Signs and Symptoms of Diarrhea

Signs and Symptoms of Diarrhea - Diarrhea is a troublesome discomfort that affects most individuals in the United States at some point in their lives and can be thought of as both a symptom and a sign. Usually diarrheal episodes begin abruptly and subside within 1 or 2 days without treatment. Acute diarrhea is commonly defined as <14 days’ duration, persistent diarrhea as more than 14 days’ duration, and chronic diarrhea as more than 30 days’ duration.

To understand diarrhea, one must have a reasonable definition of the condition; unfortunately, the literature is extremely variable on this. Simply put, diarrhea is an increased frequency and decreased consistency of fecal discharge as compared to an individual’s normal bowel pattern. Frequency and consistency are variable within and between individuals. For example, some individuals defecate as often as three times per day, whereas others defecate only two or three times per week. 

A Western diet usually produces a daily stool weighing between 100 and 300 g, depending on the amount of nonabsorbable materials (mainly carbohydrates) consumed. Patients with serious diarrhea may have a daily stool weight in excess of 300 g; however, a subset of patients experience frequent small, watery passages. Additionally, vegetable fiber-rich diets, such as those consumed in some Eastern cultures, such as those in Africa, produce stools weighing more than 300 g/day.

Diarrhea may be associated with a specific disease of the intestines or secondary to a disease outside the intestines. For instance, bacillary dysentery directly affects the gut, whereas diabetes mellitus causes neuropathic diarrheal episodes. Furthermore, diarrhea can be considered as acute or chronic disease. Infectious diarrhea is often acute; diabetic diarrhea is chronic. Congenital disorders in gastrointestinal ion-transport mechanisms are another cause of chronic diarrhea. Whether acute or chronic, diarrhea has the same pathophysiologic causes that help identification of specific treatments.

Physiology

In the fasting state, 9 L of fluid enters the proximal small intestine each day. Of this fluid, 2 L are ingested through diet, while the remainder consists of internal secretions. Because of meal content, duodenal chyme is usually hypertonic. When chyme reaches the ileum, the osmolality adjusts to that of plasma, with most dietary fat, carbohydrate, and protein being absorbed. The volume of ileal chyme decreases to about 1 L/day upon entering the colon, which is further reduced by colonic absorption to 100 mL daily. If the small intestine water absorption capacity is exceeded, chyme overloads the colon, resulting in diarrhea. In humans, the colon absorptive capacity is about 5 L daily.

Colonic fluid transport is critical to water and electrolyte balance. Absorption from the intestines back into the blood occurs by three mechanisms: active transport, diffusion, and solvent drag. Active transport and diffusion are the mechanisms of sodium transport. Because of the high luminal sodium concentration (142 mEq/L), sodium diffuses from the sodium-rich gut into epithelial cells, where it is actively pumped into the blood and exchanged with chloride to maintain an isoelectric condition across the epithelial membrane. Hydrogen ions are transported by an indirect mechanism in the upper small intestine. As sodium is absorbed, hydrogen ions are secreted into the gut. 

Hydrogen ions then combine with bicarbonate ions to form carbonic acid, which then dissociates into carbon dioxide and water. Carbon dioxide readily diffuses into the blood for expiration through the lung. The water remains in the chyme. Paracellular pathways are major routes of ion movement. As ions, monosaccharides, and amino acids are actively transported, an osmotic pressure is created, drawing water and electrolytes across the intestinal wall. This pathway accounts for significant amounts of ion transport, especially sodium. Sodium plays an important role in stimulating glucose absorption. Glucose and amino acids are actively transported into the blood via a sodium dependent cotransport mechanism. Cotransport absorption mechanisms of glucose-sodium and amino acid-sodium are extremely important for treating diarrhea.

Gut motility influences absorption and secretion. The amount of time in which luminal content is in contact with the epithelium is under neural and hormonal control. Neurohormonal substances, such as angiotensin, vasopressin, glucocorticoid, aldosterone, and neurotransmitters also regulate ion transport.

Clinical Presentation of Diarrhea

A medication history is extremely important in identifying drug-induced diarrhea. Many agents, including antibiotics and other drugs, cause diarrhea or, less commonly, pseudomembranous colitis. Self-inflicted laxative abuse for weight loss is popular. Most acute diarrhea is self-limiting, subsiding within 72 hours. However, infants, young children, the elderly, and debilitated persons are at risk for morbid and mortal events in prolonged or voluminous diarrhea. These groups are at risk for water, electrolyte, and acid–base disturbances, and potentially cardiovascular collapse and death. The prognosis for chronic diarrhea depends on the cause; for example, diarrhea secondary to diabetes mellitus waxes and wanes throughout life.

General
• Usually, acute diarrheal episodes subside within 72 hours of onset, whereas chronic diarrhea involves frequent attacks over extended time periods.
Signs and symptoms
• Abrupt onset of nausea, vomiting, abdominal pain, headache, fever, chills, and malaise.
• Bowel movements are frequent and never bloody, and diarrhea lasts 12 to 60 hours.
• Intermittent periumbilical or lower right quadrant pain with cramps and audible bowel sounds is characteristic of small intestinal disease.
• When pain is present in large intestinal diarrhea, it is a gripping, aching sensation with tenesmus (straining, ineffective, and painful stooling). Pain localizes to the hypogastric region, right or left lower quadrant, or sacral region.
• In chronic diarrhea, a history of previous bouts, weight loss, anorexia, and chronic weakness are important findings.
Physical examination
• Typically demonstrates hyperperistalsis with borborygmi and generalized or local tenderness.
Laboratory tests
• Stool analysis studies include examination for microorganisms, blood, mucus, fat, osmolality, pH, electrolyte and mineral concentration, and cultures.
• Stool test kits are useful for detecting gastrointestinal viruses, particularly rotavirus.
• Antibody serologic testing shows rising titers over a 3- to 6-day period, but this test is not practical and is nonspecific.
• Occasionally, total daily stool volume is also determined.
• Direct endoscopic visualization and biopsy of the colon may be undertaken to assess for the presence of conditions such as colitis or cancer.
• Radiographic studies are helpful in neoplastic and inflammatory conditions.

Drugs Causing Diarrhea

Laxatives
Antacids containing magnesium
Antineoplastics
Auranofin (gold salt)
Antibiotics
Clindamycin
Tetracyclines
Sulfonamides
Any broad-spectrum antibiotic
Antihypertensives
Reserpine
Guanethidine
Methyldopa
Guanabenz
Guanadrel
Angiotensin-converting enzyme inhibitors
Cholinergics
Bethanechol
Neostigmine
Cardiac agents
Quinidine
Digitalis
Digoxin
Nonsteroidal antiinflammatory drugs
Misoprostol
Colchicine
Proton pump inhibitors
H2-receptor blockers

Salam

by Umaee

Sign and Symptoms of Diarrhea

Source: Pharmacotherapy 7th

New Role For Public Health

New Role For Public Health - With the spiraling costs of medical care and the corresponding interest in cost containment and accountability, it is reasonable to avoid duplications. We need a closer link of clinical and public health disciplines and activities.

A recent example of the control of a new epidemic by the collaborative efforts of the World Health Organization (WHO), basic scientists and clinicians followed the outbreak of SARS—Severe Acute Respiratory Syndrome. WHO forcefully assumed international leadership, coordinated scientific investigations, and quickly reported all new advances from the laboratory and field epidemiological studies to clinicians. In medical schools it is propitious for these disciplines jointly to develop curricula and research projects.

In the health service arena, closer ties between clinicians and public health officials will be efficient and effective for the good of the population. A special role for public health officials could be to “translate” important epidemiological data for clinicians giving primary care. This could be particularly important and useful in enhancing prevention. Examples of useful data would be the risk ratios for becoming an alcohol abuser for persons with and without a family history of abuse; cigarette smoking for the smoker, those nearby, and the unborn fetus; and for fatal versus nonfatal injury in persons driving with and without a seat belt.

In the field of communicable diseases it is useful to know the risk of AIDS in those practicing intravenous drug abuse or unprotected sexual activities, the relative risk of Lyme disease in those using effective insect repellents versus those not using such agents, and the relative risk of hepatitis B in healthcare workers who have received the vaccine and those who have not. In 2006, a key role for a public health-clinicians partnership is the continual education of the public about the real risks of avian (H5N1) influenza and the progress toward its prevention and control.

An epidemiological approach to community-wide education about local health risks, perhaps with a well-designed periodical, would further link the clinician and public health official. The Centers for Disease Control and Prevention (CDC) has done this successfully with Morbidity and Mortality Weekly Report. A community-wide modification for consumption by local practitioners would be helpful. Such networking is feasible and desirable.

Networking with schools, businesses, health clubs, and senior citizen groups might increase compliance with behavior designed to enhance resistance to environmental hazards. Fundamentals of general and dental hygiene, nutrition, exercise, and stress control would be essential components. It would be reasonable to reinforce such basic principles as maintaining immunizations and proper use of antibiotics. In summary, we need a proactive and integrative role in education, one that involves networking with clinicians and the public directly. Improving environmental safety has been the focus and strength of public health. Essentially, the goal has been to reduce the microbial hazards to humans. For the most part, this is carried out by systematic measurement or a series of inspections of the environment. 

Good general sanitation and safe air, water, and food are hallmarks of public health. Environmental activist groups have heightened interest in environmental safety. This is an opportune time to build a coalition between informed public health officials and interested and energetic activists genuinely concerned with improving the environment. From infectious diseases point of view, an important goal would be to reduce the degree of exposure while preserving the vitality of the ecosystem. The government of Brazil was reported to have instituted a $200 million program to control malaria in the Amazon region by spraying dichlorodiphenyltrichloroethane (DDT) in thousands of rain forest huts. As McCoy pointed out, however, the chemical has been banned in over 40 countries because of its lethal effect on birds and fish.

Moreover, in India, although it had a remarkable short-term effect initially (75 million annual cases of malaria reduced in the 1950s to 50,000), the number of cases rose to 65 million by 1976, the result of resistance in mosquito vectors. Moreover, bottled milk sampled in India in April 1990 had 10 times the permissible limit of DDT. DDT is fat soluble and has been carried in food chains to countries all over the world. The lesson we have learned from the Russian nuclear accident at Chernobyl, the AIDS epidemic, and the DDT experience and the SARS epidemic is that radiation, viruses, and pollutants respect no national borders.

The response to such lessons needs to be an enhanced commitment by individuals, communities, and nations to solve the problems of others and to view the world as a global village. Limiting the survival of important infection agents, their animal reservoirs, or hosts requires careful examination of the implications of such approaches in collaboration with veterinarians, entomologists, and toxicologists.

Salam

by Umaee

New Role For Public Health

Source: public health & preventive medicine

Treatment Nausea and Vomiting

Treatment Nausea and Vomiting - Nausea and vomiting are common complaints among many individuals with gastrointestinal (GI) disorders. However, because of the variable etiologies of these problems, management can be quite simple or detailed and complex, essentially innocuous or associated with therapy-induced adverse reactions. This chapter  provides an overview of nausea and vomiting, two multifaceted problems. Nausea and vomiting may be associated with a variety of clinical presentations. In addition to GI diseases, either or both may accompany cardiovascular, infectious, neurologic, or metabolic disease processes. Nausea and vomiting may be a feature of such conditions as pregnancy, or may follow operative procedures or administration of certain medications, such as those used in cancer chemotherapy.

Psychogenic etiologies of these symptoms may be present, especially in young women with an underlying emotional disturbance. Anticipatory etiologies may be involved, such as in patients who have previously received cytotoxic chemotherapy. Table below lists specific etiologies associated with nausea and vomiting. In addition to identifying conditions associated with nausea and vomiting, it is important to address the specific causative medical problems. For example, nausea and vomiting may occur in as many as 70% of patients with inferior myocardial infarction or diabetic ketoacidosis. Eighty percent to 90% of patients with an Addisonian crisis, acute pancreatitis, or acute appendicitis may present with nausea and vomiting.

The etiology of nausea and vomiting may vary with the age of the patient. For example, vomiting in the newborn during the first day of life suggests upper digestive tract obstruction or an increase in intracranial pressure. Other illnesses associated with vomiting in children include pyloric stenosis, duodenal ulcer, stress ulcer, adrenal insufficiency, septicemia, and diseases of the pancreas, liver, or biliary tree. Also, the hepatocellular failure seen in Reye syndrome may lead to profound cerebral edema followed by persistent emesis.

A common etiology of vomiting in children is viral gastroenteritis caused by rotavirus. Vomiting in infants may be associated with something as simple as overfeeding, rapid feeding, inadequate burping, or lying down too soon after feeding. These types of vomiting are usually indicative of minor problems and may be altered by changing the approach to feeding.

General Approach to Treatment

Treatment options for nausea and vomiting include drug and nondrug modalities. The treatment of nausea and vomiting is quite varied depending on the associated medical situation. Even though a number of potentially effective measures are available, most patients receive a medication at some point in their care. For simple nausea and vomiting, patients may choose to do nothing or to select from a variety of nonprescription drugs. As symptoms become worse or are associated with more serious medical problems, patients are more likely to benefit from prescription antiemetic drugs. When prescribed according to reliable clinical information, these agents often provide acceptable relief; however, some patients will never be totally free of symptoms. 

This lack of relief is most disabling when it is associated with an unresolved medical problem or when the necessary therapy for this condition is the cause of the nausea or vomiting, as in the case of patients who are receiving chemotherapy of moderate or high emetic risk.

Nonpharmacologic Management

Nonpharmacologic management of nausea and vomiting may include a variety of dietary, physical, or psychological changes consistent with the etiology of symptoms. For patients with simple complaints, perhaps resulting from excessive or disagreeable food or beverage consumption, avoidance or moderation in dietary intake may be preferable. Patients suffering symptoms of systemic illness may improve dramatically as their underlying condition resolves. Finally, patients in whom these symptoms result from labyrinthine
changes produced by motion may benefit quickly by assuming a stable physical position.

Cancer patients who are undergoing chemotherapy may experience nausea and/or vomiting despite receiving prophylactic antiemetics. Anticipatory nausea or vomiting rarely occurs unless the patient has previously experienced posttreatment nausea or vomiting, suggesting that the mechanism for anticipatory nausea and vomiting is a learned process involving elements of classic conditioning. This conditioning model may also be important in understanding the development of pregnancy-related nausea. Nonpharmacologic interventions are classified as behavioral interventions and include relaxation, biofeedback, self-hypnosis, cognitive distraction, guided imagery, and systematic desensitization.

The management of psychogenic vomiting is greatly dependent on psychological intervention. However, because the underlying problems are so complex and intertwined in personal relationships, psychological therapy may require lengthy, in-depth treatment. Pharmacologic therapy offers only minimal benefit in these patients. Surgery, such as gastroenterostomy, is of no value.

Presentation of Nausea and Vomiting

General
Depending on severity of symptoms, patients may present in mild to severe distress

Symptoms
Simple: Self-limiting, resolves spontaneously and requires only symptomatic therapy
Complex: Not relieved after administration of antiemetics; progressive deterioration of patient secondary to fluid–electrolyte imbalances; usually associated with noxious agents or psychogenic events

Signs
Simple: Patient complaint of queasiness or discomfort 

Complex: Weight loss; fever; abdominal pain

Laboratory tests
Simple: None
Complex: Serum electrolyte concentrations; upper/lower GI evaluation

Other information
Fluid input and output
Medication history
Recent history of behavioral or visual changes, headache, pain, or stress
Family history positive for psychogenic vomiting

Pharmacologic therapy

Although many approaches to the treatment of nausea and vomiting have been suggested, antiemetic drugs (nonprescription and prescription) are most often recommended. These agents represent a variety of pharmacologic and chemical classes, as well as dosage regimens and routes of administration. With so many treatment possibilities available, factors that enable the clinician to discriminate among various choices include (a) the suspected etiology of the symptoms; (b) the frequency, duration, and severity of the episodes; (c) the ability of the patient to use oral, rectal, injectable, or transdermal medications; and (d) the success of previous antiemetic medications. Table below gives information concerning commonly available antiemetic preparations.

The treatment of simple nausea and vomiting usually requires minimal therapy. For these symptoms, patients may choose from a lengthy list of nonprescription products. Both nonprescription and prescription drugs useful in the treatment of simple nausea and vomiting are usually effective in small, infrequently administered doses. Side effects and toxic effects in these settings are also usually minimal. Although suitable for occasional simple nausea and vomiting, nonprescription agents are often abandoned by the patient as symptoms continue or become progressively worse. As the patient’s condition warrants, prescription medications may be chosen, either as single-agent therapy or in combination.

The management of complex nausea and vomiting, for example, in patients who are receiving cytotoxic chemotherapy, may require combination therapy. In combination regimens, the goal is to achieve symptomatic control through administration of agents with different pharmacologic mechanisms of action.

Salam

by Umaee

Treatment Nausea and Vomiting

Source: Pharmacotherapy 7th

Image:  wikinoticia.com

Algorithm For Treatment of Peptic Ulcer Disease

Algorithm For Treatment of Peptic Ulcer Disease - The clinical presentation of PUD varies depending on the severity of epigastric pain and the presence of complications (presentation of peptic ulcer disease). Ulcer-related pain in duodenal ulcer often occurs 1 to 3 hours after meals and is usually relieved by food, but this is variable. In gastric ulcer, food may precipitate or accentuate ulcer pain. Antacids usually provide immediate pain relief in most ulcer patients. Pain usually diminishes or disappears during treatment; however, recurrence of epigastric pain after healing often suggests an unhealed or recurrent ulcer.

Epigastric pain does not define an ulcer. The absence of pain does not preclude the diagnosis especially in the elderly who may present with “silent” ulcer complications. The reasons for this are unclear, but may relate to differences in the way the elderly perceive pain or the analgesic effect of NSAIDs. Dyspepsia in itself is of little clinical value when assessing subsets of patients who are most likely to have an ulcer. Patients taking NSAIDs often report dyspepsia, but dyspeptic symptoms do not directly correlate with an ulcer. 

Patients with dyspeptic symptoms may have either uninvestigated (no upper endoscopy) or investigated (underwent upper endoscopy) dyspepsia. If an ulcer is not confirmed in a patient with ulcer-like symptoms at the time of endoscopy, the disorder is referred to as nonulcer dyspepsia. Ulcer-like symptoms may occur in the absence of peptic ulceration in association with H. pylori gastritis or duodenitis. There is no one sign or symptom that differentiates between H. pylori-associated and NSAID-induced ulcer.

Presentation of Peptic Ulcer Disease

General
• Mild epigastric pain or acute life-threatening upper gastrointestinal complications Symptoms
• Abdominal pain that is often epigastric and described as burning, but may present as vague discomfort, abdominal fullness, or cramping
• A typical nocturnal pain that awakens the patient from sleep (especially between 12 AM and 3 AM)
• The severity of ulcer pain varies from patient to patient, and may be seasonal, occurring more frequently in the spring or fall; episodes of discomfort usually occur in clusters, lasting up to a few weeks and followed by a pain-free period or remission lasting from weeks to years
• Changes in the character of the pain may suggest the presence of complications
• Heartburn, belching, and bloating often accompany the pain
• Nausea, vomiting, and anorexia, are more common in patients with gastric ulcer than with duodenal ulcer, but may also be signs of an ulcer-related complication

Signs
• Weight loss associated with nausea, vomiting, and anorexia
• Complications, including ulcer bleeding, perforation, penetration, or obstruction Laboratory tests
• Gastric acid secretory studies
• Fasting serum gastrin concentrations are only recommended for patients who are unresponsive to therapy, or for those in whom hypersecretory diseases are suspected
• The hematocrit and hemoglobin are low with bleeding, and stool hemoccult tests are positive
• Tests for Helicobacter pylori 

Other diagnostic tests
• Fiberoptic upper endoscopy (esophagogastroduodenoscopy) detects more than 90% of peptic ulcers and permits direct inspection, biopsy, visualization of superficial erosions, and sites of active bleeding
• Routine single-barium contrast techniques detect 30% of peptic ulcers; optimal double-contrast radiography detects 60% to 80% of ulcers

General Approach to Treatment

The treatment of PUD centers on healing the ulcer and reducing the risk of ulcer recurrence and related complications. Drug regimens containing antimicrobials such as clarithromycin, metronidazole, amoxicillin, and bismuth salts and antisecretory drugs (PPIs or H2RAs) relieve ulcer symptoms, heal the ulcer, and eradicate H. pylori infection. Successful eradication will alter the natural history of PUD and cure the disease. PPIs are preferred to H2RAs or sucralfate for healing H. pylori-negative NSAID ulcers because they accelerate ulcer healing and provide more effective relief of symptoms. Treatment with a PPI should be extended to 8 to 12 weeks if the NSAID must be continued. A PPI-based H. pylori eradication regimen is recommended in H. pylori-positive patients with an active ulcer who are also taking an NSAID. 

Prophylactic cotherapy with either a PPI or miso-prostol decreases ulcer risk and upper GI complications in patients taking nonselective NSAIDs. A COX-2 inhibitor may be used as an alternative to a nonselective NSAID, but the risk of adverse cardiovascular effects must be weighted against the gastroprotective benefits in each patient. The optimal therapeutic strategy for patients at very high risk of NSAID-related GI events is not known, but selected patients may benefit from the use of a COX-2 inhibitor and a PPI.

Dietary modifications are important for patients who are unable to tolerate certain foods and beverages. Lifestyle modifications such as reducing stress and decreasing or stopping cigarette smoking is encouraged. Some patients may require radiographic or endoscopic procedures for a definitive diagnosis or for complications such as bleeding. Surgery may be necessary in patients with ulcer-related complications.

Nonpharmacologic Therapy

Patients with PUD should eliminate or reduce psychological stress, cigarette smoking, and the use of nonselective NSAIDs (including aspirin). Although there is no “antiulcer diet,” the patient should avoid foods and beverages (e.g., spicy foods, caffeine, and alcohol) that cause dyspepsia or that exacerbate ulcer symptoms. If possible, alternative agents such as acetaminophen, nonacetylated salicylate (e.g., salsalate), or COX-2 inhibitors should be used for relief of pain. Elective surgery for PUD is rarely performed today because of highly effective medical management such as the eradication of H. pylori and the use of potent acid inhibitors. A subset of patients, however, may require emergency surgery for bleeding, perforation, or obstruction. In the past, surgical procedures were performed for medical treatment failures and included vagotomy with pyloroplasty or vagotomy with antrectomy.

Vagotomy (truncal, selective, or parietal cell) inhibits vagal stimulation of gastric acid. A truncal or selective vagotomy frequently results in postoperative gastric dysfunction and requires a pyloroplasty or antrectomy to facilitate gastric drainage. When an antrectomy is performed, the remaining stomach is anastomosed with the duodenum (Billroth I) or with the jejunum (Billroth II). A vagotomy is unnecessary when an antrectomy is performed for gastric ulcer. The postoperative consequences associated with these procedures include postvagotomy diarrhea, dumping syndrome, anemia, and recurrent ulceration.

Salam

by Umaee

Algorithm For Treatment of Peptic Ulcer Disease

Source: Pharmacotherapy 7th

Severe Asthma Attack

Severe Asthma Attack - Uncontrolled asthma, with its inherent variability, can progress to an acute state where inflammation, airways edema, excessive accumulation of mucus, and severe bronchospasm result in a profound airways narrowing that is poorly responsive to usual bronchodilator therapy (see Clinical Presentation: Severe Acute Asthma). Although this progression is the most common scenario, some patients experience rapid onset or hyperacute attacks.

Hyperacute attacks are associated with neutrophilic as opposed to eosinophilic infiltration and resolve rapidly with bronchodilator therapy, suggesting that smooth muscle spasm is the major pathogenic mechanism. In most cases, emergency department visits for severe acute asthma represent the failure of an adequate therapeutic regimen for persistent asthma. Underuse of antiinflammatory drugs and excessive reliance on short-acting inhaled β2-agonists are the major risk factors for severe exacerbations. A blunted perception of airway obstruction may predispose certain individuals to fatal asthma attacks.

Clinical Presentation

General

■ An episode can progress over several days or hours (usual scenario) or can progress rapidly over 1 to 2 hours.

Symptoms

■ The patient is anxious in acute distress and complains of severe dyspnea, shortness of breath, chest tightness, or burning. The patient is only able to say a few words with each breath. Symptoms are unresponsive to usual measures (inhaled shortacting β2-agonist administration).

Signs

■ Signs include expiratory and inspiratory wheezing on auscultation (breath sounds may be diminished with very severe obstruction), dry hacking cough, tachypnea, tachycardia, pale or cyanotic skin, hyperinflated chest with intercostal and supraclavicular retractions, and hypoxic seizures if very severe.

Laboratory

■ PEF and/or FEV1 less than 50% of normal predicted values. Decreased arterial oxygen (PaO2), and O2 saturations by pulse oximetry (SaO2 less than 90% on room air is severe). Decreased arterial or capillary CO2 if mild, but in the normal range or increased in moderate to severe obstruction.

Other Diagnostic Tests

■ Blood gases to assess metabolic acidosis (lactic acidosis) in severe obstruction. Complete blood count if there are signs of infection (fever and purulent sputum). Serum electrolytes as therapy with β2-agonist and corticosteroids can lower serum potassium and magnesium and increase glucose.Chest radiograph if signs of consolidation on auscultation.

Factors Contributing to Asthma Severity

Viral Respiratory Infections

Viral respiratory infections are primarily responsible for exacerbations of asthma, particularly in children younger than age 10 years. Infants are particularly susceptible to airways obstruction and wheezing with viral infections because of their small airways. The most common cause of exacerbations in both children and adults is the common rhinovirus. Other viruses isolated include respiratory syncytial virus, parainfluenza virus, coronavirus, and influenza viruses. The inflammatory response to viral infection is thought to be associated directly with the increasing BHR. Certain viruses (respiratory syncytial virus and parainfluenza virus) are capable of inducing specific IgE antibodies, and rhinovirus can activate eosinophils directly in asthmatics.

The increase in asthma symptoms and BHR that occurs may last for days or weeks following resolution of the symptoms of the viral infection. Recent evidence does not support a beneficial effect of influenza vaccine for preventing asthma exacerbations from subsequent influenza infections.

Envirenmental And Occupational

Table below lists the agents, events, and mechanisms that are known to trigger asthma. The general mechanisms are unknown but presumably are the result of epithelial damage and inflammation in the airway mucosa. Ozone and sulfur dioxide, common components of air pollution, have been used to induce BHR in animals. Exposure to 0.2 parts per million ozone for 2 to 3 hours can induce bronchoconstriction and increase BHR in asthmatics. Sulfur dioxide in the ambient atmosphere is highly irritating. It presumably induces bronchoconstriction through mast cell or irritantreceptor involvement. 

Asthma produced by repeated prolonged exposure to industrial inhalants is a significant health problem. It has been estimated that occupational asthma accounts for 2% of all asthmatic persons. Persons with occupational asthma have the typical symptoms of asthma with cough, dyspnea, and wheeze. Typically, the symptoms are related to work and improve on weekends and during vacations. In some instances, symptoms may persist even after termination of exposure.

Stress, Depression, And Psychosocial

Observational studies demonstrate an association between increased stress and worsening asthma, but the role is not clearly defined. Bronchoconstriction from psychological factors appears to be mediated primarily through excess parasympathetic input. Atropine has been shown to block experimental psychogenic bronchoconstriction. It is most important to emphasize to both patients and parents that asthma is not an emotional disease; however, coping skills may benefit the patient who becomes emotionally distraught during an asthma attack.

Rhinitis And Sinusitis

Disorders of the upper respiratory tract, particularly rhinitis and sinusitis, have been linked with asthma for many years. As many as 40% to 50% of asthmatics have abnormal sinus radiographs. However, chronic sinusitis may just represent a nonbacterial coexisting condition with allergic asthmatics because the histologic changes in the paranasal sinuses are similar to those seen in the lung and nose. Treatment of upper airway disease may optimize overall asthma control. The mechanism by which sinusitis aggravates asthma is unknown. The treatment of allergic rhinitis with inhaled corticosteroids and cromolyn but not antihistamines will reduce BHR in asthmatic patients. It has been postulated that transport of mucus chemotactic factors and inflammatory mediators from nasal passages during allergic rhinitis into the lung may accentuate BHR.

Gastroesophageal Reflux Disease

Symptoms of gastroesophageal reflux disease are common in both children and adults who have asthma. Nocturnal asthma may be associated with nighttime reflux. Reflux of acidic gastric contents into the esophagus is thought to initiate a vagally mediated reflex bronchoconstriction. Also of concern is that most medications that decrease airways smooth muscle tone also have a relaxant effect on gastroesophageal sphincter tone. Although a systematic review concluded there was no significant improvement in asthma symptoms from medical management of gastroesophageal reflux disease, the standard approach is to initiate standard antireflux therapy in those patients who are exhibiting symptoms of reflux (particularly with nocturnal asthma) and observe the asthma symptoms.

Female Hormones And Asthma

Premenstrual worsening of asthma has been reported in as many as 30% to 40% of women in some studies, whereas worsening of pulmonary functions has been reported even in women who are unaware of worsening symptoms. The pathophysiology is uncertain because estrogen replacement in postmenopausal women worsens asthma, whereas estradiol and progesterone administration have been variably reported to improve or have no effect on asthma in women with premenstrual asthma. The clinical significance of menstruation-related asthma is still unclear because some studies report that up to 50% of emergency department visits by women were premenstrual, whereas others report no association with menstrual phase. Studies indicate that, in general, BHR and symptoms improve in asthmatics during pregnancy.

Treatment

The primary goal is prevention of life-threatening asthma by early recognition of signs of deterioration and early intervention. As such, the principal goals of treatment include

• Correction of significant hypoxemia.

• Rapid reversal of airflow obstruction

• Reduction of the likelihood of relapse of the exacerbation or future recurrence of severe airflow obstruction

• Development of a written asthma action plan in case of a further exacerbation

These goals are best achieved by early initiation or intensification of treatment and close monitoring of objective measures of oxygen-ation and lung function. Early response to treatment as measured by the improvement in FEV1 at 30 minutes following inhaled β2-agonists is the best predictor of outcome. Providing adequate oxygen supplementation to maintain oxygen (O2) saturations above 90% (or above 95% in pregnant women and those who have coexistent heart disease) is essential. In children younger than 6 years of age, in whom lung function measures are difficult to obtain, a combination of objective (e.g., oxygen saturation, capillary CO2, respiratory rate, and heart rate) and subjective measures may be used to assess severity.

Salam

by Umaee

Severe Asthma Attack

Source: Pharmacotherapy 7th

Image: babble.com

How to Treatment Gastric Reflux

How to Treatment Gastric Reflux - Patients with GERD (Gastroesophageal Reflux Disease) may display symptoms described as (a) typical, (b) atypical, or (c) alarm. Table 34–2 summarizes each of these clinical presentations of GERD. The severity of the symptoms of gastroesophageal reflux does not always correlate with the degree of esophagitis, but it does correlate with the duration of reflux. Patients with nonerosive disease may have symptoms as severe as those with endoscopic findings. It is important to distinguish GERD symptoms from those of other diseases, especially when chest pain or pulmonary symptoms are present. Interestingly, close to half of patients presenting with chest pain who have a normal electrocardiogram have GERD. Similarly, approximately half of patients with asthma have GERD.

Patients presenting with asthma (especially nocturnal asthma) that is poorly responsive to standard medical therapies should be evaluated to determine if GERD contributes to their symptoms. Pulmonary symptoms result from either direct irritation of the vagus nerve when refluxed acid comes in contact with the esophageal mucosa, causing bronchospasm (the reflex theory) or, less commonly, from aspiration of the refluxate into the lungs, causing chemical irritation that manifests as pneumonia or pulmonary fibrosis (the reflux theory). As previously mentioned, patients who are inadequately treated for GERD may go on to develop complications from long-term acid exposure.

Long-term, recurrent reflux symptoms that are not ade quately treated may lead to the development of Barrett’s esophagus and may be an independent risk factor for the development of esophageal adenocarcinoma. Esophageal strictures may be present in patients presenting with dysphagia. However, these symptoms may occur in other esophageal disorders such as esophageal diverticulum, achalasia, obstruction, esophageal spasm, esophageal infections, scleroderma, and malignancy. The presence of alarm symptoms should be further investigated to differentiate other diseases as the cause.

The most useful tool in the diagnosis of gastroesophageal reflux is the clinical history, including both presenting symptoms and associated risk factors. Patients presenting with mild, typical symptoms of reflux (heartburn and regurgitation) do not usually require invasive esophageal evaluation. These patients generally benefit from an initial empiric trial of acid-suppression therapy. A clinical diagnosis of GERD can be assumed in patients who respond to appropriate therapy.1 Further diagnostic evaluation should be performed in those patients do not respond to therapy, for those who present with alarm symptoms (e.g., dysphagia, weight loss), and in those with long-standing GERD symptoms. Alarm symptoms may indicate more complicated disease and long-standing GERD symptoms increase the risk for Barrett’s esophagus.

Useful tests in diagnosing GERD include endoscopy, ambulatory reflux monitoring, and manometry. Endoscopy is the preferred technique for assessing the mucosa for esophagitis, identifying Barrett’s esophagus and diagnosing complications. It enables visualization and biopsy of the esophageal mucosa. Although endoscopy is a highly specific test, it is not extremely sensitive. In mild cases of GERD, the esophageal mucosa may appear relatively normal. In addition, noninflammatory GERD and major motor disorders may be missed by endoscopy. A camera-containing capsule swallowed by the patient offers the newest technology for visualizing the esophageal mucosa. The PillCam ESO is less invasive and takes less than 15 minutes to perform in the clinician’s office. Images of the esophagus are downloaded through sensors placed on the patient’s chest that are connected to a data collector. The camera-containing capsule is passed in the stool.

Although less expensive than endoscopy, barium radiography lacks the sensitivity and specificity needed to accurately determine the presence of mucosal injury or to distinguish between Barrett’s esophagus and esophagitis. For these reasons, barium radiography has limited use in the routine diagnosis of GERD. Unfortunately, the presence or absence of mucosal damage does not prove the patient’s symptoms are reflux related; for that, ambulatory reflux monitoring is useful.

Ambulatory pH testing identifies patients with excessive esophageal acid exposure and helps determine if symptoms, both typical and atypical, are acid related. However, pH monitoring may be less reliable in confirming laryngopharyngeal reflux. Interestingly, patients may have severe symptoms, including esophagitis, even when total acid exposure is considered normal.1 Ambulatory pH testing may also be useful in patients who are on what is considered adequate therapy, but whose symptoms are not improving. However, GERD that is truly refractory to medical therapy is uncommon. Ambulatory pH testing can be performed by passing a small pH probe transnasally and placing it approximately 5 cm above the LES. Patients are asked to keep a diary of symptoms that later are correlated with the pH measurement corresponding to the time the symptom was reported. 

In addition to correlating symptoms to abnormal esophageal acid exposure, ambulatory pH testing also documents the percentage of time the intraesophageal pH is below 4 and determines the frequency and severity of reflux. Two recent developments related to ambulatory reflux monitoring include (a) the use of combined impedance and acid testing and (b) the use of a tubeless method of acid monitoring. Whereas ambulatory pH testing only measures acid reflux, combined impedance and acid testing measures both acid and nonacid reflux. This may be useful when evaluating patients on acid suppression therapy.

The second method involves the attachment of a radiotelemetry capsule to the esophageal mucosa. The advantages of this method are that a longer period of monitoring is possible (48 hours) and it is more comfortable for the patient because a nasogastric tube is unnecessary. The empiric use of standard- or even double-dose proton pump inhibitor (specifically omeprazole) as a therapeutic trial for diagnosing the presence of GERD may be useful in patients with atypical symptoms. This approach is less expensive, more convenient, and more readily available than ambulatory reflux monitoring. Problems with using a proton pump inhibitor as a diagnostic tool include lack of a standardized dosing regimen and duration of the diagnostic trial.

Esophageal manometry may be used to ensure the proper placement of esophageal pH probes and to evaluate esophageal peristalsis and motility prior to antireflux surgery. To perform manometry, a multilumen pressure sensing tube is passed into the stomach and the pressures are measured as the tube is pulled back across the lower esophageal sphincter, esophagus, and pharynx. The recent advancement of the tubeless pH monitoring system using endoscopic landmarks for placement may negate the need for manometry

for ensuring proper placement of esophageal pH probes.

General Approach to Treatment

The treatment of GERD is categorized into one of the following modalities: (a) lifestyle modifications and patient-directed therapy with antacids, nonprescription H2-receptor antagonists, and/or nonprescription proton pump inhibitors; (b) pharmacologic intervention with prescription-strength acid suppression therapy; (c) and interventional therapies (antireflux surgery or endoscopic therapies; Table 34–3). The initial therapeutic modality used is in part dependent on the patient’s condition (frequency of symptoms, degree of esophagitis, and presence of complications).

Historically, a step-up approach was used, starting with  noninvasive lifestyle modifications and patient-directed therapy, and progressing to pharmacologic management or interventional approaches (Table 34–4). A step-down approach, starting with a proton pump inhibitor given once or twice daily instead of an H2-receptor antagonist, and then stepping down to the lowest degree of acid suppression needed to control symptoms, is also effective. Neither the “step-up” nor the “step-down” approach has superior efficacy over the other.

The clinician should determine the most appropriate approach for the individual patient. Every attempt should be made to aggressively control symptoms and to prevent relapses early in the course of the patient’s disease in order to prevent the complications that are seen with long-standing symptomatic GERD. In patients with moderate to severe GERD, especially those with erosive disease, starting with a proton pump inhibitor as initial therapy is advocated because of its superior efficacy over H2-receptor antagonists. 

Dietary and lifestyle modifications with education about factors that may worsen GERD symptoms is reasonable to discuss with the patient even though they are unlikely to control the patient’s symptoms in most cases. Table 34–5 lists many of the lifestyle modifications that can be recommended. Although most patients do not respond to lifestyle changes alone, education about their potential benefits should be stressed on a routine basis. Patients with mild or infrequent symptoms may see improvement with the inexpensive nonprescription H2- receptor antagonists, proton pump inhibitors, antacids, or alginic acid.

Patients who do not respond to lifestyle modifications and patientdirected therapy after 2 weeks should seek medical attention and are generally started on empiric therapy consisting of an acid-suppression agent. Acid-suppression therapy with proton pump inhibitors or H2- receptor antagonists is the mainstay of GERD treatment. Patients presenting with moderate to severe symptoms (with or without esophageal erosions) should be started on a proton pump inhibitor as initial therapy because it provides the most rapid symptomatic relief and healing in the highest percentage of patients. H2-receptor antagonists in divided doses are effective in patients with mild GERD. Standard H2-receptor antagonist doses may be increased to 2 to 4 times the normal dose in patients who do not respond to standard doses. However, if this is necessary, it is more cost-effective to switch to a proton pump inhibitor.

Promotility agents are not as effective as acid-suppression agents. Combining promotility agents with acid-suppression drugs offers only modest improvements in symptoms over standard doses of H2- receptor antagonists and should not be routinely recommended. In addition, the availability of a promotility agent that has an acceptable adverse effect profile is lacking. Mucosal protectants, such as sucralfate, have a very limited role in the treatment of GERD. Maintenance therapy is generally necessary to control symptoms and to prevent complications. In patients with more severe symptoms (with or without esophageal erosions), or in patients with other complications, maintenance therapy with a proton pump inhibitor is most effective.

Routine use of combination therapy has no role in maintenance therapy of GERD. GERD that is refractory to adequate acid suppression is rare. In these cases, the diagnosis should be confirmed through further diagnostic tests before longterm, high-dose therapy or interventional approaches (antireflux surgery or endoscopic therapies) are considered.

Salam

by Umaee

How to Treatment Gastric Reflux

Source: Pharmacotherapy 7th

image: realresultswsl.com

Algorithm for Treatment of Heart Failure

Algorithm for Treatment of Heart Failure - Heart failure can result from any disorder that affects the ability of the heart to contract (systolic function) and/or relax (diastolic dysfunction); Table 16–1 lists the common causes of heart failure. Heart failure with impaired systolic function (i.e., reduced LVEF) is the classic, more familiar form of the disorder, but current estimates suggest up to 50% of patients with heart failure have preserved left ventricular systolic function with presumed diastolic dysfunction. 

In contrast to systolic heart failure that is usually caused by previous myocardial infarction (MI), patients with preserved LVEF typically are elderly, female, obese, and have hypertension, atrial fibrillation, or diabetes. Recent data indicate that survival is similar in patients with impaired or preserved LVEF. Frequently, systolic and diastolic dysfunction coexist. The common cardiovascular diseases, such as MI and hypertension, can cause both systolic and diastolic dysfunction; thus many patients have heart failure as a result of reduced myocardial contractility and abnormal ventricular filling. 

Coronary artery disease is the most common cause of systolic heart failure, accounting for nearly 70% of cases. Myocardial infarction leads to reduction in muscle mass as a consequence of death of affected myocardial cells. The degree to which contractility is impaired will depend on the size of the infarction. In an attempt to maintain cardiac output, the surviving myocardium undergoes a compensatory remodeling, thus beginning the maladaptive process that initiates the heart failure syndrome and leads to further injury to the heart. 

Myocardial ischemia and infarction also affect the diastolic properties of the heart by increasing ventricular stiffness and slowing ventricular relaxation. Thus, myocardial infarction frequently results in systolic and diastolic dysfunction. Impaired systolic function is a cardinal feature of dilated cardiomyopathies. Although the cause of reduced contractility frequently is unknown, abnormalities such as interstitial fibrosis, cellular infiltrates, cellular hypertrophy, and myocardial cell degeneration are seen commonly on histologic examination. Genetic causes of dilated cardiomyopathies may also occur.

General Approach to Treatment

Treatment of Stage A Heart Failure

Patients in stage A do not have structural heart disease or heart failure symptoms but are at high risk for developing heart failure because of the presence of risk factors. The emphasis here is on identification and modification of these risk factors to prevent the development of structural heart disease and subsequent heart failure. Commonly encountered risk factors include hypertension, diabetes, obesity, metabolic syndrome, smoking, and coronary artery disease. Although each of these disorders individually increases risk, they frequently coexist in many patients and act synergistically to foster the development of heart failure. 

Effective control of blood pressure reduces the risk of developing heart failure by approximately 50%, thus current hypertension treatment guidelines should be followed. Control of hyperglycemia reduces the risk of end-organ damage and the risk of developing heart failure. Appropriate management of coronary disease
and its associated risk factors is also important, including treatment of hyperlipidemia according to published guidelines and smoking cessation. Although treatment must be individualized, ACE inhibitors or ARBs should be strongly considered for antihypertensive therapy in patients with multiple vascular risk factors. Diuretics and β-blockers may also useful in this setting.

Treatment of Stage B Heart Failure

Patients in stage B have structural heart disease, but do not have heart failure symptoms. This group includes patients with left ventricular hypertrophy, recent or remote MI, valvular disease, or reduced LVEF (less than 40%). These individuals are at risk for developing heart failure and treatment is targeted at minimizing  additional injury and preventing or slowing the remodeling process. In addition to the treatment measures outlined in stage A, ACE inhibitors and β-blockers are important components of therapy. Patients with a previous MI should receive both ACE inhibitors and β-blockers, regardless of the LVEF.1 Similarly, patients with a reduced LVEF should also receive both these agents, whether or not they have had a MI. ARBs are an effective alternative in patients intolerant to ACE inhibitors.

Treatment of Stage C Heart Failure

Patients with structural heart disease and previous or current heart failure symptoms are classified in stage C. In addition to treatments in stages A and B, most patients in stage C should be routinely treated with three medications: a diuretic, an ACE inhibitor, and a β-blocker (see Drug Therapies for Routine Use below). The benefits of these medications on slowing heart failure progression, reducing morbidity and mortality, and improving symptoms are clearly established. Aldosterone receptor antagonists, ARBs, digoxin, and hydralazine-isosorbide dinitrate are also useful in selected patients.

Nonpharmacologic therapy with devices such as an implantable cardiac-defibrillator (ICD) or cardiac resynchroni zation therapy (CRT) with a biventricular pacemaker is also indicated in certain patients in stage C (see Nonpharmacologic Therapy below). Other general measures are also important, including moderate sodium restriction, daily weight measurement, immunization against influenza and pneumococcus, modest physical activity, and avoidance of medications that can exacerbate heart failure. Recent evidence suggests that careful followup and patient education that reinforces dietary and medication compliance can prevent clinical deterioration and reduce hospitalization.

Treatment of Stage D Heart Failure

Stage D heart failure includes patients with symptoms at rest that are refractory despite maximal medical therapy. This includes patients who undergo recurrent hospitalizations or who cannot be discharged from the hospital without special interventions. These individuals have the most advanced form of heart failure and should be considered for specialized therapies including mechanical circulatory support, continuous intravenous positive inotropic therapy, cardiac transplantation, or hospice care. 

Salam

by Umaee

Algorithm for Treatment of Heart Failure

Source: Pharmacotherapy 7th

Image: zeenews.india.com