Pet Hyperbaric Oxygen Chamber Treatment Therapy in Florida

HBOT…What Hyperbaric Oxygen Therapy Can Do For Your Patients

by Ronald Lyman, DVM, DACVIM
from University of Florida College of Veterinary Medicine August 19th 2011

Introduction to Pet Hyperbaric Oxygen Therapy

Hyperbaric oxygen therapy [HBOT] has transcended from its traditional place in treatment of decompression illness ["the bends"] to a variety of clinical applications globally. Basic science studies have demonstrated HBOT effects and mechanisms of action. Clinical studies on practical applications are abundant in the human medical literature. Book chapters describing clinical applications of HBOT have been included in the most recent editions of Ettinger's "Textbook of Veterinary Internal Medicine" and Bonagura's "Current Veterinary Therapy XIV". The June 2010 Veterinary Emergency and Critical Care Journal featured HBOT as the subject in it's 'State of the Art' articles. Recently, Dr. Colin Kaide [ from The Ohio State University Medical Center] discussed HBOT and its role in the therapy of human infectious diseases in The Emergency Medicine Clinics of North America. He concluded with the statement "in our opinion withholding HBOT because of a lack of randomized trials in the face of a huge body of clinical experience and in vitro studies, especially in these devastating disease processes, would be bordering on unethical". The Veterinary Hyperbaric Medicine Society [VHMS] has developed didactic material and test questions for hyperbaric oxygen therapy technical certification. The Animal Emergency and Referral Center of Florida is conducting a prospective clinical study on the effects of different HBOT pressures on the clinical outcome of small breed canine "no deep pain" acute thoracolumbar intervertebral disc disease. This manuscript and today's discussion will focus on HBOT treatment methods, physiologic effects, therapeutic effects, clinical uses, and safety issues in veterinary medical cases. Specific examples of patients treated with HBOT will be presented.

HBOT Chambers and ancillary hardware

Therapeutic chambers are now available from veterinary medical manufacturers and suppliers. Experienced professionals are available to assist in designing systems, obtaining and installing chambers, training hospital personnel regarding operation and safety issues, and servicing HBOT equipment. Clinical chambers range in size from monoplace [single patient] design, to chambers accommodating multiple patients / caregivers, operating suites, and "walk in" equine chambers. Most chambers require an oxygen supply system capable of large gas volumes delivered at a rapid flow rate. Liquid oxygen tanks and a medical grade oxygen pipeline of large diameter satisfy these requirements. A passive discharge pipeline directs the exhaust gases outside the hospital building. Some chambers have ports allowing [specific] IV lines and/ or tubing for assisted ventilation to be connected to the patient during an HBOT session. Current oxygen costs to operate a small animal monoplace chamber may range from approximately $8 to $20 per treatment session depending on chamber design, length of session, pressure employed, and oxygen supply system. The large animal [equine] chambers consume $20 to $40 of oxygen per session.

Hyperbaric Oxygen Treatment Protocol ["The Dive"]

The patient is prepared by examination and body temperature determination. HBOT is generally not given when the small animal's patient's body temperature is greater than 103 degrees Fahrenheit. Equine sessions are not initiated if an adult horse has a temperature above 102 degrees, or a young horse above 103 degrees. Theoretically, excessive hyperthermia may increase oxygen uptake by tissues, and enhance the chance of oxygen toxicity. The vast majority of patients are quiet and relaxed during HBOT. Occasional patients are given sedation. Acepromazine is the usual drug of choice for small animals. Occasionally, benzodiazepines or barbiturates are employed in canines. Detomidine is sometimes used in the initial sessions for the equine patient. Cotton bandages cover IV catheters. Metal collars are removed. A static inhibitor ground line is secured on a leg [in the small animal chamber]. The session begins with a gradual pressure increase to the designated treatment pressure over approximately 15 minutes. The desired treatment pressure may range from 1.5 to 3 atmospheres absolute [ATA] in a 100% oxygen environment. The treatment period "at pressure" may range from 45 minutes to 2 hours. Then, a gradual decompression over approximately 15 minutes is made, and the patient is removed from the chamber. Currently, most of our small animal patients are treated at 1.5 or 2 ATA for 45 minutes "at pressure". In patients perceived to be at reduced threshold for seizures, we may employ the low range [1.5 ATA] for the "at pressure" treatment period. The patients are rested at room atmospheric pressure for at least 4 hours between HBOT sessions to minimize the chances of CNS or pulmonary oxygen toxicity. We treat most patients with BID sessions, and continue HBOT acutely until marked and progressive improvement occurs [for example, the tetraparetic, paraparetic, or monoparetic patient is using the affected limb[s] with improving strength and function over several days, or the wound is well on its way to resolution]. We treat selected patients with follow up sessions after initial discharge from the hospital. In many cases dogs or cats may be treated as outpatients. Patients may receive as little as 1 session [for example, after orthopedic surgery or venomous insect bite when administered to reduce inflammation and swelling] to as many as 40 or more sessions in extremely critical or chronic disease entities. One canine patient with multifocal CNS inflammatory disease has received over 600 treatment sessions in 3 years as her sole method of therapy for this clinical issue. Her neurologic signs begin to return if she goes beyond 7-8 days without an HBOT session.

Physiology of Cat/Dog HBOT

At normal atmospheric pressures [1 ATA] and while breathing room air, insignificant amounts of oxygen are dissolved and delivered to the tissues via the plasma. Mild increases are possible when oxygen is administered via mask, oxygen cage, intranasally, or intubation. The effects of HBOT are based upon the fact that oxygen delivered to the alveoli under increased atmospheric pressure results in large increases in the amount dissolved in plasma. This can increase the plasma arterial oxygen content from 0.32 vol % [ml 02/ dl whole blood] breathing room air at 1 ATA , to 4.44 vol % at 2 ATA breathing 100% oxygen, and up to 6.8 vol % at 3 ATA breathing 100% oxygen. This dramatic increase in dissolved oxygen [for example, breathing 100% oxygen at 3 ATA] allows diffusion and delivery via the plasma up to 4 times further through the tissues than is possible while breathing room air at 1 ATA. This delivery is independent of the hemoglobin system. Tissue PO2 measurement devices have demonstrated that oxygen tension remains elevated at > 10% of normal for up to 3 hours following a 1 hour HBOT session. Thus, cells and mitochondria in areas where nearby capillary blood flow has been compromised by traumatic, ischemic, or inflammatory processes may receive oxygen subsequent to HBOT which would otherwise be denied by the underlying pathological disease process. Hyperbaric oxygen at 2 ATA has been shown to reduce cerebral blood flow up to 25% [by effecting vasoconstriction], reduce nitric oxide production, yet concurrently increase [X 10] cerebral oxygen content. Intracranial pressure and cerebral edema are reduced following HBOT. In addition to the direct effect of supplying oxygen necessary for mitochondrial metabolic processes, HBOT results in the following:

Three recent textbooks and other publications offer detailed discussions of the physiology of oxygenation, its relation to HBOT, and effects on the CNS , PNS, and pathological disease states including the wound healing process.

Your Pet's Hyperbaric Chamber Treatment: Therapeutic Effects and Uses

The most common case types treated with HBOT at our small animal facility include intervertebral disc disease, pre and post op spinal and orthopedic surgical cases, acute severe anemia, ischemic syndromes, post cardiopulmonary arrest, immune mediated diseases, fibrocartilagenous emboli, pancreatitis, head trauma, snake bite, and wound care. We will illustrate case examples with associated literature references in the remainder of this discussion.

Snakebite

Snakebite pit viper envenomation is the classic example of the clinical situation where the anti-inflammatory, tissue sparing and tissue healing effects of HBOT come together to create dramatic changes in many patients. If a canine snakebite patient is rapidly placed into an HBOT chamber within a few hours of the bite event, grossly visible swelling is often markedly reduced during and after the treatment session [with or without anti-venon administration]. HBOT is also effective in many cases even if not initiated immediately after the bite.

Complete Global Cerebral Ischemia

A 1992 paper described a controlled study from Japan where 20 dogs with complete global cerebral ischemia of 15 minutes duration were randomized and divided into two groups. One group received 1 hour sessions of HBOT at 3 ATA in 100% oxygen at 3, 24, and 29 hours after recirculation was established. The control group received room air at 1 ATA. Both groups received nursing support. The HBOT treated group's mean neurologic recovery score was > 65/100 after 5 days, with neurologic recovery scores of > 95/100 reached in two dogs from the HBOT group [range: 0=brain dead to 100= normal]. In contrast, in the group not receiving HBOT, the mean neurologic score remained < 60/100 throughout the 14 day follow up, and only 1 of 10 dogs from the non HBOT group recovered to a score of > 65/100. 7 of the HBOT group survived to the 14 day follow up, whereas 3 of the non HBOT group survived to the 14 period.

Case example: A 1 year old M/I Shih-Tzu canine fell off a grooming table while the groomer was distracted, and was accidentally hung by the lead around the neck. CPR was successful. Acute cortical blindness followed. The patient was given IV methylprednisolone immediately following the resuscitation, and referred for hyperbaric therapy the following day. Low dose oral prednisolone was continued. BID HBOT [45 minute sessions at 2 ATA] was given for 7 days. After the second session vision began to return as evidenced by obstacle course performance. Two week follow up confirmed improving vision based on owner interview and obstacle course examination. Consultation by an ophthalmologist confirmed resolving cortical blindness. In human cases [near hanging, near drowning, neonatal asphyxia, stroke, cardiopulmonary arrest, etc.] SPECT brain blood flow imaging has been used to demonstrate abnormalities in cerebral perfusion and subsequent improvement following immediate and long term HBOT. HBOT is employed in cases of birth asphyxia in foals.

Referral for HBOT therapy after cardiopulmonary arrest during anesthesia or after injury has become more frequent as primary care veterinarians recognize the option exists.

Head Trauma

Many studies have shown that HBOT reduces elevations in intracranial pressure resulting from head trauma in animals and in human head trauma patients.4 Clinical trials have demonstrated improved survival rates and neurologic recovery scores in human head trauma patients . In addition, improved glucose utilization in rat brain tissue has been demonstrated to persist for up to 24 hours following the last HBOT. There is much contemporary focus and research on the role of matrix metalloproteinases [MMPs] in traumatic brain injury and inflammatory CNS and PNS diseases, including Multiple Sclerosis [MS] in humans. A change in the balance of certain types of these proteases is associated with cellular infiltrates, apoptosis, and gliosis in traumatic, inflammatory, and neoplastic CNS disease. A 2006 rat model study of traumatic brain injury demonstrated that subjects treated with HBOT had reduced expression of certain MMPs, milder neutrophilic inflammatory infiltrates, and decreased secondary cell death when compared to controls.

Case example: 3 month old F/I canine Yorkshire Terrier hit by a recliner chair. The patient presented obtunded and able to posture only when placed sternally. IV mannitol and ICU oxygen unit therapy were given, and a neck brace placed overnight by the E/CC clinicians. BID HBOT was begun the following morning [45 minute sessions at 2 ATA] and continued for 5 days. Marked neurologic improvement was obvious as the patient exited the chamber after the first session, and progressed rapidly until discharge.

Fibrocartilagenous Emboli

Some HBOT studies performed on dogs date back several decades. A 1965 study demonstrated that spinal cord pO2 could be raised by HBOT as long as 72 hours after tissue hypoxia was created in a model of spinal cord injury in canines. Canine cases of fibrocartilagenous emboli often show rapid improvement when promptly treated by HBOT. It is especially important for nursing care and physical therapy purposes to get these primarily large breed patients ambulatory as soon as possible.

Case examples: 1] 8 year old M/N Labrador mix . Acutely monoparetic, then paraparetic. 2] 8 year old F/S Boxer. Acutely monoparetic. Clinical diagnoses were based on neurologic examinations, CSF analysis, and myelograms within a few hours of emergency presentation. Both patients received one dose of parenteral corticosteroids, then low dose short term oral prednisolone. Both patients were given BID HBOT [45 minute sessions at 2 ATA] . The Lab received 14 HBOT treatments, the Boxer 10. It is interesting to note in this acute ischemic myelopathy that patients will often improve markedly as they exit the chamber session, then regress, presumably as p02 in the affected cord region drops off. Patients who exhibit this pattern typically improve for longer periods after each session, and eventually maintain their neurologic improvement.

Spinal cord trauma, Intervertebral disc disease, and other compressive spinal cord lesions

In a 1972 canine model of spinal cord compression, spinal cord tissue p02 in the normal cord rose when the subjects were breathing 100% oxygen at 1 ATA. After compressive trauma, the cord p02 dropped to near zero on room air, and did not rise when the subjects were breathing 100% oxygen at 1 ATA. When HBOT at 2 ATA was given with 100% oxygen, tissue p02 rose sharply even during the compressive period. Neurologic recovery of the HBOT treated group was improved compared to the control group.

Case example: 11 year old Bichon M/N. Acute upper motor neuron tetraparesis with severe neck pain. Normal CSF protein and cytology. Spinal stenosis at a C2-3 fusion site [no history of previous surgery or trauma] and a C3-4 disc extrusion were found on myelographic examnination. Initial treatment was with HBOT [2 ATA, 45 minutes], prior to the diagnostics. At this point the patient became strongly ambulatory. Diagnostics were performed, followed immediately by a limited continuous dorsal laminectomy. Low dose oral prednisolone and HBOT were given post operatively for 6 days. Progressive clinical improvement was rapid. A desirable effect in neurosurgical cases treated with post op HBOT is rapid surgical wound healing, with reduced swelling, inflammation, seroma, and scar formation. HBOT has become standard pre and post neurosurgical adjunctive therapy in our practice, for both spinal and brain surgical cases. We have used HBOT in conservative treatment of documented or presumed spinal cord compressive diseases.

Inflammatory CNS Diseases

We have discussed some of the mechanisms of HBOT anti-inflammatory effects above. The reader should note that in the UK, there are 64 centers [distributed to cover the population density] which are dedicated solely to the treatment of MS in human patients. Over 1.7 million sessions have been completed in the last 24 years without serious incident. Patients generally manage their own long term treatment schedule, and many find that their symptoms, especially frequency of micturition, are controlled only by regular HBOT sessions. Some schedule their holidays to be near a "Center". The reader is referred to a detailed chapter on rationale for HBOT in inflammatory disease, including MS in a recent HBOT textbook.2 A 2006 symposium presentation from a Russian HBOT research clinician described the use of combined HBOT and cyclosporine in the treatment of inflammatory CNS disease in humans.

Case example: 9 ½ year old M/N mixed canine presented for persistent fever, sudden loss of coordination and slight personality change. Neurologic exam supported multifocal CNS lesions. CSF cisternal and lumbar puncture protein and cytology were normal. MRI revealed multiple small mixed size hyperintense T2-weighted lesions throughout the thalamus and rostral brainstem. Most remain hyperintense on T2-weighted FLAIR sequencing. Multiple serologies and PCR's, PARR [LSA] were submitted. A 1/164 positive serology for E equi was the only notable laboratory finding. BID treatments of HBOT [45 minute sessions at 2 ATA over 7 days] were initiated along with cyclosporine, prednisolone, imidocarb, and doxycycline. Neurologic signs improved over a 7 day period, with the owner commenting on a marked improvement at home at the two week recheck exam. The immunosuppressive therapy was tapered very slowly over several weeks.

Major Organ Ischemia

HBOT may be employed in cases with major organ ischemia, such as post-surgical correction GDV in the canine, where the ischemia- reperfusion injury complex often results in serious clinical complications.

Pancreatitis

This inflammatory process is often severe, effusive, and fatal to canine and feline patients. Recent publications describing experimental rat pancreatitis models demonstrate reduced histopathologic severity and improved survival rate in the groups exposed to HBOT when compared to controls. 14,15,16 Our clinical experience is that now even cases with severe, effusive pancreatitis can be given a prognosis which includes a good chance for survival when HBOT is employed along with intensive supportive care. Case example. 12 year old Fe spayed Lab who ate a "rotted carcass" in a nearby yard. History, clinical signs, physical exam, radiographs, ultrasound exam, fluid analysis, and PLI all supported a diagnosis of pancreatitis. Severe pleural effusion was also present. BID HBOT for 45 minutes at 2 ATA was given. By hospitalization day 3 the pleural and peritoneal effusions were nearly resolved. A total of nine sessions were given, and rapid clinical improvement resulted in discharge by day 5. Physical exam one week after discharge was normal. Follow up PLI and ultrasound exam of the chest and abdomen 3 months later were normal.

Smoke inhalation/ CO toxicity/ Burn wounds from exposure to a fire

This combination of pathology is a unique opportunity to treat three different clinical issues with one form of adjuvant therapy, HBOT.

Osteomyelitis/ Infectious agents

This disease entity often has devastating consequences in the equine. Lesions developing in critical locations such as the fetlock sesamoids usually result in breakdown and subsequent euthanasia despite aggressive antibiotic therapy. The anti-inflammatory and angiogenic effects of HBOT are ideal here. HBOT potentiates the effect of certain antibiotics [for example, the quinolones], and is directly bacteriocidal to anaerobic bacteria. At 2.4 ATA HBOT is bacteriocidal to Borrelia burgdorfi [the Lyme disease spirochete].

Delayed or Non healing wounds

HBOT is widely accepted in human medicine for its adjuvant effect in wound healing, especially in diabetes mellitus or vascular occlusive disorders. It is a coded and reimbursed treatment modality for radiation induced tissue damage and non healing wounds. Cases in veterinary medicine are presented here.

Other clinical applications of HBOT

Other cases treated with HBOT therapy include acute tetraparesis secondary to Atlanto-axial [A/A] luxation, acute peripheral nerve injury, and brain lesions pre and post operatively. Decubital ulcers, thermal burns, shearing wounds, and near drowning are a few of the other clinical applications for which we have employed HBOT. Human medical practice is often limited by "approved indication lists" and diagnosis "codes". For example, in the U.S., there are currently 14 indications approved by Medicare, and thus typically funded by third party payers. HBOT for Non- healing wounds of certain types is funded by some third party payers. The U.K. has 13 "approved" indications, Japan 20, China 53, and Russia 85. In the latter three countries the "approved" lists contain disease indications which translate as "severe spinal cord disorders", "acute and severe hypoxic brain disorders", "severe spinal cord injury", "Bell's palsy", "Multiple Sclerosis", "cranial traumas", "viral encephalitis", "illeus", "sepsis", "non - healing wounds, " "osteomyelitis", "burns", "mountain sickness", etc.

Safety Issues

Pet HBOT should not be administered to patients with pneumothorax, certain older type pacemakers, within 48 hours of doxorubricin, or in a patient currently receiving cis-platinum or bleomycin. Acetazolamide, Zonisamide, or other carbonic anhydrase inhibitors should be tapered prior to HBOT, as they inhibit oxygen induced vasoconstriction and increase blood flow to the brain, increasing the chance of oxygen toxicity. Transdermal patches should be temporarily removed. Conservative dosages of narcotic analgesics should be employed prior to HBOT, as increased CO2 tension secondary to respiratory depression can cause cerebral vasodilatation and predispose to oxygen induced seizures. Insulin dosages should be tapered prior to HBOT therapy. Patients with hyperthyroidism also may have an increased chance for oxygen induced seizures. Vestibular signs may be aggravated due to barostimulation of the ear structures. This said, we have witnessed less than 30 mild motor seizures in over fifteen thousand HBOT treatment sessions at our hospital. The seizures all ended rapidly, and gradual reduction in treatment pressure was initiated in these individuals. No sequellae were recognized as a result of those seizures. The previously cited textbooks are a good source of detailed information on potential contraindications and specific interactions of HBOT with other therapeutic measures.

The chamber contains 100 % oxygen under pressure. Measures should be taken to reduce the chance of fire. The chamber should be grounded. A static grounding limb strap should be considered in small animals. Hair coats should be gently wiped with a wet cotton towel. Cotton towels and bandages generate less static than polyester fibers. No flammable materials or electronic devices should be placed in the chamber. No metal collars or skin staples should be used. No alcohol, Vaseline, or flammable based dressings should be used. An emergency master oxygen shut off valve should be installed and known by all personnel. A CO2 fire extinguisher should be close and functional. A textbook on hyperbaric safety is recommended.

HBOT in Equine Racing Athletes

Under the care and direction of veterinarians some horses receive post-race HBOT as a method to reduce the inflammatory sequellae of a supreme racing effort, or in the treatment of orthopedic or neurologic injuries.

In the spring of 1999 equine treatment chambers in trailers began appearing near racetracks in New York and California, as some trainers of equine athletes around the world began to use HBOT in their horses. No governing body was consulted initially, which resulted in New York racing officials issuing an immediate 7 day ban on HBOT for racing horses. After consultation with veterinarians familiar with HBOT, Maryland and New York have settled on a 48 hour pre- race moratorium on HBOT. Kentucky requires a 24 hour HBOT- free period prior to any race.

Conclusion

Over the past six years it has been very rewarding for the doctors and staff to observe the clinical improvement of many cases treated by HBOT at our hospital. The addition of this treatment modality has resulted in an obvious enhancement of our ability to successfully treat many critically ill patients.

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