Chapter V

PulmonGlpgy

Chronic obstructive pulmonary disease (COPD) means that the |'i:y ,/THV ratio is less than normal (0,75-0.BO, usually given value), whereas in restrictive lung disease, the l l'V /f-TV ratio is often normal. FEV, may be equal in both conditions; it is the ITV,/(TV ratio that is different.

Emphysema almost always is due to smoking (even if second-hand). In a young person wi th minimal smoke exposure (< 5 years of smoking), think of'alpha, antitrypsin deficiency.

Asthma: look for wheezing in children. Treat with beta > agonists in the emergency department. Use steroids if asthma is severe or does not respond to beta. agonists. Cromolyn is for prophylaxis, not acute attacks. The new leiikotriene inhibitors (zaifrfukast, zileuton) are used regularly, not usually for acute attacks. Phosphodiesterase inhibitors (theophylline, amino phyiline) are older, second -l ine agents.

Note: Do not put patients with asthma or COPD on beta blockers, which block the beta.: receptors needed to open the airways.

Wheezing in children under age 2 is often due to respiratory syncytial virus, especially in die winter. Look for coexisting fever.

Important points:

1. Beware the asthmatic who no longer hyperventilates or whose C02 is normal or rising (the patient should hyperventilate, which causes low ('(),). Do not think that patients who seem calm or sleepy are okay. They arc probably crashing and need an immediate arterial blood gas analysis and possible intubation. Fatigue alone is enough reason to intubate an asthmatic.

2. A patient with COPD may normally live at a higher CO, and lower O ,; treat the patient, not the lab value. If the patient is asymptomatic and talking to you, the lab value should not make you panic.

3. As a rough rule of thumb, you should prepare to intubate any patient whose CO? is > 50 nnnl lg or whose 0? is < SO mini Ig, especially if the pi I i n either ease is < 7.30 whi le the patient is breathing room air. Usually, unless the patient is crashing rapidly, a trial of 0? by nasal cannula is given first;, if this approach docs riot work or if the patient becomes too tired (use of accessory muscles is a good clue to the work of breathing,), intubate.

With a solitary pulmonary nodule, the first step is to check for old films. If the lesion has not changed in more than 1 year, it is likely to be benign. Certain clues point to the etiology:

a Immigrant: think tuberculosis (do a skin test). b Southwest U.S.: think Coa'idioiikv imniitis.

■ Cave explorer, exposure to bird droppings, or Ohio/Mississippi River valleys: think histoplasmosis.

¡a Smoker over the age of 50: think lung cancer (bronchoscopy and biopsy), a Person under 40 with none of the above: think hamartoma,

A baseline chest x-ray is standard preoperative evaluation for patients over 60 and patients with known pulmonary or cardiovascular disease, but when to order pulmonary function tests is not as clear. Overall, the best indicator of possible postoperative pulmonary complications is preoperative pulmonary function. Overall, the best way to reduce pulmonary postoperative complications is to stop smoking preoperative!). Aggressive pulmonary toileting, incentive spirometry, minimal narcotics, and early ambulation help to prevent or minimize postoperative pulmonary complication.

Note: The most common cause of a postoperative fever hi the first 24 hours is atelectasis.

Adult respiratory distress syndrome (ARDS): acute lung injury that results in noncardiogenic pulmonary edema, respiratory distress, and hypoxemia. Common causes are sepsis, major trauma, pancreatitis, shock:, near drowning, and drug overdose. Look for ARDS to develop within 24-48 hr of the initial insult. Classic symptoms include mottled/cyanotic skin, intercostal retractions, rales/rhonchi, and no improvement of hypoxia with 0} administration. X-ray shows pulmonary edema with normal cardiac silhouette (no congestive heart failure).Treat with intubation, mechanical ventilation with high percentage of 02 and positive end-expiratory pressure (PEEP).

The diagnosis of pneumonia usually is based on clinical findings plus elevated wh ite blood cell count and chest x -ray abnormalities. On physical exam, look to differentiate between typical (Staphylococcus pneumoniae) and atypical (other bugs) pneumonia, although the distinction is not always clear-cut:

TYPICAL PNEUMONIA ATYPICAL PNEUMONIA

Prodrome Short (< ?. days). Long (> 3 days)--4teadache, rnabise, other aches

Fever High (> 30?,° F) ■ Low (< 10>/5 F)

Chest x-ray One distinct lobe involved Diffuse or multilobe involvement

Infective- agent . S, pneumonmc Many (e.g., Haemophilus' influenzae, Mycoplusma sp.. Chlamydia sp.)

Medications* . Penicillin, third-generation cephalosporin Virythroinycm

* Avoid the temptation to pull out the "big gmt" antibiotics (very wide spectrum) unless the patient is crashing or unstable.

Certain clinical clues should make yon think of certain bugs:

& College student: think Mycoplasma sp. (look for cold agglutinins) or Chlamydia sp.

m Alcoholic: think Klebsiella sp. (currant jelly sputum), Staphylococcus aureus, other enteric bugs (aspiration).

® Cystic fibrosis: think Pscuiiornonris sp. or S. aureus.

a Immigrant: think tuberculosis.

® COPD: think H. influenzae, Moraxella sp.

» Patient: with known tuberculosis and pulmonary cavitation: think Aspergillus sp.

■ Patient with silicosis (metal, granite, pottery workers): think tuberculosis.

■ Exposure; to air conditioner/aerosolized water: think Legionella sp.

* HIV/AIDS: think Pneumocystis carinii or cytomegalovirus (if shown a picture of koilocytosis). ■» Exposure to bird droppings: think CJilamyditi psiUad or HistopJasma sp.

■ Child < 1 yr: think respiratory syncytial virus.

■ Child 2-5 yr: think parainfluenza (croup) or epiglottitis.

Recurrent pneumonia in a child, if it always occurs in the right middle and/or right lower lobe, is most likely due to foreign body aspiration (a foreign body is most likely to go down the right bronchus). It should be a consideration especially if the patient has no other signs of iminimodeficiency (e.g., other types of infections, cystic fibrosis symptoms) before or during the episodes.

Sinusitis: usually S. pneumoniae or Haemophilus sp. Look for purulent (green/yellow) nasal discharge with tenderness over the involved sinus. Associated symptoms are headache and/or toothache (maxillary sinusitis).You cannot transilhrnvinate the sinuses, and an x-ray or CT scan shows opacification of the frontal or maxillary sinuses (order a sinus x-ray to confirm the diagnosis if it has not already been done). Treatment is with penidihn/amoxieillin or erythromycin for 10—14 days.

Note: The most common cause of epistaxis in children is nose-picking (do not assume low or defective platelets without evidence.

Respiratory distress syndrome, due to atelectasis from deficiency of surfactant , almost al ways occurs in premature infants and infants of diabetic mothers. Look for rapid, labored respirations, substernal retractions, cyanosis, grunting, and/or nasal flaring. Arterial blood gases show hypoxemia and hyperearbia, whereas x -ray shows diffuse atelectasis.Treat, with O,, give surfactant, and intubate if needed (often). Complications include intraventricular hemorrhage and pneumothorax/bronchopulmonary dysplasia (acute or chronic mechanical ventilation complications).

Diaphragmatic hernia commonly causes respiratory problems because bowel herniated into the chest pushes on developing lung and causes lung hypoplasia on the affected side. Look for scaphoid abdomen and bowel sounds in the chest (herniated bowel also may be seen on the chest x-ray; 90% are left-sided).

Note: Look for meconium aspiration if the infant is covered with meconium when delivered. Suction the nose first (bulb suction); then suction the oropharynx under direct visualization. Intubate if necessary.

The most common type (85%) of tracheoesophageal fístula is an esophagus with a blind pouch proximally and a fistula between a bronchus or the carina and the distal esophagus. Look for a neonate with excessive oral secretions, coughing and cyanosis with attempted feedings, abdominal distention, and aspiration pneumonia. Diagnosis is made by inability to pass a nasogastric tube; contrast x-ray shows the proximal esophagus only.Treatment is early surgical correct ion.

Cystic: fibrosis: autosomal recessive inheritance; the most common lethal genetic disease in white children. Always suspect it in children with rectal prolapse, meconium ileus, esophageal varices, a "salty" taste, recurrent pulmonary infections, and/or failure to thrive. Diagnosis is made by an abnormal increase in tire electrolytes of the patient's sweat (sodium and chloride).

Patients also have pancreatic insufficiency (give pancreatic enzyme replacements and iat-solu-ble vitamin supplements) and infertility (98% of affected males and many females) and may develop cor pulmonale (right heart failure). Look for S. (lureus and Pseudomonas sp. as the causes of the many respiratory infections.Treat with chest physical therapy, annual influenza vaccine, fat-soluble vitamin supplements, pancreatic enzyme replacement, and aggressive treatment of infections with, antibiotics.

Pleural effusion: if you do not know the cause, always consider thoracentesis and examine the fluid with Gram stain, culture and sensitivity (including tuberculosis culture), cell count wit.lv differential, glucose (low in infection), and protein (high in infection).

Gastroesophageal reflux disease (GBRD) is due to inappropriate, intermittent lower esophageal sphincter (LES) relaxation. The incidence is greatly increased in patients with a hiatal hernia. GERD presents as "heartburn," often related to eating and lying supine. Initial treatment is to elevate the head of the bed and to avoid cofiee, alcohol, tobacco, spicy and fatty foods, chocolate, and medications with anticholinergic properties. If this approach fails, antacids, H2-blockers, and proton-purnp inhibitors may be tried. Surgery is reserved for severe or resistant eases (Nisserr fundoplication). Sequelae of GERD include esophagitis, esophageal stricture (may mimic esophageal cancer), esophageal ulcer, hemorrhage, and Barrett's metaplasia/ esophageal adenocarcinoma.

Hiatal hernia, as the term is commonly used, implies a sliding hiatal hernia; that is, the entire gastroesophageal junction moves above the diaphragm, pulling the stomach with it—a common and benign finding. A paraesophageal hiatal hernia means that the gastroesophageal junction stays below the diaphragm, but the stomach herniates through the diaphragm into the thorax. This is an uncommon, serious type of hernia thai: may become strangulated and should be repaired surgically.

Sliding hernia

Esophagus

Diaphragmatic hiatus

Normal

Esophagus

Diaphragmatic hiatus

GE junction

Normal

Hiatal hernias. In the sliding typo, the gastroesophageal junction slides freely above arid below the diaphragmatic hiatus, In a paraesophagaai hernia, the gastroesophageal junction is fixed below the diaphragm, allowing part of the stomach to herniate into the chest, (From Crapo JD, Hamilton MA, tidsman S: Medicine & Pfttiiatries, Philadelphia, HanleyHi (ielfus, 1988, with permission.)

GE junction

Paraesophageal hernia

Arid wavNun ; M 3,iri_ ICtfeifogyi i:

Peptic ulcer disease presents with chronic, intermittent, epigastric pain—burning, gnawing, or aching—that is localized and often relieved by antacids or milk. Look for epigastric tenderness. Patients may have occult blood in stool and nausea or vomiting. Peptic ulcer disease is more common in males. The two types are gastric and duodenal.

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