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Saturday, March 7, 2009

Bronchitis

Bronchitis

Description

· Hyperemia and edema of the mucous membranes

· Production of mucopurulent exudates

· Impairment of the productive function of the cilia, lymphatics, and phagocytes

· Airway obstruction from:

o Edema

o Secretions

o Bronchial muscle spasm

Etiology

  • Viral infections are the primary cause of bronchitis:
    • Parainfluenza
    • Influenza A and B
    • Respiratory syncytial virus
    • Human meta pneumovirus
    • Echovirus
    • Coronavirus
    • Adenovirus
    • Coxsackievirus
    • Rhinovirus
    • Measles and herpes viruses (can cause severe viral bronchitis)
  • Particularly severe or long-lasting bronchitis:
    • Mycoplasma pneumoniae
    • Chlamydia pneumoniae
    • Bordetella pertussis:
      • Rates of pertussis are increasing, even in the fully immunized population (little protection remains after 10 years).
  • Other bacteria have not been conclusively proven to cause bronchitis except in those with chronic lung disease.

Diagnosis

Signs and Symptoms

History

  • Complaints that may precede upper respiratory tract infection (URTI) symptoms:
    • Malaise
    • Chills
    • Myalgias
    • Coryza
    • Sore throat
  • Onset of URTI symptoms:
    • Mile dyspnea
    • Cough, initially dry and nonproductive
    • Cough, later becomes mucoid or mucopurulent
    • Chest pain or burning related to cough
    • Initial symptoms improve after 3-5 days, with 1-3 weeks of residual cough and malaise

Physical Exam

  • Fever, not usually above 102°F (38.5°C)
  • Tachypnea
  • Mild hemoptysis
  • Wheezing
  • Rales
  • Scattered rhonchi
  • Pulmonary function tests are frequently abnormal

Essential Workup

  • The diagnosis is clinical
  • Pulse oximetry
  • Influenza A and B testing if identification of these organisms is required for treatment or reporting
  • Evaluate for pertussis:
    • Acute cough illness lasting 14 days or more in a person with paroxysmal cough, posttussive vomiting, or inspiratory whoop
    • 14 days or more of cough within an outbreak setting

Tests

Lab

  • Influenza A and B testing may help immediately confirm clinical suspicion.
  • In most cases, no specific test will help make the diagnosis immediately.
  • Viral or bacterial cultures are rarely helpful.
  • CBC may show leukocytosis, but this is a nonspecific finding.
  • Pertussis may be confirmed using polymerase chain reaction (PCR) testing, but diagnosis will be delayed.

Imaging

Chest radiograph:

  • No evidence of consolidation
  • Indications:
    • Shortness of breath
    • Hypoxia
    • Chest pain
    • Heart rate >100 beats/minute
    • Respiratory rate 24 breaths/minute
    • Temperature 38 °C
    • Focal findings on chest examination
    • Elderly patient with multiple comorbid conditions
    • Hypoxia
    • 14 days or more of cough

Diagnostic Procedures/Surgery

None specific

Differential Diagnosis

  • Acute and subacute <8>
    • Pneumonia
    • Reactive airway disease
    • Aspiration
    • Acute sinusitis
    • Bacterial tracheitis
    • Occupational exposure
  • Chronic >8 weeks:
    • Asthma
    • Gastroesophageal reflux disease
    • Chronic bronchitis
    • Bronchiectasis
    • ACE inhibitor use
    • Bronchogenic carcinoma
    • Carcinomatosis
    • Sarcoidosis
    • Left ventricular failure
    • Aspiration syndrome
    • Psychogenic/habit

Pediatric Considerations

  • Aggressive initial management of these patients is seldom required.
  • Administer oxygen if the patient is hypoxic.
  • Fluids may be administered if the patient is dehydrated.

Treatment

Pre Hospital

  • Maintain adequate oxygenation
  • Bronchodilators if wheezing is present

Initial Stabilization

  • Aggressive initial management of these patients is seldom required.
  • Administer oxygen if the patient is hypoxic.
  • Fluids may be administered if the patient is dehydrated.

ED Treatment

  • Bronchitis is usually a viral process; treatment is symptomatic.
  • Cough suppressants may be considered.
  • β-adrenergic inhaler for patients with severe cough or wheezing
  • Amantadine may be used in known outbreaks of influenza A.
  • Oseltamivir (Tamiflu) and zanamivir (Relenza) may be considered in patients with recent onset of influenza.
  • Antibiotics:
    • Generally, antibiotics are not indicated (even when secretions are purulent).
    • Antibiotics do not improve overall illness duration, activity limitation, or work loss in healthy patients with no underlying lung disease.
    • Consider use in those patients who have recurrence of fever after initial improvement.
  • Symptomatic control with antipyretics and analgesics
  • Although patients should be encouraged to stop smoking, the use of tobacco is not an indication for antibiotics unless the patient has a known history of emphysema.

Medication (Drugs)

  • Albuterol: 0.5 mL in a 0.5% solution nebulized q6h
  • Amantadine: 100 mg PO per day, must be given within 48 hours of symptom onset
  • Oseltamivir (Tamiflu) and zanamivir (Relenza) within 48 hours of symptom onset for influenza-related bronchitis:
    • Zanamivir: 10 mg inhalation q12h — 5 days (no pediatric dosing)
    • Oseltamivir: 75 mg PO b.i.d. (peds: 2 mg/kg) — 5 days
  • Erythromycin should be given to proven cases of pertussis and to household contacts of those with proven pertussis.
  • Yearly influenza vaccinations should be encouraged in health care providers and in the high-risk population (elderly, immunocompromised, chronic lung disease).

Pediatric Considerations

  • Use of acetaminophen rather than aspirin for analgesia.
  • Repeated bouts in children should lead to referral for complete evaluation of the respiratory tract.

Follow-Up

Disposition

Admission Criteria

  • Underlying significant cardiopulmonary compromise
  • Significant hypoxia
  • Ill patient with unclear diagnosis

Discharge Criteria

  • No pulmonary compromise should be present.
  • Instruct patients, particularly high-risk patients, to return if no improvement or worsening of symptoms occurs.
  • Bed rest
  • Fluids
  • Aspirin or acetaminophen

References

1. Aagaard E, Gonzales R. Management of acute bronchitis. Infect Dis Clinic N Am. 2004; 18:919-937.

2. Gonzoles R, Sande MA: Uncomplicated acte bronchitis. Ann Intern Med. 2000;133:981-991.

3. Hirschmann JV: Antibiotics for common respiratory tract infections in adults. Arch Intern Med. 2002; 162:256-264.

4. Linder JA, Sims I: Antibiotic treatment of acute bronchitis in smokers. A systemic review. J Gen Inern Med. 2002;17:230-234.

5. Stephens MM, Nashelsky J: Do inhaled beta-agonists control cough in URIs or acute bronchitis? J Fam Prac. 2004;53:662-663.

6. Ward MA: Emergency department management of acute respiratory tract infections in adults. Sem Resp Infec. 2002:17:65-71.

Miscellaneous

SEE ALSO: Cough; Shortness of Breath

Codes

ICD9-CM

466

490

ICD10

J40

Asthma, Adult

Asthma, Adult

Description

  • Increased expiratory resistance:
    • Bronchospasm
    • Airway inflammation
    • Mucosal edema
    • Mucous plugging
  • Consequences:
    • Air trapping
    • Increased dead space
    • Hyperinflation
  • Risk factors for life-threatening disease:
    • Prior intubations
    • Intensive care unit admissions
    • Chronic steroid use
    • Hospital admission for asthma during the past year
    • Inadequate medical management
    • Increasing age
    • Ethnicity (African Americans)
    • Lack of access to medical care

Etiology

Mechanism

  • Pollen
  • Dust mites
  • Molds
  • Animal dander
  • Other environmental allergens
  • Viral upper respiratory infections
  • Occupational chemicals
  • Tobacco smoke
  • Environmental change
  • Cold air
  • Exercise
  • Emotional factors
  • Drugs:
    • Aspirin
    • NSAIDs
    • Beta-blockers

Diagnosis

Signs and Symptoms

  • Wheezing
  • Dyspnea
  • Chest tightness
  • Cough
  • Tachypnea
  • Tachycardia
  • Respiratory distress:
    • Posture sitting upright or leaning forward
    • Use of accessory muscles
    • Inability to speak in full sentences
    • Diaphoresis
    • Poor air movement
  • Altered mental status

Essential Workup

  • Primarily a clinical diagnosis
  • Measure and follow severity with peak expiratory flow rate (PEFR)
  • Assess for underlying disease
  • Pneumonia:
    • Pneumothorax

Tests

Lab

  • Arterial blood gas:
    • Not helpful during the initial evaluation
    • The decision to intubate should be based on clinical criteria.
    • Mild-moderate asthma: respiratory alkalosis
    • Severe airflow obstruction and fatigue: respiratory acidosis
  • Pulse oximetry:
    • Less than 90% is indicative of severe respiratory distress
    • Patients with impending respiratory compromise may still maintain saturation above 90% until sudden collapse.
  • WBC:
    • Leukocytosis is nonspecific
    • Pneumonia
    • Chronic steroid use
    • Stress of an asthma exacerbation
    • Demargination occurs after administration of epinephrine and steroids.

Imaging

  • Peak expiratory flow rate:
    • Estimates the degree of airflow obstruction:
      • Normal peak flow in an adult is 400–600
      • Between 100 and 300 indicates moderate airway obstruction.
      • <100>
      • Use serially as an objective measure of the response to therapy
  • Forced expiratory volume (FEV):
    • More reliable measure of lung function than PEFR
    • More operator dependent
    • Difficult to use as a screening tool
    • Often unavailable in the ED
    • Severe airway obstruction: FEV1 less than 30–50%
  • Chest radiograph:
    • Indications:
      • Fever
      • Suspicion of pneumonia
      • Suspicion of pneumothorax or pneumomediastinum
      • Foreign body aspiration
      • First episode of asthma
      • Comorbid illness
      • Diabetes
      • Renal failure
      • AIDS
      • Cancer
    • Findings:
      • Hyperinflation
      • Scattered atelectasis
  • ECG:
    • Indicated in patients at risk for cardiac disease:
      • Dysrhythmias
      • Myocardial ischemia
    • Transient changes in severe asthma:
      • Right axis deviation
      • Right bundle branch block
      • Abnormal P waves
      • Nonspecific ST-T wave changes

Differential Diagnosis

  • Congestive heart failure
  • Myocardial ischemia
  • Pulmonary embolus
  • Pneumonia
  • Bronchitis
  • Bronchiolitis
  • Croup
  • Foreign body aspiration
  • Upper airway obstruction
  • Angioedema
  • Allergic reaction
  • Chronic obstructive pulmonary disease
  • Chronic cor pulmonale
  • Chemical pneumonitis
  • Carcinoid tumors
  • Smoke inhalation
  • Immersion injury
  • Venous air embolus

Treatment

Pre Hospital

  • Recognize the ‘quiet chest’ as respiratory distress.
  • Supplemental oxygen
  • Continuous nebulized β2-agonist
  • Administration of subcutaneous epinephrine
  • Severe disease with decreased breath sounds

Initial Stabilization

  • Immediate initiation of inhaled β2-agonist treatment
  • Intubate for fatigue and respiratory distress.
  • Steroids

ED Treatment

β2Adrenergic Agonist

  • Mild-moderate asthmatic:
    • Administer every 20 minutes
  • Severe asthmatic:
    • Continuous nebulized treatment
  • Selective β2-agonists (albuterol)
  • Subcutaneous β-agonist:
    • Severe exacerbations
    • Limited inhalation of aerosolized medicine
    • More side effects because of systemic absorption:
      • Tachycardia
      • Tremors
    • Relative contraindications: age >40 years and coronary disease
  • Corticosteroids:
    • Reduce airway wall inflammation
    • Administered early
    • Onset of action may take 4-6 hours
    • Administer intravenously or orally
    • IV Solu-Medrol in the treatment of severe asthma exacerbation
    • Mild-moderate exacerbations may be treated with oral prednisone.
    • Inhaled corticosteroids are currently not recommended as initial therapy.
  • Oxygen:
    • Maintain an oxygen saturation above 90%
  • Aminophylline:
    • Rare utility in acute management
    • Toxicity:
      • Nausea
      • Tremor
      • Anxiety
      • Palpitations
      • Tachycardia
  • Anticholinergic agents:
    • If minimal response to initial β2-agonist treatment
    • Severe airflow obstruction
    • Inhaled anticholinergic agents should be used in conjunction with β2-agonists.
  • Magnesium sulfate:
    • No benefit in mild-moderate asthma
    • Benefit of magnesium remains unclear in severe asthma
  • Heliox:
    • Mixture of helium and oxygen (80:20, 70:30, 60:40)
    • Less dense than air
    • Decrease airway resistance.
    • Decrease in respiratory exhaustion
    • Not currently recommended for routine use:
      • Consider in severe asthma
  • Ketamine:
    • Bronchodilator and an anesthetic agent
    • Useful as an induction agent during intubation
    • Contraindications:
      • Hypertension
      • Coronary disease
      • Pre-eclampsia
      • Increased intracranial pressure
  • Halothane:
    • Inhalation anesthetics are potent bronchodilators.
    • Refractory asthma in intubated patients
  • Intubation of the asthmatic patient:
    • Rapid sequence intubation:
      • Lidocaine to attenuate airway reflexes
      • Etomidate or ketamine as an induction agent
      • Succinylcholine should be administered to achieve paralysis.
      • A large endotracheal tube >7 mm should be used to facilitate ventilation.
      • May need to mechanically exhale for the patient
      • Permissive hypercapnia

Medication (Drugs)

  • β2-agonists
    • Albuterol: 2.5 mg in 2.5 mL normal saline q20min inhaled (peds: 0.1-0.15 mg/kg/dose q20min [minimum dose 1.25 mg])
    • Epinephrine: adult: 0.3 mg (1:1,000) SC q0.5h-q4.0h × three doses (peds: 0.01 mg/kg up to 0.3 mg SC)
    • Terbutaline: 0.25 mg SC q0.5h × two doses (peds: 0.01 mg/kg up to 0.3 mg SC)
  • Corticosteroids:
    • Methylprednisolone: 60-125 mg IV (peds: 1-2 mg/kg/dose IV or PO q6h × 24 hours)
    • Prednisone: 40-60 mg PO (peds: 1-2 mg/kg/day in single or divided doses)
  • Anticholinergics
    • Ipratropium bromide: 0.5 mg in 3 mL NS q1h × three doses
  • Magnesium: 2 g IV over 20 minutes
  • Aminophylline: 0.6 mg/kg/h IV infusion
  • Rapid sequence intubation:
    • Etomidate: 0.3 mg/kg, or ketamine: 1-1.5 mg/kg
    • Lidocaine: 1-1.5 mg/kg
    • Succinylcholine: 1.5 mg/kg

Follow-Up

Disposition

Admission Criteria

  • Persistent respiratory distress
  • PEFR <100>
  • Intubated patients

Medical Wards or Observation Unit

  • PEFR <40%>
  • Patients without subjective improvement
  • Patients with continued wheeze and diminished air movement
  • Patients with moderate response to therapy and no respiratory distress:
    • Factors that should favor admission
    • Prior intubation
    • Recent ED visit
    • Multiple ED visits or hospitalizations
    • Symptoms for more than 1 week
    • Failure of outpatient therapy
    • Use of steroids
    • Inadequate follow-up mechanisms
    • Psychiatric illness
  • Complications:
    • Pneumothorax
    • Pneumomediastinum
    • Pneumonia
    • Fatigue

Discharge Criteria

  • Patient reports subjective improvement
  • Clear lungs with good air movement
  • PEFR or FEV1 greater than 70% of predicted
  • Peak flow should be greater than 300.
  • Adequate follow-up within 48–72 hours

References

1. Corbridge TC, Hall JB. The assessment and management of adults with status asthmaticus. Am J Respir Crit Care Med. 1995;151:1296-1316.

2. Guidelines for the diagnosis and management of asthma: National Asthma Education Program Expert Panel Report. Bethesda, MD: Department of Health and Human Services; 1991. NIH 91-3042.

3. Jagoda A, Shepherd SM, Spevitz A, et al. Refractory asthma, part 1: epidemiology, pathophysiology, pharmacologic interventions. Ann Emerg Med. 1997;29:262-274.

4. Jagoda A, Shepherd SM, Spevitz A, et al. Refractory asthma, part 2. Airway interventions and management. Ann Emerg Med. 1997;29:275-281.

5. Manthous CA. Management of severe exacerbations of asthma. Am J Med. 1995;99:298-308.

Codes

ICD9-CM

493

ICD10

J45.9

Acidosis

Acidosis

Description

Respiratory Acidosis

  • Reduced pH owing to alveolar hypoventilation with elevated PaCO2
  • Defined as PaCO2 >45 mm Hg or higher than expected for calculated respiratory compensation for metabolic acidosis
  • Divided into three broad categories:
    • Primary failure in central nervous system drive to ventilate:
      • Sleep apnea
      • Anesthesia
      • Sedative overdose
    • Primary failure in transport of CO2 from alveolar space:
      • Chronic obstructive pulmonary disease
      • Myasthenic crisis
      • Severe hypokalemia
      • Guillain-Barre syndrome
    • Primary failure in transport of CO2 from tissue to alveoli:
      • Severe heart failure

Metabolic Acidosis

  • Process that reduces serum pH by decreasing plasma bicarbonate levels
  • Primarily caused by:
    • Gain of a strong acid through ingestion or metabolism
    • Loss of bicarbonate from the body
  • Metabolic acidosis is clinically evaluated by dividing into two main groups:
    • Elevated anion gap metabolic acidosis:
      • Bicarbonate reduced through buffering of added strong acid
      • Anion gap is increased owing to retention of the unmeasured anion from the titrated strong acid.
    • Normal anion gap metabolic acidosis owing to:
      • Kidneys fail to reabsorb or regenerate bicarbonate.
      • Losses of bicarbonate from gastrointestinal tract (diarrhea)
      • Ingestion or infusion of substances that release hydrochloric acid
    • No anion gap is observed owing to the absence of any unmeasured anion of a titrated acid and secondary chloride retention with HCO3- loss.

Etiology

Anion Gap Acidosis

To remember possible causes, use mnemonic A CAT MUD PILES:

  • Alcohol ketoacidosis
  • Carbon monoxide or cyanide
  • Aspirin
  • Toluene
  • Methanol
  • Uremia
  • Diabetic ketoacidosis
  • Paraldehyde
  • Iron/isoniazid
  • Lactic acidosis
  • Ethylene glycol
  • Starvation

Increased Osmolar Gap

To remember possible causes, use mnemonic ME DIE:

  • Methanol
  • Ethylene glycol
  • Diuretics (mannitol; no acidosis)
  • Isopropyl alcohol (no acidosis)
  • Ethanol

Non-Anion Gap Metabolic Acidosis

  • Gastrointestinal losses of bicarbonate:
    • Diarrhea
    • Villous adenoma
    • Removal of small bowel, pancreatic or biliary secretions
    • Tube drainage
    • Small bowel/pancreatic fistula
  • Anion exchange resins (i.e., cholestyramine):
    • Ingestion of calcium chloride or magnesium chloride
  • Renal loss of bicarbonate
  • Renal tubular acidosis:
    • Type I (distal): hypokalemic hyperchloremic metabolic acidosis:
      • Decreased ability to secrete hydrogen
      • Serum HCO3 <15>
      • Potassium low
      • Renal stones common
    • Type II (proximal): hypokalemic hyperchloremic metabolic acidosis:
      • Decreased proximal reabsorption of HCO3-.
      • Acidosis limited by reabsorptive capacity of proximal tubule for HCO3-
      • Serum HCO3 typically 14–18 mEq/L
      • Low/normal potassium.
    • Type IV (hypoaldosteronism): hyperkalemic hyperchloremic acidosis:
      • Aldosterone deficiency or resistance causing decreased H+ secretion
      • Serum bicarb >15 mEq/L
      • Normal/elevated potassium
  • Carbonic anhydrase inhibitors
  • Tubulointerstitial renal disease
  • Hypoaldosteronism
  • Addition of hydrochloric acid such as:
    • Ammonium chloride
    • Arginine hydrogen chloride
    • Lysine hydrogen chloride

Diagnosis

Signs and Symptoms

  • Nonspecific findings
  • Vital signs:
    • Tachypnea or Kussmaul respirations with metabolic acidosis
    • Hypoventilation with respiratory acidosis
    • Tachycardia
  • Somnolence
  • Confusion
  • CO2 narcosis
  • Myocardial conduction and contraction disturbances

Essential Workup

  • Electrolytes, BUN, creatinine, glucose:
    • Decreased bicarbonate with metabolic acidosis
    • Hyperkalemia and hypercalcemia with severe metabolic acidosis
  • Arterial blood gases:
    • pH
    • CO2 retention in respiratory acidosis
    • CO level
  • Calculate anion gap: Na+ - (HCO3- + Cl-):
    • Correct anion gap for hypoalbuminemia:
      • For every 1 g/dL decrease in albumin (from 4.0 g/dL), add 2.5 points to calculated anion gap.
    • Normal range = 5-12 ± 3 mEq/L
    • Anion gap >25 mEq/L is seen only with:
      • Lactic acidosis
      • Ketoacidosis
      • Toxin-associated acidoses
  • Calculate the degree of compensation:
    • Expected PaCO2 = 1.5[HCO3-] + 8
    • If PaCO2 inappropriately high, patient has a concomitant respiratory acidosis and inadequate compensation
  • Respiratory acidosis:
    • Acute: expected HCO3- increased by 1 mEq/L for every 10 mm Hg increase in PaCO2
    • Chronic: expected HCO3- increased by 4 mEq/L for every 10 mm Hg increase in PaCO2
  • Evaluate the delta gap:
    • For every one-point increase in anion gap, HCO3- should decrease by 1 mEq/L in simple acid/base disorder.
  • Evaluate by comparing the change in the anion gap (ΔAG) with the change in the HCO3- (ΔHCO3-) from normal:
    • If ΔAG > ΔHCO3-, then patient has a concomitant metabolic alkalosis.
    • If ΔHCO3- > ΔAG, then patient has concomitant non-anion gap acidosis.

Tests

Lab

  • Urinalysis for glucose and ketones
  • Measure serum osmolality:
    • Calculated serum osmolality = 2 Na + glucose/18 + blood urea nitrogen/2.8
  • Osmolal gap = difference between calculated and measured osmolality:
    • Normal = <10
  • Toxicology screen:
    • Methanol, ethylene glycol, ethanol, and isopropyl alcohol if increased osmolality gap
    • Aspirin or iron levels for suspected ingestion
  • Co-oximetry for CO exposure
  • Serum ketones or β-hydroxybutyrate level
  • Serum lactate

Alert

  • Failure to appreciate acidosis in mixed acid/base disorders
  • Failure to appreciate inadequate respiratory compensation for metabolic acidosis and need for ventilatory support

Differential Diagnosis

  • Anion gap acidosis:
    • To remember possible causes, use mnemonic A CAT MUD PILES:
      • Alcohol ketoacidosis
      • Carbon monoxide or cyanide
      • Aspirin
      • Toluene
      • Methanol
      • Uremia
      • Diabetic ketoacidosis
      • Paraldehyde
      • Iron/isoniazid
      • Lactic acidosis
      • Ethylene glycol
      • Starvation
  • Increased osmolar gap:
    • To remember possible causes, use mnemonic ME DIE:
      • Methanol
      • Ethylene glycol
      • Diuretics (mannitol)
      • Isopropyl alcohol
      • Ethanol

Treatment

Initial Stabilization

Airway, breathing, circulation (ABCs):

  • Early intubation for severe metabolic acidosis with progressive/potential weakening of respiratory compensation
  • Naloxone, D50W (or Accu-Chek) and thiamine if mental status altered

ED Treatment

  • Respiratory acidosis:
    • Treat underlying disorder.
    • Provide ventilatory support for worsening hypercapnia.
    • Identify and correct aggravating factors (pneumonia) in chronic hypercapnia.
  • Metabolic acidosis:
    • Identify if concurrent osmolal gap.
    • Treat underlying disorder:
      • Diabetic ketoacidosis
      • Lactic acidosis
      • Alcohol ketoacidosis
      • Ingestion
    • Correct electrolyte abnormalities.

IV Fluids

Rehydrate with 0.9% normal saline if patient hypovolemic.

Medication (Drugs)

  • Dextrose: D50W 1 amp (50 mL or 25 g); (peds: D25W 4 mL/kg) IV
  • Naloxone (Narcan): 2 mg (peds: 0.1 mg/kg) IV or IM initial dose
  • Thiamine (vitamin B1): 100 mg (peds: 50 mg) IV or IM

Follow-Up

Disposition

Admission Criteria

  • Worsening metabolic acidosis
  • ICU admission if pH <7.1>
  • Respiratory acidosis

Discharge Criteria

Resolving or resolved anion gap metabolic acidosis

References

1. Adrogue HJ, Madias NE. Management of life-threatening acid-base disorders. New Engl J Med. 1998;338:26.

2. Swenson ER. Metabolic acidosis. Respir Care. 2001;46:342.

3. Whittier WL, Rutecki GW. Primer on clinical acid-base problem solving. Dis Mon. 2004;50:122.

Codes

ICD9-CM

276.2 Acidosis

ICD10

E87.2