idris

2012-05-16T03:05:00.002-07:00

WHAT CAUSES KIDNEY STONES?

Kidney stones develop as a result of a complicated interaction of biologic events that are most likely triggered by genetic susceptibility coupled with dietary factors. The process is not completely known.

General Biologic Events Leading to Kidney Stones

The key process in the development of kidney stones is supersaturation.

This process involves salts that are carried in urine. Such salts may include calcium oxalate, uric acid, cystine, or xanthine.
These salts can become extremely concentrated under certain circumstances: if the volume of urine is significantly reduced; or if abnormally high amounts of crystal-forming salts are present.
When concentration levels reach the point at which the salts no longer dissolve, they precipitate out and form crystals.

Different factors may be involved in either reducing urine volume or increasing the levels of the salts.

Deficiencies in Protective Factors. Normally, urine contains protective factors that include magnesium, citrate, pyrophosphate, and various proteins and enzymes. These compounds may protect against stone formation in various ways:

Allowing salt in the urine to be at higher-than-normal concentrations without forming crystals.
Preventing crystal formation.
Coating the crystals and preventing them for adhering to the tube surface.

Deficiencies in these protective substances therefore cause stones.

Changes in the Acidity of the Urine. Changes in the balance of acid to alkaline in the urine can affect stone precipitation.

Uric acid and cystine stones thrive in acidic urine
Calcium phosphate and struvite stones thrive in alkaline.

Factors that Bind Crystals to the Kidney Tubules. Researchers are studying the cells lining the kidney tubules in order to understand how and why early crystals bind to the tubes long enough to form stones. Under investigation are elevated levels of substances that either cause crystals to adhere to the tubes or deficiencies in those that prevent them from sticking.

Causes of Calcium Stones

Often, the cause of calcium stones is not known, a condition called idiopathic nephrolithiasis. In general, calcium stones form when there are imbalances of components in the urine that either promote or inhibit formation of the stone. Genetic factors may play a role in 45% of calcium-stone cases.

Excess Calcium in the Urine (Hypercalciuria). Hypercalciuria, in which there is too much calcium in the urine, is responsible for about 70% of calcium-combining stones. A number of conditions may produce hypercalciuria. Many are due to genetic factors, but most causes are unknown. Here are some theories and actual causes:

Overly efficient intestinal absorption of calcium. In more than half of cases, the source of excess calcium overload in urine is from the intestine, not the kidney. In most cases, a combination of genetic factors conspires to increase calcium absorption. Researchers are investigating a number of suspects, including a possible defective gene that regulates calcitriol, a form of vitamin D, which, in excess levels, may increase intestinal absorption of calcium.
Excessive chloride. Chloride has a negative charge and calcium a positive one, so they are often used by the body to balance each other. Excess chloride, then, may lead to excess calcium. A gene known as CLCN5, which regulates chloride in the urine, is defective in many patients with calcium stones.
Renal calcium leak. This is a condition in which the filtering processes in the kidney fail, causing an increase of calcium in the urine.
Excessive sodium. Calcium absorption in the kidney tubules follows the absorption of sodium and water. High urinary levels of sodium then results in increased levels of calcium. Defects in the kidney tubules transport system can cause imbalances in sodium and phosphate that result in elevated calcium in the urine. A high salt diet can also produce this effect.
Certain cancers and sarcoidosis (a chronic disorder marked by small lumps on organs) can cause excess calcium.
Many drugs, including thyroid hormones and loop diuretics (drugs that increase urination), can increase calcium concentration in urine. Stones are an uncommon side effect of these medications, however.

Excess Oxalate in the Urine (Hyperoxaluria). Oxalate, also called oxalic acid, combines with calcium to form calcium oxalate which is the most common stone-forming compound. Excessive oxalate in the urine (hyperoxaluria) is responsible for about 30% of calcium stones and is a more common cause of stones than too much calcium in the urine. A number of conditions can contribute to hyperoxaluria:

Primary hyperoxaluria (type I or type II). This is an inherited disorder associated with kidney stones.
Deficiencies of pyridoxine (vitamin B6). Severe vitamin B6 deficiencies (usually due to genetic disorders) can result in overproduction of oxalic acid.
Short bowel syndrome. Short bowel syndrome is the result of surgery in the small intestine that results in malabsorption. This disorder is the inability of the intestines to absorb fat and nutrients. In such cases, calcium may bind to unabsorbed fat instead of to oxalates. This leaves excess oxalate, which is absorbed by the intestine and excreted into the kidney. People with Crohn's disease, intestinal infections, and children with structural abnormalities in the small intestine are at risk for these procedures and short bowel syndrome.
Dietary oxalates. Whether eating foods rich in oxalates or taking too much vitamin C plays any major role in hyperoxaluria is unproven. One Swiss study suggests that certain people may be hypersensitive to meat protein, rendering them susceptible to mild hyperoxaluria. [For foods containing oxalates, see How Can Kidney Stones Be Prevented?, below.]
Hormones. One 1999 animal study suggested that male hormones may account for the greater risk for kidney stones in men. Androgens (male hormones) were associated with a higher risk for calcium oxalate crystals formation while estrogens (female hormones) decreased it. This finding is consistent with others, suggesting that estrogen may protect against the formation of calcium stones by keeping urine alkaline and raising citrate levels. Whether hormone replacement actually prevents stones in older women is not yet determined, however.

Excessive Calcium in the Bloodstream (Hypercalcemia). Hypercalcemia generally occurs when bones break down and release too much calcium into the bloodstream. This is a process called resorption, which can occur because of the following:

Hyperparathyroidism. Overactive parathyroid glands are the causes of about 5% of calcium stones. And people with this disorder have at least a 20% chance of kidney stones. Women are more likely to have this disorder than men are.
Immobilization.
Renal tubular acidosis, disorder that causes acid and alkaline imbalance. It not only increases calcium in the blood stream, it also reduces citrate levels [ see below ].

Low Urine Levels of Citrate (Hypocitraturia) and Other Stone-Inhibiting Compounds. Citrate is the primary agent for removal of excess calcium. Low levels in the urine, known as hypocitraturia, are a significant risk factor for calcium (and also uric acid) stones. Many conditions can reduce citrate levels, but often the causes of hypocitraturia severe enough to cause stones are unknown:

Renal tubular acidosis. This disorder results in abnormalities in the acid and alkaline balance in the body's fluids, which causes a reduction of citrate in the urine. To make matters worse, the disorder also causes bone resorption and increases calcium levels in the blood.
Potassium or magnesium deficiency.
Urinary tract infection.
Kidney failure.
Chronic diarrhea.

In addition to citrate, other substances in urine also prevent calcium from precipitating out or forming calcium stones. Some of these include nephrocalcin-A and uropontin (molecules known as glycoproteins), glycosaminoglycan, magnesium, and pyrophosphate.

Nanobacteria Infection. An interesting focus of investigation is the discovery of extremely tiny bacteria, termed nanobacteria, which are able to pass from the blood into urine. Such bacteria coat themselves with mineral deposits that resemble the composition of kidney stones. Cells infected with the bacteria develop mineral deposits both on the inside and outside. Researchers hypothesize that such bacteria may provide the core kidney stones in many people.

Causes of Uric Acid Stones

Excessive Amounts of Uric Acid (Hyperuricuria). Uric acid stones most often form out of high concentrations of uric acid crystals (hyperuricuria). Such crystals are made from purine, a nitrogen end product of dietary protein. They are not related to the acidity of the urine itself, although in the majority of uric acid stones, the urine is so persistently acidic that even normal amounts of uric acid can precipitate and form stones. (About 10% to 20% of cases of uric acid stones are found in urine with normal pH values.) A number of conditions contribute to hyperuricuria:

Genetic factors.
Diets overly rich in animal proteins.
Gout.
Certain medications (chemotherapy agents, diuretics, and salicylates).
Binge drinking.
Fasting.
Lead toxicity.
Blood diseases (leukemia, certain uncommon anemias, multiple myeloma, and lymphomas).
Chronic diarrhea.

Note: Hyperuricuria may also play a role in some calcium oxalate stones. In this case, urate (the salt formed from uric acid) creates a crystal nidus (the nucleus of a crystal), around which calcium oxalate crystals form and grow. Such stones tend to be severe and recurrent.

Causes of Struvite Stones

Struvite stones are almost always caused by urinary tract infections due to bacteria that secrete certain enzymes. These enzymes, in turn, raise urine concentrations of the ammonia that composes the crystals forming struvite stones. The stone-promoting bacteria are usually Proteus, but may also include Pseudomonas, Klebsiella, Providencia, Serratia, and staphylococci. Women are twice as likely to have struvite stones than men are.

Causes of Other Stones

Other stones, including cystine and xanthine stones, are usually due to genetic abnormalities.

Causes of Cystine Stones. Cystine stones are found in patients with an inherited disorder that causes abnormal transport in the kidney and gastrointestinal system of the amino acids cystine, ornithine, lysine, and arginine.

Causes of Xanthine Stones. In some cases, xanthine stones may develop in patients being treated with allopurinol for gout.

Q. What causes kidney stones?
Dr. Green: The exact causes of kidney stone formation are not completely known; however, most credible sources believe that stones are the result of mineral supersaturation and crystallization in the urine. Heredity, environment, age, sex, urinary infection, diet, and metabolic diseases are probably involved in stone formation. The primary known causes are: 1) inadequate urinary drainage, 2) dehydration and lack of sufficient fluid ingestion, 3) foreign bodies in the urinary tract, 4) diet with excess oxalates, calcium, and vitamin abnormalities, e.g., Vitamin A deficiencies, Vitamin D excess, 5) urinary infections, 6) metabolic diseases, e.g., hyperparathyroidism, cystinuria, gout, intestinal dysfunction, and 7) use of certain medications, e.g., diuretics, that increase levels of uric acid.

SNAKE BITES

2012-02-08T04:01:00.005-08:00

At presentation of casualty A,B,C of resuscitation ,some of the venomous snakes can complicate with hemorrhagic shock,cardiotoxicity

Secondary survey

1-History of the snake bites and if possible establishes whether it was venomous or not.

2-Examination of the wound inflicted can give indication whether the snake was venomous or not. Nonvenomous snakes do not produce fang marks, but rather rows of tiny puncture wounds or scratches.

3-Removal of any tight clothing on the limb or tourniquet that had been applied.

4- Obtain IV access in the non-affected limb and keep on IV fluids

5-Take vital signs continuously monitor

6-Clean the bitten part and irrigate with copious amounts of water.

7-Elevate the limb as much as possible.

8-Provide analgesia

9-Administer tetanus toxoids

10-Give prophylactic antibiotics

11-Measure circumference of the bitten part at several levels, comparing these with similar measurements carried out once on the unaffected side.

-Monitor for any continued swelling.

12-If anti venom available this can be given in the IV fluid infusion and run slowly looking out for any allergic reactions.

13-If there is continued swelling of the limb even with elevation, then fasciotomy may be necessary to prevent occurrence of compartment syndrome.

Initial investigations

1.Full blood count-Hb ,can draw blood for GXM

2.LFT-Liver transaminases ,serum bilirubin

3.Urea,electrolyte and creatinine

Urinalysis-protenuria and hematuria

4.Creatine kinase

5.Coagulation profile- platelet count, clotting time, prothrombin time, partial thromboplastin time, fibrinogen level

6. ECG studies.

Manage any complications as appropriate:

Abnormal coagulation profile-Fresh frozen plasma transfusion.

Hemolytic anemia-Whole blood transfusion

Shock-IV fluid –crystalloids and Colloids

STATUS ASTHMATICUS

2012-02-08T03:15:00.000-08:00

STATUS ASTHMATICUS

Introduction

-Status asthmaticus is an acute exacerbation of asthma that remains unresponsive to initial treatment with bronchodilators.

-Patients report chest tightness, rapidly progressive shortness of breath, dry cough, and wheezing.

-Typically, patients present a few days after the onset of a viral respiratory illness, following exposure to a potent allergen or irritant, or after exercise in a cold environment.

Pathophysiology

-Allergic inflammation in asthma begins with the development of a predominantly helper T2 lymphocyte–driven, as opposed to helper T1 lymphocyte–driven, immune milieu, perhaps caused by certain types of immune stimulation early in life.

-This is followed by allergen exposure in a genetically susceptible individual. Specific allergen exposure (eg, dust mites) under the influence of helper T2 lymphocytes leads to B-lymphocyte elaboration of immunoglobulin E (IgE) antibodies specific to that allergen.

-The IgE antibody attaches to surface receptors on airway mucosal mast cells.

-Subsequent specific allergen exposure leads to cross-bridging of IgE molecules and activation of mast cells, with elaboration and release of a vast array of mediators. -These mediators include histamine; leukotrienes C4, D4, and E4; and a host of cytokines.

-These mediators cause:

ü Bronchial smooth muscle constriction

ü Vascular leakage

ü Inflammatory cell recruitment (with further mediator release)

ü Mucous gland secretion

-These processes lead to airway obstruction by constriction of the smooth muscles, edema of the airways, influx of inflammatory cells, and formation of intraluminal mucus.

-In addition, ongoing airway inflammation is thought to cause the airway hyperreactivity characteristic of asthma. -Physiologically, asthma has 2 components: an early acute bronchospastic aspect marked by smooth muscle bronchoconstriction and a later inflammatory component resulting in airway swelling and edema.

Early bronchospastic response

Mediators, including histamine, prostaglandin D2, and leukotriene C4. These substances cause airway smooth muscle contraction, increased capillary permeability, mucus secretion, and activation of neuronal reflexes. Early asthmatic response is characterized by bronchoconstriction that is generally responsive to bronchodilators, such as beta2-agonist agents

Clinical presentation

History

-The symptoms of asthma consist of a triad of

§ Dyspnea

§ Cough

§ wheezing

§ Chest tightness

-Wheezing regarded as the sine qua non for asthma.

-Cough is non productive initially then thick sputum later

- Personal or family history of allergic diseases such as eczema, rhinitis, or urticaria is valuable contributory evidence.

-Worsening of symptoms after exposure to recognized triggers such as pollens, dust, feathered or furry animals, exercise, viral infections, chemicals, and environmental tobacco smoke

-Worsening of symptoms after taking aspirin/non-steroidal anti-inflammatory medication or

use of β-blockers.

-An extremely common feature of asthma is nocturnal awakening with dyspnea and/or wheezing

The hallmark of asthma is that these symptoms tend to be:

􀂄 Variable

􀂄 Intermittent

􀂄 Worse at night

􀂄 Provoked by triggers including exercise

Physical

-Respiratory distress

-Patients present with tachypnea, tachycardia, and mild systolic hypertension.

-Severe asthma may give paradoxical pulse. paradoxical pulse depends on the generation of large negative intrathoracic pressures

-The lungs rapidly become overinflated, and the anteroposterior diameter of the thorax increases. –barrel chest.

-If the attack is severe or prolonged, there may be a loss of adventitial breath sounds, and wheezing becomes very high pitched.

-The end of an episode is marked by a cough that produces thick, stringy mucus, which often takes the form of casts of the distal airways (Curschmann's spirals) and, when examined microscopically, often shows eosinophils and Charcot-Leyden crystals.

- Very severe attack may cause air trapping with the chest and cause silent chest. These findings imply extensive mucus plugging and impending suffocation. Ventilatory assistance by mechanical means may be required.

-Atelectasis due to inspissated secretions occasionally occurs with asthmatic attacks.

- Spontaneous pneumothorax or pneumo-mediastinum occur but are rare.

Diagnosis

The diagnosis of asthma is made principally on clinical grounds and laboratory data are utilized in a supplementary or confirmatory fashion. A history of episodic wheezing in a nonsmoking patient, with findings of wheezing on physical examination is strongly suggestive of asthma.

5.Serology

Total IgE is frequently elevated in serum in asthmatics.

6.Hematology

Blood counts may reveal evidence of eosinophilia, which is usually mild, representing 5%-15% of the differential count. Profound eosinophilia (25% or greater, 3000 per ul or greater) should suggest another cause.

Staging:

The 4 stages of status asthmaticus are based on ABG progressions in status asthma.

Patients in stage 1 or 2 may be admitted to the hospital, depending on the severity of their dyspnea, their ability to use accessory muscles, and their PEF values or FEV₁ after treatment (>50% but <70% of predicted values). Patients with ABG determinations characteristic of stages 3 and 4 require admission to the ICU. The PEF value or FEV₁ is less than 50% of the predicted value after treatment.

Stage 1

-Patients not hypoxemic, but they are hyperventilating and have a normal PO₂.

-Recent data suggest that to possibly facilitate hospital discharge, these patients may benefit from ipratropium treatment via a handheld nebulizer in the emergency setting as an adjunct to beta-agonists.

Stage 2

This stage is similar to stage 1, but patients are hyperventilating and hypoxemic.

Such patients may still be discharged from the emergency department, depending on their response to bronchodilator treatment, but will require systemic corticosteroids.

Stage 3

-These patients are generally ill and have a normal PCO₂ due to respiratory muscle fatigue.

-Their PCO₂ is considered a false-normal value and is a very serious sign of fatigue that signals a need for expanded care.

-This is generally an indication for elective intubation and mechanical ventilation, and these patients require admission to the ICU.

-Parenteral corticosteroids are indicated, as is continued aggressive use of an inhaled beta2-adrenergic bronchodilator.

-These patients may benefit from theophylline.

Stage 4

This is a very serious stage marked by

-PO₂ is low (hypoxia) and PCO₂ is high (hypercapnea) signifying respiratory failure.

-Less than 20% lung function or FEV₁

-Patients require intubation and mechanical ventilation.

-Patients in stage 4 should be admitted to the ICU.

-Switching from inhaled beta-2 agonists and anticholinergics to metered-dose inhalers (MDIs) via mechanical ventilator tubing is indicated.

-Parenteral steroids are essential, and theophylline may be added, as with patients in stage 3.

Monitoring:

-Severe asthmatics should be monitored for heart rate, blood pressure, O2 saturation, and arterial pH and PaCO2.

-Ventilator monitoring must be meticulous, because increases in peak inspiratory pressure or decreases in pulmonary compliance may signal worsening bronchoconstriction or an extrapleural air leak.

Other definitions of asthma

Near fatal asthma

Raised PaCO2 and/or requiring mechanical ventilation

with raised inflation pressures 223mmHg

Life threatening asthma –Stage 4

Any one of the following in a patient with severe asthma:

1- PEF <33% best or predicted

2- SpO2 <92%

- PaO2 <8 kPa

3-Raised Pco2- normal PaCO2 (4.6 – 6.0 kPa)

4-Silent chest

5-Cyanosis

6-Feeble respiratory effort-with exhaustion-

7-Hypoventilation

8-Bradycardia and Dysrhythmia

9-Hypotension

10-Confusion, irritability and anxiety

11-Coma

Acute severe asthma Any one of:-Stage 3

- PEF 33-50% best or predicted

- respiratory rate ≥25/min

- heart rate ≥110/min

- inability to complete sentences in one breath

Moderate asthma exacerbation

- Increasing symptoms

- PEF >50-75% best or predicted

- no features of acute severe asthma

Brittle asthma

- Type 1: wide PEF variability (>40% diurnal variation for >50% of the time over a period >150 days) despite

intense therapy

- Type 2: sudden severe attacks on a background of

apparently well controlled asthma

Complications

Complications of asthma include

§ Exhaustion

§ Dehydration

§ airway infection

§ cor pulmonale

§ tussive syncope

§ Pneumothorax occurs but is rare

§ Acute hypercapnic and hypoxic respiratory failure occurs in severe disease.

Late inflammatory response

Release of inflammatory mediators prime adhesion molecules in the airway epithelium and capillary endothelium, which then allows inflammatory cells, such as eosinophils, neutrophils, and basophils, to attach to the epithelium and endothelium and subsequently migrate into the tissues of the airway.

Eosinophils release eosinophilic cationic protein (ECP) and major basic protein (MBP). Both ECP and MBP induce desquamation of the airway epithelium and expose nerve endings. This interaction promotes further airway hyperresponsiveness in asthma.

The 2 phases of asthma lead to:a

ü increased airway resistance and obstruction.

ü Air trapping results in lung hyperinflation

ü Ventilation/perfusion (V/Q) mismatch

ü Increased dead space ventilation.

ü Decreased compliance and increased work of breathing.

-The increased pleural and intra-alveolar pressures that result from obstruction and hyperinflation, together with the mechanical forces of the distended alveoli, eventually lead to a decrease in alveolar perfusion.

-The combination of atelectasis and decreased perfusion leads to V/Q mismatch within lung units. The V/Q mismatch and resultant hypoxemia trigger an increase in minute ventilation.

The early stages of acute asthma, hyperventilation may result in respiratory alkalosis but later respiratory acidosis occurs V/Q mismatch.

Sex: In infants, males generally have more severe disease than females.

In older children, males and females are equally affected.

Asthma has a higher incidence among adult females.

Age:

Asthma is well distributed among people of all age groups.

Children who have asthma in the first year of life and those aged 9-16 years tend to have much more severe disease.

DDx

-Pulmonary Hypertension, Primary

-Congestive heart failure- Orthopnea, moist basilar rales, gallop rhythms, blood-tinged sputum
-Croup
-Stridor
-Upper airway obstruction
-Foreign-body aspiration

-Neoplasm

-Bronchial stenosis.

-Recurrent episodes of bronchospasm can occur with carcinoid tumors

-Recurrent pulmonary emboli

- Chronic bronchitis

- Eosinophilic pneumonias are often associated with asthmatic symptoms, as are various chemical pneumonias and exposures to insecticides and cholinergic drugs.

-Bronchospasm occasionally is a manifestation of systemic vasculitis with pulmonary involvement.

INVESTIGATIONS

1-Spirometry

-The diagnosis of asthma is established by demonstrating reversible airway obstruction.

-The evaluation for asthma should include spirometry (FEV1, FVC, FEV1/FVC) before and after the administration of a short-acting bronchodilator.

-Reversibility is traditionally defined as a 15% or greater increase in FEV1 after two puffs of a b-adrenergic agonist

-In severe airflow obstruction with significant air trapping, the FVC may also be reduced, resulting in a pattern that suggests a restrictive ventilatory defect.

-Airflow obstruction is indicated by a reduced FEV1/FVC ratio (< 75%).

-Peak expiratory flow (PEF) meters are handheld devices designed as monitoring tools to be used at home.

- PEF monitoring can establish peak flow variability and assist in the determination of asthma severity in patients with asthma symptoms and normal spirometry.

- PEF is generally lowest on first awakening and highest several hours before the midpoint of the waking day (diurnal variation).

-Ideally, PEF should be measured in the morning before the administration of a bronchodilator and in the afternoon after taking a bronchodilator; 20% variability in PEF values from morning to afternoon or over time suggests asthma. Predicted values for PEF vary with gender, age, and height.

2- Arterial blood gases

-During moderately severe exacerbations pulse oximetry may be of value.

-During severe exacerbations arterial blood gases are indicated.

-Hypoxemia is a frequent finding in this setting and is caused by a mismatch of ventilation and perfusion associated with bronchoconstriction, with a resultant increase in the alveolar-arterial oxygen difference.

-Mild to moderate obstruction hyperventilate , and thus the arterial PCO2 is decreased

-During prolonged and severe episodes respiratory muscle fatigue and the PCO2 may normalize or become elevated.

A normal PCO2 during a severe exacerbation of asthma is thought to be an ominous sign, suggesting impending respiratory failure. Early intubation is recommended to avoid profound respiratory muscle fatigue or respiratory arrest.

3-Chest X-ray

Hyperinflation of the lung may be present during severe exacerbations,

Complications of their disease such as pneumonia, pneumothorax, or pneumomediastinum.

Infiltrates may be seen in allergic bronchopulmonary aspergillosis.

4-Sputum examination

Usually reveal inflammatory cells, including neutrophils and eosinophils, in the sputum of asthmatics, although this finding is of little diagnostic value.

MANAGEMENT

1.Oxygen therapy

-Administered via a nasal canula or mask.

-With the advent of pulse oximetry, oxygen therapy can be easily titrated to maintain the patient's oxygen saturation above 92% (>95% in pregnant patients or those with cardiac disease).

2.Beta-2 Adrenergic agonists

-The first line of therapy is bronchodilator treatment with a beta-2 agonist, typically albuterol.

-Nebulizer treatments may be administered either continuously (10-15 mg/h) or by frequent timing (eg, q5-20min), depending on the severity of the bronchospasm.

-The dose of albuterol for intermittent dosing is 0.3-0.5 mL of a 0.5% formulation mixed with 2.5 mL water for injection

NB. Patients resistant to beta-2 agonists may be given nonselective beta-2 agonists (eg, epinephrine [0.3-0.5 mg] or terbutaline [0.25 mg]) administered subcutaneously.

3.Ipratropium bromide treatment

-Ipratropium, can be synergistic with albuterol or other beta-2 agonists.

-Ipratropium is administered every 4-6 hours.

-Because children appear to have more cholinergic receptors, they are more responsive to parasympathetic stimulation than adults

4.Glucocorticosteroids

Steroids are the most important treatment for status asthmaticus.

The usual dose is oral prednisone at 1-2 mg/kg/d.

Methylprednisolone provides excellent efficacy when given intravenously at 1 mg/kg/dose every 6 hours

Loading dose: 125-250 mg IV
Maintenance dose: 4 mg/kg/d IV divided q4-6h

5.Fluid replacement

Intravenous fluids are administered to restore euvolemia.

6.Aminophylline

-Conflicting reports on the efficacy of aminophylline therapy have made it controversial.

-Starting intravenous aminophylline may be reasonable in patients who do not respond to medical treatment with bronchodilators, oxygen, corticosteroids, and intravenous fluids within 24 hours.

-Recent data suggest that aminophylline may have an anti-inflammatory effect in addition to its bronchodilator properties.

-The loading dose is usually 5-6 mg/kg, followed by a continuous infusion of 0.5-0.9 mg/kg/h.

6.Antibiotics

The routine administration of antibiotics is discouraged. Patients are administered antibiotics only when they show evidence of infection (eg, pneumonia, sinusitis).

DDX

Upper airway disorders that mimic asthma include

§ vocal cord paralysis

§ vocal cord dysfunction syndrome

§ foreign body aspiration

§ laryngotracheal masses

§ Tracheal narrowing

§ Tracheomalacia

§ Airway edema as in the setting of angioedema or inhalation injury.

Lower airway disorders include

§ Nonasthmatic chronic obstructive pulmonary disease (chronic bronchitis or emphysema), bronchiectasis

§ Allergic bronchopulmonary mycosis

§ Cystic fibrosis

§ Eosinophilic pneumonia

§ Bronchiolitis obliterane

§ Systemic vasculitides that often have an asthmatic component include Churg-Strauss syndrome and other systemic vasculitides with pulmonary involvement.

medical conditions

2012-01-13T08:22:00.000-08:00

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