gastroenterology observership 2

40 year old female has hepA infection, jaundice at young age, no family history of liver disease, she had her liver enzyme up and down since 10 years ago, recently high alt ast, high cholesterol, TG, her weight is stable, recently ultrasound show mild fatty liver
NASH? LIVER BIOPSY?

NASH nonalcoholic steatohepatitis (NASH)
Patients with nonalcoholic fatty liver disease (NAFLD) have hepatic steatosis, with or without inflammation and fibrosis. In addition, no secondary causes of hepatic steatosis are present.
NAFLD is subdivided into nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH). In NAFL, hepatic steatosis is present without evidence of significant inflammation, whereas in NASH, hepatic steatosis is associated with hepatic inflammation that may be histologically indistinguishable from alcoholic steatohepatitis.

Prevalence — Nonalcoholic fatty liver disease (NAFLD) is seen worldwide and is the most common liver disorder in Western industrialized countries, where the major risk factors for NAFLD, central obesity, type 2 diabetes mellitus, dyslipidemia, and metabolic syndrome are common.
In the United States, studies report a prevalence of NAFLD of 10 to 46 percent, with most biopsy-based studies reporting a prevalence of NASH of 3 to 5 percent.
Worldwide, NAFLD has a reported prevalence of 6 to 35 percent (median 20 percent).

Patients with NAFLD (particularly those with NASH) often have one or more components of the metabolic syndrome.
■Obesity
■Systemic hypertension
■Dyslipidemia
■Insulin resistance or overt diabetes

Laboratory findings — Patients with NAFLD may have mild or moderate elevations in the aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Patients with NAFLD may have an elevated serum ferritin concentration or transferrin saturation . There is evidence that a serum ferritin greater than 1.5 times the upper limit of normal in patients with NAFLD is associated with a higher nonalcoholic fatty liver disease activity score (and thus, NASH) and with advanced hepatic fibrosis.

Rule out other disorders — Differentiating NAFLD from the other items in the differential diagnosis begins with a thorough history to identify potential causes such as significant alcohol use, starvation, medication use, and pregnancy-related hepatic steatosis.

We test all patients with hepatic steatosis for hepatitis C virus infection. We also test for hepatitis A and B. We do this to both to rule out these infections in patients with elevated aminotransferases and to determine immunity to guide future immunizations.
We also rule out other chronic liver diseases such as autoimmune hepatitis and hemochromatosis.
We obtain the following tests in all patients:
■Anti-hepatitis C virus antibody
■Hepatitis A IgG
■Hepatitis B surface antigen, surface antibody, and core antibody
■Plasma iron, ferritin, and total iron binding capacity
■Serum gammaglobulin level, antinuclear antibody, antismooth muscle antibody, and anti-liver/kidney microsomal antibody-1

Radiographic examinations:obtain an ultrasound

Role of liver biopsy: While liver biopsy is the gold standard for diagnosing NAFLD, in many cases a presumptive diagnosis can be made based upon the patient's history, laboratory tests, and imaging findings, provided other disorders have been excluded. However, some patients will continue to have an unclear diagnosis following a noninvasive evaluation. In such cases, a liver biopsy is indicated.

STAGES OF FIBROSIS — Noninvasive tests of hepatic fibrosis attempt to predict the stage of hepatic fibrosis that would be seen histologically. There are several histologic scoring systems for chronic liver disease. Many use five-point scales, such at the Metavir score (see "Histologic scoring systems for chronic liver disease", section on 'Metavir score'):
■F0: No fibrosis
■F1: Portal fibrosis without septa
■F2: Few septa
■F3: Numerous septa without cirrhosis
■F4: Cirrhosis 
Patients are typically considered to have significant fibrosis if their fibrosis score is ≥F2.

SEROLOGIC TESTS for fibrosis— A variety of serologic markers have been evaluated to predict the degree of fibrosis in the liver, and panels have been developed that combine assays of multiple markers to improve predictive ability.

The most studied panels are the aspartate aminotransferase (AST) to platelet ratio (APRI), FibroTest/FibroSure, Hepascore, and FibroSpect.

Panels of indirect markers of fibrosis: AST to platelet ratio index — The APRI is based on the AST level and platelet count and is easy to calculate. The APRI is calculated using the AST elevation (which is the AST level divided by the upper limit of normal [ULN] for the lab) and the platelet count per mm3 divided by 1000.
APRI = (AST elevation/platelet count) x 100
As an example, a patient with an AST level of 90 int. unit/L in a lab with an ULN = 45 int. unit/L and a platelet count of 120,000/mm3 would have an APRI of: (2/120) x 100 = 1.67

FibroTest, FibroSure, and ActiTest:FibroTest involves assessment of alpha-2-macroglobulin, alpha-2-globulin (haptoglobin), gammaglobulin, apolipoprotein A1, GGT, and total bilirubin Hepascore — Hepascore involves a combination of bilirubin, GGT, hyaluronic acid, alpha-2-macroglobulin, age, and sex. 

AST/ALT ratio — The AST/ALT ratio is approximately 0.8 in normal subjects. Some studies have suggested that a ratio >1 suggests the presence of cirrhosis.

RADIOLOGIC TESTS: Ultrasound-based transient elastography Magnetic resonance elastography (MRE) Acoustic radiation forse impulse (ARFI) imaging

COMBINING TESTS — Using multiple serologic panels or combining serologic panels with radiographic imaging may improve the ability to correctly assess the degree of a patient's fibrosis [14,166,167]. In addition, it may be possible to improve the diagnostic performance of these panels if they are used in stepwise combination. We typically use a combination serologic testing and tissue elastography. The specific tests chosen will depend on local availability. (See 'Choice of test' above.) The aspartate aminotransferase (AST) to platelet ratio (APRI) has been combined with FibroTest/FibroSure, a strategy referred to as "SAFE" biopsy (sequential algorithm for fibrosis evaluation). In one study, the combination had good overall accuracy for significant fibrosis and reduced the need for liver biopsy in patients with chronic hepatitis C virus (HCV). (See 'FibroTest, FibroSure, and ActiTest' above.) FibroTest has also been evaluated in combination with ultrasound-based transient elastography. In a study of 183 patients with chronic HCV, the combination of these tests demonstrated an area under the ROC curve of 0.88 for F ≥2, 0.95 for F ≥3, and 0.95 for F = 4. When the elastography and FibroTest results agreed, liver biopsy examination confirmed the stage of fibrosis in 84 percent of cases for F ≥2 fibrosis, in 95 percent for F ≥3 fibrosis, and in 94 percent for F = 4 fibrosis. Thus, it is likely that a combination of serum biomarkers and elastography will improve the accuracy of fibrosis detection.

Which patients to biopsy — Specifically, we obtain a biopsy if the patient:
■Has peripheral stigmata of chronic liver disease (suggestive of cirrhosis)
■Has splenomegaly (suggestive of cirrhosis)
■Has cytopenias (suggestive of cirrhosis)
■Has a serum ferritin >1.5 times the upper limit of normal (suggestive of NASH and advanced fibrosis)
■Is >45 years of age with associated obesity or diabetes (increased risk of advanced fibrosis)

NAFLD activity score — The NAFLD activity score (NAS) is a validated score that is used to grade disease activity in patients with NAFLD. The NAS is the sum of the biopsy's individual scores for steatosis (0 to 3), lobular inflammation (0 to 2), hepatocellular ballooning (0 to 2), and fibrosis (0 to 4). An NAS of 1 or 2 corresponds to NAFL, 3 to 4 corresponds to borderline NASH, and a score ≥5 corresponds to NASH.

DIFFERENTIAL DIAGNOSIS Alternative causes of hepatic steatosis — There are multiple causes of hepatic steatosis that should be considered in a patient with suspected nonalcoholic fatty liver disease (NAFLD).
Causes of hepatic steatosis in addition to NAFLD include:
■Alcoholic liver disease
■Hepatitis C (particularly genotype 3)
■Wilson disease
■Lipodystrophy
■Starvation
■Parenteral nutrition
■Abetalipoproteinemia
■Medications (amiodarone, methotrexate, tamoxifen, glucocorticoids, valproate, anti-retroviral agents for HIV)
■Reye syndrome
■Acute fatty liver of pregnancy
■HELLP (hemolytic anemia, elevated liver enzymes, low platelet count) syndrome
■Inborn errors of metabolism (LCAT deficiency, cholesterol ester storage disease, Wolman disease) A standard drink in the United States (12 oz [360 mL] of beer, 5 oz [150 mL] of wine, 1.5 oz [45 mL] of 80-proof spirits) contains approximately 14 grams of alcohol (figure 1), so the limits above roughly translate to >15 drinks per week for men and >10 drinks per week for women.

SUMMARY AND RECOMMENDATIONS
■Nonalcoholic fatty liver disease (NAFLD) refers to the presence of hepatic steatosis when no other causes for secondary hepatic fat accumulation (eg, heavy alcohol consumption) are present. NAFLD may progress to cirrhosis and is likely an important cause of cryptogenic cirrhosis. (See 'Definitions' above.) NAFLD is subdivided into nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH). In NAFL, hepatic steatosis is present without evidence of significant inflammation, whereas in NASH, hepatic steatosis is associated with hepatic inflammation that may be histologically indistinguishable from alcoholic steatohepatitis.
■Most patients with NAFLD are asymptomatic, although some patients with NASH may complain of fatigue, malaise, and vague right upper abdominal discomfort. Patients are more likely to come to attention because laboratory testing revealed elevated liver aminotransferases or hepatic steatosis was detected incidentally on abdominal imaging.
■Patients with NAFLD may have mild or moderate elevations in the aspartate aminotransferase and alanine aminotransferase, although normal aminotransferase levels do not exclude NAFLD.
■Radiographic findings in patients with NAFLD include increased echogenicity on ultrasound, decreased hepatic attenuation on computed tomography, or an increased fat signal on magnetic resonance imaging.
■A definitive diagnosis of NAFLD requires all of the following: •Demonstration of hepatic steatosis by imaging or biopsy •Exclusion of significant alcohol consumption •Exclusion of other causes of hepatic steatosis
■Other causes of hepatic steatosis include (see 'Differential diagnosis' above): •Significant alcohol use •Hepatitis C (particularly genotype 3) •Wilson disease •Lipodystrophy •Starvation •Parenteral nutrition •Abetalipoproteinemia •Medications •Reye syndrome •Acute fatty liver of pregnancy •HELLP (hemolytic anemia, elevated liver enzymes, low platelet count) syndrome •Inborn errors of metabolism
■Radiologic findings are often sufficient to make a diagnosis of NAFLD, provided other causes of hepatic steatosis have been excluded. However, liver biopsy may be indicated if the diagnosis is not clear or to assess the degree of hepatic injury.

gastroenterology observership 1

colonoscopy 
medicine: midazolam+fentanyl (most common)
patient with a lot of pain medication, use propofol for deeper sedation

Barrette esophagus:

 A, Lower esophageal sphincter and squamocolumnar junction; B, endoscopic view.

A, Normal esophageal epithelium; B-D, variants of Barrett’s esophagus.

                                        A, Short-segment and B, long-segment Barrett’s esophagus; A’, B’, endoscopic views.

 Histology of Barrett’s esophagus; A, no dysplasia, B, low-grade dysplasia, and C, high- grade dysplasia.

base on visual change under endoscopy+pathologic diagnosis, if see visual change but pathology not supporting, it is not barrette esophagus.
Barrett's esophagus is the condition in which any extent of metaplastic columnar epithelium that predisposes to cancer development replaces the stratified squamous epithelium that normally lines the distal esophagus.

The condition develops as a consequence of chronic gastroesophageal reflux disease (GERD), and predisposes to the development of adenocarcinoma of the esophagus.

EPIDEMIOLOGY — Barrett's esophagus is usually discovered during endoscopic examinations of middle-aged and older adults whose mean age at the time of diagnosis is approximately 55 years
Barrett's esophagus appears to be uncommon in blacks and Asians.
Obesity is a risk factor for gastroesophageal reflux disease (GERD) and may be a risk factor for Barrett's esophagus
44 percent of patients lacked "troublesome heartburn and/or acid regurgitation during the past three months" suggesting that screening programs based upon reflux symptoms alone may be inadequate to identify patients with Barrett's esophagus.
Familial aggregation of Barrett's esophagus has been described. It is unclear if this is due to common environmental exposures and/or an inherited predisposition. Germline mutations in the MSR1, ASCC1, and CTHRC1 genes have been associated with the presence of Barrett's esophagus and esophageal adenocarcinoma. However, large cohort studies are needed to validate these findings.

CLINICAL FEATURES:  symptoms of associated gastroesophageal reflux disease (GERD), such as heartburn, regurgitation, and dysphagia.

DIAGNOSTIC CRITERIA — Endoscopic examination generally is required to diagnose Barrett's esophagus.
Two criteria must be fulfilled:
■The endoscopist must document that columnar epithelium lines the distal esophagus.
■Histologic examination of biopsy specimens from that columnar epithelium must reveal intestinal metaplasia. Some data suggest that gastric cardiac-type epithelium in the esophagus also might predispose to cancer and thus might be considered "Barrett's esophagus," but most authorities still require the presence of intestinal metaplasia for an unequivocal diagnosis

SUMMARY AND RECOMMENDATIONS
■Barrett's esophagus is usually discovered during endoscopic examinations of middle-aged and older adults whose mean age at the time of diagnosis is approximately 55 years. The specialized intestinal columnar metaplasia typical of Barrett's esophagus causes no symptoms. Most patients are seen initially for symptoms of associated gastroesophageal reflux disease (GERD), such as heartburn, regurgitation, and dysphagia. (See 'Epidemiology' above.)
■Two criteria must be fulfilled to make a diagnosis of Barrett's esophagus: (See 'Diagnostic criteria' above.) •The endoscopist must document that columnar epithelium lines the distal esophagus. •Histologic examination of biopsy specimens from that columnar epithelium must reveal specialized intestinal metaplasia. Some data suggest that gastric cardiac-type epithelium in the esophagus also might predispose to cancer and thus might be considered "Barrett's esophagus," but most authorities still require the presence of specialized intestinal metaplasia for an unequivocal diagnosis.
■It has been proposed that patients with GERD symptoms should be screened endoscopically for Barrett's esophagus. We suggest that patients with multiple risk factors for esophageal adenocarcinoma undergo screening for Barrett's esophagus. However, the evidence supporting this recommendation is weak, and we feel that decisions on when to recommend endoscopic screening should be individualized. Factors known to increase the risk for Barrett's esophagus include white ethnicity, older age, obesity (especially central obesity), and long duration of GERD symptoms.

some info and pics are from
https://gi.jhsps.org/GDL_DiseaseLibrary.aspx?CurrentUDV=31

useful study materials

http://courses.washington.edu/med610/radiology/Luks&TakasugiX-rayTutorial6-8-10.ppt

38 wk pregnant present w/ SOB

ABG 7.32/36/65/18/90%RA it seems like a metabolic acidosis, but in a pregnant woman, normally has respiratory alkalosis, so combine with this patient, it should be a respiratory acidosis diagnosis is asthma exacerbation

liver enzyme

Child Pugh Score, is the best indicator in cirrhosis. Child Turcotte classification of patients with cirrhosis

Child-Pugh classification of severity of cirrhosis

Child Pugh classification

Parameter	Points assigned
	1	2	3
Ascites	Absent	Slight	Moderate
Bilirubin	<2 mg/dL (<34.2 micromol/liter)	2 to 3 mg/dL (34.2 to 51.3 micromol/liter)	>3 mg/dL (>51.3 micromol/liter)
Albumin	>3.5 g/dL (35 g/liter)	2.8 to 3.5 g/dL (28 to 35 g/liter)	<2.8 g/dL (<28 g/liter)
Prothrombin time
Seconds over control	<4	4 to 6	>6
INR	<1.7	1.7 to 2.3	>2.3
Encephalopathy	None	Grade 1 to 2	Grade 3 to 4

Modified Child-Pugh classification of the severity of liver disease according to the degree of ascites, the serum concentrations of bilirubin and albumin, the prothrombin time, and the degree of encephalopathy. A total Child-Turcotte-Pugh score of 5 to 6 is considered class A (well-compensated disease); 7 to 9 is class B (significant functional compromise); and 10 to 15 is class C (decompensated disease). These classes correlate with one- and two-year patient survival: class A: 100 and 85 percent; class B: 80 and 60 percent; and class C: 45 and 35 percent.


remember, MI can has elevated AST+LDH, although it is non-specific.
When you see both elevated, beware of MI.

AST/ALT ratio 2:1 indicate alcoholic, because AST exists in both cytoplasm and mitochondrial, and ALT only exists in cytoplasm. Alcohol will damage mitochondrial, that is the reason why AST can be higher. 

Elevated GGT can help hepatic/non-hepatic for elevation of ALP.

If patient has chronic ALT, AST elevation, work up include:
ANA(autoimmune hepatitis),
iron study(hematochromatosis),
alpha 1 anti-trypsin,
and hepatitis B and C

when you see the isolated elevation of ALP, suspect PBC, check the antimitochondrial, and ultrasound

if liver enzyme is 10 times higher >400, 400-800, >1000 (think about ischemic injury, drug toxin, viral hepatitis augmentin(amoxicillin/clavulanate potassium) and unasyn(ampicillin sodium/sulbactam sodium) are MCC medication for cholestasis.

MELD score (Model for End-stage Liver Disease) MELD = 3.8[Ln serum bilirubin (mg/dL)] + 11.2[Ln INR] + 9.6[Ln serum creatinine (mg/dL)] + 6.4

COPD exacerbation

80 year old female with past history of moderate COPD( 3L oxygen all the time), HTN, hyperlipidemia, osteoporosis, glaucoma and CAD present with shortness of breath since yesterday morning. Patient is getting SOB every day in the morning since last month. She has been taking Proair(albuterol) and Duoneb (albuterol/ipratropium), SOB normally can improve and go back to baseline within 1 hour. yesterday morning, her SOB couldn't improve with same medications, therefore, she came to ER. She had COPD exacerbation in Dec 2012, Mar 2013. She has always cough with clear phlegm. there is no fever, chills, no chest pain, orthopnea, paroxysmal nocturnal dyspnea. She smoke all her life for 60-70 years, but quit smoking 2 weeks ago. at ER, she received solu medrol 125 mg IV once, and Duoneb once. vital, RR 22, SaO2 95% on 3L, cxr no acute infiltrate, EKG is normal sinus rhythm. assessment and plan: 1, COPD exacerbation, solu medrol 60mg IV q8h, for 1-2 days, then transtion to po steroid, plus azithromycin 500mg once for 3 days. 2, HTN, continue lisinopril and metoprolol 3, CAD, continue ACEi, beta blocker, aspirin and statin 4, start omeprazol as she will be on steroid. Management of acute exacerbations of chronic obstructive pulmonary disease defines an exacerbation of chronic obstructive pulmonary disease (COPD) as an acute increase in symptoms beyond normal day-to-day variation. This generally includes an acute increase in one or more of the following cardinal symptoms: ■Cough increases in frequency and severity ■Sputum production increases in volume and/or changes character ■Dyspnea increases Constitutional symptoms, an unchanged chest radiograph, a variable decrease in pulmonary function, and tachypnea are typical in acute exacerbations Rapid overview: Emergency management of severe acute COPD exacerbations General points Chronic obstructive pulmonary disease (COPD) exacerbations are most often precipitated by infection (viral or bacterial) Differential diagnosis includes: Acute decompensated heart failure, pulmonary embolism (PE), pneumonia, pneumothorax Clinical manifestations Cardinal symptoms: Increase or change in character of dyspnea, cough, sputum production Diagnostic testing Assess oxygen saturation with pulse oximetry Obtain arterial blood gas in severe exacerbations Obtain chest radiograph to assess for signs of pneumonia, acute heart failure, pneumothorax Obtain complete blood count and measures of basic electrolytes and renal function Obtain electrocardiogram Pharmacotherapy Oxygen to target saturation of 90 to 94 percent and PaO2 of 60-70 mmHg; Venturi mask can be useful for titrating FiO2; high FiO2 usually not needed and can contribute to hypercapnia (high FiO2 requirement should prompt consideration of alternative diagnosis (eg, PE)) Inhaled beta agonist (eg, albuterol 2.5 mg diluted to 3 mL via nebulizer) Inhaled anticholinergic agent (eg, ipratropium 500 micrograms via nebulizer) Systemic corticosteroid (eg, methylprednisolone 60 mg IV) Antibiotic therapy: Levofloxacin (750 mg IV) or alternative based on likely pathogens (including risk of pseudomonas infection) and local patterns of antibiotic resistance Noninvasive Positive Pressure Ventilation (NPPV) Indicated for moderate to severe exacerbations Use only if tracheal intubation not immediately necessary and no other contraindications Contraindications to NPPV include: Severely impaired consciousness, inability to clear secretions or protect airway, high aspiration risk Initial settings for bilevel NPPV: 8 cm H2O inspiratory pressure (may increase up to 15 cm H2O if needed to aid ventilation); 3 cm H2O expiratory pressure Monitoring and initial interventions Perform continual monitoring of oxygen saturation, cardiac rhythm, and vital signs Place two peripheral IV catheters Tracheal intubation For patients with severe respiratory distress in whom NPPV is contraindicated or who fail to improve with NPPV and aggressive pharmacotherapy Disposition Criteria for hospitalization include: Patients with high-risk comorbidities (pneumonia, cardiac arrhythmia, heart failure, diabetes mellitus, renal failure, liver failure) Inadequate improvement of symptoms with initial therapies Marked increase in dyspnea Inability to eat or sleep due to symptoms Worsening hypoxemia or hypercapnea PRECIPITANTS — It is estimated that 70 to 80 percent of COPD exacerbations are due to respiratory infections, including: Haemophilus influenzae 13 to 50 Moraxella catarrhalis 9 to 21 Streptococcus pneumoniae 7 to 26 Pseudomonas aeruginosa 1 to 13 The remaining 20 to 30 percent are due to environmental pollution or have an unknown etiology. The single best predictor of exacerbations was a history of exacerbations, regardless of COPD severity. The GOLD guidelines suggest using a combination of an individual’s FEV1 and history of exacerbations to assess the exacerbation risk [1]. The number of exacerbations in the previous 12 months is stratified: a history of zero or one exacerbation suggests a low future risk of exacerbations, while two or more suggest a high future risk. Severity of airflow limitation in COPD (based on postbronchodilator FEV1) In patients with FEV1/FVC <0.7: GOLD 1 Mild FEV1 ≥80 percent predicted GOLD 2 Moderate 50 percent ≤FEV1 <80 percent predicted GOLD 3 Severe 30 percent ≤FEV1 <50 percent predicted GOLD 4 Very severe FEV1 <30 percent predicted ■Low risk: Typically GOLD 1 or 2 (mild to moderate airflow limitation) and/or 0 to 1 exacerbation per year ■High risk: Typically GOLD 3 or 4 (severe or very severe airflow limitation) and/or ≥2 exacerbations per year DIFFERENTIAL DIAGNOSIS — Patients with COPD who present to the hospital with acute worsening of dyspnea should be evaluated for potential alternative diagnoses, such as heart failure, pulmonary thromboembolism, and pneumonia. TREATMENT: OXYGEN THERAPY — Supplemental oxygen is a critical component of acute therapy. It should target an arterial oxygen tension (PaO2) of 60 to 70 mmHg, with an oxyhemoglobin saturation of 90 to 94 percent. PHARMACOLOGIC TREATMENT — The major components of managing an acute exacerbation of COPD include inhaled short-acting bronchodilators (beta adrenergic agonists and anticholinergic agents), glucocorticoids, and antibiotics. Beta adrenergic agonists — Inhaled short-acting beta adrenergic agonists (eg, albuterol) are the mainstay of therapy for an acute exacerbation of COPD.These medications may be administered via a nebulizer or a metered dose inhaler (MDI) with a spacer device. Despite evidence that MDI devices may have equal efficacy during acute exacerbations of COPD, many clinicians prefer nebulized therapy on the presumption of more reliable delivery of drug to the airway [1]. We favor nebulized therapy because many patients with COPD have difficulty using proper MDI technique in the setting of an acute exacerbation. Patients with severe COPD are at risk for hypercapnia with administration of supplemental oxygen, so concern has been raised about the risk of hypercapnia during bronchodilator treatments using oxygen-driven nebulizers.We concur with the British Thoracic Society guidelines that suggest using air-, rather than oxygen-driven bronchodilator nebulization, or limiting oxygen-driven treatments to 6 minutes. Anticholinergic agents — Inhaled short-acting anticholinergic agents (eg, ipratropium bromide) are used with inhaled short-acting beta adrenergic agonists to treat exacerbations of COPD. Glucocorticoids Route — Oral glucocorticoids are rapidly absorbed (peak serum levels achieved at one hour after ingestion) with virtually complete bioavailability and appear equally efficacious as intravenous glucocorticoids for treating most exacerbations of COPD. As an example, a randomized trial assigned 210 patients hospitalized with a COPD exacerbation to receive oral or intravenous prednisolone (60 mg daily) for five days and found no difference between the two groups in the rate of treatment failure, length of hospital stay, improvement in spirometry, or improvement in quality of life. However, intravenous glucocorticoids are typically administered to patients who present with a severe exacerbation, who respond poorly to oral glucocorticoids, who are unable to take oral medication, or who may have impaired absorption due to decreased splanchnic perfusion (eg, patients in shock). Antibiotics — Antibiotics are indicated for many patients having a COPD exacerbation. CHEST PHYSIOTHERAPY — Mechanical techniques to augment sputum clearance, such as directed coughing, chest physiotherapy with percussion and vibration, intermittent positive pressure breathing, and postural drainage, have not been shown to be beneficial in COPD and may provoke bronchoconstriction. Their use in acute exacerbations of COPD is not supported by clinical trials. MECHANICAL VENTILATION Noninvasive ventilation — Noninvasive positive pressure ventilation (NPPV) refers to mechanical ventilation delivered through a noninvasive interface, such as a face mask, nasal mask, or nasal prongs. It improves numerous clinical outcomes and is the preferred method of ventilatory support in many patients with an acute exacerbation of COPD. Invasive ventilation — Invasive mechanical ventilation should be administered when patients fail NPPV, do not tolerate NPPV, or have contraindications to NPPV. PROGNOSIS — Acute exacerbations of COPD are associated with increased mortality after hospital discharge. ■It is estimated that 14 percent of patients admitted for an exacerbation of COPD will die within three months of admission [47,48]. ■Among 1016 patients with an acute exacerbation of COPD and a PaCO2 of 50 mmHg or more, the 6 and 12 month mortality rates were 33 and 43 percent, respectively [49]. ■In a study of 260 patients admitted with a COPD exacerbation, the one year mortality was 28 percent [50]. Independent risk factors for mortality were age, male gender, prior hospitalization for COPD, PaCO2 ≥45 mmHg (6 kPa), and urea >8 mmol/L. ■Patients hospitalized for a COPD exacerbation who have a Pseudomonas aeruginosa in their sputum have an increased risk of mortality at three years than those without (59 versus 35 percent, HR 2.33, 95% CI 1.29-3.86), independent of age, comorbidity, or COPD severity SUMMARY AND RECOMMENDATIONS ■A table to assist with emergency management of severe acute exacerbations of COPD is provided (table 1). ■An acute exacerbation of COPD is characterized by an acute increase in symptoms beyond normal day-to-day variation. (See 'Introduction' above.). ■We recommend that all patients having a COPD exacerbation receive both an inhaled short-acting beta adrenergic agonist and an inhaled short-acting anticholinergic agent, rather than either medication alone (Grade 1B). (See 'Beta adrenergic agonists' above and 'Anticholinergic agents' above.) ■We recommend that all patients having a COPD exacerbation receive systemic glucocorticoids (Grade 1A). A reasonable dose for patients not requiring intensive care unit admission is prednisone 30 to 60 mg orally once daily, or the equivalent, for 10 to 14 days, although preliminary data suggest that a 5 day course may be an acceptable alternative. (See 'Glucocorticoids' above.) ■Antibiotics are indicated for many patients having a COPD exacerbation. (See "Management of infection in acute exacerbations of chronic obstructive pulmonary disease", section on 'Summary and recommendations'.) ■Mucoactive agents, mechanical techniques to augment sputum clearance, and methylxanthines have not been shown to confer benefit for patients with a COPD exacerbation. (See 'Mucoactive agents' above and 'Chest physiotherapy' above and 'Methylxanthines' above.) ■We suggest that all patients who are hypoxemic be given supplemental oxygen targeting a PaO2 of 60 to 70 mmHg, with an oxyhemoglobin saturation of 90 to 94 percent (Grade 2C). (See 'Oxygen therapy' above.) ■Noninvasive positive pressure ventilation (NPPV) improves numerous clinical outcomes and is the preferred method of ventilatory support in many patients with an acute exacerbation of COPD. Invasive mechanical ventilation is required in patients with respiratory failure who fail NPPV, do not tolerate NPPV, or have contraindications to NPPV. Both NPPV and invasive mechanical ventilation for patients with an acute exacerbation of COPD are discussed separately.

Initial management of animal and human bites

INTRODUCTION — Animal and human bites are a common problem. Proper care requires wound inspection for injury to deeper structures; meticulous wound care at the initial encounter; and decisions regarding primary closure, the provision of prophylactic antibiotics for wounds at high risk for infection, and prophylaxis for tetanus and rabies as indicated. EPIDEMIOLOGY — Animal bites are common. In the United States, there is an annual incidence of two to five million occurrences which account for about 1 percent of all visits to emergency departments. Approximately 10 percent of bite wounds presenting for medical attention require suturing and follow-up care, and 1 to 2 percent result in hospitalization. MICROBIOLOGY — The predominant pathogens in animal bite wounds are the oral flora of the biting animal and human skin flora. Infection usually results from a mixture of organisms. Common pathogens (in order of prevalence) include Pasteurella species, staphylococci, streptococci, and anaerobic bacteria. Capnocytophaga canimorsus, a fastidious gram-negative rod, can cause bacteremia and fatal sepsis after animal bites, especially in asplenic patients, chronic alcohol abusers, or those with underlying hepatic disease. Cat bites can also transmit Bartonella henselae, the organism responsible for cat scratch disease. Cat bites — Two-thirds of cat bites involve the upper extremities; scratches typically occur on the upper extremities or face. Deep puncture wounds are of particular concern because cats have long, slender, sharp teeth. When the hand is the target of such a puncture wound, bacteria can be inoculated below the periosteum or into a joint and result in osteomyelitis or septic arthritis INITIAL MANAGEMENT: Stabilization — Direct pressure should be applied to actively bleeding wounds and a neurovascular assessment should be performed in areas distal to the wound. Deep wounds to vital structures should be treated as major penetrating trauma. Wound preparation — Appropriate local anesthesia facilitates adequate wound cleansing. To reduce the counts of bacteria present in the wound, the surface should be cleaned with 1 percent povidone iodine or 1 percent benzalkonium chloride, and the depths irrigated with copious amounts of saline using pressure irrigation. Debridement of devitalized tissue is important to remove any nidus for infection. Primary closure — A clinician with prior training and experience in laceration repair may perform primary wound closure of simple lacerations due to dog bites. In contrast, most cat or human bites are left open to heal by secondary intention. In addition to these indications for primary wound closure of open lacerations, we suggest that the laceration meets ALL of the following criteria: ■Clinically uninfected ■Less than 12 hours old (24 hours on the face) ■NOT located on the hand or foot In particular, wounds to the face are usually closed promptly because good cosmesis is especially important, and infection of these wounds is uncommon Wounds at high risk for the development of infection should NOT be closed primarily in most cases [3,5,8,29,30]. These include: ■Crush injuries ■Puncture wounds ■Bites involving the hands and feet ■Wounds more than 12 hours old (24 hours old on face) ■Cat or human bites, except those to the face ■Bite wounds in compromised hosts (eg, immunocompromised, absent spleen or splenic dysfunction, venous stasis, diabetes mellitus [adults]) Surgical consultation — Surgical consultation is usually necessary for the following wounds [30]: ■Deep wounds that penetrate bone, tendons, joints, or other major structures ■Complex facial lacerations ■Wounds associated with neurovascular compromise ■Wounds with complex infections (eg, abscess formation, osteomyelitis, or joint infection) Antibiotic prophylaxis — Prophylactic antibiotics reduce the rate of infection due to some animal bites, especially cat bites. Although routine antibiotic prophylaxis is not recommended, prophylaxis is warranted in certain high-risk wounds . ■Deep puncture wounds (especially due to cat bites) ■Moderate to severe wounds with associated crush injury ■Wounds in areas of underlying venous and/or lymphatic compromise ■Wounds on the hand(s), genitalia, face, or in close proximity to a bone or joint (particularly the hand and prosthetic joints) ■Wounds requiring closure ■Bite wounds in compromised hosts (eg, immunocompromised, absent spleen or splenic dysfunction, and adults with diabetes mellitus) Tetanus and rabies prophylaxis — Viral prophylaxis after human bites — Any unvaccinated patient or individual negative for anti-HBs antibodies who is bitten by an individual positive for HBsAg should receive both hepatitis B immune globulin (HBIG) and hepatitis B vaccine Infected bites — To successfully manage an infected wound, the clinician must recognize early signs of infection and be aware of the likely pathogens. (See 'Infected wound' above.) If a bite wound appears to be infected, the following actions should be taken: ■Remove suture material, if previously repaired. ■Obtain Gram stain and aerobic and anaerobic cultures from the depth of an infected puncture or laceration prior to the initiation of antibiotics. The laboratory requisition should note that an animal or human bite wound is the culture source. ■Draw aerobic and anaerobic blood cultures prior to antibiotic therapy in patients with signs of systemic infection. ■Consult a surgeon for possible operative exploration, debridement, and drainage if abscess formation or suspected infection of bone, joint, or other major underlying structure (eg, clenched fist infections and other hand infections) is present. Debrided material should be sent for aerobic and anaerobic culture. ■Hospitalize patients with systemic symptoms or progression or development of infection despite receiving oral antibiotics. Empiric antibiotic therapy — Once a bite becomes infected, it is crucial to perform aggressive debridement and abscess drainage, as indicated, and to administer intravenous broad-spectrum antibiotics to cover probable infecting bacteria in patients with dog or cat bites (table 1) or human bites (table 2). A common approach involves initial IV therapy until infection is resolving followed by oral therapy to complete a course of 10 to 14 days. Empiric intravenous antibiotic therapy for animal bites Adults Children Options for empiric gram-negative and anaerobic coverage include: Monotherapy with a beta-lactam/beta-lactamase inhibitor, such as one of the following: Ampicillin-sulbactam (unasyn) 3 g every six hours 50 mg/kg per dose (based on ampicillin component) every six hours* Piperacillin-tazobactam (zosyn)4.5 g every eight hours 125 mg/kg per dose (based on piperacillin component) every eight hours* Ticarcillin-clavulanate (timentin)3.1 g every four hours 50 mg/kg per dose (based on ticarcillin component) every four hours* A third generation cephalosporin such as ceftriaxone 1 g IV every 24 hours PLUS Metronidazole 500 mg IV every eight hours A third generation cephalosporin such as ceftriaxone 100 mg/kg per dose every 24 hours* PLUS Metronidazole 10 mg/kg per dose every eight hours* COMPLICATIONS — The most serious complications of animal bites include trauma to deep structures, and infections, either transmitted or arising in the wound. In addition children who have suffered dog bites requiring at least minor surgical intervention may develop symptoms of post-traumatic stress disorder (PTSD) [40]. ■Systemic infections – Any infected bite wound can progress to infection of underlying structures (eg, bone, joint, tendon) and to bloodstream infection. Human bites can transmit numerous other infections, including hepatitis viruses B (HBV) and C (HCV), primary syphilis (rare), and herpes simplex virus [33,41]. The risk for transmitting HIV through saliva is extremely low but is of concern if there is blood in the saliva. Counseling regarding post-exposure HIV prophylaxis is appropriate in this setting [34]. (See "Management of healthcare personnel exposed to HIV".) Any patient negative for anti-HBs antibodies who is bitten by an individual positive for HBsAg should receive both hepatitis B immune globulin (HBIG) and hepatitis B vaccine (table 7). Individuals who work in facilities where the risk for human bites is high, such as institutions for the cognitively impaired, should be given the hepatitis B vaccine series upon employment. (See "Hepatitis B virus vaccination", section on 'Indications'.) ■Post-traumatic stress disorder – Children who have suffered dog bites requiring at least minor wound repair, particularly if the wounds are deep or multiple, may develop symptoms of post-traumatic stress disorder (PTSD) [40]. In one prospective study, the parents of 22 children who presented to an emergency department for minor surgical treatment of dog bites agreed to complete a questionnaire and undergo a telephone and/or personal interview about the circumstances of the injury and the child's behavior before and after it occurred. The interviews took place between two and nine months after the incident. Among the 22 children, 12 had symptoms of PTSD for at least one month (five children met all of the DSM-IV criteria and seven met only some) (table 8). SUMMARY AND RECOMMENDATIONS ■Most animal bites are caused by dogs, cats, and humans. The predominant organisms in animal bite wounds are the oral flora of the biting animal as well as human skin flora (such as Staphylococci and Streptococci). (See 'Epidemiology' above and 'Microbiology' above and "Soft tissue infections due to dog and cat bites" and "Soft tissue infections due to human bites".) ■The typical location and nature of the injury differs depending upon the animal inflicting the bite. (See 'Clinical manifestations' above.) Wound assessment ■After appropriate local anesthesia, the wound should be carefully explored to identify injury to underlying structures and the presence of a foreign body. Appropriate imaging should be obtained for deep bite wounds near bone and/or joints and when a foreign body is suspected (eg, plain radiograph or ultrasound). (See 'Plain radiographs and ultrasound' above and "Infiltration of local anesthetics" and "Topical anesthetics in children".) ■Head computed tomography is warranted in patients with a deep dog bite to the scalp, including puncture wounds, especially in children less than two years of age. (See 'Head computed tomography' above.) ■If a bite wound appears to be infected, Gram stain and aerobic and anaerobic cultures should be obtained prior to the initiation of antibiotics. Wound cultures are NOT indicated in clinically uninfected bite wounds as results do not correlate with the likelihood of infection or the pathogen that is present in patients with subsequent infection. (See 'Infected wound' above and 'Wound culture' above.) Wound management ■Wound irrigation and debridement of devitalized tissue are essential components in the initial management of bite wounds. The wound should be carefully explored to identify injury to underlying structures and the presence of a foreign body. (See 'Wound preparation' above and "Minor wound preparation and irrigation".) ■We suggest primary closure of open lacerations in healthy patients that meet all of the following criteria (Grade 2B): •Cosmetically important (eg, facial lacerations) •Wounds that are clinically uninfected •Wounds less than 12 hours old (24 hours on the face) •Wounds NOT located on the hand or foot ■Sealing the wound with cyanoacrylate tissue adhesive ("glue") should be avoided. (See 'Primary closure' above and 'Wound preparation' above.) ■We suggest NOT closing wounds at high risk for the development of infection including the following types of wounds (Grade 2C): •Crush injuries •Puncture wounds •Bites involving the hands or feet •Wounds more than 12 hours old (24 hours old on face) •Cat or human bites (except those to the face) •Bite wounds in compromised hosts (eg, immunocompromised, absent spleen or splenic dysfunction, venous stasis, diabetes mellitus [adults]) (see 'Primary closure' above) ■Tetanus and rabies prophylaxis should be provided as indicated. (See 'Tetanus and rabies prophylaxis' above.) ■Surgical consultation may be indicated in selected circumstances. (See 'Surgical consultation' above.) ■Patients who are discharged after initial care should follow-up with their primary care provider or other appropriate clinician within 48 to 72 hours to assess wound status. (See 'Follow-up care' above.) Antibiotic therapy ■Prophylaxis with oral antibiotics should be given for patient circumstances as outlined above (table 3 and table 4). (See 'Antibiotic prophylaxis' above and "Soft tissue infections due to dog and cat bites", section on 'Prophylaxis' and "Soft tissue infections due to human bites", section on 'Antibiotics'.) ■Patients with deep or severe wound infections are treated with intravenous rather than oral antibiotics (table 1 and table 2). (See 'Infected bites' above and 'Empiric antibiotic therapy' above and "Soft tissue infections due to dog and cat bites", section on 'Prophylaxis' and "Soft tissue infections due to human bites", section on 'Antibiotics'.) Virus transmission after human bite ■Any patient negative for anti-HBs antibodies who is bitten by an individual positive for HBsAg should receive both hepatitis B immune globulin (HBIG) and hepatitis B vaccine (table 7). (See 'Viral prophylaxis after human bites' above.) ■The risk for transmitting HIV through saliva is extremely low but is of concern if there is blood in the saliva. Counseling regarding post-exposure HIV prophylaxis is appropriate in this setting. (See 'Viral prophylaxis after human bites' above and "Management of healthcare personnel exposed to HIV".)