Avian Respiratory Emergencies: An Approach to the Dyspneic Bird

Key Points

  • Signs of dyspnea in the avian patient include open-mouth breathing, increased sternal motion, and tail bobbing.
  • The dyspneic patient often benefits from humidifed air and 40% to 50% oxygen.
  • Tracheal obstruction is associated with acute onset of inspiratory and expiratory dyspnea, and is best managed short-term by air sac cannulation.
  • Important causes of tracheal disease are aspergillosis and seed inhalation.
  • Aspergillosis and chlamydiosis are important causes of pneumonia and air sacculitis. Onset is generally insidious, however subtle, non-specific signs of illness are often missed. Patients can present with dyspnea and prolonged expiration. Treatment frequently includes systemic therapy and nebulization.
  • Air sac compression caused by extrathoracic problems such as hepatomegaly is another important cause of respiratory compromise.
  • Low humidity and exposure to inhalant irritants such as strong fumes or cigarette smoke are important risk factors causing respiratory tract inflammation.
  • Survey radiography is a valuable diagnostic tool, particularly in medium to large-sized parrots. Additional diagnostic testing may include cytology, culture, endoscopy, hematology, and serum biochemistry.
  • Upper respiratory tract disease is common, but rarely a cause of dyspnea.

Recognizing dyspnea

Can you recognize respiratory difficulty in this bird? Clip provided by Dr. Isabelle Langlois. Note: This video has no audio.

Respirations should be hardly noticeable in the normal, calm bird. Signs of excessive respiratory effort include open-mouth breathing, increased sternal motion, and tail bobbing (Fig 1). Additional signs of respiratory distress may include tachypnea and wings held slightly away from the body. More subtle signs of respiratory difficulty may include exercise intolerance or reluctance to move around or fly, as well as a prolonged respiratory recovery rate. A bird that takes longer than 3 to 5 minutes to breathe normally after being manually restrained has a prolonged respiratory recovery rate (RRR). A prolonged RRR may be observed with a host of problems including obesity, cardiovascular diseases, and respiratory disease.

Raptor, open mouth breathing

Figure 1. Signs of dyspnea in the avian patient include open-mouth breathing, increased sternal motion, and tail bobbing. Image provided by Dr. Ed Ramsay. Click image to enlarge.

Initial response to the dyspneic bird

After recognizing a dyspneic bird, the clinician’s initial response should be: Hands Off!! Dyspneic birds can die soon after presentation with the additional stress of restraint and handling. Therefore minimize handling and place the bird in an oxygen-rich cage. Humidify air and provide 40 to 50% oxygen. As in mammals, oxygen therapy is potentially toxic if given for prolonged periods at high levels.

Keep the dyspneic bird in a quiet, calm environment. Provide some form of visual security such as a towel draped over part of the oxygen cage, and consider supplemental heat (80-85°F or 27-29°C) if the patient is fluffed and ruffled or thin. Be cautious when providing heat to overweight birds since overheating may exacerbate respiratory distress.

Anamnesis

While the patient is being cage rested in oxygen, obtain a complete history. Confirm signalment, and if the species is sexually monomorphic be sure to confirm how gender has been determined. Discuss the presenting complaint and the progression of clinical signs. For any bird presented with respiratory disease, be sure to ask if there has been a change in or loss of voice since this may localize lesions to the trachea, or more specifically the syrinx or “voice box” of the bird, a collection of muscles and membranes located at or near the tracheal bifurcation. Also obtain detailed husbandry information. For instance, is the bird on an all-seed diet, which would promote vitamin A deficiency?

Distinguishing upper and lower respiratory disease

Signs of upper respiratory disease such as rhinitis and sinusitis may include:

  • Oculonasal discharge, plugged nares
  • Sneezing
  • Swollen cere
  • Dried discharge on the feathers around the nares
  • Evidence of scratching or rubbing around the cere, nares, and/or eyes.
  • Frequent head shaking or yawning
  • Periorbital swelling, redness (Fig 2): The infraorbital sinus is the only true paranasal sinus of the bird. Located ventromedial to eye, the infraorbital sinus has numerous air-filled diverticula that extend forward into the beak, back around the ear, to the back of the neck, and even into the skull.

    Suborbital swelling in a canary

    Figure 2. Suborbital swelling in a canary (Serinus canaria). Image provided by Dr. M. Scott Echols. Click image to enlarge.

Tracheal disease may be associated with a change in or loss of voice or a squeaking or clicking sound. Marked inspiratory and expiratory dyspnea may be observed.

Signs of lower respiratory tract disease such as air sacculitis or pneumonia rarely include dyspnea until disease is quite advanced. More frequently non-specific signs of illness, weight loss, exercise intolerance, and a prolonged respiratory recovery rate are observed. Advanced disease may be associated with a prolonged expiratory phase.

Physical examination

After resting in an oxygen-rich environment, the bird’s clinical condition may allow an abbreviated exam. Have oxygen by mask nearby and ready for use. Cursory examination generally includes the oropharynx, crop, pectoral muscle mass, coelom, vent, and any other areas of particular interest.

During a complete physical examination, it is particularly important to:

  • Carefully study the patient’s head straight on to look for any sign of asymmetry.
  • Open the oropharynx to carefully evaluate the choana, glottis, and mucous membrane color. The choana is a slit in the roof of the mouth that communicates with the nasal cavity. The glottis is the opening to the trachea. Evaluate the choana for evidence of choanal discharge, swelling, as well as loss or blunting of choanal papillae. Evaluate the glottis for evidence of redness or discharge.
  • Auscult the lungs over the back. Breath sounds usually cannot be heard unless the patient is extremely stressed or severe pulmonary disease is present.
  • Companion birds often vocalize during the entire exam. Note any abnormalities or changes in the voice.

Differential diagnoses for respiratory disease

Dyspnea may be associated with tracheal disease, lower respiratory tract disease, or severe upper respiratory tract disease. Important differentials for primary respiratory disease may be categorized using the “DAMNIT” scheme: Degenerative,Anomalous,Metabolic, and Neoplastic causes of primary respiratory disease are rare in the bird.

Nutritional

Vitamin A deficiency develops in birds on an all-seed diet without supplementation. Hypovitaminosis A leads to epithelial squamous metaplasia of the conjunctiva, nasolacrimal duct, and respiratory epithelium lining the sinus and syrinx. Therefore hypovitaminosis A may be associated with recurrent bacterial respiratory infections such as chronic sinusitis.

Goiter or iodine deficiency develops in budgerigar parakeets on all-seed diets without supplementation. Clinical signs are secondary to extraluminal compression of the trachea and/or crop by the hyperplastic thyroid gland. Affected birds may demonstrate a clicking respiratory noise, dyspnea, and regurgitation. Owners may also complain of a change in or loss of voice. . It is extremely rare to find a treatment of choice in modern avian medicine that includes mediation in the water. However there is significant risk of toxicity in parakeets given parenteral iodine supplementation. Instead Lugol’s iodine is placed in the water. The stock solution consists of 2 ml of Lugol’s iodine added to 30 ml of water. Then mix one drop of stock solution with 250 ml of drinking water. Provide this as the only form of drinking water.

Infectious

An important cause of infectious respiratory disease in parrots, doves, and pigeons is Chlamydophila psittaci. Affected birds may suffer from acute or chronic rhinitis, sinusitis, keratoconjunctivitis, pneumonia, and/or air sacculitis. Specific testing for psittacosis should combine antigen and antibody detection tests. (See Compendium of Measures to Control Chlamydophila.)

Bacterial infection is an important cause of rhinitis and sinusitis, although there are often significant underlying factors such as hypovitaminosis A or poor husbandry. Bacterial pathogens most frequently include gram-negative bacteria, however gram-positive bacteria (Streptococcus, Staphylococcus, Enterococcus), spirochetes (Borrelia anserina), and Mycoplasma have also been implicated. Important gram-negative pathogens include E. coli,Klebsiella, Pseudomonas, Aeromonas, Pasteurella, and Proteus sp. Additional pathogens that have been reported include: Yersinia, Bordetella, Salmonella, Hemophilus, and Enterobacter.

Fungal infection caused by Aspergillus fumigatus is a very important cause of acute or chronic tracheitis, air sacculitis and pneumonia in raptors (Fig. 3). Aspergillosis is less common in psittacines, however disease appears most prevalent in Amazon parrots and African grey parrots. There is an increased risk of aspergillosis when the birds are exposed to poor ventilation or climatic extremes. Aspergillosis may also occur with concurrent illness or long-term antibiotic administration. Profound heterophilic leukocytosis may be measured in some individuals. Antigen and antibody detection tests exist but interpretation may be difficult. (See Aspergillus serology.) Treatment of aspergillosis is often very difficult, and prognosis is frequently grave. Other causes of fungal respiratory disease such as Candida and Cryptococcus are rare.

Aspergillus fumigatus

Figure 3. Aspergillus fumigatus is an important cause of tracheitis, air sacculitis, and/or pneumonia. The photograph below shows fungal plaques. Photograph provided by Dr. Isabelle Langlois.

The most important viral cause of avian respiratory disease in the United States is poxvirus. Of pet bird species, juvenile lovebirds, canaries, and pigeons are most commonly affected. Birds are usually housed outdoors or at least have exposure to insect vectors. Wet poxvirus causes diphtheritic lesions of the eyelids, conjunctiva, and oropharynx. Lesions are often complicated by secondary bacterial infections. Extensive lesions may obstruct airflow. Cytologic diagnosis is confirmed by identification of Bollinger bodies.

Parasitic disease may be an important cause of respiratory disease in ground birds housed outdoors. Syngamus trachea or gapeworm is also occasionally seen in songbirds or passerines. Affected birds may die peracutely, or open-mouth breathing and blood coming from the trachea may be observed (Fig 4). Perform a fecal exam to look for parasite eggs (Fig 5).

Figure 4. Sygnamus trachea in the trachea of a ringnecked pheasant. Photo credit: Milton Friend via Wikimedia Commons.

Figure 4. Sygnamus trachea in the trachea of a ringnecked pheasant. Photo credit: Milton Friend via Wikimedia Commons.

Bioperculate egg of Syngamus trachea

Figure 5. The bioperculate egg of Syngamus trachea. Arrows point to each operculum. Image from nematode2011.

Trichomonas gallinae is an important cause of disease in pigeons, doves, and accipiter hawks. Oropharyngeal plaques may block the trachea, and lesions sometimes extend down into the lungs.

Sarcocystis falcatula may infect passerines and Old World psittacines like the cockatoo (Cacatua sp). Clinical signs are secondary to encephalitis and/or pneumonia. Disease is often fatal in psittacine birds.

Sternostoma tracheacolus mites of the trachea, air sacs, and lungs are seen in the Gouldian finch (Chloebia gouldiae), and less frequently in canaries (Serinus canaria). Clinical signs may include dyspnea, wheezing, squeaking, sneezing, nasal discharge, loss of voice, and head shaking.

Inflammatory

Low humidity is an important environmental factor, particularly during the winter months when warmed air is not humidified or during summer months with air conditioning. Birds from tropical rainforests such as Amazon parrots and macaws are particularly susceptible to the adverse effects of dry air.

Chronic obstructive pulmonary disease, also known as macaw pulmonary hypersensitivity or allergic pneumonitis, is an important cause of respiratory disease in the blue and gold macaw (Ara ararauna). Blue and gold macaws seems particularly sensitive to respiratory irritants like powder down, smoke, strong odors, aerosols, and dust, especially in poorly ventilated surroundings. This chronic, insidious condition eventually leads to polycythemia. There are no proven treatments, however anti-inflammatories and antihistamines are frequently tried.

Toxins

The efficiency of the avian respiratory system places birds at high risk to the effects of environmental gases. Exposure to strong household fumes such as overheated Teflon (polytetrafluoroethylene), undiluted sodium hypochlorite, self-cleaning ovens, and cigarette smoke can all lead to peracute death or respiratory distress. Supportive care for such cases includes oxygen supplementation, non-steroidal anti-inflammatory agents, diuretics, and broad-spectrum antibiotics, fluid therapy, and supplemental heat.

Trauma

Unfortunately aspiration pneumonia is an important cause of respiratory disease in the nestling, hand-raised parrot. Inhalation of formula is associated with a poor to grave prognosis despite the administration of antifungals and broad-spectrum antibiotics.

Mechanical obstruction of the trachea may occur secondary to inhalation of seed hulls. Inhalation of millet seems to occur most commonly in cockatiels or similarly sized birds. History with seed foreign body is often of an animal that is completely fine, and then while eating, is suddenly in respiratory distress. Papillomatosis of the oropharynx may also mechanically obstruct the airway, however the onset of signs should be more gradual.

Non-respiratory tract conditions associated with respiratory signs

As in mammals, an important differential diagnosis for the patient with respiratory signs is cardiovascular disease. In the avian patient, another important set of differential diagnoses includes conditions that cause air sac compression. Air sac compression caused by organomegaly, coelomic masses, egg binding, or ascites frequently leads to respiratory compromise. Obesity may also be an important contributory factor to air sac compression.

Diagnostics

If the patient is strong enough, perform diagnostic tests in stages.

  1. Survey radiographs may be one of the most valuable initial diagnostic tests, particularly in medium to large-sized parrots. Be sure to use high- or ultra-detail film and table top technique. Carefully evaluate the trachea, lungs, air sacs, and coelomic cavity. Normal avian lungs possess a prominent honeycomb pattern best visualized on the lateral view. Cells, fluid, or fat may obscure this pattern or make it less distinct. The caudal air sacs are best visualized on the ventrodorsal view. Normal air sacs are so thin-walled that they should not be visible on survey films.Manual restraint may work well for birds that are not struggling or handle restraint well, (i.e. smaller species up to the size of a cockatiel). Hooded raptors may also handle manual restraint well. Careful positioning is crucial for proper evaluation of the respiratory tract, however, and if the patient is struggling the resultant films may be non-diagnostic. Radiographs may be quicker, less stressful, and more diagnostic when performed under anesthesia when the bird’s clinical condition allows. Birds may be mask induced with isoflurane (3 to 5%) or sevoflurane (incremental increases up to 7%), or induced with careful intravenous administration of propofol (5 mg/kg IV) followed by intubation and maintenance on gas.
  2. Perform bloodwork when clinical condition allows. Leukocytosis may be seen with Chlamydophilosis or aspergillosis. Biochemistry panel results may indicate conditions such as liver disease.
  3. Cytology is often a valuable diagnostic test in the dyspneic patient. Roll swabs from diagnostics samples onto sterile glass slides, and use modified wright-geimsa stain and/or gram stain for evaluation. Include wet mount cytology to identify protozoa such as Trichomonas. Perform fecal testing to search for parasite eggs such as Syngamus.
    • Nasal flushes and choanal swabs may provide some information about the upper respiratory tract, however these samples may not be very representative of upper respiratory tract flora. If the sinus is involved, perform a sinus aspirate instead.
      Sinus aspirates collect samples from the infraorbital sinus cranioventral to the globe. The beak should be held open to increase sinus space. Insert a 25- to 22-gauge needle with a 3 to 6 ml syringe attached into the sinus space. To enter the ventral sinus space, insert the needle perpendicular to the skin just underneath the jugal arch. Watch the eye carefully for movement since the needle can penetrate the globe if directed incorrectly.To perform a choanal swab, gently roll a moistened swab in the rostral-most portion of the choana. Carefully avoid touching the swab to other oral mucosal surfaces.The nasal flush is both a diagnostic and therapeutic procedure. Flush warm saline or eyewash solution with some force through the nares essentially blowing the bird’s nose for it and relieving congestion. The presence of the choanal slit allows fluid flushed through the nares to be collected in a Petri dish or some other sterile container for cytology and culture/sensitivity. Recommended volumes for nasal flush are 2 to 3 ml for budgerigar parakeets, 4 to 6 ml for cockatiels, 8 to 12 ml for birds the size of an Amazon or African grey parrot, and 15 to 20 ml for large cockatoos and macaws. Restrain the bird with the head facing the floor or at least held parallel with the floor. Place the syringe securely against the nares, then push fluid through with force (Fig. 5)

      Nasal flush of an avian patient

      Figure 5. Nasal flush of an avian patient. Image provided by Dr. Ed Ramsay.

    • Cytologic samples of the lower respiratory tract include tracheal swabs, tracheal wash, as well as the air sac swab or air sac wash.
      Tracheal cytology may be obtained with use of a tracheal swab in larger birds. Insert and gently roll a moistened swabs into the proximal trachea while minimizing contact with oropharyngeal mucosa. The tracheal wash collects a more representative sample of the lower respiratory tract. Tracheal wash is usually done in the anesthetized bird. It may be performed through a sterile endotracheal tube or a soft, sterile tube may be passed directly into the trachea. Infuse 1 to 2 ml/kg. Severely dyspneic patients may require ventilation through an air sac cannula during this procedure.To perform an air sac swab or air sac wash, restrain the bird in lateral recumbency as one would for laparoscopy. Identify the last rib at the level of the pubis. Insert a sterile, rigid laparoscope into the caudal thoracic or abdominal air sac behind the last rib. Identify and swab lesions within the air sac space. Alternatively, a cytologic sample may be obtained by inserting a soft sterile catheter into the air sac space to infuse sterile saline. Keep the head elevated to maximize recovery of fluid and prevent fluid from getting into the lungs.
    • Cytologic evaluation may identify changes consistent with infectious disease or vitamin A deficiency. Hypovitaminosis A may be associated with irregularly shaped, basophilic epithelial cells that have frequently lost their nucleus.
  4. Endoscopic evaluation of the trachea, air sacs, and lungs can yield valuable diagnostic information in larger birds (Fig 6). Endoscopy is also a great way to obtain samples for cytology and culture.

    Laparoscopic view of the caudal thoracic air sac space

    Figure 6. Laparoscopic view of the caudal thoracic air sac space (small arrow: ostium or opening into the lung). Image provided by Dr. Stephen Divers. Click image to enlarge.

Therapeutics

Treatment of the bird with respiratory disease is ideally based on the results of diagnostic testing, however diagnostics are not always possible in the dyspneic bird. Sometimes treatment must be empirically based on signalment and history.

Non-specific therapy

  • Fluid therapy
  • Improve plane of nutrition.
  • Supplement vitamin A as needed
  • Reduce exposure to inhalant irritants in the environment. Consider an air purifier with a HEPA filter.
  • Humidify air to soothe dry, irritated respiratory epithelium, particularly species derived from tropical climates. On an outpatient basis, birds may receive humidified air through bathroom steam treatments or frequent baths. Placing a cool air evaporative humidifier in the bird room may also be beneficial as long as the humidifier is kept scrupulously clean.

Treatment of upper respiratory tract disease may include:

  • Nasal flushing (see diagnostics above) essentially “blows the bird’s nose” thereby relieving congestion, at least temporarily.
  • Gently clean nares impacted with debris using moistened swabs or a small bone curet being careful of the vascular operculum. (The operculum is a keratinized structure found just within the rostral-most portion of the nasal cavity).
  • Very firm impactions may first be softened with several drops of saline flushed into the nares 5 minutes before curettage.
  • Ophthalmic drops directly applied to the nares every 8 to 12 hours for 7 to 14 days. Frequent empirical choices for topical treatment include ciprofloxacin, gentamicin, and tobramycin.
  • See systemic drug treatment and nebulization below.
  • Sinus flushing
  • Chronic cases of sinusitis frequently require surgical curettage.

Management of tracheitis can include:

  • Tracheal/syringeal obstruction requires air sac cannulation in the caudal thoracic or abdominal air sac. Following tube placement, dyspnea should stop immediately. The tube can also be used to maintain anesthesia while the obstruction is treated (Fig. 7).
  • Birds suffering from tracheal disease may benefit from tracheal injections. Intratracheal injections may be performed in the conscious bird using a small diameter metal feeding needle or a red rubber catheter. Infuse up to 2 ml/kg of water-soluble medication such as amphotericin B or clotrimazole, then release the bird and allow it to clear its throat.
  • See nebulization and systemic drug treatment below.

    Tracheal obstruction is associated with acute onset of inspiratory and expiratory dyspnea

    Figure 7 Tracheal obstruction is associated with acute onset of inspiratory and expiratory dyspnea, and is best managed short-term by air sac cannulation. Photograph provided by Dr. Isabelle Langlois. Click image to enlarge.

Systemic antibiotic, antifungal, and anthelmintic medication

Systemic drug therapy is indicated in almost all cases of respiratory disease although mild or early rhinitis may respond to topical therapy alone. Antibiotic choice should ideally be based on culture and sensitivity, although drugs may also be empirically selected depending on history, signalment, and physical exam findings. Antifungals frequently used include itraconazole and amphotericin B.

Table 1. Systemic drug therapy
Drug Dose Route Freq Comments
Amikacin sulfate
(Amiglyde, Aveco)
10-15 mg/kg SC, IM, IV q8-12h Least nephrotoxic of the amingolycosides
Amphotericin B
(Fungizone, Squibb)
1.5 mg/kg IV q8h Potentially nephrotoxic
1 mg/kg IT q8-12h
Azithromycin
(Zithromax, Pfizer)
50-80 mg/kg PO q24h Chlamydophila psittaci
Cefotaxime sodium
(Claforan, Hoechst-Roussel)
50-100 mg/kg IM q8h
Ceftiofur sodium
(Naxcel, Pharmacia)
50-100 mg/kg IM q8h
Ceftriaxone sodium
(Rocephin, Roche)
75-100 mg/kg IM q4-8h
Ciprofloxacin
(CIpro, Bayer)
15-20 mg/kg PO q12h
Doxycycline
(VIbramycin, Pfizer)
25-50 mg/kg PO q12-24h Drug of choice for Chlamydophila psittaci
Enrofloxacin
(Baytril, Bayer)
10-15 mg/kg PO, SC, IM q12h Parenteral formulation is extremely alkaline and should not be given repeatedly
15 mg/kg PO, IM q24h Some large species like raptors
Fenbendazole
(Panacur, Hoechst)
10-15 mg/kg PO Syngamus trachea; Use with caution in a novel species, may be toxic for some species, including raptors, lories, and storks
Itraconazole
(Sporanox, Janssen)
5-10 mg/kg PO q12-24h Azole of choice for treatment of aspergillosis
Ivermectin
(Ivomec, Merial)
0.2 mg/kg PO, SC Once Sternostoma tracheolum; treatment must often be repeated in 7 to 14 days
Metronidazole
(Flagyl, Searle)
25 mg/kg PO q12h Trichomoniasis
Oxytetracycline
(LA-200, Pfizer)
50-100 mg/kg
50-100 mg/kg
IM
SC
q24h
q48-72h
Piperacillin
(Piperacil, Lederle)
50-100 mg/kg SC, IM q8-12h
Pyrimethamine
(Fansidar, Roche)
0.5-1.0 mg/kg PO q12h Used in conjuction with sulfa antibiotics for treatment of sarcocystis
Sulfa-trimethoprim See trimethoprim
Thiabendazole 100 mg/kg x 7-10 days PO q24h Syngamus trachea
Ticarcillin
(Ticar, SmithKline Beecham)
150-200 mg/kg IM, IV q6-8h
Trimethoprim/ sulfadiazine
(Tribrissen, Schering-Plough)
30 mg/kg PO q12h Sarcocystis
5 mg/kg IM q12h Sarcocystis
Tylosin
(Tylan, Elanco)
20 mg/kg PO q8h Mycoplasmosis, Chlamydophila psittaci
20-30 mg/kg IM q8h

Nebulization

Nebulization, another form of topical treatment, is a valuable part of respiratory disease management. In order for nebulized material to extend into the avian parabronchi, nebulizers should be capable of producing particles ranging from 3 to 10 µm in diameter. Nebulize patients within a small enclosure for 15 to 30 minutes two to four times daily. Saline may be used to soothe irritated respiratory epithelium or antibiotics may be delivered to the lower respiratory tract. Monitor patients carefully, since excessive nebulization may over hydrate airways and flood the respiratory tract.

Table 2. Drugs used for nebulization.
Drug Dose Frequency Comments
Amikacin sulfate
(Amiglyde, Aveco)
5-6 mg/ml sterile water or saline x 15 min q8-12h Aminoglycoside active against gram-negative bacteria including Pseudomonas; discontinue if polyuria develops
Amphotericin B
(Fungizone, Squibb)
1 mg/ml sterile water or saline x 15 min q12h Treatment of aspergillosis
Cefotaxime sodium
(Claforan, Hoechst-Roussel)
10 mg/ml saline x 10-30 min q6-12h
Ceftriaxone sodium
(Rocephin, Roche)
40 mg/ml sterile water q12h
Clotrimazole
(Lotrimin, Schering)
10 mg/ml propylene glycol x 30-45 min q24h x 3 days Treatment of aspergillosis
F10 Super Concentrate
(Health and Hygiene Ltd, South Africa)
1:250 dilution q8-24h Antifungal and antibacterial activity
Gentamicin
(Garamycin, Schering)
5 mg/ml saline or sterile water x 15 min q8h Aminoglycoside active against gram-negative bacteria including Pseudomonas; discontinue if polyuria develops
Piperacillin
(Piperacil, Lederle)
10 mg/ml saline x 10-30 min q6-12h Extended spectrum penicillin with broad-spectrum activity
Saline 6 ml q6-8h
Sterile water 6 ml q6-8h Viscosity of respiratory secretions may be decreased by hydration
Terbinafine
(Lamasil, Novartis)
1 mg/ml distilled water Treatment of aspergillosis

References