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TWU FHN 2 module 2

TWU FHN 2 Module 2

QuestionAnswer
Referred from outside of abdomen Sources of pain: Pneumonia Myocardial infarction
Sources of pain: Intra-abdominal causes causes can be referred to other areas Pain of acute cholecystitis referred to right scapula Stomach pain to shoulders Pancreatic pain to back and L shoulder Ovaries/uterine- inner thighs
Acute abdominal pain is pain of sudden onset and is not always a surgical emergency
Chronic abdominal pain is intermittent or continuous abdominal pain/discomfort lasting longer than 3 to 6 months
Acute abdomen is a sudden (acute) condition of the abdomen requiring immediate surgical intervention
Children under 5 Appendicitis uncommon Diagnosis often missed or delayed Perforation more common Disproportionately high percentage of deaths due to appendicitis Difficult to determine unless abdominal tenderness, guarding, doubling up or vomiting present
Intussusception peak incidence 6 months
Children age 5-12 Recurrent abdominal pain Psychosomatic most common Organic cause found in less than 10% Always rule out constipation in children-common cause of GI complaint
Acute appendicitis Common from age 5-15
Abdominal Pain - Adolescence Inflammatory bowel disease Screen for STD/pregnancy risk Acute appendicitis Peak incidence from age 10-15
abdominal pain - adult PUD from 30-50 Nonspecific abdominal pain (NSAP) most common under 40
Cholecystitis higher incidence obese females on estrogen
PUD higher incidence males
Women of childbearing age with lower abdominal pain LMP Sexual history to assess risk for preg/STD Contraception use Vaginal discharge
Women of reproductive age at risk for: Ectopic pregnancy Endometriosis Adenexal/Ovarian torsion More common for UTI/pyelonephritis PID Pregnant female: Appendicitis difficult to diagnose due to upward displacement of vermiform appendix
Elderly Difficult to elicit accurate description of the pain Concurrent illnesses, complaints make it hard for patient to differentiate new symptoms Malignancies-assess weight loss Strangulated hernias Intestinal obstruction Diverticulitis
Blacks, Mediterranean descent- sickle cell crisis
Native Americans higher incidence gallbladder disease
Biliary colic typically develops in the evening
Abdominal pain child under 5 Consider poison
abdominal pain child 5-15 consider constipation
appendicitis Colicky, crampy periumbilical progressing to constant pain in RLQ
ureterolithiasis Excruciating pain in R, LUQ, or flank radiating to groin or medial thigh-
pain Radiating to L shoulder renal calculi, splenic rupture, ectopic pregnancy
GB disease RUQ pain radiating to R scapula
Surgical scars possible adhesions
Silver colored stools stools-Carcinoma of Ampulla of Vater
Hernias strangulation, obstruction
obstruction Distention, abnormal peristalsis
Bluish periumbilical discoloration (Cullen sign)— intraabdominal bleeding
Ecchymosis of flanks (Gray Turner sign)— intraabdominal bleeding or pancreatitis
peritonitis, ileus Absent or hypoactive bowel sounds-
Absent bowel sounds RLQ- intussusception
Light percussion produces localized pain in presence of peritoneal inflammation
Palpable gall bladder, Murphy’s sign inspiratory halt
Blumberg rebound tenderness
Positive McBurney sign rebound tenderness over the McBurney point
Positive obturator sign ruptured appendix or pelvic abscess causes irritation of the obturator muscle) With R leg flexed 90 degrees at the hip and knee rotate leg laterally and medially to elicit pain in hypogastric (pubic) region
Positive iliopsoas sign Pain with raising the R leg from the hip while the examiner pushed downward
Positive Rovsing sign RLQ pain intensified with LLQ palpation
Positive Markle (heel drop test) Heel jar raises up to tip toes pain with relaxation when heel touches the floor
rectal Tenderness laterally to left Diverticulitis with abscess
rectal Tenderness laterally to rt Acute appendicitis Intussusception
Upright chest free intraperitoneal air under diaphragm (pneumoperitoneum
Suspected intestinal obstruction Enlarged loops of bowel/ fluid levels
Suspected perforation (intestinal or gastric) Free air in peritoneum
CBC with differential Never diagnostic of acute appendicitis Rising leukocyctosis supportive of acute infectious or inflammatory process Anemia (acute/chronic) (may need corrected prior to surgery)
C Reactive Protein Elevated in acute inflammation states Nonspecific for location Sensitivity for acute appendicitis 91%
Amylase, lipase, liver function tests Elevated AST/ALT results from hepatocellular necrosis or inflammation-hepatitis Elevated alkaline phosphatase seen in cholestasis or infiltrative liver disease Elevated amylase and lipase associated with pancreatic pathology
If suspecting ectopic-order quantitative BhCG Abnormal pregnancy usually associated with abnormally low beta-hCG (Remember, qualitative BhCG reveals only positive or negative test result)
Stool O &P, C&S Infection, parasites
Fecal occult blood GI blood loss
Role of NP Perform history and physical, form clinical impression, triage appropriately, order initial noninvasive studies and lab, and consult/refer to physician/surgeon
RUQ common causes Cholecystitis, cholelithiasis Leaking duodenal ulcer Renal cell carcinoma/hydronephrosis Hepatomegaly-Hepatitis CHF
LUQ common causes Gastroenteritis Irritable colon Splenic infarct Pancreatitis Aortic aneurysm (also in epigastric region) Renal pathology
Diagnostics to consider in RUQ/LUQ Chest x-ray and EKG Upright abdominal films Upper abdominal US Serum amylase, lipase, transaminases Radionuclide scan (HIDA) Upper GI endoscopy
Epigastric pain Most common causes GERD Peptic Ulcer Disease Pancreatitis
Diagnostics to consider in epigastric pain C-xray, EKG Obtain upright abdominal films Upper GI endoscopy RUQ ultrasound
Generalized Abdominal Pain Common causes Peritonitis Pancreatitis Sickle cell crisis Early appendicitis
Diagnostics to consider in generalized abdomial pain: Abdominal films CT scan Abdominal angiogram
Periumbilical Abdominal Pain Common causes Appendicitis Small bowel obstruction Gastritis
Diagnostics to consider in periumbilical pain: Lab-CBC, Chemistry (CMP) Abdominal x-rays and ultrasound Contrast enema (consult with surgeon first) Colonoscopy if indicated CT scan
RLQ causes appendicitis ectopic pregnancy Renal calculi Ovarian cyst/torsion Colon cancer
LLQ causes Most common cause is diverticulitis Ulcerative colitis/Crohns Colon cancer Ovarian cyst/torsion Endometriosis uterine fibroids Renal calculi
Diagnostics to consider in RLQ/LLQ pain: Pelvic and rectal exam is mandatory UA, C & S, cervical cultures, wet prep, CBC, preg. test Abodominal/Pelvic sono CT abdomen/pelvis IVP if indicated
Pelvic pain-pain in hypogastrium or suprapubic region Common causes Prostatitis-also mid sacral pain PID-referred to midline Ectopic pregnancy-referred to midline Acute cervicitis-also midsacral pain
PUD ulcer is a break in the gastric or duodenal mucosa that arises when the normal mucosal defensive factors are impaired.
Peptic Ulcer Three major causes: H-pylori NSAID use Hypersecretory states such as Zollinger-Ellison
Other causes of PUD Stress/trauma Severe burns CNS trauma
Disease associated with PUD Cirrhosis Chronic pulmonary disease Renal failure Renal transplant
Helicobacter pylori infection spread person to person, may be fecal-oral route or as a reservoir in water sources.
H-pylori causes chronic active inflammation may resolve spontaneously may progress to gastritis, PUD, gastric adenocarcinoma or mucosa-associated lymphoid tissue lymphoma
PUD symptoms Epigastric pain gnawing or burning 1-3 hrs after eating-relieved by food or antacids-may radiate to the back Nausea/Vomiting may or may not be present Heartburn Chest discomfort Hematemeis or melena
PUD Diagnosis May have anemia with blood loss Elevated serum amylase in patient with severe epigastric pain suggests ulcer penetration into the pancreas. Testing for H-pylori Serum gastrin to screen for Zollinger-Ellison Syndrome
PUD Differential Diagnosis GERD Biliary tract disease Pancreatitis Musculoskeletal Gastric cancer/pancreatic cancer Crohn’s Disease
Invasive Testing for H-pylori endoscopy for biopsy and histology
Testing for H-pylori Noninvasive Serum: Screen for H-pylori IgM, IgA antibodies for active disease- Urea Breath Test Fecal antigen test
Urea Breath Test H. pylori produce urease-urea changes to ammonia causing a rise in pH which results in a color change best for determination between active and resolved infection & is considered the gold standard-useful to confirm eradication
Fecal antigen test The H-pylori antigen is shed in the stool of clients with active disease Appears to be as sensitive as the breath test. Should be obtained14 days post treatment for PPI treatment regimens, 1 month for bismuth
Treatment for H-pylori Combination AntibioticTherapy Advised Due to drug resistance to metronidazole (50%) and clarithromycin (7%) resistance Amoxicillin and tetracycline with less resistance Now recomending to save metronidazole for PCN allergic patients
Histamine (H2) receptor antagonist Work by reversing the competitive inhibition of histamine that stimulates parietal cells to release gastric acid
Histamine (H2) receptor antagonist Cimetidine (Tagamet) 400-800 po bid Famotidine (Pepcid) 20mg QD Ranitidine (Zantac) 150 mg bid Nizatidine (Axid) 150mg po bid
Proton Pump Inhibitors Provide decrease in acid secretion resulting in faster healing rates and symptom control. Inhibit parietal H+,K+ ATPase blocking gastric secretion Slightly more effective than H2 receptor antagonists (Tagamet, Pepcid, Zantac
PPI Use to treat PUD Uncomplicated treat for 4 wks, 6 wks with complications Omeprazole (Prilosec) 20-40mg Lansoprazole (Prevacid) 15-30mg Pantoprazole (Protonix) 40mg Esomeprazole (Nexium) 20-40mg Rabeprazole (Aciphex) 20mg
Agents to enhance mucosal defenses Sucralfate, bismuth, misoprostol and low doses of aluminum-containing antacids have all been shown to promote ulcer healing through the enhancement of mucosal defensive mechanisms. Bismuth also has direct antibacterial properties
Combination Drug Therapy for H. pylori PUD Triple or quadruple therapies available Example: Proton Pump Inhibitor bid Bismuth Subsalicylate 2 tabs qid Tetracycline 500mg qid Metronidazole 250mg qid
Prevpac 1 dose bid x 14 days lansoprazole (Prevacid) 30mg 1 tab. bid amoxicillin 500mg 2 tabs. bid clarithromycin 500mg 1 tab bid
NSAID Induced PUD Prevention: With chronic conditions that require use of NSAID -give with PPI Take NSAID with meals
Treatment of NSAID PUD Stop NSAIDs and offending agents: ETOH, smoking Treat with PPI Uncomplicated for 4 weeks Complicated treat for 8 weeks
Zollinger-Ellison Syndrome Caused by gastrin-secreting tumors which result in hypergastrinemia and acid hypersecrection. 90% of pts with syndrome develop PUD < 1% of PUD is caused by Zollinger-Ellison Syndrome 2/3 are malignant
Reflux: normal physiologic occurrence produced by proximal gastric distention resulting in transient relaxation of the lower esophageal sphincter (LES) with symptoms of heartburn and acid regurgitation (dyspepsia)
Gastroesophageal Reflux Disease (GERD): inappropriate relaxation of the LES with accompanying symptoms Heartburn and acid reflux Acid regurgitation Non-cardiac chest pain Chronic cough or asthma Chronic laryngitis and hoarseness Dysphagia
Obesity: doubles risk for GERD Obesity: increased risk for GERD related complications Erosive esophagitis Barrett’s Esophagus Esophageal adenocarcinoma
Lifestyle risk factors that reduce sphincter tone: Smoking Alcohol consumption Coffee and chocolate Estrogen or progesterone Other drugs
GERD Associated diseases: Irritable bowel syndrome Connective tissue disorders (scleroderma) COPD
GERD Presentation: Pediatrics Vomiting is most common presentation Hyperirritability Refusal of feeding Asthma in children Although reflux is usually harmless; may lead to FTT or esophagitis
GERD Alarm Symptoms: Adults Weight loss Persistent vomiting Difficulty swallowing (dysphagia) Symptoms of GI bleeding (hematemesis or melena) Anemia Refer to gastroenterologist for further evaluation or ER if volume depletion
GERD Alarm Symptoms: Children Failure to gain weight at an appropriate rate Developmental delays Projectile vomiting Persistent respiratory symptoms Changes in neurobehavior
GERD Essentials of diagnosis Diagnosis is based on patient’s symptom report alone (clinical diagnosis) CBC and stool for occult blood on all CBC: Identify anemia Fecal occult blood: Identify GI bleeding If anemia or GI bleed (alarm) refer to gastroenterology
GERD Diagnostic testing recommended for: Patients not responding to initial medical therapy Alarm symptoms Persistent symptoms
GERD Diagnostic Studies Endoscopy with biopsy is recommended study Demonstrates abnormalities in < 50% of patients some normal Ambulatory esophageal pH monitoring-pH probe placed above esphageal sphincter-24hr ph monitoring Esophageal manometry-to assess esophageal motility
GERD Differential diagnosis Myocardial infarction Esophageal spasm Cholelithiasis Angina pectoris Children: pyloric stenosis; infections Peptic ulcer disease Reflux erosive esophagitis: pill induced damage, radiation esophagitis
GERD Complications Barrett’s esophagus normal squamous epithelium of esophagus replaced by a metaplastic columnar epithelium 10% of patients Peptic stricture 10% of patients solid food dysphagia
GERD Lifestyle Changes Avoid lying down within 3 hrs of eating Elevate HOB 4-6 inches or foam wedge, (worse with pillows) Decrease abdominal pressure Avoid constricting clothing. Avoid NSAID, ASA Avoid agents that relax the LES Alcohol/smoking Avoid acidic foods-
GERD Treatment for infants/children In 85% self-limited, disappearing between 6-12 months Frequent small feedings Burp after each feeding; hold upright 15-30 minutes Prone position not recommended due to danger of SIDS Some authorities recommend thickening agents (rice cereal)
GERD 2005 American College of Gastroenterology (ACG) guidelines For patients with history of uncomplicated GERD, 4 week trial of empiric therapy with a proton pump inhibitor Lifestyle changes alone usually not able to adequately control symptoms
ProtonPump Inhibitors Weak bases that are converted to the active form in highly acidic environments. substantially decreases acid secretion of the parietal cells. Can take with antacids Food decreases absorption. Much more expensive than H2 blockers
Proton Pump Inhibitors dosing for GERD Once a day dosing Before breakfast for best efficacy Switch to bedtime if nocturnal symptoms BID dosing if incomplete response to once daily If no response with BID dosing, considered a treatment failure and referral for further investigation
Drug-drug Interactions and Cardiac Events Some PPIs may interfere with clopidogrel (antiplatelet drug) reducing the antiplatelet effect Conflicting studies FDA warning in 2009 of possible interaction between clopidrogel and omeprazole and esomeprazole
PPI Dosing for GERD Omeprazole (Prilosec) starting 20mg QD Lansoprazole (Prevacid) 15-30 mg QD Rabeprazole sodium (Aciphex) 20 mg QD Pantoprazole sodium (Protonix) 40 mg QD Esomeprazole magnesium (Nexium) 40mg QD Dexlansoprazole (Kapidex) 30-60 mg QD
Caution for use of PPIs in liver impairment Dosage adjustment necessary
GERD Long-term maintenance therapy Erosive esophagitis must have long-term acid suppression to maintain healing Once daily dose of PPI Majority need once daily or on-demand PPI therapy Can try to step-down to H2blocker
H2 Receptor Antagonists Can be used if cost of PPIs is prohibitive Bind to H2 receptors inhibit histamine and acid secretion on gastric parietal cells Onset of action-30minutes Bid dosing Provide heartburn relief for about 8 hours Reduce 24 hour acidity by 60%
GERD Antacids Provide the most rapid symptom relief (immediate) Useful for occasional mild symptoms. Duration only 2 hours Caution magnesium antacids with renal damage. Can help with diagnosis if symptoms are controlled with antacids
GERD Surgical treatment Refer children for possible surgery if persistent vomiting with FTT, esophagitis or esophageal stricture, apneic spells or chronic pulmonary disease Surgical fundoplication: relief of symptoms and healing of esophagitis in > 90% of selected patients
GERD Follow up by FNP Re-evaluate adult in 1-2 weeks; if symptoms controlled, continue full course of therapy If still symptomatic after course of therapy refer to gastroenterology for further evaluation If control with Rx after 4-6 weeks, can discontinue and re evaluate.
GERD full course of therapy 4 weeks therapy for proton pump inhibitors 6-8 weeks if H2 blockers
Cholelithiasis The presence of stones within the gallbladder
Cholelithiasis - High risk patient Female Pregnancy Crohn’s disease Obesity Rapid weight loss Status post-bariatric surgery Spinal cord injury Pima Indian Diabetes mellitus Increasing age
High risk medications for Cholelithiasis Estrogen OCPs and HRT Fibric acid agents (Lopid) Gemfibrozil Ceftriaxone Furosemide Cyclosporine Opiates TPN
Risk reducers for cholelithiasis Low-carbohydrate diet and physical activity may decrease risk. Aspirin and NSAIDs may decrease risk
Clinical presentation Asymptomatic gallstones No symptoms; gallstones visualized on radiologic exam done for another cause Previously, cholecystectomy performed on only high risk patients Currently, cholecystectomy NOT indicated for most asymptomatic patients
Symptomatic gallstones Biliary colic Transient Steady intense pain in RUQ that subsides gradually over 30 minutes to 2-3 hours Nausea and vomiting May be referred to R shoulder or scapula Midepigastrum or other abdominal area Atypically, chest pain No associated lab findings
% of acute cases of biliary colic will resolve spontaneously 60 Recurrent attacks common for years
Differential diagnosis of biliary colic Peptic ulcer disease Acute hepatitis Renal colic Appendicitis Ileitis Colitis
diagnosis of biliary colic CBC with diff Liver function testing (liver profile), CMP (chem profile) for hepatic enzymes RUQ Ultrasound to confirm presence of gallstones (sensitivity >95%)
Management of biliary colic Referral to surgeon for cholecystectomy 90% of all cholecystectomy is now laparoscopic
Medical Management of Biliary colic - referral then Medical therapy may be indicated for patients at high risk for surgery (10% of symptomatic) Oral dissolution agents (UDCA, CDCA) Extracorporeal shock wave lithotripsy (ESWL)
Acute cholecystitis Acute or chronic inflammation of the gallbladder
Pathophysiology of cholecystitis Stone impaction within the cystic duct Produces inflammation of gallbladder and adjacent peritoneum
Clinical presentation of cholecystitis (similar to episode of biliary colic, but additional as underlined): History of biliary colic Biliary colic symptoms >6 hours Nausea/Vomiting Low grade fever Tender RUQ Localized rebound Positive Murphy’s sign Mild jaundice (20%)
Cholecystitis Labs Elevated bilirubin levels (jaundice rare) Transaminase levels (ALT, AST) usually < 3 times the normal Check CBC: Leukocytosis (12,000-15,000)
Complications of cholecystitis Gangrenous cholecystitis (necrosis of GB wall) Emphysematous cholecystitis (Severe form cholecystitis from gas-forming bacteria) Gallbladder perforation caused by above
Cholecystitis Treatment Most respond to conservative treatment IV’s, antibiotics Percutaneous cholecystostomy Cholecystectomy recommended due to high rate of recurrence and complications
Choledocholithiasis The presence of gallstones within the biliary tract Choledocholithiasis develops in 15 % of patients with cholelithiasis
Choledocholithiasis pathophysiology Stones originate from GB and obstruct ducts Stones can develop in the ducts (especially if chronically infected)
Choledocholithiasis Clinical presentation Jaundice
Choledocholithiasis Labs Bilirubin 20-30 times normal Alkaline phosphatase mild to 3-6 times normal
Choledocholithiasis Diagnosis Ultrasound-shows bile duct dilatation, not initial finding so repeat in 2 weeks Magnetic resonance cholangiography (MRCP) Cholangiography most sensitive test Percutaneously, surgically, or endoscopically (ERCP)
Choledocholithiasis Treatment Remove stones at time of endoscopy via basket Choledocholithotomy
Cholangitis: Inflammation and infection of the biliary tree due to obstruction. Carries 10% mortality rate
Suppurative cholangitis Severe form of cholangitis. Emergency requiring immediate surgical intervention
Cholangitis patho Stone or malignancy obstructs biliary tree Impairment of biliary excretion Jaundice Spilling of conjugated bilirubin into the urine
Cholangitis Bacteria - proliferate in resultant closed system E. coli Klebsiella pneumoniae Bacteriodes fragilis Enterococcus faecalis
Cholangitis - Clinical Presentation Charcot’s triad Jaundice Abdominal pain Intermittent fever and rigors
Charcot's Triad Jaundice Abdominal pain Intermittent fever and rigors
Reynold’s pentad Charcot’s triad PLUS Hypotension Altered mental status
Gallstone pancreatitis Pancreatitis produced by gallstones
Gallstone pancreatitis Clinical presentation Similar to acute cholecystitis Epigastric pain radiating to back Nausea vomiting
Gallstone pancreatitis Laboratory Amylase, alk phosphatase, bilirubin elevated
Coronary heart disease Most common cause of CVD and death in the US Men are more often affected than women Peak incidence for women is age 60-70, men age 50-60 4:1 before age 40 8 to 1 after age 40 over age 70 1 to 1
Ischemic Heart Disease Risk factors Positive family history (onset prior to age 55 in men and 65 in women) Age Male gender Blood lipid abnormalities HTN Physical inactivity Cigarette smoking Diabetes mellitus Elevated blood homocysteine levels Possibly chronic infection
Ratio of LDL to HDL Ratios below 3 indicate lower risk Ratios above 5 indicate higher risk
Ischemic Heart Disease Other possible risk factors Elevated apolipoprotein(a) Small dense LDL particles Hypertriglyceridemia possibly now independent risk factor: usually associated with low levels of HDL Elevated serum homocysteine
High level of C-reactive protein associated with higher rate of ischemic events Elevated serum CRP levels with High sensitivity assays i. e., hsCRP 1 mg/L – low risk for vascular events 1-3 mg/L- intermediate risk, > 3 mg /L – high risk
Possible inflammatory process in vessel wall In healthy pts without hyperlipidemia but with hsCRP > 2mg/L Statin therapy has been shown to reduce the risk for MI, Stroke , unstable angina
Coronary arterial calcification correlates with the presence and severity of CAD. Electron Beam CT or multidetector CT can accurately quantify coronary calcification and can be used as screening tests in asymptomatic patients.
Kawasaki disease in kids cause coronary vasculitis and aneurysms which in the setting of a hematological disorder can cause coronary embolism.
Other causes for myocardial ischemia Spontaneous coronary spasm resulting in Prinzmetal angina Cocaine use Thyrotoxicosis, aortic stenosis, aortic insufficiency, tachyarrhythmia or sepsis: Myocardial O2 Demand significantly exceeds supply
ANGINA PECTORIS Increased oxygen demand is the most frequent mechanism
ACUTE CORONARY SYNDROME-Unstable angina and myocardial infarction Plaque disruption, platelet plugging and coronary thrombosis
Stable angina - fairly good prognosis Typically, chest pain, pressure, or heaviness Can radiate to jaw, arm, back, abdomen Silent angina expressed as dyspnea Atypical symptoms Nausea, diaphoresis, lightheadedness, anxiety Occurs predictably with exertion Resolves within minutes with rest
Progressive angina Increase in frequency, severity, or duration of anginal episodes during the last 6 weeks but not enough to require hospitalization.
Unstable angina-poorer prognosis Described as a “crescendo” pain which occurs with exertion, or at rest, less responsive to medication-may result in complete occlusion or infarction Episodes usually prolonged greater than 20 min. Unable to walk 1-2 blocks, climb 1 flight of stairs
Stable Angina: Increased oxygen demand-vessels cannot meet demand-responds well to meds and rest. Normal ECG at rest or may show ST or T abnormalities ECG abnormalities (depression or elevation of ST segment) with angina episode or with stress testing
unstable angina Large blockages or artery; ruptured plaque Blood clot may form which impedes or blocks flow ECG shows ST segment depression
In MI plaque or thrombus completely blocks major coronary artery Irreversible necrosis and cellular death
Essentials of diagnosis- stable angina Precordial chest pain Stress or exertion precipitates Nitrates or rest relieves ECG or scintigraphic evidence of ischemia during pain or stress testing Angiographic demonstration of significant obstruction of major coronary vessels
Prinzmetal’s Variant Angina Clinical syndrome where chest pain occurs without usual precipitating factors-associated with ST segment elevation rather than depression. Associated more with coronary arterial vasoconstrictions (spasms).
Women < 50 Early morning symptoms associated with arrhythmia or conduction defects Avoid precipitants smoking and cocaine Responds to calcium channel blockers alone or in combo with nitrate preparations. Avoid betablockers unless fixed stenosis
Costochondritis pain with palpation borders of sternum, may increase with movement
Aortic dissection (asymmetry of pulses and blood pressure in both arms
Pulmonary emboli pleuritic chest pain, tachypnea, wheezing, and hemoptysis
If suspect acute MI Troponin rises at 3-4 hours after will peak at 12-16 hours. It is found that measuring troponin increased the number of patients diagnosed with AMI by 10.4% over patients diagnosed using CK and CK-MB levels CK and CK-MB q 8h 3 negatives exclude MI
Angina Pectoris: Evaluation Lab Lipids Other as indicated by H & P CBC (check for anemia) TSH (underlying hypo or hyperthyroidism) Glucose, complete metabolic profile
Angina Pectoris: Evaluation Chest x-ray Heart size Heart failure Helps to R/O pulmonary edema, pleural effusion, and aortic aneurysm
Angina Pectoris: Evaluation ECG 1/4 have normal; remainder may have Changes associated with old MI Nonspecific ST-T changes A-V or intraventricular conduction defects Left ventricular hypertrophy
Angina Pectoris: Evaluation During attack Characteristic change is horizontal or downsloping ST segment depression Reverses after ischemia disappears T wave flattening or inversion ST segment elevation suggests severe ischemia (coronary spasm)
Angina Pectoris: Evaluation Exercise ECG Most useful noninvasive procedure Carries risk of 1 infarct or death/1000 tests Aortic stenosis is contraindication for testing Beta Blockers affect test results
Indications for Stress Testing To confirm the diagnosis of angina To determine the severity of limitation of activity due to angina To assess the progression of disease To evaluate response to therapy Less frequently??--to screen asymptomatic populations for silent coronary disease
Angina Pectoris Evaluation Coronary Angiography Definitive diagnostic procedure for CAD Low mortality/morbidity High cost With other noninvasive techniques it is usually not indicated solely for diagnosis
Angina Pectoris: Evaluation Coronary radionuclide angiography Radioactive isotope is injected IV and sequential images are obtained to visualize vessels and chambers-evaluates ejection fractions and pulmonary blood volumes.
Angina Pectoris: Treatment Primary prevention Smoking cessation Lipid management Control HTN AHA Step II Diet Regular exercise as tolerated High intensity exercise especially in the cold (skiing, shoveling snow etc) is not advisable Ideal body weight
Angina Pectoris: Treatment Antiplatelet agents ASA-- 80-325 mg/day (cheap) Plavix 75 mg (clopidogrel bisulfate)-- slight edge over ASA in reducing of atherosclerotic events (expensive) ACE inhibitors to patients who have DM or LV dysfunction unless contraindicated.
Hormone Replacement Therapy is NOT ADVISED FOR PREVENTION or TREATMENT OF CAD - BLACK BOX WARNING Recent study has indicated an increase risk of heart disease in men who use testosterone therapy. This is under FDA review
Angina Pectoris: Treatment Infrequent anginal attacks--stable angina Nitrostat 1 tab (0.3 -0.4 mg) SL or Nitrolingual 1-2 sprays onto or under tongue DO NOT USE NITRATES WITH VIAGRA Causes precipitous drop in blood pressure! Can take prophylactically--5-10 minutes prior to activity or sex
Angina Pectoris: Treatment Correct treatable conditions HTN Anemia Valvular disease Hyperthyroidism Heart failure
Angina Pectoris: Treatment Daily attacks--stable angina Initially Nitrate or B-blocker B-blocker decreases heart rate and contractility
B-blocker First-line therapy in most patients with chronic angina Advantages: efficacious in prophylaxis Initial therapy after MI due to cardioprotective effects
B-blocker Examples for angina tx Atenolol (Tenormin) 50mg QD; increase to 100mg after 1 wk Nadolol (Corgard) 40mg QD; increase in 3-7d to 80 (Max dose 240 mg QD)
B-blocker Disadvantages: Serious SE’s in patients with COPD, sinus or AV block Contraindication: severe bronchospastic diseases bradyarrhythmias decompensated heart failure Contraindicated in vasospastic angina
Angina Pectoris: Treatment Long acting nitrates Contraindications Migraine or cluster h/a Orthostatic hypotension
Angina Pectoris: Treatment Long acting nitrates Isosorbide dinitrate (Isordil titradose) Needs 8-10 h nitrate free interval daily Initial h/a will abate in 1-2 wk Isosorbide mononitrate (Ismo) 20mg on awakening and in 7 hrs Nitroglycerine 2% ointment Nitroglycerine patch
Angina: Treatment Calcium Channel Blockers Block the inward movement of calcium through smooth and cardiac muscle. Decrease the force of myocardial contraction Increase exercise tolerance Improve artery blood flow Avoid in recent MI and with reduced LV function
Angina: Treatment Calcium Channel Blockers Diltiazem HCl (Cardizem CD) Verapamil HCl (Calan) Dihydropyridines Amlodipine (Norvasc); Nifedipine (Procardia XL)
Angina: Treatment Calcium Channel Blockers Disadvantages: Disadvantages: Constipation, peripheral edema; no cardioprotective effect after MI; may worsen heart failure , serious SE’s
Angina: Treatment Calcium Channel Blockers Advantages: Effective, useful with coronary artery spasm; possible anti-atherogenic effect
Angina: Treatment Calcium Channel Blockers Dihydropyridine group-do not affect the cardiac conduction system. Nifedipine (Procardia XL) Amlopidine (Norvasc)-less edema, decrease systolic B/P Felodipine (Plendil) Isradipine (DynaCirc) Nicardipine SR (Cardene SR) Nisoldipine (Sular)
Calcium Channel Blockers NOT usually first choice for stable angina unless unable to tolerate beta blockers and diuretics
Calcium Channel Blockers May be first line for Prinzmetal’s angina- dihydropydines-do not affect the conduction system verapamil and diltazem-less reflex tachycardia
may have AV and SA nodal blockade-don’t give with Beta Blockers: Verapamil (Calan), Diltiazem (Cardizem)
Ranolazine (Ranexa) Selective Inhibitor of late sodium influx: Reduces sodium induced calcium overload in myocytes- antianginal /anti ischemic No effects of HR or BP. May be used as a first line or second line agent for stable angina. 500-1000mg PO BID
Myocardial Infarction Irreversible necrosis of myocardial tissue as a result of inadequate blood flow for critical period of time.
Myocardial Infarction May result from: Occlusive coronary thrombus *most common cause More rarely prolonged vasospasm inadequate blood flow-shock cocaine embolic occlusion, vasculitis, aortic pathology
Thrombus Pathophysiology Fibrous cap of an atherosclerotic plaque ruptures, which activate local hemostatic mechanism with the formation of platelet-fibrin thrombus. Thrombus abruptly occludes the atherosclerotic coronary arteries, resulting in an MI.
Symptoms of acute MI Occur at rest, usually in early AM Similar to angina but more severe NTG has little effect Cold sweat, feels weak and apprehensive Move about seeking position of comfort Lightheaded, syncopal Dyspnea, orthopnea Cough, wheeze, nausea & vomiting
Signs of acute MI Brady to tachycardia BP high or low Low grade fever after 12 hours Heart sounds may be normal or include murmurs, gallops
Acute Myocardial Infarction Lab findings Leukocytosis of 10,00-20,000 on day 2, resolving in 1 week Serial cardiac enzymes--CK-MB isoenzymes may be positive within 6 hrs Troponin I--sensitive at 10-14 hours Elevated for 5-7 days Troponin T
Acute Myocardial Infarction Essentials of Diagnosis Sudden (but not instantaneous) development of anterior chest discomfort >30 minutes that may produce Arrhythmias, Hypotension,Shock or Cardiac failure Rarely painless, masquerades as Acute congestive heart failure Syncope, stroke or shock
Acute Myocardial Infarction ECG ST segment elevation or depression Evolving Q waves Symmetric inversion of T waves
Acute Myocardial Infarction Essentials of Diagnosis Elevation of cardiac enzymes CK-MB Troponin T or Troponin I Appearance of segmental wall motion abnormality by imaging techniques
Acute Myocardial Infarction In Primary Care Setting KNOW THIS Immediate transport-call 911 or EMS ASA 325 mg (if not allergic) Chew if enteric coated O2 @ 2-4 liters by nasal cannula Nitro SL or spray ECG-12 LEAD IV if available See ACLS Guidelines
Acute Myocardial Infarction In Emergency Department Setting Termed Acute Coronary Syndrome EKG within 5 minutes ST segment elevation—repeat in 5-10 minutes if no elevation (to R/O a late occurring ST segment elevation) Determine if ST segment elevation (STEMI) Determine if non-ST segment elevation
Acute ST Segment Elevation MI (STEMI) Treatment Angioplasty in 90 minutes Currently first choice in therapy Reduces fatality rate better than thrombolysis alone Thrombolytics in 30 minutes Only if NO angioplasty services
Unstable Angina and Non ST Segment Elevation MI (NSTEMI) Acutely presenting: Partial occlusion At high risk for ST Segment Elevation MI (STEMI) and sudden death Immediate referral to ED Admit if ischemia on ECG ST segment deviation new T wave abnormalities new Left BBB
Unstable Angina and Non ST Segment Elevation MI-Chronic Tx In chronic phase, typically following revascularization Aspirin 75-324 mg daily Clopidogrel (Plavix) 75 mg daily for 9-12 months Statins ACE inhibitors Beta blockers Smoking cessation Lo-fat low carb diet Diabetes control
Anti-thrombolytics (used in STEMI) Accelerates the formation of plasmin from plasminogen Plasmin degrades: Fibrin Plasma proteins Fibrinogen, prothrombin factors V and VIII Produces a defective hemostasis Drugs are clot specific or non-clot specific
Anti platelet agents Prevent platelet aggregation ASA Partially effective Plavix (clopidogrel) Acts by blocking ADP receptor Potent irreversible antiplatelet drug Others Intravenous glycoprotein IIb/IIIa inhibitors Specific indications prior to revascularization procedures or in ischemia
Antithrombin drugs Heparin Xarelto (oral factor Xa inhibitor) This a new drug being suggested for use in dual antiplatlet therapy in patients with ACS. There are many outcomes studies supporting but it is not yet listed as indicated Low-molecular-weight heparin (LMW)
Nursemaid Elbow Result of being lifted or pulled by the hand May be symptom of child abuse if recurrent Symptoms Presents with painful, fully pronated elbow Complaint that child’s elbow will not bend
Nursemaid Elbow Clinical findings Normal radiograph of elbow Point tenderness over radial head Usually normal x ray Ask about trauma as usually not x rayed to rule out fracture if was trauma
Nursemaid Elbow Treatment Place elbow extended in full supination; move to full flexion; Palpable click felt at level of radial head with instant relief of pain/crying May immobilize briefly in sling for comfort; immobilize longer if symptoms last for several days
Hip: Evaluation General information for hip evaluation NOTE: Hip pain often refers to the knee KNEE PAIN should trigger an examination of the hip
Legg-Calve-Perthes Legg-Calve-Perthes disease (LCPD) Vascular supply of proximal femur is precarious, and if interrupted can result in necrosis Highest incidence is ages 3-12; mean of age 7 Atraumatic, persistent pain and limp or limited motion; more common in boys
Legg-Calve-Perthes Symptoms : Atraumatic, persistent pain and limp or limited motion; more common in boys
Hip: Legg-Calve-Perthes Clinical findings Radiologic A-P and frog-leg views: Early findings: effusion of joint, widening of joint space, periarticular swelling Later findings: decreased bone density or collapse of femoral head; necrotic ossification center with patchwork replacement
Hip: Legg-Calve-Perthes Treatment referral to pediatric orthopedist
Hip: Slipped Capital Femoral Epiphysis SCFE (pronouncec skif-ee) displacement of proximal femoral epiphysis due to disrupted growth plate ORTHOPEDIC EMERGENCY! obese adolescent males fall or direct trauma weakened epiphyseal area due to hormonal change Hypothyroidism or endocrine disorder are risk factors
Slipped Capital Femoral Epiphysis Stable--Able to bear weight Symptoms Hip or knee pain, limp or inability to ambulate Clinical findings Limitation of internal rotation of hip A-P and frog-let radiographs show widened epiphysis and decreased height of the epiphysis Mismatch between epiphysis and metaphysis
“Toeing-in” major causes Internal tibial torsion Internal femoral torsion (femoral anteversion
Internal tibial torsion: Rotation of the leg between the knee and the ankle Normally about 20 degees at birth, but decreases to neutral rotation by age 16 months. Most common cause of in-toeing in child younger than 2 years document improvement Refer if no improvement by age 2
Internal femoral torsion Children 2 years or older Worst at ages 4-6, then typically resolves Incidence twice as high in girls Congenital and common in individuals that sit in W-sitting position
Internal femoral torsion Symptoms Kissing kneecaps Running may have egg-beater gain where legs flip laterally
Internal femoral torsion Clinical Findings Internal rotation of hip increased with limited external rotation Radiography not indicated
Internal femoral torsion Treatment No orthoses required Active external rotation such as skating or bicycle riding encouraged Resolves by ages 7-8 Refer only if no external rotation of hip in extension
Genu varum (bowleg) Normal from infancy thru age 2 Criteria for referral to pediatric orthopedist Persisteng bowing beyond age 2 Bowing that is increasing rather than decreasing Bowing of one leg only
Genu valgum (knock-knee) (hint for memorizing: gum sticks things together) Typical from age 2 thru age 8 Criteria for referral to pediatric orthopedist Knock-knee associated with short stature
Osgood Schlatter disease Common cause of knee pain at insertion of patellar tendon on tibial tuberosity (tubercle) Quadriceps muscle stresses on developing tibial tubercle Partial avulsion fracture or micro fracture in the ossification center of tibial tuberosity
Rates over 150 SVT
Junctional No P wave rate of 40-60
Accelerated Junctional No P wave rate of 60-100
Atrial Flutter Saw tooth pattern but regular qrs complexes
A fib always irregular P waves difficult to identify
Afib patients must be anticoagulated
PVC - Premature Ventricular contraction Check electrolyte and medications - something is wrong. Non perfusion
Upper Respiratory Infection (URI)- Definition An illness caused by an acute infectious agent which involves the upper respiratory tract, including the nasopharynx and sinuses, and larynx commonly including tonsillitis, pharyngitis, laryngitis, sinusitis, acute otitis media, and the common cold
The majority of URI are caused by a virus Bacteria cause about 25% of the cases
Over 200 different viruses have been isolated in patients with URI; the most common is rhinovirus; others include coronavirus, parainfluenza virus, adenovirus, enterovirus and RSV
Streptococcus is a bacterial cause of URI resulting in tonsillitis, pharyngitis and otitis media and account for more than 20 million primary care provider visits annually; up to 15% of acute pharyngitis may be caused by Group A streptococcus
Incubation period for most URI is 1-4 days with onset of symptoms 1-3 days after exposure and lasting 7-10 days
Acute Bronchitis Definition Infection of the tracheobronchial tree that causes reversible bronchial inflammation
Treatment of CAP Clinical factor Points Confusion (new disorientation 1 BUN > 19mg/dl 1 Respiratory rate >30 1 BP systolic <90; diastolic <60 1 Age > 65 1 Scoring 0-1 - low risk; consider home treatment 2 - short in-patient hospitalization or closely monitored outpatient treat >3 - Sever pneumonia, hospitalize, consider ICU
Streptococcus pneumoniae Penicillin nonresistant Penicillin G, amoxicillin Alternative Macrolide, cephalosporins (oral [cefpodoxime,cefprozil, cefuroxime, cefdinir, cefditoren] or parenteral [cefuroxime, ceftriaxone, cefotaxime]), clindamycin, doxycyline, respiratory fluoroquinolone
Streptococcus pneumoniae Penicillin resistant Agents chosen on the basis of susceptibility, including cefotaxime, ceftriaxone, fluoroquinolone Alternative Vancomycin, linezolid, high-dose amoxicillin (3 g/day with penicillin)
Haemophilus influenzae Non–b-lactamase producing Amoxicillin Alternative Fluoroquinolone, doxycycline, azithromycin, Clarithromycin
Haemophilus influenzae b-lactamase producing 2nd or 3rd generation cephalosporin, amoxicillin-clavulanate alternate Fluoroquinolone, doxycycline, azithromycin, Clarithromycin
Mycoplasma pneumoniae/ Chlamydophila pneumoniae Macrolide, a tetracycline alternate Fluoroquinolone
Legionella species Fluoroquinolone, azithromycin alternate Doxycyline
CAP Antibiotic Recommendations Outpatient Management For previously healthy patients who have not taken antibiotics with the past 3 months: A Macrolide (clarithromycin, 500 mg orally bid; or Azithromycin, 500 mg day 1, then 250 mg daily x 4 days or 500 mg daily x 3 days or Doxycycline, 100 mg po bid
CAP Antibiotic Recommendations Outpatient Management For patients with such comorbid medical conditions as chronic hear, lung, liver, or renal disease, DM, alcoholism, malignancy, asplenia, immunosuppressant conditions or use of immunosuppressive drugs A respiratory fluoroquinolone (moxifloxacin, 400 mg po daily; Gemifloxacin 320 mg qd, Levofloxacin 750 mg qd or A macrolide plus a B-lactam (amoxicillin, 1 g po tid; amoxicillin-clavulante, 2 g po bid are preferred to cefpodoxime, 200 mg bid:
Acute Life Threatening Event Observer of event brings infant to ER or clinic Apnea, cyanosis or pallor, limpness, choking or gagging Event is frightening to observer; fears infant has died
ALTE Peak age 2-4 months (same as SIDS)
Cough is an important reflex in clearing the lungs of debris and secretions. The loss of the ability to cough results in decreased secretion clearance and predisposes to atelectasis and pneumonia.
Ventilation inadequate to keep Pco2 from increasing above normal is hypoventillation
The lungs are repeatedly exposed to particles and infectious particles. The ________ is responsible for filtering larger particles. nasopharynx
Hypoxemia reduction in the oxygen content of the blood.
Airway resistance is influenced by the diameter and length of the airways, the viscosity of gas and the nature of the airflow.
Functional residual volume is the volume of gas in the lung when mechanical forces acting on the lung are at equilibrium (at the end of a normal relaxed breath).
Lung compliance is a measure of the ease at which the lung can be inflated.
Residual volume (RV) is the volume of gas left in the lungs at the end of a maximal exhalation.
Total lung capacity (TLC) is the volume of gas in the lungs at the end of maximal inhalation.
Vital capacity (VC) is the maximal amount of air that can be expelled from the lungs.
Acute Life Threatening Event Etiology Gastroesophageal reflux and laryngospasm are the most common causes of ALTE Epidemiology Peak age 2-4 months (same as SIDS)
Differential Diagnosis for ALTE Viral: RSV and others Bacterial: sepsis, pertussis, chlamydia GERD with or without obstructive apnea, midgut volvulus, shockHypoglycemia, medium-chain acyl-coenzyme A dehydrogenase deficiency, carnitine deficiency, urea cycle defect
Subjective Data for ALTE Careful history most important element of exam Chronically ill or essentially well, pre-term, prior apnea Feeding pattern, febrile, respiratory or GI symptoms “Trying or struggling to breathe” implies airway obstruction Association with feeding or crying, breath-holding
Subjective Data for ALTE Careful history most important element of exam Social situation of the family Episodes of sleep apnea Duration of episode (often difficult to assess) Resuscitative measures at home
Objective Data for ALTE Fever or hypothermia suggests infection Bruising or injury Nutritional status Altered state of consciousness suggests seizure or overdose Respiratory distress implies cardiac or pulmonary involvement
Diagnostics:ALTE CBC, metabolic profile, ABG’s, CXR, RSV, pertussis, chlamydia, fiber optic bronchoscopy, CT or barium swallow, esophageal pH monitoring, EEG, MRI brain, polysomnographs (sleep studies)
Treatment Plan for ALTE Infant is hospitalized for observation and prompt evaluation and continuous cardiorespiratory monitoring for 12-24 hours Alleviate parental fears and anxiety surrounding event Reassess home situation Treatment in directed at underlying cause
Oxygen, nasal CPAP for reduction of periodic breathing; immature breathing pattern causing desaturation
Caffeine or aminophylline for central apnea or periodic breathing
Sudden Infant Death Syndrome (SIDS) is the unexplained death of an infant younger than one year of age in which the cause cannot be determined either by autopsy, death scene investigation and review of clinical history.
greatest risk for SIDS. Premature, low-birth-weight infants, infants of young impoverished mothers of cigarette smokers, African-American and Native-American infants and infants born to mothers who have abused drugs
Incidence of SIDS Highest during the winter months Increases 3-5 fold to infants whose siblings have died of SIDS Most common between 2-4 months of age
Incidence has dramatically decreased since the 1990’s since the AAP educational promotion of “Back to Sleep” where supine sleeping positions are advocated
A variety of causes for SIDS have been proposed, however none have been proven to explain SIDS SIDS is associated with the prone position and soft bedding Cellular brainstem abnormalities and maturational delays Prolongation of Q-T interval resulting in dysrhythmias Abnormal CNS control of respiration
SIDS Pathological Findings Intrathoracic petechiae Mild inflammation and congestion of the respiratory tract Other, subtler changes suggest an intermittent or chronic hypoxia before death
Upper Airway Obstruction Foreign Body Aspiration Blockage of any part of the airway located above the thoracic inlet, ranging from nasal obstruction due to the common cold to life-threatening obstruction of the larynx or upper trachea (subglottic space) Epidemiology: children 6 months to 4 years of age
Upper Airway Obstruction Foreign Body Aspiration Presentation and diagnosis: Acute onset of cyanosis or choking Inability to vocalize or cough (complete obstruction) More pronounced on inspiration Drooling and stridor (partial obstruction)
Epiglottitis (Supraglottitis) inflammation of the soft tissue above the glottis This illness is relatively rare but it is a medical emergency that requires immediate lifesaving intervention due to the risk of total airway obstruction Early recognition is critical
Clinical Presentation of Epiglottitis Abrupt onset of severe sore throat usually voice is muffled sniffing position Difficulty swallowing Copious oral secretions or drooling Symptoms may progress to stridor and respiratory distress, anxiety, sternal retractions and later exhaustion
sniffing position Have a preference for sitting with head held forward, hyperextended, the mouth open and the jaw thrust forward;
If epiglottitis is suspected , DO NOT attempt to examine the pharynx with a tongue depressor because this may result in occlusion of the airway; also do not attempt to place the patient in the supine position; keep the patient in the sitting position
Treatment Plan - Epiglottitis Immediate ACLS transport to the hospital Keep the patient in the sitting position Attempt to keep the patient calm Alleviate parental fears
Croup Definition Laryngeal obstruction caused by subglottic edema Laryngotracheal airway inflammation disproportionately affects children because a small decrease in diameter secondary to mucosal edema and inflammation
Croup Pathophysiology The most common causes of croup are parainfluenza viruses (type 1,2 and 3) RSV in younger children Influenza virus and Mycoplasma pneumoniae are other causes
Croup Epidemiology Most common in children 3 months to 5 years with a peak at 2 years Higher incidence in males Occurs in fall and winter months It typically follows a common cold
Presentation of Croup Onset 3-5 days Absent or low grade fever Barking cough Inspiratory stridor Hoarseness Is usually worse at night
Treatment of Croup For mild symptoms with no stridor at rest give oral hydration, minimal handling, provide comfort measures to calm child, breathing of cool, dry, night air, acetaminophen for fever reduction,
Treatment of Croup Consider hospitalization if severe symptoms such as stridor at rest, dehydration, hypoxia, respiratory distress For significant airway compromise nebulized racemic epinephrine 0.05ml/kg/dose diluted to 3 ml NS over 15 minutes not to exceed q 1-2 hour dosing; may cause HTN, cardiac arrhythmias; a rebound effect may occur, with worsening of symptoms after dissipates
Treatment of Croup - Pharmacological Oxygen therapy if hypoxic or desaturating Dexamethasone 0.6 - 1 mg/kg once IM or 0.6 - 1mg/kg po once or oral prednisalone 2mg/kg in 2-3 divided doses Nebulized Budesinide (Pulmicort) 0.5 – 1 mg daily or bid
Treatment of Croup Education of parents Assess for respiratory distress, changes in level of activity, increased somnolence Assess for hydration When to return to ER if symptoms intensify
Treatment of Croup Follow-up Phone contact in 8-24 hours Return visit if no improvement in 48 hours
Treatment of Croup Prognosis Most children clinically improve in a few days Recurrence of croup implies airway hyperreactivity (asthma) Viral pneumonia may occur in 1 – 2% of children with croup and in immunocompromised children, parainfluenza viral pneumonia or secondary bacterial
Bronchiolitis - etiology Inflammation of the bronchioles resulting in small airway obstruction leading to inadequate expiratory airflow A term used for first time wheezing with a viral respiratory infection Bronchiolitis is potentially life threatening
Respiratory synctial virus (RSV) is the primary cause of bronchiolitis
Bronchiolitis is extremely contagious spread by contact with infected respiratory secretions through coughing and hand carriage of contaminated secretions
Bronchiolitis Epidemiology Bronchiolitis is the leading cause of hospitalization of infants Approximately 50% of children will experience bronchiolitis during the first 2 years of life with a peak age at 2-6 months.
Bronchiolitis - Clinical presentation Usually presents as a progressive respiratory illness similar to the common cold in its early phase associated with cough, coryza and rhinorrhea
Young infants with RSV may not have prodromal symptoms and can present with apnea as the first sign of infection
Bronchiolitis Treatment Plan Indications for hospitalization include infants <6mos, marked respiratory distress, hypoxemia with PO2 < 60mm Hg or SaO2 < 92% on room air; intolerability of oral feeding and inadequate care at home
environmental irritants tobacco smoke, wood burning fires, stoves
Bronchiolitis Prevention Palivizumab (Synagis) 15 mg/kg/ IM once per month November-April Palivizumab is a RSV monoclonal antibody
correlation between RSV infection future airway hyperreactivity as well as abnormalities in pulmonary function tests (incidence of asthma is higher in hospitalized children)
Treatment Plan CAP Neonates, age < 1 month: Ampilcillin +Gentamicin + Cefotaxime If MRSA is a concern add Vancomycin For Chlamydia trachomatis – Erythromycin 12.5 mg/kg po or IV x 14 days
Treatment Plan CAP Infants age 1-3 months
Created by: kcorkinsnctc