Rotavirus Infection in Children

Diarrhea is a leading cause of childhood mortality in the world, accounting for 5–10 million deaths per year. In early childhood, the single most important cause of severe dehydrating diarrhea is rotavirus infection.

Epidemiology:
Rotaviruses, which are in the Reoviridae family, cause disease in virtually all mammals and birds. The virus is a wheel-like, triple-shelled icosahedron containing 11 segments of double-stranded RNA. The diameter of the particles by electron microscopy is approximately 80 nm. Rotaviruses are classified by serogroup (A, B, C, D, E, F, and G) and subgroup (I or II).
Occasional human outbreaks of group C rotavirus are reported. The other serogroups infect only nonhumans.
Rotavirus infection is most common in winter months in temperate climates. In the United States, the annual winter peak spreads from west to east
Disease tends to be most severe in patients 3–24 mo of age, although 25% of the cases of severe disease occur after 2 yr of age, with serologic evidence of infection developing in virtually all children by 4–5 yr of age. Infants younger than 3 mo are relatively protected by transplacental antibody and possibly breast-feeding. Infections in neonates and in adults in close contact with infected children are generally asymptomatic

Clinical Features:
Rotavirus infection typically begins after an incubation period of <48 hr (range 1–7 days) with mild to

Clinical Manifestations of Measles

Measles is a serious infection characterized by high fever, an enanthem, cough, coryza, conjunctivitis, and a prominent exanthem.

After an incubation period of 8–12 days, the prodromal phase begins with a mild fever followed by the onset of conjunctivitis with photophobia, coryza, a prominent cough and increasing fever.

The enanthem, Koplik spots, is the pathognomonic sign of measles and appears 1 to 4 days prior to the onset of the rash . They first appear as discrete red lesions with bluish white spots in the center on the inner aspects of the cheeks at the level of the premolars. They may spread to involve the lips, hard palate, and gingiva. They also may occur in conjunctival folds and in the vaginal mucosa. Koplik spots have been reported in 50–70% of measles cases but probably occur in the great majority.

Symptoms increase in intensity for 2–4 days until the 1st day of the rash.

The rash begins around the forehead (around the hairline), behind the ears, and on the upper neck as a red maculopapular eruption. It then spreads downward to the torso and extremities, reaching the palms and soles in up to 50% of cases. The exanthem frequently becomes confluent on the face and upper trunk

With the onset of the rash, symptoms begin to subside and the rash fades over about 7 days in the same progression as it evolved, often leaving a fine desquamation of skin in its wake.

Of the major symptoms of measles, the cough lasts the longest, often up to 10 days. In more severe cases, generalized lymphadenopathy may be present, with cervical and occipital lymph nodes especially prominent.

Approach to the Neonate With Poor Feeding

Clinical Presentation and Physical Examination

• A term infant does not feed by mouth.
• Examine the infant. Is he or she ill or well appearing?

Diagnosis and Treatment

• In an ill-appearing infant, evaluate for sepsis, respiratory distress, and congestive heart failure. Appropriate evaluation depending on signs and symptoms would be then indicated.
  
  
• In a well-appearing infant, consider whether he or she is (has):
  • Borderline preterm? Telltale signs include thin red skin, poorly developed breast tissue, undescended testes or poorly developed scrotal rugae (prominent labia minora), and few creases on the anterior third of the feet. A detailed Ballard score would also be helpful
  • Not feeding because he or she has never fed so far or may be very young (only a few hours old) and not learned how to feed. Tincture of time is all that may be required.
  • Very sleepy from just being a normal infant or from maternal magnesium sulphate or narcotics? Cold? Hypoglycemic? All these are easily reversible and require observation.
  • Anatomical barriers to feeding (cleft palate, small chin)?
  • Topical infection (oral thrush)? Tongue tie is not a cause of

Aplastic Crises In Sickle Cell Anemia

Because sickle cell anemia is a congenital hemolytic anemia, there is ongoing red cell destruction, which must be supported by endogenous erythropoiesis manifest as reticulocytosis. Any concurrent illness that suppresses endogenous erythropoiesis will result in reticulocytopenia and a decrease in hemoglobin level and hematocrit.

Acute aplastic crises are characterized by a decrease in the level of hemoglobin of >3.0 g per dL in the setting of reticulocytopenia.

Causes :
These crises often occur in association with an infection that leads to transient bone marrow suppression; human parvovirus B19, the etiologic agent of erythema infectiosum (fifth disease), is notorious for causing this complication.

Management:
Patients should be given supportive red cell transfusions when they have hemodynamic instability, which may present with tachycardia, tachypnea, postural hypotension, and unstable blood pressure. Symptomatic anemia, indicative of the need for transfusion, includes dyspnea, dizziness, excessive fatigue, and difficulty in concentrating. Clinical management depends on the degree of anemia and cardiovascular compromise. Aggressive transfusions should be avoided, because transfusion to levels much above the patient's baseline hematocrit may suppress endogenous erythropoiesis further

Acute Splenic Sequestration Crises In Sickle Cell Anemia

Acute splenic sequestration is the sudden pooling of blood in the spleen resulting in anemia, which may be life threatening. This type of crisis occurs most often in young children between 10 and 27 months of age in whom autoinfarction of the spleens has not yet happened.
The cause of this syndrome is unclear; it may be seen in the setting of concurrent bacterial or viral infection.

Diagnostic criteria
The diagnostic criteria for acute splenic sequestration include an acutely enlarging spleen, a decrease in hemoglobin level of at least 2 g per dL below baseline, thrombocytopenia often with a platelet count <100,000 per mm,³ leukopenia, and evidence of bone marrow compensation with reticulocytosis.

In its most severe form, acute splenic sequestration results in life-threatening anemia, hypovolemia, and shock. Decreases in the levels of hemoglobin <4 g per dL are associated with 35% mortality rates. It is estimated that as much as 50% of the patient's red cells can be sequestered in the spleen. Approximately 50% of patients who survive an episode of acute splenic sequestration will experience a recurrence.

Mangement
Emergency management is aimed at restoring circulatory blood volume and hemodynamic stability. Although

Acute Larynotracheitis (Viral Croup)

Acute laryngotracheitis is the most common cause of acute stridor that is encountered in pediatric practice. It usually occurs in the late fall and winter months, when viral respiratory infections reach their peak incidence. It is more common in boys than in girls, and occurs more often in children between 6 months and 6 years of age who have had an upper respiratory infection for 2 to 3 days before inspiratory stridor develops.

Clinical Features:
Fever usually is present, but the child generally does not appear to be very ill. On cautious examination of the posterior pharynx, the epiglottis may be slightly red and mildly edematous, which is quite different from the gross swelling of acute epiglottitis. The obstruction in acute laryngotracheobronchitis is primarily subglottic in location

Etiology:
Parainfluenza type 1 viruses are the most common cause of viral croups, accounting for up to 65% of the incidents, and parainfluenza type 3, influenza A and B viruses, adenoviruses, respiratory syncytial virus, and echovirus cause most of the rest. Mycoplasma pneumoniae also can produce croup symptoms in older children.

Management:
Most children with croup do not require hospitalization. Treatment at home consists of air humidification, avoidance of agitation, and reduction of fever

If signs of severe obstruction develop, treatment with

Spina Bifida Occulta

This common anomaly consists of a midline defect of the vertebral bodies without protrusion of the spinal cord or meninges. Most individuals are asymptomatic and lack neurologic signs, and the condition is usually of no consequence. In some cases, patches of hair, a lipoma, discoloration of the skin, or a dermal sinus in the midline of the lower back suggests a more significant malformation of the spinal cord .

A spine roentgenogram in simple spina bifida occulta shows a defect in closure of the posterior vertebral arches and laminae, typically involving L5 and S1; there is no abnormality of the meninges, spinal cord, or nerve roots. Spina bifida occulta is occasionally associated with more significant developmental abnormalities of the spinal cord, including syringomyelia, diastematomyelia, and a tethered cord. These are best identified with MRI . Some consider the term spina bifida occulta to denote merely a posterior vertebral body fusion defect. This simple defect does not have an associated spinal cord malformation.
 Other clinically more significant forms are more correctly termed occult spinal dysraphism.
In most of these cases, there are cutaneous manifestations such as a hemangioma, pit, lump, or hairy patch .
A dermoid sinus usually forms a small skin opening, which leads into a narrow duct, sometimes indicated by protruding hairs, a hairy patch, or a vascular nevus. Dermoid sinuses occur in the midline at the site of where meningoceles or encephaloceles may occur: the lumbosacral region or occiput. Dermoid sinus tracts may pass through the dura, acting as a conduit for the spread of infection. Recurrent meningitis of occult origin should prompt careful examination for a small sinus tract in the posterior midline region, including the back of the head. Lower back sinuses are usually above the gluteal fold and are directed cephalad. Tethered spinal cord syndrome may also be an associated problem.

Treatment Options for Duchenne Muscular Dystrophy

There is neither a medical cure for this disease nor a method of slowing its progression. Much can be done to treat complications and to improve the quality of life of affected children.


Cardiac decompensation often responds initially well to digoxin.
Pulmonary infections should be promptly treated. Patients should avoid contact with children who have obvious respiratory or other contagious illnesses. Immunizations for influenza virus and other routine vaccinations are indicated.
Preservation of a good nutritional state is importantBecause sedentary children burn fewer calories than active children and because of depression as an additional factor, these children tend to eat excessively and gain weight. Obesity makes a patient with myopathy even less functional because part of the limited reserve muscle strength is dissipated in lifting the weight of excess subcutaneous adipose tissue. Dietary restrictions with supervision may be needed.
Physiotherapy delays but does not always prevent contractures.

Other treatment of human patients with Duchenne dystrophy involves the use of prednisone, prednisolone, deflazacort, or other steroids. Glucocorticoids decrease the rate of apoptosis or programmed cell death of myotubes during ontogenesis and may decelerate the myofiber necrosis in muscular dystrophy
One protocol gives prednisone (0.75 mg/kg/day) for the first 10 days of each month to avoid

Clinical Manifestations of Hereditary spherocytosis

Hereditary spherocytosis may be a cause of hemolytic disease in the newborn and may present as anemia and hyperbilirubinemia sufficiently severe to require phototherapy or exchange transfusions. Hemolysis may be more prominent in the newborn because hemoglobin F binds 2,3-diphosphoglycerate poorly, and the increased level of free 2,3-diphosphoglycerate destabilizes spectrin-actin-protein 4.1 interactions in the RBC membrane .

The severity of symptoms in infants and children is variable. Some children remain asymptomatic into adulthood, but others may have severe anemia, with pallor, jaundice, fatigue, and exercise intolerance. Severe cases may be marked by expansion of the diploë of the skull and the medullary region of other bones, but to a lesser extent than in thalassemia major.

 After infancy, the spleen is usually enlarged, and pigmentary (bilirubin) gallstones may form as early as age 4–5 yr. At least 50% of unsplenectomized patients ultimately form gallstones, although they may be asymptomatic. Because of the high RBC turnover and heightened erythroid marrow activity, children with hereditary spherocytosis are susceptible to aplastic crisis, primarily as a result of parvovirus infection, and to hypoplastic crises associated with various other infections .

The erythroid marrow failure may result rapidly in profound anemia (hematocrit <10%), high-output heart failure, hypoxia, cardiovascular collapse, and death. White blood cell and platelet counts may also fall .

Clinical features of gasroesophegeal reflux disease

GERD is the most common esophageal disorder in children of all ages. Gastroesophageal reflux (GER) signifies the retrograde movement of gastric contents across the lower esophageal sphincter (LES) into the esophagus. Although occasional episodes of reflux are physiologic, exemplified by the regurgitation of normal infants, the phenomenon becomes pathologic (GERD) in children who have episodes that are more frequent or persistent, and thus produce esophagitis or esophageal symptoms, or in those who have respiratory sequelae.

CLINICAL MANIFESTATIONS.

Most of the common clinical manifestations of esophageal disease can signify the presence of GERD.

Infantile reflux manifests more often with regurgitation (especially postprandially), signs of esophagitis (irritability, arching, choking, gagging, feeding aversion), and resulting failure to thrive; symptoms resolve spontaneously in the majority by 12–24 mo.

Older children, in contrast, may have regurgitation during the preschool years; complaints of abdominal and chest pain supervene in later childhood and adolescence.

Occasional children present with neck contortions (arching, turning of head) designated Sandifer syndrome.

The respiratory presentations are also age dependent: GERD in infants may manifest as obstructive apnea or as stridor or lower airway disease in which reflux complicates primary airway disease such as laryngomalacia or bronchopulmonary dysplasia. Otitis media, sinusitis, lymphoid hyperplasia, hoarseness, vocal cord nodules, and laryngeal edema have all been associated with GERD. In contrast, airway manifestations in older children are more frequently related to asthma or to otolaryngologic disease such as laryngitis or sinusitis.

Pathopysiology of Portal Hypertension

The primary hemodynamic abnormality in portal hypertension is increased resistance to portal blood flow. This is the case whether the resistance to portal flow has an intrahepatic cause such as cirrhosis or is due to portal vein obstruction.

Portosystemic shunting should decompress the portal system and thus significantly lower portal pressures. Despite the development of significant collaterals deviating portal blood into systemic veins, portal hypertension is maintained by an overall increase in portal venous flow and thus maintenance of portal hypertension. A hyperdynamic circulation is achieved by tachycardia, an increase in cardiac output, and decreased systemic vascular resistance. Splanchnic dilatation also occurs. Overall, the increase in portal flow likely contributes to an increase in variceal transmural pressure. The increase in portal blood flow is related to the contribution of hepatic and collateral flow; the actual portal blood flow reaching the liver is reduced. It is also likely that hepatocellular dysfunction and portosystemic shunting lead to the generation of various humoral factors that cause vasodilatation and an increase in plasma volume.

Many of the portal hypertension complications can be accounted for by the development of a remarkable collateral circulation.

Collateral vessels may form prominently in areas in which absorptive epithelium joins stratified epithelium, particularly in the esophagus or anorectal region. The superficial submucosal collaterals, especially those in the esophagus and stomach and, to a lesser extent, those in the duodenum, colon, or rectum, are prone to rupture and bleeding under increased pressure. In portal hypertension, the vascularity of the stomach is also abnormal and demonstrates prominent submucosal arteriovenous communications between the muscularis mucosa and dilated precapillaries and veins. The resulting lesion, a vascular ectasia, has been called congestive gastropathy and contributes to a significant risk of bleeding from the stomach.

Pathology of Glomerular Diseases

The glomerulus may be injured by several mechanisms but has only a limited number of histopathologic responses; accordingly, different disease states may produce similar microscopic changes.

Proliferation of glomerular cells occurs in most forms of glomerulonephritis and may be generalized, involving all glomeruli, or focal, involving only some glomeruli while sparing others. Within a single glomerulus, proliferation may be diffuse, involving all parts of the glomerulus, or segmental, involving only some areas but not others. Proliferation commonly involves the endothelial and mesangial cells and is frequently associated with an increase in the mesangial matrix (see Fig. 508-7 ). Mesangial proliferation may result from immune complex deposition within the mesangium. The resultant increase in cell size and number and in mesangial matrix may increase glomerular size and narrow the lumens of glomerular capillaries, leading to renal insufficiency.

Crescent formation in Bowman's space (capsule) is a result of proliferation of parietal epithelial cells. Crescents develop in several forms of glomerulonephritis (termed rapidly progressive) and are thought to be a response to fibrin deposited in Bowman's space. New crescents contain fibrin, the proliferating epithelial cells of Bowman's space, basement membrane-like material produced by these cells, and macrophages that may have a role in the genesis of glomerular injury. In days to weeks, the crescent is invaded by connective tissue (fibroepithelial crescent); this generally results in glomerular obsolescence. Crescent formation is frequently associated with glomerular cell death. The necrotic glomerulus has a characteristic eosinophilic appearance and usually contains nuclear remnants. Crescent formation is usually associated with generalized proliferation of the mesangial cells and with either immune complex or anti-GBM antibody deposition in the glomerular capillary wall.

Certain forms of acute glomerulonephritis show glomerular exudation of blood cells, including neutrophils, eosinophils, basophils, and mononuclear cells. The thickened appearance of GBM may result from a true increase in the width of the membrane (as seen in membranous glomerulopathy), from massive deposition of immune complexes that have staining characteristics similar to the membrane (as seen in systemic lupus erythematosus), or from the interposition of mesangial cells and matrix into the subendothelial space between the endothelial cells and the GBM. The latter may give the basement membrane a split appearance, as seen in type I membranoproliferative glomerulonephritis and other diseases.

Sclerosis refers to the presence of scar tissue within the glomerulus. Occasionally, pathologists use this term to refer to an increase in mesangial matrix.Tubulointerstitial fibrosis is present in all patients with glomerular disease who develop progressive renal injury. This fibrosis is initiated by injury to the renal tubules, resulting in mononuclear cell infiltrates that release soluble factors that have fibrosis-promoting effects. Additionally, matrix proteins of the renal interstitium begin to accumulate, leading to eventual destruction of renal tubules and peritubular capillaries. The actual transformation of tubular epithelium to mesenchymal tissue may contribute to progressive tubulointerstitial fibrosis.

Multiple Sclerosis

MS is a chronic and generally remitting-relapsing disorder characterized by multiple white lesions in the CNS separated by time and location in the brain. The condition is rare in the pediatric population; 5% of all cases of MS occur before age 18 yrEtiology:

The cause of MS is unknown, but interactive genetic, immunologic, and infectious factors are probably responsible. A family history of MS in a first-degree relative is present in ?20%

Clinical Features:

The most frequent presenting signs are unilateral weakness with upper motor neuron signs, sensory abnormalities, visual complaints, or ataxia. Paresthesias involving the lower extremities, distal portions of the hands and feet, and the face are common.

Visual symptoms including diplopia, nystagmus, or sudden visual loss due to optic neuritis are also important early manifestations of MS.

Headache, fatigue, dysarthria, or myelopathy with a sensory level and neurogenic bladder can also be present, but impaired consciousness and encephalopathy are uncommon

Pathology:

The pathology of MS consists of demyelination with the formation of plaques

Diagnosis:

No reliable laboratory test unequivocally confirms the diagnosis of MS, except for a biopsy or an autopsy. MRI is the neuroimaging technique of choice; small plaques of 3–4 mm can be identified, particularly those located in the brainstem and spinal cord

A high percentage of pediatric patients have T2 enhancing lesions in the corpus callosum and periventricular white matter. The cerebrospinal fluid (CSF) often contains oligoclonal bands

Etiology of Pseudotumor cerebri

There are many explanations for the development of pseudotumor cerebri, including alterations in CSF absorption and production, cerebral edema, abnormalities in vasomotor control and cerebral blood flow, and venous obstruction.

The causes of pseudotumor are numerous and include

metabolic disorders (galactosemia, hypoparathyroidism, pseudohypoparathyroidism, hypophosphatasia,

prolonged corticosteroid therapy or too rapid corticosteroid withdrawal,

possibly growth hormone treatment,

refeeding of a significantly malnourished child,

hypervitaminosis A,

vitamin A deficiency,

Addison disease,

obesity,

menarche,

oral contraceptives, and pregnancy),

infections (roseola infantum, sinusitis, chronic otitis media and mastoiditis, Guillain-Barré syndrome),

drugs (nalidixic acid, doxycycline, minocycline, tetracycline, nitrofurantoin),

isotretinoin used for acne therapy especially when combined with tetracycline,

hematologic disorders (polycythemia, hemolytic and iron-deficiency anemias, Wiskott-Aldrich syndrome),

obstruction of intracranial drainage by venous thrombosis (lateral sinus or posterior sagittal sinus thrombosis),

head injury, and

obstruction of the superior vena cava.

When a secondary cause is not identified, the condition is classified as “idiopathic intracranial hypertension.”

Disorders of Malabsorption

Disorders of malabsorption constitute a broad spectrum of diseases with multiple etiologies and varied clinical manifestations. All are associated with diminished intestinal absorption of one or more dietary nutrients.

Malabsorption can result from either a defect in the nutrient digestion in the intestinal lumen or mucosal absorption

CLINICAL APPROACH TO A CHILD WITH SUSPECTED MALABSORPTION

The clinical features depend on the extent and type of the malabsorbed nutrient.

The common presenting features, especially in toddlers with malabsorption, are diarrhea, abdominal distention, and failure to gain weight, with a fall in growth chart percentiles.

Physical findings include the disappearance of the subcutaneous fat, muscle wasting, and the appearance of skin being too loose for the child

Specific findings on examination may guide toward a particular disorder;

edema is usually associated with protein-losing enteropathy,

digital clubbing with cystic fibrosis and celiac disease,

perianal excoriation and gaseous abdominal distention with carbohydrate malabsorption,

perianal and circumoral rash with acrodermatitis enteropathica,

abnormal hair with Menkes syndrome, and

the typical facial features diagnostic of the Johannson-Blizzard syndrome.

Clinical history alone may not be sufficient to make a specific diagnosis, but can direct the pediatrician toward a more structured and rational investigative approach. Diarrhea is the main clinical expression of malabsorption The nature of the diarrhea may be helpful:

explosive watery diarrhea suggests carbohydrate malabsorption;

loose, bulky stools are associated with celiac disease; and

pasty and yellowish offensive stool suggests an exocrine pancreatic insufficiency.

Investigations:

The choice of investigative studies is usually guided by the history and physical examination. In a child presenting with diarrhea, the initial work-up should include

stool occult blood and leukocytes to exclude inflammatory disorders,

stool microscopy and antibody tests for parasites such as Giardia,

stool pH and reducing substance for carbohydrate malabsorption, and

quantitative stool fat examination to identify fat malabsorption

A complete blood count including peripheral smear for microcytic anemia, lymphopenia (lymphangiectasia), neutropenia (Shwachman syndrome), and acanthocytosis (abetalipoproteinemia) is useful.

If celiac disease is suspected, serum immunoglobulin A (IgA) and tissue transglutaminase levels should be determined.

Depending on the initial investigation results, more specific investigations can be planned

Approach to pt with polyuria , polydipsia and hyponatremia

The cause of pathologic polyuria or polydipsia (exceeding 2 L/m2/24 hr) may be difficult to establish in children. Infants may present with irritability, failure to thrive, and intermittent fever.

History:

Patients with suspected DI should have a careful history taken, which should quantify the child's daily fluid intake and output and establish the voiding pattern, nocturia, and primary or secondary enuresis

Examination:

A complete physical examination should establish the patient's hydration status, and the physician should search for evidence of visual and central nervous system dysfunction as well as other pituitary hormone deficiencies

Investigations:

If pathologic polyuria or polydipsia is present, the following should be obtained:

serum for osmolality,

serum sodium, potassium, blood urea nitrogen, creatinine, glucose, and calcium;

urine for osmolality, specific gravity, and glucose determination.

The diagnosis of DI is established if the serum osmolality is greater than 300 mOsm/kg and the urine osmolality is less than 300 mOsm/kg.

If the patient's serum osmolality is less than 300 mOsm/kg (but greater than 270 mOsm/kg) and pathologic polyuria and polydipsia are present, a water deprivation test is indicated to establish the diagnosis of DI and to differentiate central from nephrogenic causes.

In the inpatient post-neurosurgical setting, central DI is likely if hyperosmolality (serum osmolality >300 mOsm/kg) is associated with urine osmolality less than serum osmolality. It is important to distinguish between polyuria resulting from postsurgical central DI and polyuria resulting from the normal diuresis of fluids received intraoperatively. Both cases may be associated with a large volume (>200 mL/m2/h) of dilute urine, although in patients with DI, the serum osmolality is high in comparison with patients undergoing postoperative diuresis

Introduction to Infective Endocarditis

INTRODUCTION

Infective endocarditis includes acute and subacute bacterial endocarditis, as well as nonbacterial endocarditis caused by viruses, fungi, and other microbiologic agents. It is a significant cause of morbidity and mortality in children and adolescents despite advances in the management and prophylaxis of the disease with antimicrobial agents

ETIOLOGY.

Viridans-type streptococci (?-hemolytic streptococci) and Staphylococcus aureus are the leading causative agents for endocarditis in pediatric patients. Other organisms cause endocarditis less frequently and, in ?6% of cases, blood cultures are negative for any organisms

EPIDEMIOLOGY.

Infective endocarditis is often a complication of congenital or rheumatic heart disease but can also occur in children without any abnormal valves or cardiac malformations. In developed countries, congenital heart disease is the overwhelming predisposing factor

In ?30% of patients with infective endocarditis, a predisposing factor is recognized. A surgical or dental procedure can be implicated in ?65% of cases in which the potential source of bacteremia is identified. Poor dental hygiene in children with cyanotic heart disease results in a greater risk for endocarditis

CLINICAL MANIFESTATIONS

Early manifestations are usually mild, especially when viridans group streptococci are the infecting organisms.

Prolonged fever without other manifestations (except, occasionally, weight loss) that persists for as long as several months may be the only symptom. Alternatively, the onset may be acute and severe, with high, intermittent fever and prostration. Usually, the onset and course vary between these two extremes

New or changing heart murmurs are common, particularly with associated heart failure.

Splenomegaly and petechiae are relatively common.

Serious neurologic complications such as embolic strokes, cerebral abscesses, mycotic aneurysms, and hemorrhage are most often associated with staphylococcal disease and may be late manifestations.

Many of the classic skin findings develop late in the course of the disease; they are seldom seen in appropriately treated patients. Such manifestations include Osler nodes (tender, pea-sized intradermal nodules in the pads of the fingers and toes), Janeway lesions (painless small erythematous or hemorrhagic lesions on the palms and soles), and splinter hemorrhages (linear lesions beneath the nails).

Acute Renal Failure

Acute renal failure (ARF) is a clinical syndrome in which a sudden deterioration in renal function results in the inability of the kidneys to maintain fluid and electrolyte homeostasis.

Pathogenesis:

ARF has been conventionally classified into 3 categories:

prerenal,
intrinsic renal, and
postrenal
Prerenal ARF, also called prerenal azotemia, is characterized by diminished effective circulating arterial volume, which leads to inadequate renal perfusion and a decreased glomerular filtration rate (GFR). Evidence of kidney damage is absent. Common causes of prerenal ARF include dehydration, sepsis, hemorrhage, severe hypoalbuminemia, and cardiac failure. If the underlying cause of the renal hypoperfusion is reversed promptly, renal function returns to normal. If hypoperfusion is sustained, intrinsic renal parenchymal damage may develop.

Intrinsic renal ARF includes a variety of disorders characterized by renal parenchymal damage, including sustained hypoperfusion/ischemia

Postrenal ARF includes a variety of disorders characterized by obstruction of the urinary tract. In neonates and infants, congenital conditions such as posterior urethral valves and bilateral ureteropelvic junction obstruction account for the majority of cases of ARF. Other conditions such as urolithiasis, tumor (intra-abdominal or within the urinary tract), hemorrhagic cystitis, and neurogenic bladder may cause ARF in older children and adolescents. In a patient with 2 functioning kidneys, obstruction must be bilateral to result in ARF. Relief of the obstruction usually results in recovery of renal function except in patients with associated renal dysplasia or prolonged urinary tract obstruction