry mucous membrane, oliguria/ anuria) or of congestive heart failure (hepatomegaly, pulmonary edema, peripheral edema, gallop) may be present.

Laboratory studies will demonstrate hemoconcentration with an increase in hematocrit, uric acid, and total protein and a markedly elevated BUN. The BUN/SCr ratio usually is more than 20. Urinalysis will show a trace to + 1 protein, and sediment usually is normal, but hyaline and fine granular casts may be present as well. Urinary indices will reflect a maximally concentrated urine (specific gravity >1.016 to 1.030, urine osmolality >400 mOsm per kg H2O), preserved tubular integrity (urine/ plasma osmolality ratio > 1.5, urine/ plasma creatinine ratio >40, urine/ plasma urea ratio >20), and salt conservation (urine sodium <720 mEq/L, FENA <1%). In the case of metabolic alkalosis, a spot urine chloride of less than 20 mEq/L usually indicates perserved tubular function.

The chest radiograph may evidence signs of heart failure. Findings on renal ultrasonography usually are non specific, and kidney size is normal.


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Acute Renal Failure (ARF) in Children

Acute Renal Failure in Children

Acute Renal Failure (ARF) is relatively uncommon, its mortality rate is potentially so high that it is important to recognize this condition in children. Rapid deterioration of renal function is caused by numerous insults and results in typical findings, including extracellular volume expansion, hyperkalemia, hypertension, metabolic acidosis, and azotemia. It usually is reversible, with the majority of patients recovering completely. However, ARF can lead to residual impairment of renal function and progress to end-stage renal disease and death. Conservative medical treatment often is life-saving.

Definition

Acute Renal Failure (ARF) represents the rapidly progressive (within several hours or days) cessation of renal function, which results in the inability of the kidney to control body homeostasis, manifesting in retention of nitrogenous waste products (azotemia) and fluid and electrolyte imbalance. On the basis of pathophysiologic process, ARF has been divided broadly into three diagnostic categories: prerenal, intrarenal (organic-intrinsic), and postrenal failure. Prerenal and early postrenal failures are renal functional disorders and responses of a structurally intact kidney to extrarenal processes. These forms of renal dysfunction recover rapidly as soon as the cause is reversed. However, if these two disorders are not recognized in time, persist too long, or are treated inadequately, they can result in intrinsic renal failure. Intrinsic or organic renal failure is caused by structural changes within the kidney. It is potentially reversible but requires an extended period of recovery.

Etimology
Prerenal failure is the most common form of Acute Renal Failure (ARF) in children. The main process in the development of prerenal failure is hypoperfusion of the kidney, secondary to reduced effective plasma volume or heart failure. Numerous underlying conditions can lead to prerenal failure. In children, the most common causes are hypovolemia secondary to gastrointestinal losses, the state of shock, and postoperative conditions. For example, ARF may occur after heart surgery when the aorta is cross-clamped or following prolonged cardiopulmonary bypass time.
A variety of renal disorders and insulting events can contribute to the development of intrinsic renal failure. Among these are acute glomerulonephritis and vasculitis of childhood, acute tubular necrosis, and acute interstitial nephritis.
Acute tubular necrosis (ATN) is the most common cause of intrinsic renal failure. It is associated with necrosis of the tubular epithelium following hypoxic or nephrotoxic injury. Various substances, including ethylene glycol, heavy metals, hydrocarbons, and certain antibiotics, including cephalosporins, aminoglycosides, sulfonamides, methicillin, and colistin, are potent nephrotoxins. Aminoglycoside-induced acute renal failure occurs typically 5 days after drug administration and represents a dose-dependent phenomenon.
Radiologic contrast material of the ionic type can cause ARF, usually within 24 hours after exposure, especially in individuals who are dehydrated, have diabetes mellitus, or have preexisting renal insufficiency. Primary diseases of the glomeruli and small blood vessels of the kidney may present with rapidly progressive ARF. Large vessel diseases (renal artery thrombosis or embolism, renal vein thrombosis) are uncommon. Acute interstitial nephritis usually results from immune-mediated drug sensitivity or infection.
Postrenal failure is a less frequent cause of ARF in children. It presents as an abrupt decline in glomerular filtration rate (GFR) secondary to lower tract obstruction or bilateral upper tract obstructions, unless the patient has a single kidney. Obstruction can be secondary to structural, congenital, or acquired anomalies of the urinary tract, including posterior urethral valve, ectopic ureter, aberrant vessels, or stones, or may result from functional abnormalities such as neurogenic bladder. Uric acid, the end product of purine metabolism, is insoluble at high concentrations in an acidic medium; during rapid cellular lysis before or after chemotherapy it often will precipitate in a distal nephron and cause renal obstruction. Depending on localization, obstruction can be extrinsic or intrinsic, at the level of the collecting duct, pelvis, ureter, bladder, urethra, or meatus.

Pathophysiology
Prerenal dysfunction can lead to development of renal failure and is characterized by a decline in renal blood flow (RBF), GFR, and urine flow. After an acute reduction in effective intravascular volume, compensatory mechanisms of both the organism and the kidney will operate to counteract the volume loss and restore renal perfusion. Central activation of several neural and humoral responses occurs, including increased activity of the sympathetic system and the renin-angiotensin II-aldosterone system and enhanced release of antidiuretic hormone.
Hemodynamic alterations within the kidney develop. An initial, short response of maximum dilatation of afferent arteriole is replaced by vasoconstriction. Blood flow is redistributed away from the renal cortex to juxtamedullary nephrons, which results in extensive tubular reabsorption of sodium, water, and urea.
With intense vasoconstriction, the kidney, acting as a blood reservoir, will shunt additional volumes of blood to the most vital organs (brain and heart); this response actually may be lifesaving in states of shock, blood loss, or severe dehydration. When the kidney has used these compensatory mechanisms fully, and the delivery of oxygen to the kidney remains critically impaired, acute necrosis of tubular cells occurs.
Injury due to ischemia or toxins is manifested by alterations in cellular metabolism. Cell detachment, desquamation, necrosis, and generation of intratubular debris and cast formations develop. The backward leak of tubular fluid across the injured tubular membrane and tubular obstruction results in further hemodynamic changes. Finally, decreased filtration rate leads to oliguria or anuria, defined as follows:

• · Oliguria-urine output less than 0.5 mL/kg per hour in infants or less than 500 mL/1.73 m² per day) in older children
• · Anuria-total cessation of urinary output

Although intrinsic renal failures generally present as oliguria or anuria, the entity of nonoliguric ARF (sometimes called nonoliguric vasomotor nephropathy) is being increasingly recognized. Nonoliguric renal failure typically consists of azotemia in the face of a normal urine output (> 1 mL/kg per hour). It occurs primarily as a result of exposure to a nephrotoxic drug, especially an aminoglycoside.
Postrenal failure is a result of a total or partial obstruction of the urinary tract that affects the flow of normally produced urine. In the case of partial obstruction, the patient usually is nonoliguric and may even be polyuric. With the development of an obstruction, pressure proximal to the site of obstruction rises, which results in increased intratubular pressure and dilatation of the collecting system (hydronephrosis). Vasodilatation occurs only in the first 1 to 3 hours after obstruction and is followed by a period of intense vasoconstriction that leads to the ultimate damage of the tubular cells.



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Carpal Tunnel Syndrome: Clinical Findings and Treatment

Carpal Tunnel Syndrome: Clinical Findings and Treatment

What is Carpal Tunnel Syndrome?

 Here's Carpal Tunnel Syndrome definition:
Carpal tunnel syndrome is a common disorder characterized by pain, burning , and tingling of the palmar surface of the hand, resulting from compression of the median nerve between the carpal ligament and other structures within the carpal tunnel (entrapment neuropathy). The volume of the contents of the tunnel can be increased by organic lesions such as synovitis of the tendon sheaths or carpal joints, recent or malhealed fractures, tumors, and occasionally congenital anomalies. Even though no anatomic lesion is apparent, flattening or even circumferential constriction of the median nerve may be observed during operative section of the ligament. The disorder may occur in pregnancy, is seen in individuals with a history of repetitive use of the hands, and may follow injuries of the wrists. A familial type of carpal tunnel syndrome has been reported in which no etiologic factor can be identified.
Carpal tunnel syndrome can also be a feature of many systemic diseases: rheumatoid arthritis and other rheumatic disorders (inflammatory tenosynovitis); myxedema, amyloidosis, sarcoidosis, and leukemia (tissue infiltration); acromegaly; hyperparathyroidism, hypocalcemia, and diabetes mellitus.

Clinical Findings of Carpal Tunnel Syndrome

Pain in the distribution of the median nerve, which may be burning and tingling (acroparesthesia), is the initial symptom. Aching pain may radiate proximally into the forearm and occasionally proximally to the shoulder, neck, and chest. Pain is exacerbated by manual activity, particularly by extremes of volar flexion or dorsiflexion of the wrist. It may be most bothersome at night. Impairment of sensation in the median nerve distribution may not be apparent. Subtle disparity between the affected and opposite sides can be demonstrated by testing for two-point discrimination or by requiring the patient to identify different textures of cloth by rubbing them between the tips of the thumb and the index finger. Tinel's or Phalen's sign may be positive. (Tinel's sign is tingling or shock-like pain on volar wrist percussion; Phalen's sign, pain or paresthesia in the distribution of the median nerve when the patient flexes both wrists to 90 degrees with the dorsal aspects of the hands held in apposition for 60 seconds.) The carpal compression test, performed by applying direct pressure on the carpal tunnel, may be more sensitive and specific than the Tinel and Phalen tests. Muscle weakness or atrophy, especially of the abductor pollicis brevis, appears later than sensory disturbances. Useful special examinations include electromyography and determinations of segmental sensory and motor conduction delay. Distal median sensory conduction delay may be evident before motor delay.

Differential Diagnosis of Carpal Tunnel Syndrome

This syndrome should be differentiated from other cervicobrachial pain syndromes, from compression syndromes of the median nerve in the forearm or arm, and from mononeuritis multiplex. When left-sided, it may be confused with angina pectoris.

Carpal Tunnel Syndrome Treatment

Treatment is directed toward relief of pressure on the median nerve. When a primary lesion is discovered, specific treatment should be given. When soft tissue swelling is a cause, elevation of the extremity may relieve symptoms. Splinting of the hand and forearm at night may be beneficial. Injection of corticosteroid into the carpal tunnel can alleviate symptoms in some patients, particularly those with synovitis of the wrist. To reduce the chance of nerve injury, this injection should be performed by a physician thoroughly familiar with the anatomy of the carpal tunnel. Operative division of the volar carpal ligament gives lasting relief from pain, which usually subsides within a few days. Muscle strength returns gradually, but complete recovery cannot be expected when atrophy is pronounced.



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BreastFeeding Benefits

BreastFeeding Benefits

Breast milk is universally recognized as the preferred source of infant nutrition, and the nutritional advantages of breast milk have been well documented. Colos-trum, the first milk produced after delivery, provides an initial dose of enzymes that promote gut maturation, facilitate digestion and stimulate passage of meco-nium. Colostrum is also high in protein, primarily because of high levels of im-munoglobulins and secretory IgA. The protein in human milk is ideal not only for absorption, but also for utilization, especially by the rapidly developing infant brain. Human milk also contains predominantly polyunsaturated fats with stable amounts of cholesterol, an important constituent of brain and nerve tissue.

Human milk also protects against infection by providing cellular immunity through macrophages and humoral factors, such as antibodies. Numerous studies have verified that breast-fed infants have a lower incidence of bacterial and viral illnesses than bottle-fed infants. This low incidence is of particular clinical significance in developing nations? Ongoing research suggests that breast feeding may provide immuno-logic protection against diabetes mellitus, cancer and lymphoma. Finally, breast feeding has been found to provide protection from allergic diseases, including eczema, asthma and allergic rhinitis. This protection is most likely the result of breast milk decreasing intestinal permeability to large, allergenic molecules.

Recognizing these as well as other advantages, the American Academy of Family Physicians (AAFP) and the American Academy of Pediatrics (AAP) have identified breast milk as the preferred source of infant nutrition. In addition, the U.S. Public Health Service (USPHS) has established a national goal that, by the turn of the century, 75 percent of new mothers will be breast-feeding at the time of hospital discharge. Despite an emphasis on breast feeding by both private and government organizations, only 54 percent of U.S. mothers initiate breast feeding, and fewer than half of these mothers continue nursing for at least six months. Clearly, all health care providers should actively promote breast feeding if the goal set by the USPHS is to be accomplished.

To successfully promote breast feeding, family physicians should consider the influence of marketing campaigns aimed at expectant and new mothers by the manufacturers of infant formulas. Historically, their dogged marketing efforts have included the distribution of free cases of infant formula to expectant mothers, as well as the inclusion of formula samples in commercial hospital discharge packs designed for breast-fed infants. Physicians must work proactively to weigh the risks and benefits of promotional materials and develop appropriate policies governing their distribution in their hospitals or academic institutions.



image source: http://healthynaturalbaby.org/breastfeeding-shown-to-reduce-crib-death-in-infants-by-50/

Heart disease: Problem diseases in pregnancy

Heart disease: Problem diseases in pregnancy

Most heart disease in women of childbearing age is rheumatic in origin despite the recent great reduction in the prevalence of rheumatic fever. Better living conditions in the UK and the more prompt treatment of streptococcal sore throats with antibiotics in childhood have reduced rheumatic damage to the heart valves and myocardium. An increasing proportion of pregnant women have congenital heart lesions that have been treated previously.
Pregnancy puts an increased load on the cardiovascular system. More blood has to be circulated so that cardiac output increases by up to 40% by mid-pregnancy, staying steady until labour, when it increases further. This increased cardiac work cannot be done as effectively by a damaged heart; if the heart is compromised a woman would be wise to avoid other increased loads that might precipitate cardiac failure. The most frequently encountered are:

• Household work
• Recrudescence of rheumatic fever
• Paid work outside the home
• Care of other family members
• Respiratory infection
• Pre-eclampsia
• Urinary infection
• AnaemiaBacterial endocarditis

Care should be taken just after delivery: with the uterine retraction up to a litre of blood can be swiftly shunted from the uterine veins into the general venous system.


References:
Geoffrey Chamberlain. 2002. ABC of Antenatal Care. London: BMJ Books.
Image Source: http://www.nhs.uk/Conditions/Congenital-heart-disease/Pages/Complications.aspx